Veterinary News - Medical Veterinary - Animal Health

Veterinary Technician Jobs at Animal Kingdom and Puppies 'N Love

2008-10-12T08:48:00.000-07:00

Animal Kingdom and Puppies 'N Love is a Phoenix, Az. based family owned and operated company that has been in the retail pet business for over 40 years. We have built our outstanding reputation by providing quality companion pets to our customers and standing behind them in every way possible.
This is a great opportunity for a Qualified Experienced Vet Technician to care for our Puppies to include, Give IV and IM injections, intravenous catheterizations, etc. Provide care to critical pups, administers medication, monitors effectiveness of medications, drawing blood, restraining pups, monitoring recovery, documentation of health, phone calls, general cleaning.
Find more vet jobs at veterinary and animal health jobs website

Learn how to stitch up wounds

2008-09-19T04:29:00.000-07:00

Whether acute or chronic, wounds can compromise an individual’s wellbeing, self-image, working capacity, and independence. Good wound management is necessary not only for the individual, but also for the community. While appropriate wound management by qualified health care professionals is an integral part of treatment success, dressing choice and specification is equally important.
Wound healing can be delayed when microorganisms are present in large enough numbers. Therefore, reducing the bacterial load of a wound may be necessary to facilitate wound healing, as well as reduce local inflammation and tissue destruction. An ideal agent for the prevention and control of wound infection would therefore be one that directly destroys pathogens, while also stimulating immune activity.
To Learn how to stitch up wounds, The Apprentice Doctor provides a Suturing Course and Kit. The course material comes on an interactive CD-ROM, and teaches students the basic principles of suturing and wound care. The course contains video clips, illustrations, detailed instructions, and games of tutorials Learn how to stitch up wounds. With an 18-piece suture kit included, you will gain both theoretical knowledge and practical skills while performing 26 practical fun projects.
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Veterinary Technician Job, Westford Animal Hospital

2008-08-27T15:59:00.000-07:00

Westford Animal Hospital is looking for a veterinary technician to join our health care team. Certification or comparable veterinary technician education and skill is preferred. Specialization is a plus. Excellent salary and benefits (including continuing education) package. Room for advancement for the right candidate. Find more Veterinary Jobs at Veterinary & Animal Health Jobs Website...

the profession of veterinary medicine

2008-05-23T03:38:00.000-07:00

Today's veterinarians are members of an important health profession. In taking the veterinarian's oath, a doctor solemnly swears to use his or her scientific knowledge and skills "for the benefit of society, through the protection of animal health, the relief of animal suffering, the conservation of animal resources, the promotion of public health, and the advancement of medical knowledge."

Today more than 67,000 veterinarians are professionally active in the United States. They provide a wide variety of services in private clinical practice, teaching, research, government service, public health, military service, private industry, and other areas.

In recent years, the profession of veterinary medicine has become ever more sophisticated and complex. The public expects state-of-the-art veterinary care for its animals. To provide high quality service, today's veterinarians utilize the skills of trained professionals known as veterinary technicians.

We dedicated to provide the best online veterinary job marketplace services. Our services are completely free for veterinary job seekers.

Provide by: Veterinary Jobs Directory

Daily Dog Magazine

2008-03-31T18:44:00.000-07:00

The Best Dog Magazine is now online, right here! The most useful information… the most entertaining and helpful stories from 18 years of Best Dog Magazine are now available for you to search, browse, read and enjoy.

Hemorrhagic Septicemia

2008-02-15T03:15:00.000-08:00

Hemorrhagic septicemia (HS) is an acute pasteurellosis, caused by particular serotypes of Pasteurella multocida and manifested by an acute and highly fatal septicemia principally in cattle and water buffaloes; the latter are thought to be more susceptible. HS is seen infrequently in swine and even less commonly in sheep and goats. It has been reported in bison, camels, elephants, horses, and donkeys, and there is evidence of its occurrence in yak. An acute pasteurellosis indistinguishable from HS is seen infrequently in deer, elk, and probably other feral ruminants. Laboratory rabbits and mice are highly susceptible to experimental infection.
HS is a major disease of cattle and water buffalo in Asia, Africa, and some countries of southern Europe and the Middle East. Although it may be seen at any time of year, the worst epidemics occur during the rainy season. It is most common in the river valleys and deltas of southeast Asia among buffaloes used in rice cultivation. The only true outbreaks in North America have occurred in bison in Yellowstone National Park. Occurrence in Central and South America has not been confirmed.
The HS serotypes of P multocida have not been recovered from human infections. However, because many serotypes of P multocida have the potential to infect humans, appropriate precautions should be taken.
Etiology:
Epidemic HS is caused by 1 of 2 serotypes of P multocida , designated B:2 and E:2. Serotype E:2 has been recovered only in Africa; B:2 causes the disease elsewhere and also has been recovered from cases in Egypt and the Sudan. Serotypes closely related antigenically to serotype B:2 have been implicated in limited outbreaks of a disease indistinguishable from HS in deer and elk. P multocida is an extracellular parasite, and immunity is primarily humoral.
Animals are infected by direct or indirect contact. The source of infective bacteria is thought to be the nasopharynx of bovine or buffalo carriers. As many as 5% of cattle and water buffaloes may be carriers in endemic regions.
It is hypothesized that animals become susceptible as a result of various stresses, eg, the inanition seen in cattle and water buffalo at the beginning of the rainy season. Natural infection is acquired by ingestion or inhalation. The initial site of proliferation is thought to be the tonsillar region. In susceptible animals, a septicemia develops rapidly, and death due to endotoxemia ensues within 8-24 hr after the first signs develop. Exotoxins have not been demonstrated.
The mortality rate is high when the agent is introduced to virgin or nonendemic regions. Losses vary widely in endemic areas. The heaviest losses occur during the monsoon rains in southeast Asia, and it is thought that the organisms, which can survive for hours and probably days in the moist soil and water, are transmitted widely at this time.
Most cases are acute or peracute, resulting in death within 8-24 hr after onset. Because the course is so short, clinical signs may easily be overlooked. Animals first evince dullness, then reluctance to move, fever, salivation, and serous nasal discharge. Edematous swelling is frequently seen, beginning in the throat region and spreading to the parotid region, neck, and brisket. Mucous membranes are congested. There is respiratory distress, and usually the animal goes down and dies within hours. Occasional cases linger for several days. Recovery is rare. There appears to be no chronic form. the merck

Blue Tongue

2008-02-15T03:14:00.000-08:00

Bluetongue is an infectious, noncontagious arthropodborne viral disease primarily of domestic and wild ruminants. Infection with bluetongue virus is common worldwide but is usually subclinical or mild in most infected ruminants. Bluetongue is almost exclusively a disease of sheep, particularly the fine-wool and mutton breeds, although white-tailed deer ( Odocoileus virginianus ), and pronghorn ( Antilocapra americana ) and desert bighorn sheep ( Ovis canadensis ) may develop severe clinical disease in North America.
Etiology and Transmission:
Bluetongue virus is the type-species of the genus Orbivirus in the family Reoviridae. There are 24 serotypes worldwide, although not all serotypes exist in any one geographic area, eg, only 5 serotypes (2, 10, 11, 13, and 17) have been reported in the USA. Distribution throughout the world parallels the spatial and temporal distribution of vector species of Culicoides biting midges, which are the only significant natural transmitters of the virus. Of more than 1,400 Culicoides species worldwide, fewer than 20 are actual or possible vectors of bluetongue virus. Continued cycling of the virus among competent Culicoides vectors and susceptible ruminants is critical to viral ecology. In the USA, the principal biologic vector is C variipennis sonorensis , which limits distribution of the virus to southern and western regions. In Australia the principal vector is C brevitarsis , while in Africa, Europe, and the Middle East it is C imicola . In each geographic region, secondary vector species may attain local importance. Vectors become infected with bluetongue virus by imbibing blood from infected vertebrates; transovarial transmission has not been reported. High affinity of the virus to blood cells, especially the sequestering of viral particles in invaginations of RBC membranes, contributes to prolonged viremia in the presence of neutralizing antibody. The extended viremia in cattle (up to 9 wk), and the host preference of most vector species of Culicoides for cattle, provides a mechanism for year-round transmission in domestic ruminants. Mechanical transmission by other bloodsucking insects is of minor significance. Bluetongue virus is not contagious, and concentrations in secretions and excretions are minimal, making oral or aerosol transmission unlikely. However, semen from viremic bulls can serve as a source of infection for cows through natural service or artificial insemination. Embryo transfer is regarded as safe, provided that donors are not viremic and an appropriate washing procedure for embryos is used. Accidental infection has been reported in dogs in the USA following administration of a modified live virus vaccine that was contaminated with the virus. Serologic evidence of infection with bluetongue virus has been found in large carnivores in Africa, perhaps as a result of ingesting virus-infected viscera. the merck

Postweaning Multisystemic Wasting Syndrome

2008-02-15T03:12:00.000-08:00

Postweaning multisystemic wasting syndrome (PMWS) of swine was identified in western Canada in 1991; however, retrospective studies from several countries indicate PMWS was present in the previous decade. PMWS is distributed worldwide and most swine-producing countries report variable prevalence of the disease. The primary manifestations are poor growth rate, ill thrift, and/or wasting. PMWS often occurs after weaning in pigs 4-14 wk old. The disease can also be seen in older pigs, particularly finishing pigs that weigh 45-70 kg. Morbidity is typically 5-20% among cohorts in the nursery or finishing stages. Mortality in swine that show signs of PMWS often is >50%. In addition to death loss, PMWS in finishing pigs may prevent, or substantially delay, affected pigs from reaching market weight, which can result in economic loss for the producer.
Etiology and Pathogenesis:
PMWS is a multifactorial disease in which porcine circovirus type 2 (PCV2) is the necessary infectious agent. Circoviruses are small (17-22 nm in diameter), nonenveloped viruses that contain a single strand of circular DNA. There are 2 genotypes of porcine circovirus; only PCV2 has been shown to induce PMWS. Serologic cross-reaction occurs between PCV1 and PCV2, but antigenic differences between the viral genotypes allow separation of viruses using some serologic assays. Serologic surveys show that PCV2 is widespread in swine. Some reports have suggested that animals other than swine may be infected with PCV2 or PCV-like viruses. However, results of serologic studies for antibody against PCV in cattle and other livestock have been contradictory, and experimental induction of disease using PCV1 or PCV2 in species of livestock other than swine has not been successful.
Initially, PMWS was identified in high health herds that were free of most common swine pathogens but were infected with PCV2. Results from retrospective serologic studies indicate that PCV2 infected swine decades before PMWS was identified. Comparison of DNA from numerous recent isolates has shown high nucleic acid sequence homology exists among PCV2 and has not revealed a genetic determinant for virulence. Under field conditions, swine that show signs of PMWS usually are infected with multiple agents, but PCV2 is present consistently. Porcine parvovirus, porcine reproductive and respiratory syndrome virus, Actinobacillus , Pasteurella , Staphlylococcus , and Streptococcus are common pathogens frequently isolated from pigs that show signs of PMWS.
The frequent finding of mixed infection in nursery pigs with PMWS may be attributable to waning protection from colostral antibody, making the pig more susceptible to simultaneous infection with PCV2 and multiple other pathogens. Affected pigs are probably immunosuppressed. Pigs that show signs of PMWS have reduced populations of CD8+ and IgM+ lymphocytes in circulation. Microscopically, affected pigs show generalized lymphocyte depletion in lymphoid tissue. Substantial amounts of viral antigen and DNA are found in the cytoplasm of macrophages, dendritic cells, and other antigen presenting cells.
Severe disease has been reproduced in pigs co-infected with PCV2 and other viruses or immunostimulant noninfectious products; however, the mechanism of this synergy is not known. Because PCV2 replication depends on cellular enzymes expressed during the S phase of the cell cycle, it has been hypothesized that previous activation of those cells supporting viral replication (not yet fully known) may promote replication of PCV2. Enhanced viral replication might lead to extensive loss of lymphoid cells and promote onset of PMWS. However, under field conditions, stimulation of the immune system of piglets with adjuvants, or with commercially available vaccines, appears to favor induction of PMWS after infection with PCV2. the merck

Hemagglutinating Encephalomyelitis

2008-02-15T03:11:00.000-08:00

This viral disease of young pigs characterized by vomiting, constipation, and anorexia results either in rapid death or chronic emaciation. Motor disorders due to acute encephalomyelitis (hemagglutinating encephalomyelitis) also may be seen during some outbreaks.
Etiology, Epidemiology, and Pathogenesis:
The causal coronavirus, hemagglutinating encephalomyelitis virus, is of a single antigenic type, and it grows in several types of porcine cell cultures, in which it causes syncytia. It agglutinates RBC of several animal species. Pigs are the only natural host. The virus is spread via aerosol.
Infection appears to be widespread in North America, western Europe, and Australia. It usually remains subclinical. The virus is endemic in most breeding herds, and a herd immunity exists. Immune sows transfer maternal antibodies to their piglets, which are protected until they have developed an age resistance; thus, clinical outbreaks are rare. However, if the virus enters a susceptible herd with neonatal piglets, morbidity and mortality may be high.
The virus first replicates in the nasal mucosa, tonsils, lungs, and to a very limited extent, in the small intestine. From these sites of entry, the virus invades defined nuclei of the medulla oblongata via the peripheral nervous system and subsequently spreads to the entire brain stem, and possibly to the cerebrum and cerebellum. Vomiting is thought to be caused by viral replication in the vagal sensory ganglion. Wasting is due to vomiting and delayed emptying of the stomach, which is the result of virus-induced lesions in the intramural plexus. Infection of cerebral and cerebellar neurons may rarely cause motor disorders. the merck

Round Heart Disease of Turkeys

2008-02-13T04:22:00.000-08:00

Spontaneous cardiomyopathy of young turkeys is characterized by sudden death due to cardiac arrest. It has been suggested that the condition should be called spontaneous cardiomyopathy to distinguish it from round heart disease of chickens, a different syndrome that is rarely recognized today.
The exact etiology of spontaneous cardiomyopathy in turkeys is unknown. However, studies using furazolidone to produce dilated cardiomyopathy in turkeys have indicated altered membrane transport resulting in myocardial failure. Creatine kinase, glycolysis, glycogen, myofibril, Krebs cycle enzymes, fatty acid oxidation, and soluble proteins are all reduced. The calcium-transport ATPase activity of the sarcoplasmic reticulum is increased. This pattern of biochemical changes is consistent with ischemia playing a role in the pathogenesis of spontaneous cardiomyopathy in turkeys.
While most deaths occur during the brooding period, the ratio of heart weight to body weight of affected birds is increased throughout the growing period. Market body weights of affected birds are reduced an average of 3 lb (1.4 kg). Some outbreaks of the condition have been associated with hypoxia during incubation of the eggs or during transportation of poults from the hatchery to the brood farm.
Most deaths from spontaneous cardiomyopathy occur during the first 4 wk of life, with mortality peaking at 2 wk. Many poults die suddenly, but some may have ruffled feathers, drooping wings, and a general unthrifty appearance. They may show labored, gasping breathing before death. After 3 wk of age, mortality is sporadic. Characteristically, the affected poult in the first 4 wk of life has a greatly enlarged heart due to dilatation of both ventricles, congested lungs, and a swollen liver. Ascites, anasarca, pulmonary edema, and hydropericardium may or may not be present. In older poults, enlarged hearts are due to marked hypertrophy of the ventricles in addition to dilatation. Histologically, lesions of abnormal hearts are nonspecific and include congestion, damage of the myofibrils of the cardiocytes, and focal infiltration by lymphocytes.
Generally, diagnosis is based on history and gross findings at necropsy; although an ECG can be used, it is of little practical use. Sodium and polychlorinated biphenyls or related compounds may produce similar syndromes.
No treatment is available. Good brooding practices may reduce mortality. Any toxins should be eliminated. Incubation, transportation, and early brooding ventilation conditions should be reviewed. the merck

Chicken Anemia Virus Infection

2008-02-13T04:19:00.000-08:00

Chicken anemia virus (CAV), a 25 nm, nonenveloped, icosahedral virus with a single-stranded, circular DNA genome, is the only member of the genus Gyrovirus of the Circoviridae family. The genome codes for 3 viral proteins (VP). VP1 is the capsid protein, but VP2 may be needed as a scaffold protein to allow proper folding of VP1. VP3, or apoptin, is a nonstructural protein that induces apoptosis in infected cells. CAV infects only chickens, although antibodies have been detected in Japanese quail. The virus is present worldwide based on serology and virus isolation. The disease, chicken infectious anemia, has been described in most countries where chickens are raised commercially.
Horizontal transmission of CAV is by the fecal-oral route and perhaps by the respiratory route. Vertical transmission occurs when seronegative hens become infected and continues until neutralizing antibodies develop. Chicks hatched from these eggs are viremic, and CAV can rapidly spread horizontally from these chicks to susceptible, maternal antibody-negative hatchmates. Roosters shedding CAV in the semen are another source of vertical transmission. Vaccination of seronegative flocks prior to the onset of egg production is recommended to prevent vertical transmission.
Maternal antibody-negative chicks are susceptible to infection and disease until 1-2 wk of age. In contrast, maternal antibody-positive chicks are protected from disease and probably from infection. Age resistance to clinical disease, but not infection, begins at approximately 1 wk of age.
When day-old susceptible chicks are inoculated IM with CAV, viremia occurs within 24 hr. Virus can be recovered from most organs and rectal contents up to 35 days after inoculation. The principal sites of CAV replication are hemocytoblasts in the bone marrow, precursor T cells in the cortex of the thymus, and CD8 cells in the spleen. Replication in the first leads to anemia, while replication in the latter two causes immunosuppression. Neutralizing antibodies are detectable 21 days after infection and clinical, hematologic, and pathologic parameters return to normal ~35 days after infection. CAV infection has adverse effects on proliferative responses of spleen lymphocytes and on the production of interleukin-2 and interferons by splenocytes. Infection can cause a marked decrease in generation of antigen-specific cytotoxic T cells directed against other pathogens. In addition to T-cell defects, macrophage functions such as Fc-receptor expression, phagocytosis, and antimicrobial activity may be impaired. Subclinical, horizontally acquired infection with CAV in broiler progeny of seropositive parent flocks may be associated with impaired economic performance. the merck

Flip Over Disease

2008-02-13T04:18:00.000-08:00

Flip-over disease has been reported in most areas of the world that intensively raise broilers. Young, healthy, fast-growing broiler chickens die suddenly with a short, terminal, wing-beating convulsion. Many affected broilers just “flip over” and die on their backs; 60-80% are males. The condition is uncommon or unrecognized when low-density feed is used and the ratio of feed intake to weight gain is >2.5 at 6 wk, or when broilers take 8 wk to reach 2 kg.
The cause is unknown but probably is a metabolic disease related to carbohydrate metabolism, cell membrane integrity, and intracellular electrolyte balance. Death may result from ventricular fibrillation. The modern broiler tends to overeat and continues to grow rapidly while maintaining a low feed-to-gain ratio. Flip-over appears to be related to high carbohydrate intake. It is not known whether a genetic predisposition exists.
Broilers show no premonitory signs. They appear healthy and may be feeding, sparring, walking, or resting, but suddenly extend their necks, gasp or squawk, and die rapidly with a short period of wing beating and leg movement, during which they frequently flip onto their backs. They also may be found dead on their sides or breasts.
Flip-over may occur as early as day 3 and may continue until 10-12 wk in roaster flocks. Peak mortality varies but usually is between days 12 and 28, although it can be as early as day 9. It may occur after day 28, particularly if growth is restricted in young broilers. Mortality of 0.25-0.5% per day can occur for 1-3 days.
Confirmation is difficult because no specific gross or histologic lesions are present. Dead birds are well fleshed, have an empty or partially filled crop containing normal ingesta, and feed in the gizzard. The abdomen is distended because the bird is fat and because the intestines are dilated and filled with semisolid digesta and mucus (as in any broiler that dies with the intestine full of feed). There is no evidence of stasis. The muscles are mottled red and white with congestion of the dependent muscles. Organs are moderately to severely congested. There may be small hemorrhages in the liver and kidney. The ventricles of the heart are contracted (but not hypertrophied), and the atria are dilated and blood filled. (If autolysis is advanced, the ventricles may be dilated.) The lungs are congested and frequently edematous; however, pulmonary edema increases with time after death and is not prominent in broilers that are examined within a few minutes after death. The gallbladder may be small or empty (as it is in many broilers on full feed). the merck

Fatty Liver Syndrome

2008-02-13T04:16:00.000-08:00

Fatty liver syndrome was first described in the 1950s as excessive fat in the liver associated with varying degress of hemorrhage. The condition is almost universally confined to caged birds fed high-energy diets, and is most often seen in summer months. The liver is usually enlarged, yellow or putty colored, and very friable. The abdominal cavity contains large amounts of fat. Fatty liver syndrome without excessive body fat is thought to be associated with mycotoxins (eg, aflatoxins) in feed.
he affected birds may also have pale combs. The ovary is usually active and the metabolic and physical stress associated with oviposition may be factors that induce the fatal hemorrhage, although mortality generally is <5%.
Because fatty liver syndrome seems to occur only when birds are in a positive energy balance, the monitoring of body weight is a good diagnostic tool. Through force-feeding techniques, it has been shown that fatty liver syndrome is caused by an oversupply of energy rather than by an excess of any specific nutrient, such as fat or carbohydrate. The condition can be induced experimentally in layers and even male birds by the administration of estrogen, reinforcing the concept that it occurs more frequently in high-producing birds that presumably are producing estrogen from very active ovaries.
The condition is easy to recognize at necropsy due to the liver hemorrhage and also the fact that the liver is often enlarged and engorged with fat. This makes the liver friable, and it is difficult to remove each lobe in one piece. The pale yellow color of the liver, while characteristic, is not always specific to this condition. Normal layers fed appreciable quantities of yellow corn will also have a yellow liver. Also, liver color may be indicative of dietary xanthophylls rather than fatty liver syndrome, because the condition can be induced by force-feeding semi-purified diets devoid of pigment; these birds lack the characteristic yellow liver. Birds with fatty liver syndrome have 40-70% fat in the liver dry matter. In many studies, the degree of fatty liver syndrome is described via a liver hemorrhage score, which is usually based on a scale from 1-5, in which 1 = no hemorrhage, 2 = 1-5 hemorrhages, 3 = 6-15 hemorrhages, 4 = 16-25 hemorrhages, and 5 = >25 hemorrhages, including a massive, usually fatal, hemorrhage.
Attempts have been made to prevent or treat the condition through diet modification. Substituting carbohydrate with supplemental fat, while not increasing the energy content of the dietary, seems to be beneficial. Presumably such modification means that the liver needs to synthesize less fat for yolk. Replacement of corn with other cereals, such as wheat and barley, is often beneficial. However, this substitution may involve a reduction in dietary energy level or may necessitate the use of additional fat to maintain isoenergetic conditions, and these 2 factors are known to influence fatty liver syndrome. The syndrome has reportedly been reduced through the use of various byproduct feeds such as distiller’s grains and solubles, fish meal, and alfalfa meal. Although the mode of action is unclear, unintentional supplementation of selenium may be involved. Addition of 6% oat hulls to the feed has been successful at times. Fatty liver syndrome is best prevented by not allowing an excessive positive energy balance in older birds. Body weight can be monitored and when potential problems are seen, remedial action taken to limit energy intake through the use of lower energy diets and/or change in feed management. A wide energy:protein ratio in the diet will aggravate fatty liver syndrome. On farms with history of fatty liver syndrome, the diet should be supplemented with 0.3 ppm selenium, up to 100 IU vitamin E/kg diet, and appropriate levels of an antioxidant such as ethoxyquin. the merck

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2008-02-12T04:36:00.000-08:00

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Dorsal Displacement of the Soft Palate

2008-02-10T04:14:00.000-08:00

Dorsal displacement of the soft palate (DDSP) is a performance-limiting condition of the upper respiratory tract, and is a relatively common cause of upper respiratory noise during exercise. During DDSP, the caudal free margin of the soft palate moves dorsal to the epiglottis, creating a functional obstruction within the airway. The cross-sectional area of the pharynx is reduced, and airflow resistance and turbulence are increased.
DDSP may result from several pathophysiologic mechanisms. Inflammation of the upper respiratory tract due to infection may cause neuropathy of the pharyngeal branch of the vagus nerve as it traverses the floor of the medial compartment of the guttural pouch, resulting in neuromuscular dysfunction of the pharyngeal muscles that control the soft palate. The retropharyngeal lymph nodes are in direct contact with the pharyngeal branch of the vagus nerve, and retropharyngeal lymphadenopathy may result in compression and irritation. Clinical signs can be induced by local anesthesia of this nerve. Congenital hypoplasia of the epiglottis may contribute to DDSP, due to insufficient epiglottal tissue to maintain the position of the caudal border of the soft palate ventral to the epiglottis.
DDSP creates a characteristic gurgling respiratory noise, primarily during expiration, due to vibration of the soft palate. Horses may make no noise at the onset of exercise but displace their palate during high-speed exercise, causing them to “choke down.” Head position (flexed) may contribute to displacement.
The most effective treatment for DDSP in young horses (2 yr olds) and horses with evidence of upper respiratory tract infection is rest and anti-inflammatory therapy. Caudal retraction of the tongue elevates the soft palate and pushes the larynx caudally, both of which may predispose a horse to DDSP. Placing a tongue tie during exercise reduces caudal retraction of the tongue. Sternothyrohyoideus myectomy performed in horses prone to DDSP to alter the anatomy of the upper respiratory tract is successful in ~50% of horses. Soft palate resection (staphylectomy) is frequently performed in horses with DDSP and also has a success rate of ~50%; however, the mechanism of improvement after surgery is unclear. Success has been attributed to reduction in the mass of soft palate obstructing the airway, easier replacement of the shorter soft palate to the subepiglottic position, and firming of the caudal edge of the soft palate to keep it ventral to the epiglottis. the merck

Pharyngeal Lymphoid Hyperplasia

2008-02-10T04:13:00.000-08:00

Pharyngeal lymphoid hyperplasia (PLH) is a common condition of the dorsal pharyngeal wall observed in young horses (1-3 yr old). Horses do not have discrete masses of lymphoid tonsillar tissue; rather, they have many small foci or follicles of lymphoid tissue spread diffusely over the roof and lateral walls of the pharynx. In mature horses, these follicles blend with mucosal tissue and are unnoticeable. In young, maturing horses, lymphoid follicles appear as prominent, raised nodules on the surface of the pharyngeal roof and extend down the lateral walls of the pharynx and cranially into the nasopharynx. While PLH was once believed to be an important cause of poor performance in racehorses, its clincal significance is now questionable. Virtually all young horses undergo hyperplasia of pharyngeal lymphoid follicles; in most cases, this represents a normal immunologic event.
Occasionally, follicles may enlarge and coalesce with surrounding follicles. In these situations, follicles may appear hyperemic or inflamed and may exude mucoid or mucopurulent material. These cases likely represent a mild or subclinical viral infection and may be associated with impaired performance. Signs of pharyngeal pain include reduced appetite and frequent swallowing. Treatment is not necessary in the vast majority of cases; however, rest and NSAID administration are warranted in horses demonstrating pharyngeal pain. the merck

Diseases of the Nasal Septum

2008-02-10T04:04:00.000-08:00

Diseases of the nasal septum are rare. Most nasal septal disorders are congenital abnormalities that remain undetected until the horse is exercised. Traumatic injury to the bridge of the nose as a juvenile can produce nasal septal deviation and thickening. Other less common diseases of the nasal septum include amyloidosis, fungal infection, and squamous cell carcinoma.
Thickening or deviation of the nasal septum causes low-pitched stertorous breathing during exercise. Facial deformity may be observed. Septal abnormalities may be detected by palpation, visual inspection, and endoscopic examination. Dimensions of the nasal cavity are difficult to appreciate via endoscopic examination; however, abnormalities of the mucosa are easily identified. Precise dorsoventral radiographs of the skull provide definitive evidence of septal deformity, deviation, and thickening. Histologic examination of any nodules or discrete lesions on the septum will identify tumors, amyloidosis, or fungal infections.
Surgical resection of the nasal septum is the only treatment option in most cases. The entire diseased portion of the septum can be excised using obstetrical wire by transecting the septum on the dorsal, ventral, and caudal border. Hemorrhage is substantial during this procedure (4-8 L), and the nasal passages are packed with sterile gauze soaked in saline or in 1:100,000 epinephrine solution to minimize blood loss. Before the horse recovers from anesthesia, a tracheotomy is performed.
Postoperative care includes parenteral antibiotics and NSAID. The packing and tracheotomy tube should be removed 48-72 hr after surgery. All incisions heal by second intention within 3 wk. Horses should be rested for ~2 mo before returning to normal activity. After surgery, most horses make a respiratory noise during work, although less than before surgery, and exercise tolerance is improved. Shortening of the upper jaw, incisor malalignment, or nostril collapse can develop if the procedure is performed in immature horses. Ideally, the surgery should be delayed until maturity. [the merck]

Health management Interaction in Small Animals

2008-02-09T22:12:00.000-08:00

Proper management to prevent and control disease has historically been a higher priority in large animal medicine than in small animal medicine. However, appropriate management is just as important for small animals, whether their environment is that of a single or multiple-pet home or a more intensive housing situation such as a kennel or cattery.Responsible pet ownership must be emphasized to all those owning and considering owning pets. Areas of client education that should be emphasized include the following:

routine care and grooming,
preventive health care,
parasite control,
nutrition,
household hazards,
housing requirements and environmental factors.

Routine care and grooming not only help maintain pet health but also allow identification of health problems early in the course of disease. Close observation of pets allows for evaluation of changes in appetite, thirst, urination, defecation, ambulation, and general behavior. Any changes may suggest the need for a more thorough examination. Special attention should be given to hair coat, skin, ears, eyes, and teeth. Anal gland impaction and overgrowth of nails are common problems.
Preventive health care in small animals is dominated by vaccination. Vaccines are available for a variety of infectious diseases in dogs, including distemper, parvovirus, hepatitis, leptospirosis, tracheobronchitis, rabies, Lyme disease, and coronavirus. Vaccines are available against a number of infectious diseases in cats, including panleukopenia, rhinotracheitis, calicivirus, rabies, feline infectious peritonitis (FIP), and feline leukemia virus (FeLV).
Vaccination schedules vary but generally require an initial vaccination at 6-8 wk of age, followed by additional vaccinations at 3-wk intervals until the animal is 4-5 mo old. After this, most vaccines are given annually. Rabies vaccination is dictated by state law or local jurisdiction. First-time vaccination for diseases other than rabies in adult animals should include an initial vaccination followed by at least one booster.
source:the merck

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2008-02-07T00:37:00.000-08:00

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Eosinophilic Granuloma Complex

2008-01-30T08:07:00.000-08:00

The etiology of this group of diseases that affects cats, dogs, and horses has focused on an underlying hypersensitivity reaction. This is particularly true in cats and horses. Insect, environmental, and dietary hypersensitivities have been documented in cats, while insect hypersensitivity has been seen in some equine cases and in a smaller number of canine cases. Genetic predisposition and bacterial infections have also been seen in cats. In all species, idiopathic cases exist.
Clinical Findings and Diagnosis:
In cats, 3 disease entities have been grouped in the complex.
Eosinophilic Ulcer:
This well-circumscribed, erythematous, ulcerative lesion, usually not painful or pruritic, is usually found on the upper lip. Although reported to occur, progression to squamous cell carcinoma is extremely rare. Histology shows an ulcerative dermatitis, with a cellular infiltrate of neutrophils, plasma cells, and mononuclear cells predominating. Mild to moderate fibroplasia is common. Tissue or peripheral eosinophilia is uncommon.
Eosinophilic Plaque:
This well-circumscribed, erythematous, raised lesion is most commonly found in the medial thigh and abdominal regions; it is extremely pruritic. Regional lymphadenopathy can be seen. Histology shows a diffuse eosinophilic dermatitis, with marked inter- and intracellular edema and vesicles containing eosinophils in the epidermis and dermis. Mast cells may also be present. Peripheral eosinophilia is common.
Eosinophilic Granuloma:
These typically raised, well-circumscribed, yellowish to pink lesions may be found anywhere on the body but are most common on the head, face, bridge of the nose, pinnae, pads of the feet, perineal region, lips, chin, oral cavity, and caudal thighs. The caudal thigh location is usually distinctly linear. Linear lesions have been seen on other body locations, but more commonly these are papular, nodular or diffusely swollen, and firm. Histologically, a granulomatous inflammatory response surrounds degenerative collagen. Tissue and peripheral eosinophilia are marked when the lesions are in the mouth but vary when lesions are on the skin.
In dogs, the lesions reported as eosinophilic granulomas histologically resemble the eosinophilic granuloma of cats, with marked collagen degeneration surrounded by a granulomatous and eosinophilic infiltrate. These lesions may be seen as ulcerated or vegetative masses in the oral cavity or, less commonly, as plaques, nodules, or papules on the lips and other areas of the body. Any breed may be affected, but Siberian Huskies may be at greater risk.
In horses, the disease has been termed equine eosinophilic granuloma with collagen degeneration, nodular necrobiosis of collagen, and collagenolytic granuloma. The lesions are nodular, nonulcerative, and nonpruritic. They often are found in the saddle, central truncal, and lateral cervical areas and may have a gray-white central core. Older lesions may become mineralized. Both insect bites and trauma have been suggested as etiologies, although the occasional onset during winter in cold climates and in noncontact saddle or tack areas suggests multifactorial causes. Histology reveals multifocal areas of collagen degeneration surrounded by granulomatous inflammation containing eosinophils. Thus, histologically, this lesion is similar to eosinophilic granuloma of cats and dogs.
source: the merck

Fleas and Flea Allergy Dermatitis

2008-01-30T08:06:00.000-08:00

There are >2,200 species of fleas recognized worldwide. In North America, only a few species commonly infest dogs and cats: Ctenocephalides felis (the cat flea), C canis (the dog flea), Pulex simulans (a flea of small mammals), and Echidnophaga gallinacea (the poultry sticktight flea). However, by far the most prevalent flea on dogs and cats is C felis . Cat fleas cause severe irritation in animals and humans and are responsible for flea allergy dermatitis. They also serve as the vector of typhus-like rickettsiae and Bartonella sp , and are the intermediate host for filarid and cestode parasites. Cat fleas have been found to infest >50 different mammalian and avian hosts throughout the world. In North America, the most commonly infested hosts are domestic and wild canids, domestic and wild felids, raccoons, opossums, ferrets, and domestic rabbits.
Cat fleas deposit their eggs in the pelage of their host. The eggs are pearly white, oval with rounded ends, and 0.5 mm long. They readily fall from the pelage and drop onto bedding, carpet, or soil, where hatching occurs in ~1-6 days. Newly hatched flea larvae are 1-5 mm long, slender, white, segmented, and sparsely covered with short hairs. Larvae are free-living, feeding on organic debris found in their environment and on adult flea feces, which are essential for successful development. Flea larvae avoid direct light and actively move deep in carpet fibers or under organic debris (grass, branches, leaves, or soil).
Larvae are susceptible to desiccation, with exposures to relative humidity <50% being lethal. The areas within a home with the necessary humidity are limited, and suitable outdoor sites are even rarer. Flea development occurs outdoors only where the ground is shaded and moist (1-20% soil moisture content) and where the flea-infested pet spends a significant amount of time so that adult flea feces will be deposited into the larval environment. In the indoor environment, flea larvae probably survive only in the protected microenvironment deep within carpet fibers, in cracks between hardwood floors in humid climates, and on unfinished concrete floors in damp basements. The larval stage usually lasts 5-11 days but may be prolonged for 2-3 wk, depending on availability of food and climatic conditions.
After completing its development, the mature larva produces a silk-like cocoon in which it pupates. The cocoon is ovoid, ~0.5 cm long, whitish, and loosely spun. Flea cocoons can be found in soil, on vegetation, in carpets, under furniture, and on animal bedding.
Once the pupa has fully developed (1-2 wk), the adult flea emerges from the cocoon when properly stimulated by physical pressure, carbon dioxide, substrate movement, or heat. The preemerged adult (which is a fully formed adult flea) residing in the cocoon is the stage that can extend the longevity of the flea. If the preemerged adult does not receive the proper stimulus to emerge, it can remain quiescent in the cocoon for several weeks until a suitable host arrives. Emergence can be delayed up to 350 days if preemerged adults are protected from desiccation. Newly emerging fleas move to the top of the carpet pile or vegetation, where they are more likely to encounter a passing host. A newly emerged cat flea can survive 24-72 hr before requiring a blood meal. It is the newly emerged unfed fleas that infest pets and bite people. Cat fleas that have found a preferred host (eg, dog, cat, opossum, etc) generally do not leave their host unless forced off by grooming or insecticides.
Depending on temperature and humidity, the entire life cycle of the cat flea can be completed in as little as 12-14 days or can be prolonged for up to 350 days. However, under most household conditions, cat fleas complete their life cycle in 3-6 wk.
Adults begin feeding almost immediately once they find a host. Female cat fleas can consume 13.6 µL of blood daily. After rapid transit through the flea, the excreted blood dries within minutes into reddish black fecal pellets or long tubular coils (flea dirt). Fleas mate after feeding, and egg production begins within 24-48 hr of females taking their first blood meal. Female cat fleas can produce up to 40-50 eggs/day during peak egg production, averaging 27 eggs/day through 50 days, and may continue to produce eggs for >100 days.
Cat fleas are susceptible to cold. No stage of the life cycle (egg, larva, pupa, or adult) can survive exposure to <3°C (37.4°F) for several days. Therefore, cat fleas survive winters in north temperate climates as adults on untreated dogs and cats or on small wild mammals (eg, raccoons or opossums) in the urban environment. As these animals pass through yards in the spring or set up nesting sites in crawl spaces or attics, the eggs laid by surviving female fleas drop off and subsequently develop to adults. Cat fleas may also survive the winter as preemerged adults in microenvironments protected from the cold.
Fleas can cause iron deficiency anemia in heavily infested hosts, particularly in young animals. Fleas in the genus Ctenocephalides have been reported to produce anemia in poultry, dogs, cats, goats, cattle, and sheep.
Cat fleas are also involved in disease transmission. Murine typhus, caused by Rickettsia typhi and R felis , is a mild to severe febrile disease of humans characterized by headaches, chills, and skin rashes, with infrequent involvement of the kidneys and CNS. The disease occurs in humans and many small mammals along the southeastern, southwestern, and Gulf coasts. In the USA, the principal transmission cycle involves opossums and cat fleas. Cat fleas also serve as the intermediate host of the nonpathogenic subcutaneous filarid nematode of dogs, Dipetalonema reconditum . Dipylidium caninum , the common intestinal cestode of dogs and cats (and rarely children), develops as a cysticercoid in C felis , C canis , and P irritans . Flea larvae ingest the eggs of the tapeworm, which develop into cysticercoids in the body of the flea. When grooming themselves, dogs and cats may ingest infected fleas, and the cysticercoids are released.
Flea allergy dermatitis (FAD) or flea bite hypersensitivity is the most common dermatologic disease of domestic dogs in the USA. Cats are also afflicted with FAD, which is one of the major causes of feline miliary dermatitis. FAD is most prevalent in the summer, although in warm climates flea infestations may persist throughout the year. In north temperate regions, the close association of pets and their fleas with human dwellings creates conditions that permit a year-round problem. Temperature extremes and low humidity tend to inhibit flea development.
When feeding, fleas inject saliva that contains a variety of histamine-like compounds, enzymes, polypeptides, and amino acids that span a wide range of sizes (40-60 kD) and induce Type I, Type IV, and basophil hypersensitivity. Flea-naive dogs exposed intermittently to flea bites develop either immediate (15 min) or delayed (24-48 hr) reactions, or both, and detectable levels of both circulating IgE and IgG antiflea antibodies. Dogs exposed continuously to flea bites have low levels of these circulating antibodies and either do not develop skin reactions or develop them later and to a considerably reduced degree. This could indicate that immunologic tolerance may develop naturally in dogs continuously exposed to flea bites. Although the pathophysiology of FAD in cats is poorly understood, similar mechanisms may exist.
source: the merck

Definition of Q Fever

2008-01-30T08:05:00.001-08:00

Q fever is a zoonotic bacterial infection associated primarily with parturient ruminants, although domestic animals such as cats and a variety of wild animals have also been associated with human infections. Q fever occurs more frequently in persons with occupational contact with high-risk species. Q fever has a highly variable clinical presentation in humans, ranging from a self-limiting influenza-like illness to pneumonia, hepatitis, and endocarditis. It is highly infectious, and a single organism can reportedly cause infection via the aerosol route in humans. Q fever is considered a potential agent of bioterrorism due to its high rate of infectivity, stability in the environment, and potential for aerosol dispersion.
Etiology, Epidemiology, and Transmission:
Q fever is caused by the gram-negative coccobacillus Coxiella burnetii . Although classically considered a rickettsial agent, recent phylogenetic analyses suggest that C burnetii is more closely related to Legionella and Francisella than to the genus Rickettsia . It resides and reproduces in phagolysosomes of host monocytes and macrophages. Two forms exist—the large cell variant is a vegetative form found in infected cells, and the small cell variant is the extracellular infectious form that is shed in milk, urine, and feces and found in high concentration (109 ID50/g) in placental tissue and amniotic fluid. The small cell variant is resistant to heat, drying, and many common disinfectants and remains viable for weeks to months in the environment. Once a domestic ruminant is infected, C burnetii can localize in mammary glands, supramammary lymph nodes, placenta, and uterus, from which it may be shed in subsequent parturitions and lactations.
The epidemiology of C burnetii is complex because there are 2 major patterns of transmission: in one, the organism circulates between wild animals and their ectoparasites, mainly ticks; the other occurs in domestic ruminants, independent of the wild animal cycle. Ixodid and argasid ticks can act as reservoirs of the organism. Distribution is worldwide (except New Zealand) and the host range includes various wild and domestic mammals, arthropods, and birds. The disease is enzootic in most areas where cattle, sheep, and goats are kept. In the USA, seroprevalence studies have shown antibodies to C burnetii in 41.6% of sheep, 16.5% of goats, and 3.4% of cattle.
The greatest risk of transmission occurs at parturition by inhalation, ingestion, or direct contact with birth fluids or placenta. The organism is also shed in milk, urine, and feces. High-temperature pasteurization effectively kills the organism. Ticks may transmit the disease among domestic ruminants, but are not thought to play an epidemiologically important role in transmission of disease to humans.
source: the merck

Feline infectious peritonitis (FIP)

2008-01-30T08:02:00.000-08:00

Feline infectious peritonitis (FIP), caused by a feline coronavirus, is seen worldwide. Although a large number of cats may be infected with the feline coronavirus, only a few develop clinical FIP. The disease is progressive and may manifest clinically as a continuum between the effusive (serositis or wet) and noneffusive (granulomatous or dry) forms. A distinct clinical form of noneffusive FIP affecting only the eyes or brain (or both) may be seen. Mortality, even with therapy, approaches 100%. Although primarily a disease of domestic cats, FIP has been recognized in exotic Felidae, including the large and small wild cats. Among larger cats, FIP is seen in lions, leopards, jaguars, mountain lions, and especially cheetahs. Smaller cats susceptible to FIP include the sand cat, lynx, caracal, and pallas cat.
Etiology:
Field strains of feline coronavirus vary in their ability to induce FIP. Some isolates cause FIP (feline infectious peritonitis virus [FIPV]); others cause more localized GI disease ( Feline Enteric Coronavirus). Mutations from feline enteric coronavirus to FIPV occur. The exact relationship between low virulence FIPV strains and feline enteric coronavirus, which is relatively nonpathogenic, is not clear. FIPV is antigenically related to and serologically cross-reacts (by current ELISA and immunofluorescent antibody tests) with a subgroup of mammalian coronaviruses, including transmissible gastroenteritis virus of swine, human coronavirus 229-E, canine coronavirus, and feline enteric coronavirus. FIPV and canine coronavirus are very closely related antigenically and may have crossed between hosts. Strains of FIPV may differ considerably in antigenicity.
Feline coronaviruses are fairly stable in the environment and, once dry, can survive for 4-6 wk. They are enveloped viruses and are destroyed by most household disinfectants, particularly household bleach at a 1:32 dilution.
Transmission, Epidemiology, and Pathogenesis:
Most FIPV infections probably result from ingestion of the virus; however, aerosol transmission is also possible. Close contact with an infected cat or its excreta, most likely feces and saliva, is required for virus transmission. Because cats shed viral particles in feces, litter box exposure and mutual grooming are important sources of infection. Cats living in multiple cat households are at greater risk of contracting feline coronavirus and developing FIP because of sharing multiple strains of the virus and stress-associated immunosuppression. Transplacental transmission is suggested by the occasional observation of FIP in stillborn kittens, but the frequency with which this occurs is unknown. In the past, up to 50% of cats with FIP were co-infected with feline leukemia virus (FeLV); FeLV potently suppresses cell-mediated immunity, which is required for resistance to FIP. Currently, the co-infection rate is only 5%, due to FeLV testing and vaccination.
Cats of all ages and either sex can develop the disease, but incidence is highest in cats 6-24 mo old, decreased in cats 5-13 yr old, and increased in those 14-15 yr old. Kittens raised in infected colonies may contract the virus from their mothers or asymptomatic carriers when their maternal immunity wanes at 5-10 wk of age. These kittens typically may develop FIP weeks or months after they are placed in new homes. The prevalence of clinical FIP is <1% of cat-containing households, even though 20-35% of cats are infected with coronavirus. Losses are often sporadic and unpredictable, and morbidity and mortality may be greatly increased, sometimes up to 35% or more in some breeding catteries and households with multiple cats. Generally, the morbidity rate in cattery-bred kittens is 10%. The prevalence of FIPV infection in the general cat population is difficult to determine because current serologic tests for detecting FIPV antibodies cannot discriminate between FIPV and other feline coronaviruses that do not produce disease and that may be more prevalent.
After ingestion of virus or aerosol exposure, FIPV initially replicates in tonsil or intestinal epithelium and then is transported via macrophages and monocytes to primary target organs such as liver, spleen, and visceral lymph nodes. The development of FIP, and the particular clinical form of disease (ie, effusive or noneffusive) depends on the intrinsic immune responses of the cat. Cats with a strong humoral immunity and a weak or absent cell-mediated immune response against FIPV develop a persistent viremia and effusive FIP. The effusive disease results from widespread formation and deposition of immune complexes in blood vessels and from complement activation leading to vasculitis, vessel damage, and leakage of serum and protein into body cavities. Cats with partial cell-mediated immune responses along with humoral immunity develop the more chronic noneffusive FIP, which is characterized by immune-mediated (delayed hypersensitivity-like), granulomatous, frequently perivascular lesions in abdominal viscera, lungs, eyes, and brain. Cats with strong cell-mediated immune responses with or without humoral responses can either completely recover or become persistently infected asymptomatic carriers. The latter may infect contact cats and may themselves later develop FIP, usually after periods of stress or co-infection with FeLV. Some asymptomatic, seropositive carrier cats subsequently may become seronegative and stop excreting virus.
source: the merck

Definition of Zoonoses

2008-01-30T08:01:00.001-08:00

The emergence and reemergence of zoonotic diseases present challenges not only to veterinarians, but also to all professions concerned with public health. Since the 19th century, the veterinary profession in the USA has been at the forefront of control and eradication of animal diseases, including bovine pleuropneumonia, foot-and-mouth disease, Texas fever, bovine tuberculosis, brucellosis, vesicular exanthema, and classical swine fever.
The early cooperation of veterinarians and public health physicians gave impetus to the eradication of bovine tuberculosis first in Denmark, Sweden, Finland, and Norway and then in the USA and Canada. Unfortunately, bovine tuberculosis has emerged in Mexico along the border with the USA and has caused human disease and dairy cow infections from California to Texas. Bovine tuberculosis and brucellosis remain major problems in the developing world.
People with acquired immune deficiency syndrome (AIDS) are much more susceptible, in general, to zoonotic diseases, including tuberculosis and other related mycobacterial infections; toxoplasmosis; cryptosporidial enteritis, foodborne Salmonella infections, and other enteric organisms; Campylobacter ; Listeria ; and Yersinia . It is possible that other zoonotic diseases that are dormant or infrequent (eg, leptospirosis, plague, glanders, melioidosis, and pseudoglanders) may emerge in individuals with AIDS or other immunocompromising conditions. Many of these are latent or nonpathogenic serovars. AIDS-like infections have been described in lions and the tropical cats of Africa as well as in domesticated cats. None have caused human disease.
In Australia and Malaysia, new diseases have been reported in horses and swine that also affect humans. They are caused by a morbillivirus—a measles-like virus related to canine distemper and rinderpest viruses. Another virus killed many wild felids in a zoo in Egypt. Many emerging viral diseases that have a rodent or unknown animal host have caused devastating fatal diseases in humans in Africa and South America, eg, Lassa fever, an arenavirus serologically related to lymphocytic choriomeningitis, and South American hemorrhagic diseases of Argentina and Bolivia. In Africa, Ebola fever and Marburg disease, the latter a dormant monkey disease, have caused death in medical personnel and in patients. Crimean-Congo hemorrhagic fever has caused death in African travelers and in the Middle East in abattoir workers.
The death of veterinarians in the western USA from plague, and reports of serious illness in veterinary technicians and cat owners, has focused attention on both domestic and feral cats and the larger mountain lion or bobcats as carriers of this ancient disease. Dogs and wild canids are likewise involved in plague regions of the USA. The involvement of cats since the 1970s is evidence of the dynamics of zoonotic diseases in a changing environment. Human populations may be pressuring old habitats, or there may be more subtle changes. The plague bacterium ( Yersinia pestis ) may be more adept at finding new hosts or new foci, as seen in other emerging diseases.
Although Lyme borreliosis has been recognized as an important zoonotic disease in North America, other forms of borreliosis have appeared in the USA and abroad for decades.
The Hantaan virus complex was first noted in 1951 in Korea, where it caused a hemorrhagic disease with renal syndrome. Various forms of the disease exist worldwide, and it is a major public health problem in China. In the USA, 2 fatal forms of the disease have been reported, namely, nephritic and pneumonic (in addition to latent infections). Hantaan virus has caused infections in laboratory rodents, and veterinary technicians have been infected in Asia and Europe.
The naturally occurring oral bacterium of the dog and cat Capnocytophaga canimorsus can cause disease and even death in persons with other debilitating illness, eg, alcoholism. Yersinia enterocolitica in an infected dog can be a hazard to humans, as can Bartonella in infected cats.
Prion diseases have been described in North America, Europe, and Asia and are known to affect sheep, cattle, elk, and deer as well as wild and domestic felids. The bovine prion disease is reported to have caused >140 human cases with 100% mortality in the UK. Although the incidence is <1/1,000,000, the threat of prion diseases to human and animal health is of major concern.
Exposure to animals kept as pets is steadily increasing as the number of pets increases in the USA and other affluent countries. The types of animals kept as pets are also increasing. Examples of these are the “exotic pets” that have become popular in many parts of the world, eg, prairie dogs, that have brought plague, tularemia, and even monkeypox out of the wild into people’s homes. The desire of humans to touch wild animals or have contact with farm animals has resulted in the establishment of “petting zoos.” Contact with farm or wild animals may expose children or other visitors to organisms such as Escherichia coli O157:H4 or even rabies. Public health officials in the USA, Canada, and Britain are trying to control these “zoos” through inspections and rules, including microbicidal handwashing following exposures.
Another source of infection is exemplified by the severe acute respiratory syndrome epidemic caused by a novel coronavirus that appeared in southern China in 2003, first among food preparation workers exposed to civet cats and other “exotic animals” during their preparation as special foods.
The 21st century holds the threat of even more emerging diseases, nurtured by an ever-increasing human population. Control of zoonotic diseases and protection of the public health will become even more challenging as world population increases. When overpopulation and crowding occur, water shortages occur, hygiene often cannot be maintained, and malnutrition develops, leading to disease and epidemics. Surveillance and reporting of disease is the first line of defense. Knowledge of the epidemiology of the disease organisms is the first step in initiating a control program. The ultimate objective is to protect and preserve both human and animal health.
Zoonoses are generally defined as animal diseases that are transmissible to humans. However, there are several diseases listed below that occur primarily in humans and that may also be transmitted between humans and animals, with some animals serving as reservoirs for human infection (eg, Trichuris trichiura ). The following common bacterial and viral diseases of humans are not found as naturally occurring diseases in animals (ie, animals are not a reservoir): diphtheria ( Corynebacterium diphtheriae ), Legionnaires’ disease ( Legionella pneumoniae , L pneumophila , and related organisms), syphilis ( Treponema pallidum ), trachoma ( Chlamydia trachomatis ), typhoid fever ( Salmonella typhi ), poliomyelitis, hepatitis B, mumps, chickenpox, smallpox, and measles.
source: the merck

Definition of Toxicology

2008-01-30T07:59:00.000-08:00

Toxicology is the study of the harmful effects of chemical compounds on biologic systems, including their properties, actions, and effects. The toxic agent is referred to as a toxicant or poison. The term toxin refers to poisons produced by a biologic source (eg, venoms, plant toxins); the redundant term biotoxin is occasionally used. Toxicosis, poisoning, and intoxication are synonymous terms for the disease produced by a toxicant. Toxicity (sometimes incorrectly used instead of poisoning) refers to the amount of a toxicant necessary to produce a detrimental effect. Hazard describes the likelihood of poisoning under conditions of use.
If 2 poisons act via similar mechanisms on the same organs, their combined effects may be additive. Synergism is the amplification of the combined actions of 2 or more agents having the same biologic effects. Antagonism is the inhibition or elimination of the effect of one agent by another; it may be chemical or functional.
Toxicant accumulation and biomagnification occurs when absorption exceeds the capacity of the body to destroy or excrete a xenobiotic (foreign) compound. Likewise, the terms are applied to the environment, an ecosystem, species, etc, when a compound increases because of increased application or decreased destruction or disappearance. These elements are used with ecotoxicology, the study of the relation of potentially toxic chemicals in living organisms and their environment. When residual compounds are introduced into plant or animal species early in the ecosystem food chain, the levels tend to be successively higher in the next species that feeds on the contaminated plant or animal; eg, predatory birds, which are at the “end” of the food chain, often have the highest levels of certain residual chemicals.
Tolerance is the ability of an organism to show less response to a specific dose of a chemical than it demonstrated on a prior occasion; it refers to acquired, not innate, resistance.
Dose Expressions:
All toxic effects are dose dependent. (By usual standards, allergens or inducers of idiosyncratic reactions may appear to be exceptions, although even with these, presumably some dose is too small to cause detectable effects.) A dose may cause undetectable, therapeutic, toxic, or lethal effects. Further, the effective dose may differ from molecule to cell to organ or to body level (or fetus vs mother). Usually, a dose is expressed as the amount of compound per unit of body wt and the toxicant concentration as ppm or ppb. These quantitative expressions also are used for feedstuffs, water, air, tissue levels, etc.
The LD50 is the dose that is lethal to 50% of a test sample. It is an estimator of lethality and the most common expression used to rate the potency of toxicants. Other terms used for prediction of illness or lethality include: no observed effect level (NOEL), maximum nontoxic dose (MNTD), and maximum tolerated dose or minimum toxic dose (MTD).
Elimination Expressions:
The elimination or disappearance (by metabolic change) of a chemical from an organ or the body is expressed in terms of half-life (t1/2 ). This is the amount of time required for the disappearance of half the compound. The rate of elimination is usually dependent on the concentration of the compound: a constant fraction (eg, 1/2) is eliminated per unit of time (referred to as first-order kinetics); or a metabolic reaction may dictate the rate of elimination, and a constant amount is eliminated per unit of time (zero-order kinetics). Different body compartments will likely have different elimination rates. A 2-compartment system is used to describe the situation in which elimination is initially rapid, eg, from the central or plasma component, and subsequently slower from the peripheral component, eg, liver, kidney, or fat.
Acute toxicosis refers to effects during the first 24-hr period. Effects produced by prolonged exposure (≥3 mo) are referred to as chronic toxicosis . Terms such as subacute and subchronic are used to cover the large gap between acute and chronic. Regardless of terms, the duration of exposure can alter the toxicity of an agent; this is reflected by the chronicity factor (CF), the ratio of the acute to chronic LD50 dose. The biologic system may develop tolerance so that after prolonged exposure, a higher dose may be tolerated (eg, potassium cyanide, CF = 0.04). Other compounds are metabolized and eliminated in much the same manner regardless of the duration of exposure, and the lethal dose does not change appreciably (eg, caffeine, CF = 1.3). However, due to increased sensitization or cumulative effects, prolonged exposure to a toxicant may cause the chronic lethal dose to be much lower than the acute lethal dose (eg, warfarin, CF = 20).
source: the merck

Spider Bites

2008-01-30T07:57:00.000-08:00

Envenomation of animals by spiders is relatively uncommon and difficult to recognize. It may be suspected on clinical signs, but confirmatory evidence is rare. Spiders of medical importance in the USA do not inflict particularly painful bites, so it is unusual for a spider bite to be suspected until clinical signs appear. It is also unlikely that the offending spider will remain in close proximity to the victim for the time (30 min to 6 hr) required for signs to develop. Almost all spiders are venomous, but few possess the attributes necessary to cause clinical envenomation in mammals—mouth parts of sufficient size to allow penetration of the skin and toxin of sufficient quantity or potency to result in morbidity.
The spiders in the USA that are capable of causing clinical envenomation belong to 2 groups—widow spiders ( Latrodectus spp ) and brown spiders (mostly Loxosceles spp ).
Widow Spiders:
Widow spiders usually bite only when accidental skin contact occurs. The most common species is the black widow, Latrodectus mactans , characterized by a red hourglass shape on the ventral abdomen. In the western states, the western black widow, L hesperus , predominates, while the brown widow, L bishopi , is found in the south, and the red widow, L geometricus , is found in Florida.
Latrodectus venom is one of the most potent biologic toxins. The most important of its 5 or 6 components is a neurotoxin that causes release of the neurotransmitters norepinephrine and acetylcholine at synaptic junctions, which continues until the neurotransmitters are depleted. The resulting severe, painful cramping of all large muscle groups accounts for most of the clinical signs.
Unless there is a history of a widow spider bite, diagnosis must be based on clinical signs, which include restlessness with apparent anxiety or apprehension; rapid, shallow, irregular respiration; shock; abdominal rigidity or tenderness; and painful muscle rigidity, sometimes accompanied by intermittent relaxation (which may progress to clonus and eventually to respiratory paralysis). Partial paresis also has been described.
An antivenin (equine origin) is commercially available but is usually reserved for confirmed bites of high-risk individuals (very young or very old). Symptomatic treatment is usually sufficient but may require a combination of therapeutic agents. Calcium gluconate IV (10 mL of a 10% solution is the usual human dose) is reportedly helpful. Meperidine hydrochloride or morphine, also given IV, provides relief from pain and produces muscle relaxation. Muscle relaxants and diazepam are also beneficial. Tetanus antitoxin also should be administered. Recovery may be prolonged; weakness and even partial paralysis may persist for several days.
Brown Spiders:
There are at least 10 species of Loxosceles spiders in the USA, but the brown recluse spider, L reclusa , is the most common, and envenomation by it is typical. These spiders have a violin-shaped marking on the cephalothorax, although it may be indistinct or absent in some species. In the northwestern USA, the unrelated spider Tegenaria agrestis reportedly causes a clinically indistinguishable dermonecrosis in humans and presumably in other animals. Brown recluse spider venom has vasoconstrictive, thrombotic, hemolytic, and necrotizing properties. It contains several enzymes, including a phospholipase (sphingomylinase D) that attacks cell membranes. Pathogenetic mechanisms of the characteristic dermal necrosis are poorly understood, but activation of complement, chemotaxis, and accumulations of neutrophils affect (or amplify) the process.
A history of a bite by a “fiddleback” brown spider is useful but rare. A presumptive diagnosis may be based on the presence of a discrete, erythematous, intensely pruritic skin lesion that may have irregular ecchymoses. Within 4-8 hr, a vesicle develops at the bite wound, and sometimes a blanched zone circumscribes the erythematous area, imparting a “bull’s-eye” appearance to the lesion. The central area sometimes appears pale or cyanotic. The vesicle may degenerate to an ulcer that, unless treated in a timely manner, may enlarge and extend to underlying tissues, including muscle. Sometimes, a pustule follows the vesicle and, on its breakdown, a black eschar remains. The final tissue defect may be extensive and indolent and require months to heal. However, medical authorities claim that not all brown recluse spider bites result in severe, localized dermal necrosis.
Systemic signs sometimes accompany brown recluse spider envenomation and may not appear for 3-4 days after the bite. Hemolysis, thrombocytopenia, and disseminated intravascular coagulation are more likely to occur in cases with severe dermal necrosis. Fever, vomiting, edema, hemoglobinuria, hemolytic anemia, renal failure, and shock may result from systemic loxoscelism.
In known bites, early treatment can be successful, but unfortunately, many cases are not recognized until cutaneous necrosis has become extensive; treatment at that stage is less rewarding but is still of value. Immediate application of cold packs is beneficial, and if administered early, corticosteroids protect against cutaneous necrosis by stabilizing cell membranes and suppressing chemotaxis. Corticosteroids also tend to protect against systemic involvement. Radical excision has been advocated, but its value is questionable. Dapsone, an inhibitor of leukocyte function, which is frequently used in the treatment of leprosy, is currently considered the drug of choice for brown recluse spider bites. In humans, it is administered at 100 mg, bid for 14-25 days. Broad-spectrum antibiotics are useful in preventing secondary infection, and tetanus immunoprophylaxis should be considered.
source: the merck

Mercury Poisoning

2008-01-30T07:52:00.001-08:00

Mercury exists in a variety of organic and inorganic forms. The replacement of commercial mercurial compounds, including antiseptics (eg, mercurochrome), diuretics, and fungicides by other agents has decreased the likelihood of mercurial toxicosis; however, the possibility of exposure to environmental sources of organic methylmercury exists.
Inorganic Mercurials:
These include the volatile elemental form of mercury (used in thermometers) and the salted forms (mercuric chloride [sublimate] and mercurous chloride [calomel]). Ingested inorganic mercury is poorly absorbed and low in toxicity. Large amounts of these mercurials are corrosive and may produce vomiting, diarrhea, and colic. Renal damage also occurs, with polydipsia and anuria in severe cases. In rare cases of chronic inorganic mercurial poisoning, the CNS effects resemble those of organic mercury poisoning. Mercury vapor from elemental mercury produces corrosive bronchitis and interstitial pneumonia and, if not fatal, may lead to neurologic signs as do organic forms.
Emesis followed by initiation of chelation therapy (see below) is recommended after acute oral ingestion. Oral administration of sodium thiosulfate to bind mercury still in the gut may be beneficial.
Organic Mercury:
Inorganic mercury is converted to the organic alkyl forms, methylmercury and ethylmercury, by microorganisms in the sediment of rivers, lakes, and seas. Marine life accumulate the most toxic form, methylmercury, and fish must be monitored for contamination. There are reports of commercial cat food causing severe neurologic disturbances in cats fed an exclusive tuna diet for 7-11 mo.
The organic mercurials are absorbed via all routes and bioaccumulate in the brain and to some extent in the kidneys and muscle. Aryl mercurials (eg, phenylmercury fungicide) are slightly less toxic and less prone to bioaccumulation. Animals poisoned by organic mercury exhibit CNS stimulation and locomotor abnormalities after a lengthy latent period (weeks). Signs may include blindness, excitation, abnormal behavior and chewing, incoordination, and convulsions. Cats show hindleg rigidity, hypermetria, cerebellar ataxia, and tremors. Mercury is also a mutagen, teratogen, and a carcinogen, and is embryocidal. Differential diagnoses include conditions with tremors and ataxia as predominant signs, such as ingestion of other metals and insecticides and cerebellar lesions due to trauma or feline parvovirus.
Histologic lesions include degeneration of neurons and perivascular cuffing in the cerebrocortical gray matter, cerebellar atrophy of the granular layer, and damage to Purkinje cells. Laboratory diagnosis must differentiate between normal concentrations of mercury in tissue (especially whole blood, kidney, and brain) and feed (<1 ppm) and concentrations associated with poisoning.
Neurologic signs may be irreversible once they develop. Chelation therapy with dimercaprol (3 mg/kg body wt, IM, every 4 hr for the first 2 days, qid on the third day, and bid for the next 10 days or until recovery is complete) has been beneficial. When available, the water soluble, less toxic analog of dimercaprol, 2,3-dimercaptosuccinic acid, is the chelator of choice for organic mercury poisoning. Penicillamine (15-50 mg/kg, PO) may be used only after the gut is free of ingested mercury and renal function has been established.
source: the merck

Giant Kidney Worm Infection in Mink and Dogs

2008-01-23T18:35:00.000-08:00

Mink are the most common definitive host for Dioctophyma renale , the largest known nematode, which has a worldwide distribution. Many other species, including dogs and humans, can become infected. The definitive host contracts the parasite by ingesting encysted larvae in raw fish (eg, pike, bullhead) or frogs, or by ingesting an infected annelid worm. The larvae penetrate the bowel wall and migrate first to the liver and later to the kidneys. In dogs, the parasite often fails to reach the kidneys and may be found free in the abdominal cavity. Kidney worms grow larger in dogs than in mink, reaching up to 103 cm. Female worms are larger than male worms, and both are blood red. Both male and female worms must be present in the same kidney to complete the life cycle. Barrel-shaped, yellow-brown eggs with a thick pitted shell measuring 71-84 × 45-52 µm are shed into the urine.
In the kidneys, the worm(s) cause obstruction, hydronephrosis, and destruction of the renal parenchyma. The right kidney is most commonly affected in both mink and dogs. Kidney failure can result if both kidneys are parasitized. Chronic peritonitis, adhesions, and liver disease are also possible, especially in dogs. Clinical signs are hematuria, pollakiuria, weight loss, and renal or abdominal pain. Urinalysis may reveal proteinuria, hematuria, and pyuria. IV pyelography or ultrasonography shows the enlarged hydronephrotic kidney. The diagnosis is made by finding the eggs in the urine sediment if both sexes of the nematode are present in the kidney and the ureter is patent. Alternatively, exploratory laparotomy may reveal the diagnosis. Worms may be found in the peritoneal cavity, between the lobes of the liver, or within the affected kidney(s) via nephrotomy.
Unilateral nephrectomy is the treatment of choice if the opposite kidney is unaffected. Preventing ingestion of raw fish or other aquatic organisms is recommended, especially in areas where the parasite is known to infect wild animals. [themerck]

Transmission, Epidemiology, and Pathogenesis of Foot and Mouth Disease

2008-01-23T18:33:00.000-08:00

Transmission of FMD is generally by contact between susceptible and infected animals. Infected animals have a large amount of aerosolized virus in their exhaled air, which can infect other animals via the respiratory or oral routes. All excretions and secretions from the infected animal contain virus, and virus may be present in milk and semen for up to 4 days before clinical signs appear. Aerosolized FMD virus can spread a considerable distance as a plume, depending on weather conditions, particularly when the relative humidity is >60% and when the topography of the surface over which it is dispersing does not cause turbulence. FMD has been transmitted to calves via infected milk, and milk tankers carrying infected milk have been implicated in the spread of disease between farms. Fodder can become contaminated after contact with infected animals and iatrogenic spread of FMD has been reported. Although horses, dogs, and cats are not affected by FMD, they can act as mechanical vectors, as can humans. Also, avian species are not susceptible to infection, but they can carry virus on their feet and feathers and will excrete virus after ingesting infected material. Therefore, birds may carry the virus, although their role in dissemination is unclear. A typical scenario for the introduction of FMD into a previously clear area is for pigs to be fed imported food derived from an infected animal (as meat, offal, or milk); virus then spreads by aerosol from the infected pigs to cattle, which are the most likely species to be infected by the respiratory route because of their large respiratory volume. FMD virus can survive in dry fecal material for 14 days in summer, in slurry up to 6 mo in winter, in urine for 39 days, and on the soil between 3 (summer) and 28 (winter) days.
Ruminants that have recovered from infection and vaccinated ruminants that have contact with live FMD virus can serve as foci of infection and carry the virus in the pharyngeal region for up to 3.5 years in cattle, 9 mo in sheep, and ³5 years in African buffalo. Experimentally, it has not been possible to show transmission from a carrier bovid to an in-contact susceptible animal, but there is evidence that under field conditions these carrier animals initiate new outbreaks of disease. FMD virus can be recovered from carrier animals by culturing a sample of pharyngeal mucus and superficial cells (collected using a probang cup) on susceptible tissue culture, such as primary bovine thyroid cells. However, the technique is probably only 50% reliable in identifying a carrier using a single sample because the quantity of virus found in the pharynx varies on different occasions.
The primary site of infection and replication is usually the mucosa of the pharynx, although the virus can enter through skin abrasions or the GI tract. Virus is distributed through the lymphatic system to sites of replication in the epithelium of the mouth, muzzle, feet, and teats, and also to areas of damaged skin (eg, the knees and hocks of pigs kept on concrete). Vesicles develop at these sites and rupture, usually within 48 hr. The viremia persists for ~3 days. [themerck]

Definition of Foot and Mouth Disease (FMD)

2008-01-23T18:29:00.000-08:00

Foot-and-mouth disease (FMD) is a highly infectious viral disease of cattle, pigs, sheep, goats, buffalo, and artiodactyl wildlife species. It is characterized by fever and vesicles in the mouth and on the muzzle, teats, and feet. In a susceptible population, morbidity approaches 100%. The disease is rarely fatal except in young animals. All species of deer and antelope, elephant, and giraffe are susceptible to FMD, but Old World camels are resistant to natural infection. South American camelids such as alpacas and llamas, although susceptible, are probably of no epidemiologic significance. Rats, mice, and guinea pigs can be infected experimentally.
FMD is endemic in the Middle East, Iran, the southern countries of the former Soviet Union, India, and southeast Asia. Sporadic outbreaks occurred in South Korea in 2000 and 2002, Japan in 2000, and in peninsular Malaysia. FMD is restricted to Luzon island in the Philippines. Australasia and Indonesia are free of FMD, as are Central and North America. In South America, Chile, southern Argentina, Guyana, Surinam, and the region of Colombia bordering Panama are free; large outbreaks of FMD in Uruguay and central Argentina during 2001 were brought under control, and these areas together with Paraguay and large parts of Brazil are now considered free areas in which vaccination is still used. Most of sub-Saharan Africa has endemic FMD, and also Egypt, Ethiopia, and Eritrea; FMD has returned to Zimbabwe associated with economic and social changes, and sporadic outbreaks have also occurred in the previously FMD-free zones of South Africa, Namibia and Botswana. In Europe, an outbreak in Greece on the border with Turkey in 2000 was quickly eliminated, but in 2001, FMD was introduced into the UK, from where it spread to the Republic of Ireland, the Netherlands, and France. The strain causing the outbreak was the same as that found throughout Asia, and was eventually brought under control in the UK following the slaughter of >4 million animals, without the use of vaccination. Vaccination was used in the Netherlands, and all vaccinated animals were subsequently slaughtered. Europe is currently free of FMD. [themerck]

Definition of Swine Vesicular Disease

2008-01-23T18:28:00.000-08:00

Swine vesicular disease (SVD) is typically a transient disease of pigs in which vesicular lesions appear on the feet and snout and in the mouth. It does not cause severe production losses, and recent outbreaks of infection have been mainly subclinical. However, infection is of major economic importance because it must be differentiated from foot-and-mouth disease, eradication is costly, and embargoes on export of pigs and pork products are often imposed on nations not free of SVD.
Although infection in laboratory workers has occurred, and the virus may be present in sheep or cattle, pigs are said to be the only natural host. The disease was first identified in Italy in 1966 and subsequently in Hong Kong, Japan, Taiwan, and 16 countries in Europe. Although SVD virus was eradicated from Japan in the mid-1970s and most European countries by the mid-1980s, it has remained endemic in Italy and caused sporadic outbreaks of disease in other European countries during the 1990s and in Portugal in 2003 and 2004. [themerck]

What is Aspiration Pneumonia?

2008-01-23T18:16:00.000-08:00

Aspiration pneumonia is a pulmonary infection characterized by inflammation and necrosis caused by inhalation of foreign material. The severity of the inflammatory response depends on the material aspirated, the type of bacteria aspirated, and the distribution of aspirated material in the lungs.
Faulty administration of medicines is a common cause of aspiration pneumonia. Liquids administered by drench or dose syringe should not be given faster than the animal can swallow. Drenching is particularly dangerous when the animal’s tongue is drawn out, when the head is held high, or when the animal is coughing or bellowing. Administration of liquids by nasal intubation is not without risk, and careful technique is especially necessary in debilitated animals.
Inhalation of irritant gases or smoke is an infrequent cause. Aspiration of vomitus or attempts by animals to eat or drink while partially choked can result in aspiration pneumonia as well. Disturbances of deglutition, as in anesthetized or comatose animals (eg, mature cattle under general anesthesia or cows in lateral recumbency), vagal paralysis, acute pharyngitis, abscesses or tumors of the pharyngeal region, esophageal diverticula, cleft palate, megaesophagus, or encephalitis, are frequent predisposing causes.
Cats are particularly susceptible to pneumonia caused by aspiration of tasteless products such as mineral oil. In sheep, poor dipping technique may cause aspiration of fluid. Calves and lambs may inhale inflammatory debris if affected with diphtheritic laryngitis. Inhalation of milk by pail-fed calves can cause an acute necrotizing pneumonia due to the diffuse distribution of foreign material. The muscles of deglutition may be affected in lambs with nutritional myopathy. Pigs fed fine particulate food in dry environments may inhale feed granules. Aspiration pneumonia in cattle following delayed treatment for milk fever is highly fatal. In dogs with myasthenia gravis, aspiration pneumonia is the leading cause of death. [themerck]

Abnormal ingestive behavior on Dogs

2008-01-23T17:51:00.000-08:00

Abnormal ingestive behavior has the following necessary condition: consistent ingestion of abnormal amounts or types of food or nonfood material in a manner or frequency not consistent with previous behavior. The following condition is sufficient: incessant consumption of food or nonfood material, or incessant avoidance of food, in a manner that interferes with normal social functioning. Abnormal ingestive behavior includes pica (consistent ingestion of nonfood material), coprophagia (ingestion of feces that is neither accidental nor incidental), polyphagia, aerophagia, psychogenic water drinking (consumption of water in excess of that necessary to meet daily fluid balance needs or to thermoregulate or lubricate food for ingestion), anorexia, and gorging. Except for pica and aerophagia—which truly seem different from ingestion or lack of ingestion involving food—it is very difficult, although not impossible, to rule out all physiologic causal associations. It is logical that abnormal ingestion of food and abnormal ingestion of water should be classified separately because they are controlled by different, although related, physiologic systems. (The term “psychogenic” does not imply any understanding of the mechanism of the condition and is equivalent to “behaviorally idiopathic.”) The sufficient conditions for aerophagia include mechanically forced, volitional swallowing of air that is uncoupled with eating or drinking; behavior may be sufficiently frequent to interfere with normal activities, which can usually be confirmed by owners if questioned. In the extreme, pica, aerophagia, and coprophagia can be signs of obsessive-compulsive disorders. [the merck]

Fluid Therapy of Equine Emergency Medicine

2008-01-23T17:41:00.000-08:00

Injuries with blood loss, exhaustion, acute rhabdomyolysis, and overheating are conditions that require emergency fluid replacement. Fluids can be administered for maintenance purposes, when fluid intake is physically not possible, or for replacement purposes when excessive losses have been incurred or ongoing losses are anticipated.
In athletic horses, replacement therapy is the mainstay of fluid therapy. Designing a replacement fluid therapy regimen requires consideration of the volume and type of fluids required as well as the route and rate of administration. The volume of fluid to give on a daily basis can be calculated using the following: volume to administer (L) = maintenance (60 mL/kg/day) + immediate losses (body wt [kg] ¥ estimate of dehydration) + ongoing losses. Ongoing losses can be difficult to determine. Maintenance volumes are ~1L/hr for adult horses. Dehydration can be estimated by using clinical and laboratory parameters.
Ongoing losses can be difficult to estimate, as losses through the GI tract are hard to measure. The equine GI tract secretes and reabsorbs the equivalent of the extracellular volume (~30% of body wt) on a daily basis. If ileus is present, the amount of reflux can be quantitated. If the large colon is not reabsorbing water (eg, diarrhea), losses can be significant. With severe diarrhea, ~50% of extracellular fluids can be lost on a daily basis.
This calculation provides only a crude estimate; volumes should be adjusted based on objective responses to fluid administration such as heart rate, pulse quality, capillary refill time, urine production, PCV, total protein, and creatinine. These parameters should be monitored as often as dictated by the horse’s clinical condition. In a horse in severe shock, cardiovascular parameters may need to be monitored continuously, or at least every 15 min until an improvement is noted. In a horse with severe ongoing fluid losses, cardiovascular parameters should be monitored at least every 4 hr, and laboratory parameters as frequently as 4 times a day until stabilized. Following these evaluations, the estimate of fluid requirements can be adjusted.
Fluids available for administration in horses include crystalloids (fluids containing substances that freely cross the capillary membrane, including balanced electrolyte, saline, and dextrose solutions) and colloids (fluids that are retained in the vascular space for a certain number of hours because of their larger molecular size). Colloids include plasma, albumin solutions, dextrans, and hydroxyethylstarch. Crystalloids are most commonly used for replacement fluid therapy in athletic horses, whereas colloids are mostly reserved for resuscitation purposes.
Two basic types of crystalloids are available for horses: balanced electrolyte solutions (BES), which are solutions that contain electrolyte in concentrations similar to those in plasma, and saline solutions, which contain only sodium chloride. Although considered a crystalloid, dextrose solutions are rarely used alone. The decision to choose BES or saline is based, if available, on a serum chemistry profile. Saline is chosen if the sodium concentration is <125>5.9 mEq/L. Otherwise, a BES is used. If serum chemistries are unavailable, a BES is safe, unless hyperkalemic periodic paralysis is suspected, in which case saline, dextrose, and/or sodium bicarbonate should be used.
The addition of colloids to a fluid therapy regimen serves 2 purposes—preventing edema formation in hypoproteinemic states and sustaining the intravascular fluid volume. Products containing antibodies are also available for the treatment or prevention of endotoxemia, Rhodococcus equi pneumonia, West Nile virus infection, and clostridial diseases. Colloidal solutions are available in natural or synthetic forms. Natural colloids are plasma, serum products, or albumin. In general, plasma is selected when an increase in oncotic pressure is needed and coagulation factors or specific anticoagulants such as antithrombin III are required. Albumin solutions are not commonly used, as the intravascular half-life of albumin in states of compromised vascular permeability is short, and they do not have the added benefits of whole plasma. The synthetic colloid most commonly used in horses is hydroxyethylstarch. It is used to increase plasma oncotic pressure, and its effect is best evaluated either by clinical response (decreased edema) or increased oncotic pressure (measured by colloid osmometry). A refractometer cannot be used to monitor the effect of synthetic colloid administration.
The goal of fluid therapy in shock states is to rapidly expand circulating blood volume to improve perfusion and oxygen delivery. Isotonic crystalloids must be administered at a rapid rate of up to 60-80 mL/kg in the first hour (~1 blood volume) for maximal beneficial effects. Hypertonic saline can rapidly expand circulating volume by redistributing extravascular fluids into the vascular space. Because of redistribution, hypertonic solutions in horses have a short duration of effect (~45 min). Colloid solutions can be used to sustain the effect of hypertonic crystalloid solutions to several hours. For resuscitation, a combination of hypertonic saline (4 mL/kg) and hetastarch (4 mL/kg) has the most beneficial and sustained effects.
The flow rate of fluids through an administration system is directly proportional to the diameter of the line and inversely proportional to the viscosity of the fluid and the length of the line. Teflon® or polyurethane 14-gauge catheters are used routinely in adult horses. When gravity flow is used, a rate of 2-3 L/hr can be achieved when fluids are ~10 ft higher than the jugular vein. For more rapid flow, 10- or 12-gauge catheters with large-bore connecting sets can be used, but 10-gauge catheters are more thrombogenic. Finally, both jugular veins can be cannulated for increased fluid administration, and a pressure bag system or a pump used to increase the flow rate. Peristaltic pumps can cause endothelial damage and increase the risk of thrombosis. [the merck]

First Aid and Transport of Emergency Medicine

2008-01-23T17:33:00.000-08:00

Owners can provide significant medical assistance at the scene of the injury. At the time of the initial telephone call, the owner should be questioned about the level of consciousness, breathing pattern, and perfusion of the animal. The first concern is for the safety of the owner. Placing a light cloak or cloth over the head of the animal can lessen external stimuli that may cause fearful and aggressive reactions. Cats can be placed in dark boxes to minimize stress during transport; the box should have holes large enough so that the cat can be observed.
When moving the animal, motion of the head, neck, and spine should be minimized. A flat, firm board of wood, cardboard, or thick fabric can be used to provide support. Radiographs can also be taken through these materials without having to move the animal.
Mouth-to-nose resuscitation and chest compressions may provide enough respiratory and circulatory support to maintain life during transport. If the animal is unconscious and not breathing, the owner should be instructed to close the animal’s mouth, place their lips over the animal’s nostrils, and initially give 3-4 strong breaths. If the animal’s breathing does not become spontaneous, the owner should breathe for the animal 10-12 times/min. The owners can also be instructed to compress the esophagus behind the trachea so that most of the air will go down the airway instead of into the stomach. If a heart beat cannot be detected, chest compressions and ventilations at a 5:1 ratio can be performed. Of course, someone else will have to drive during transport.
Owners should be asked if hemorrhage is ongoing or if bleeding was seen at the site of injury. Pulsating arterial bleeding should be controlled by direct digital pressure and then by a pressure bandage. Any long pieces of fabric or gauze can be used. Often washcloths and hand towels are adequate when applied with mild pressure. Additional material can be placed over the original bandage if it becomes soaked with blood.
Penetrating foreign objects should be left in place, but the owner should guard against further penetration or movement of the object. When an arrow has penetrated the abdominal cavity, the shaft of the arrow should not be allowed to move during transport so that bowel segments are not lacerated by the blades. It is often necessary to stabilize the shaft of the arrow just outside the body and, holding it firmly, cut the shaft off.
In dogs with fractures below the elbow or hock with significant displacement, support should be provided. The owner can make a support splint from a rolled newspaper or magazine, which is then secured in place by long pieces of fabric.
Animals with altered mentation after trauma should be transported with the head level or elevated 20°. There should not be any jerking or thrashing motions and no compression of the neck or jugular veins.

Emergency Medicine Definition

2008-01-23T17:25:00.000-08:00

Emergency patients present special challenges because underlying problems may not be evident for 24-48 hr after initial presentation. Problems can arise from an acute illness, from a chronic illness that has decompensated, or from an unexpected complication of another illness. All postoperative patients are considered critical care patients until life-threatening anesthetic or surgical complications are ruled out. The golden rule of emergency medicine is to treat the most life-threatening problems first.
Variables that contribute to the overall success of emergency treatment include the severity of the primary illness or injury, the amount of fluid or blood lost, age of the animal, previous health problems, the number and extent of associated conditions, time delay in instituting therapy, the volume and rate of fluid administration, and the choice of fluids (eg, crystalloid, blood components, or synthetic colloids). Therapy must be done at the right time, in the right amount, and in the right order. Therapeutic failures are generally a result of failing to act expeditiously at a crucial moment.
Specialized care often begins with the owner’s initial telephone call. Instructing the owner on first aid and transport procedures can be life-saving for the animal. The clinic and staff must be in readiness, especially if more than one animal in critical condition arrives at the same time. [the merck]

PATELLA LUXATION IN DOGS

2007-09-19T01:19:00.001-07:00

Introduction
Patella luxation is probably one of the most common canine orthopedic
conditions seen in veterinary practices in New Zealand. Most patella
luxations are medial and the condition is also seen in cats. Although the
condition is predominantly seen in miniature and toy breeds of dogs it is
not uncommon in larger breeds. Left untreated patella luxation can lead to
pain, lameness, degenerative joint disease, and cranial cruciate ligament
injury. A firm understanding of the anatomy and pathogenesis of patella
luxation is required before recommending treatment options to owners of
affected dogs.
Anatomy
The patella is a large sesamoid bone that acts as a lever to decrease the
amount of force needed to extend the stifle joint. The patella is maintained
in place by the medial and lateral trochlear ridges, the stifle joint capsule,
the parapatellar fibrocartilages and fascia, and the femoropatellar ligaments.
The femoropatellar ligaments are thin bands of tissue bilaterally that connect
the patella to the lateral fabella and to the medial periosteum.
The extensor mechanism of the pelvic limb involves the quadriceps
musculature, the patella, the femoral trochlear, the patella ligament, and
the tibial tuberosity/crest. An abnormality of any of these components can
result in patella luxation.
Pathogenesis
Most patella luxation cases are congenital as the problem is evident from
a young age and generally not associated with trauma. It is recognized
that cases of mild patella luxation are predisposed to traumatic patella
luxation.

By: Dr. Richard M. Jerram
BVSc,
Diplomate, American College of Veterinary Surgeons
Registered Specialist, Small Animal Surgery
Vetscholar.org.nz

ORAL NEOPLASIA

2007-09-19T01:17:00.000-07:00

The most common canine oral tumours are fibrosarcoma (FSA),
osteosarcoma (OSA), squamous cell carcinoma (SCC), malignant melanoma
(MM) and epulides. The most common seen in cats are FSA and SCC. With
the exception of some epulides, all of these tumours are locally invasive
and often involve adjacent bone, but rarely metastasise. For this reason,
incomplete tumour resection often results in recurrence. The goal of surgical
treatment is to attain tumour-free margins because it has been shown this
has a significant positive influence on survival: One study showed dogs in
which tumour cells extended to the periphery of the excised margin (dirty
margins) were 3.6 times more likely to die from the tumour compared with
dogs where the margins were tumour free (clean margins).
The goal of surgical treatment is to attain tumour-free margins
The surgical techniques of maxillectomy and mandibulectomy offer wide
excision of oral tumours including the underlying bone. Function and
cosmetic results are good and satisfy most clients.
Pre-operative Evaluation of the Patient and Diagnosis
Oral tumours often present the same way and look the same – see below.
Owners notice the mass or halitosis, bleeding from the mouth especially
while eating or chewing a bone or some degree of dysphagia. Once an
oral mass is identified a minimum data base should be obtained including
blood work and UA. Many of these dogs are older and may have concurrent
disease.
Thoracic radiographs are taken to rule out gross pulmonary metastasis.
Fine detail radiographs of the tumour site including the dental arcade.
Check the local lymph nodes – if enlarged these should aspirated or
biopsied.
Incisional biopsy to determine the tumour type and treatment options.
Plan a definitive aggressive surgery such as maxillectomy or mandibulectomy
to achieve clean margins. The use of advanced imaging such as CT
reconstruction can aid in surgical planning.
Surgical, radiotherapy, hyperthermia, chemotherapy and immunotherapy.
Unfortunately radiotherapy is not yet available for our patients in NZ. The
main stay of treatment for oral neoplasia is aggressive en bloc surgical
resection. Chemotherapy including intralesional cisplatin is also used.

By: Alex Walker
BVSc, MACVSc
Specialist Small Animal Surgeon
Veterinary Specialist Group UNITEC.
Vetscholar.org.nz

Heatstroke or Hyperthermia

2007-08-26T17:40:00.000-07:00

Heatstroke occurs when normal body mechanisms cannot keep the body's temperature in a safe range. Animals do not have efficient cooling systems (like humans who sweat) and get overheated easily. A dog with moderate heatstroke (body temperature from 104º to 106ºF) can recover within an hour if given prompt first aid and veterinary care (normal body temperature is 100-102.5°F). Severe heatstroke (body temperature over 106ºF) can be deadly and immediate veterinary assistance is needed.
You should remove the dog from the hot area immediately. Prior to taking him to your veterinarian, lower his temperature by wetting him thoroughly with cool water (for very small dogs, use lukewarm water), then increase air movement around him with a fan. CAUTION: Using very cold water can actually be counterproductive. Cooling too quickly and especially allowing his body temperature to become too low can cause other life-threatening medical conditions. The rectal temperature should be checked every 5 minutes. Once the body temperature is 103ºF, the cooling measures should be stopped and the dog should be dried thoroughly and covered so he does not continue to lose heat. Even if the dog appears to be recovering, take him to your veterinarian as soon as possible. He should still be examined since he may be dehydrated or have other complications.

What is Euthanasia?

2007-08-23T11:04:00.000-07:00

Euthanasia is defined as an easy, painless death. In regard to animals, euthanasia is the act of killing an animal in a humane manner. The primary objectives of animal euthanasia are: 1) relieving pain and suffering of the animal(s) to be euthanized, 2) minimizing the pain, anxiety, distress, and fear the animal experiences before consciousness is lost, and 3) inducing a painless and distress-free death.
Observing the behavioral and physiologic responses of animals is beneficial in assessing whether the objectives of euthanasia are being met. A variety of behaviors and physiologic responses may be demonstrated by animals experiencing pain and/or fear, including (but not limited to) distress vocalizations, struggling, escape attempts, agitation, freezing, aggression, fearful postures or facial expressions, trembling, salivating, urinating, defecating, evacuation of anal sacs, pupillary dilation, panting, tachycardia, and sweating. Response to euthanasia procedures (handling, restraint, confinement, venipuncture, gas odors, etc) varies among species and among individuals, necessitating careful monitoring of every euthanasia.
Loss of physiologic function during euthanasia should occur in the following order to help prevent fear and distress: 1) rapid loss of consciousness, 2) loss of motor function, 3) arrest of respiratory and cardiac function, and finally, 4) permanent loss of brain function. If loss of motor or respiratory and cardiac function precedes loss of consciousness, animals become fearful and experience distress. In some species, particularly rabbits and chickens, tonic immobility may be induced by fear, and care must be taken to not confuse this behavioral response with loss of consciousness.
Before the carcass is disposed of, death must be verified by a means appropriate to the species and the method of euthanasia. Care must be taken not to confuse narcosis with death. Determination of death in ectothermic animals may be more difficult due to differences in their physiology.
Euthanasia frequently results in chemical tissue residues, necessitating proper disposal to prevent contamination of the environment or other animals (eg, scavengers, predators).
The methods used for euthanasia of animals intended for consumption by humans or other animals in the USA must meet the requirements of the USDA; chemical agents that result in chemical tissue residues cannot be used unless approved by the FDA.
Other factors that must be taken into account in animal euthanasias include the safety of operators, observers, and other animals; human psychological responses to euthanasia, eg, sadness and grief; and fear and anxiety of other animals exposed to the behaviors, vocalizations, and pheromones of animals being euthanized. Counseling services and pet loss support hotlines are available for grieving pet owners in some communities and veterinary colleges. Personnel involved in euthanasias or animal slaughter may also experience negative psychological consequences. Workplace support programs and accessibility to counseling may help alleviate the stress felt by euthanasia personnel.
The operator must be knowledgeable regarding the agent, method, equipment, and behavior and physiology of the species and individual animal(s) to be euthanized; be trained in the technique; and have demonstrated skill in the euthanasia operation to be performed.
Selection of an appropriate method and agent of euthanasia is paramount in assuring a humane death. Selection is based on the behavior, physiology, and metabolism of the species, as well as any particular characteristics of the individual animal(s) that would influence the ability to use a particular method. The setting, the available means of animal restraint, the skill and knowledge of the operator, the number of animals to be euthanized, and the purpose for which the animal(s) is to be used are also determining factors in selection of the methods and the agent. Euthanasia in circumstances other than the clinical veterinary setting, eg, wildlife in the field, may limit the euthanasia options. However, in all circumstances, humaneness to the animal should be a prevailing concern. Slaughter of animals for food, fur, or fiber, and euthanasia of wildlife and feral animals should all adhere to the same humane standards for euthanasia.
Acceptable methods and agents for euthanasia of different species of animals are listed in Table: Agents and Methods of Euthanasia by Species. It is the obligation of the operator to know the physiology and behavior of the species to be euthanized, and the specific technical information and safety precautions for the method and agent selected. The 2000 report of the American Veterinary Medical Association panel on euthanasia provides additional details, as well as references for specific technical and safety information.
Inhalant agents should not be used alone in animals <16 wk old because neonatal animals are more resistant to hypoxia and it takes longer for them to die. Reptiles, amphibians, diving birds, and diving and burrowing mammals may have a prolonged time to loss of consciousness with inhalant gases. Inhalant anesthetics are useful for small animals (<7 kg) in which injections are difficult. The order of preference of inhalant anesthetics for euthanasia is halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, and desflurane, with or without nitrous oxide.
Injectable agents are the most rapid and reliable and are preferred when venipuncture can be accomplished without causing fear to the animal or unnecessary risk to the operator. All barbituric acid derivatives are acceptable IV euthanasia agents. Certain injectable agents (eg, strychnine, nicotine, caffeine, magnesium sulfate, cleaning agents, solvents, disinfectants, other toxins or salts, potassium chloride as a sole agent, and all neuromuscular blocking agents) are absolutely not acceptable and are condemned as agents of euthanasia.
Physical methods of euthanasia, including captive bolt, gunshot, cervical dislocation, decapitation, microwave irradiation, and thoracic compression can be humane methods of euthanasia when used properly by skilled operators with well-maintained equipment and when other means of euthanasia are impractical or contraindicated by the intended use of the animal. Exsanguination, stunning, and pithing should not be used as sole methods of euthanasia but as adjuncts to other methods.

Euthanasia for Clients and Veterinarians

2007-08-23T11:02:00.000-07:00

As in any intimate relationship, when an animal companion dies or is ill, people are likely to feel stress, sorrow, and grief. This may include the animal’s family and neighbors in the community, as well as the veterinary team that has provided care. The significance of pets dying and the consequent emotional impact on clients is now clearly profiled within the veterinary profession, with educational materials and support groups, hotlines, and counseling available. The relatively short lifespan of dogs and cats means that clients face losing several animals during a lifetime. Most veterinarians themselves have painful memories of losing a particular animal and understand only too well the pain their clients feel.
An extra burden comes in assuming responsibility for the moment of death by euthanasia. The philosophical dilemma is the same as that posed by human euthanasia. One must weigh the value of mercy or the Golden Rule to relieve pain and suffering with the wrongness of killing or a religious argument for reverence for life. The difficulty of this decision overlays the loss with feelings of overwhelming guilt and the thought that there must have been some other step that could have been taken. Even with family support, these feelings are not assuaged. Among married couples in one study, about half of the wives and more than a quarter of husbands reported they were quite or extremely disturbed by the death of the family pet.
As an alternative to euthanasia, it is important to offer instruction in providing palliative care for clients who are prepared to offer it. Procedures developed in hospice care can assure high quality, end-of-life care. As in human medicine, families can combine good medical care with pain relief for the animal. The technical aspects of treatment no longer override the compassionate care, as a specific approach is offered for dealing with the family’s and animal’s distress.
Notwithstanding the anguish that veterinary clients experience, the process of animals dying, especially the act of performing euthanasia, poses a time-consuming and emotionally wearing duty for veterinarians, accounting for 2-4% of encounters. In a recent study, almost all veterinarians felt they were untrained in making explanations to clients at such times. Almost half had regretted a euthanasia, and a majority of private practice veterinarians had felt guilty after performing a euthanasia. After euthanizing their own pets, a majority felt depressed and 30% felt guilty. All of these figures were elevated among women veterinarians, suggesting that their impact may have risen in the intervening years with the gender shift of the profession.
Compassionate veterinarians include themselves in the circle of remembrance of their clients’ animals and respect the families’ regard for the animal throughout the relationship. A veterinarian can assume that many grieving clients will need a year of recovery to pass through the holidays and family traditions before somewhat accepting a loss and may consider sending a remembrance card to the family after 1 yr. [the merck]

What is Animal Welfare?

2007-08-23T11:00:00.000-07:00

Reducing or preventing the incidence of animal pain or distress and promoting animal well-being (and even pleasure) are overall goals of animal welfare. These goals pertain to animals on farms or in laboratories as well as companion animals. Aversive handling, even if infrequent, has stressful consequences for pigs and other farm animals, with resulting adverse effects on reproduction and development. Aversive handling has similar effects on animals in other settings. Veterinarians are often the first contacts when someone seeks help for animals being badly treated or receiving inadequate care.
Intentional, deliberate abuse of animals is an extreme marker of a likely pattern of abuse elsewhere within a family. Veterinarians who report suspected animal abuse sometimes can avert similar abuse of other vulnerable family members, especially children or the elderly. Two studies reported that >90% of veterinarians would report cases of suspected animal abuse to authorities. A majority agreed that animal abuse in families would tend to be linked with child or elder abuse.
Although sometimes seen by veterinarians, abuse appears less common than the neglect, poor husbandry, or lack of essential medical care of animals, some of which may be inadvertent. A more serious problem occurs with animal hoarders who may be mentally ill. Some communities routinely combine efforts of animal control and mental health agencies when dealing with such cases. The person, perhaps without awareness, acquires more animals than they can care for properly.
A major, widespread societal problem of animal welfare is the abandoning and killing of companion animals. While the incidence of animal relinquishment has decreased somewhat, the problem is still widespread. Behavioral problems of animals and owners’ lack of knowledge increase the likelihood of relinquishment. Veterinary teams can provide leadership and education about more realistic expectations of companion animals, and can encourage earlier intervention if problems arise. [the merck]

Health Benefits of Pets for Human

2007-08-23T10:57:00.000-07:00

The companionship of pets relaxes and entertains people. In coming to know their clients, veterinarians can assess the importance of the pet to a family and the extent to which the family members benefit from the potential psychosocial effects of living with an animal. During stressful periods in people’s lives, many studies have reported that pets offer meaningful comfort that is protective against depression and loneliness. Elderly women living alone score more favorably on measures of mental health; even college-aged women report less loneliness if living with companion animals rather than alone. Similar comforting effects of animal companions, whether cats or dogs, in warding off depression were reported for patients with Alzheimer’s disease who had a companion animal and were cared for at home and for men with AIDS whose social lives were shrinking. Elderly people experiencing typical life stresses are less affected (as measured by number of medical visits) when they have a companion dog, suggesting that a dog can be a stress buffer that softens the effects of adverse events on the person. The interactive caregiving exchanged with the animal allows the person to nurture and feel needed, while also feeling nurtured. The animal’s constancy bolsters courage during setbacks, as the animal’s affection is unaffected by factors such as the person’s physical capabilities or mood.
Companion animals also facilitate social interactions with other people and positive social involvement. The socializing effects of dogs have been documented in public settings and also among people with a variety of disabilities. A companion animal provides a person who has few friends with an ally in making new human acquaintances, while also creating a richer family environment with enhanced companionship. Even one person with an animal lives in a family unit, and has someone who offers a greeting or recognition when the person comes home.
The motivating role of animals is a further antidote to depression. Many people are inspired to walk their dogs, volunteer to take animals into nursing homes for visits, or just actively nurture an animal, whereas without the animal they would be less involved and engaged in living or even depressed. Walking the dog and being outdoors where other social contact arises are two healthful effects of living with a canine companion.
The daily comfort, socialization, and motivation offered by an animal also are associated with cardiovascular benefits. Blood pressure decreases transiently when a person relaxes with, talks to, or just watches an animal. When patients with elevated blood pressure were given medication, and random assignment of pets was made to some patients, those with pets performed better on stressful tasks but did not differ in blood pressure scores, indicating a lower response to stress among pet owners. Several studies show longterm health correlates with animal companionship, although the animals were not randomly assigned to the people, but rather were chosen by them or their families. Cardiovascular measures were better among pet owners than nonowners in a large Australian study. Two studies reported that pet ownership was related to decreased mortality. Recently, survival for 1 yr following heart attack was found to be more likely among people with companion dogs and human social support. [the merck]

Veterinary Family Practice

2007-08-23T10:55:00.000-07:00

The primacy of pets in clients’ lives today resembles their importance in the lives of veterinarians who entered the profession due to their involvement with animals. Clients become deeply attached to and care about the health and well-being of their companions. Their expectations for veterinary care are becoming more similar to that ideally provided in human medicine—clients anticipate superb care for both the animal and themselves. As high-tech medicine expands within veterinary specialties, a more sophisticated level of family support is required and expected by many clients. The current elevated importance of animals, often regarded as part of the family, revolutionizes the nature of veterinary practice to include the entire family. Because veterinarians now deal with the family plus the animal, and no longer just treat the animal, the style and emphasis of companion animal practices have shifted, as reflected in the terms “veterinary family practice” or “bond-centered practice.”
Such practices build lifelong relationships with families and their animals. A new animal brought into the family is the occasion to discuss the animal’s life cycle with the family and provide an overview that can optimize the likelihood of a positive relationship with few behavioral problems. Emotional needs of the family are addressed along with the medical needs of the animal. Upper-socioeconomic clients are especially likely to view their pets as companions. Many clients with companion animals are families with young children. The animals are acknowledged to play a central and formative role in children’s lives. Some studies have reported that pet-owning pre-adolescents score higher on measures of self-esteem and autonomy. Practitioners may consider giving special thought to incorporating children into their communications with the family, making it easy for families with children to be comfortable during consultation (eg, provision of play areas and planning for children to be present in or visibly near the examination room). Hospitals providing extended diagnoses and treatments to animals sometimes find entire families coming in to offer support to the animal, perhaps spending hours to be on hand when the animal is available; these hospitals may want to plan accommodation near at hand for such families.
Providing areas for relaxation, softer light in public areas, and comfortable seating in exam rooms without barriers from the medical staff are some features that improve customer satisfaction. Impeccable cleanliness also matters. In veterinary practices with these values, everyone understands that every medical intervention carries emotional consequences and that medical competence and providing emotional support go hand-in-hand. Various resources provide models for veterinary staffs based on skilled communication.
The key role of communication was revealed in a study of the medical profession showing that physicians who had never been sued laughed more with their patients, asked them more questions, and spent 3 min longer on average with patients than their colleagues who had been sued. A recent study of successful veterinarians reported that nontechnical competencies were essential, including interpersonal relationship-building skills. Using such skills, veterinarians and their staffs facilitate clients’ understanding of medical situations and preventive medicine. They can encourage clients to attend puppy socialization classes to improve retention of dogs, assist in behavioral assessments, and prepare clients for providing palliative care or dealing with end-of-life issues. Client adherence is generally lower than believed by veterinarians, but followup communication improves the level of adherence.
Despite optimal communication skills, research has shown that veterinarians inevitably encounter clients who are inattentive, neglectful, over-involved, or cost-focused, and patients who are uncontrolled, dangerous, or dirty, adding to medical and emotional problems. Almost all veterinarians feel they were not prepared by their education and training for dealing with such nonmedical issues. Making plans in advance, with specific protocols for interventions, can prepare the veterinary staff with strategies for these occasions. [the merck]

Human-Animal Bond

2007-08-23T10:54:00.000-07:00

Companion animals are now considered to be family members, no longer the outdoor dogs and cats on farms that were typical for many families a few decades ago. The human-animal bond has become a household term, reflecting the entry of dogs, cats, and other pets into our everyday lives. Cats are sharply increasing in popularity and numbers, including households with multiple cats, leading to the emergence of veterinary practices serving only cats. Yet a strong majority of Americans (73%) feel that dogs rather than cats are the better pet, as reported in a 2001 Gallup Poll. A 2002 AVMA study of household pets reported that dogs received 1.9 veterinary visits per animal in 2001, as compared with 1.0 visits per cat. Dogs had a total of 117 million veterinary visits, contrasting with 71 million for cats, but revealing the economic significance of both.
In addition to the growing awareness of the human-animal bond, the roles of animals have expanded into new applications. At the same time, the public is focused on ensuring that animals receive adequate consideration and care. Albert Schweitzer’s concept of “reverence for life” has become a standard for decision-making concerning animals. Acknowledgment of the human-animal bond is fast becoming a cornerstone of veterinary practice. [the merck]

Feeding and Management Practices of the chicken

2007-08-21T10:01:00.000-07:00

Success of the feeding program should be measured by how it achieves the breeder’s goals for proper weight and development specific to each strain. Feed and the length of time required for attaining certain weights in pullets and turkeys are presented in the growth and feed tables which can be used as a guide in estimating the amount of feed required. These figures may vary considerably due to differences in the nutrient density of feed, strain or breed of bird, amount of feed wasted, and environmental temperature.
Most diets used in feeding poultry are nutritionally “complete” diets that are commercially mixed, ie, prepared by feed manufacturing companies, most of which employ trained nutritionists. The formulation and mixing of poultry feeds requires knowledge and experience in purchasing ingredients, experimental testing of formulas, laboratory control of ingredient quality, and computer applications. Improper mixing can result in vitamin and mineral deficiencies, lack of protection against disease, or drug toxicity.
The physical form of the feed influences the expected results. Most feeds for starting and growing birds are produced as pellets or crumbles. In the pelleting process, the mash is treated with steam and then passed through a suitably sized die under pressure. The pellets are then cooled quickly and dried by means of a forced air draft. The conditions under which pelleting occurs (eg, use of an expander rather than an extruder, exposure to high temperature, use of soft pellets) have an important effect on the nutritional quality of the pellets, or of the crumbles that are produced by crushing the pellets. [the merck]

Nutritional Requirements of the Chicken

2007-08-21T09:55:00.000-07:00

Poultry continue to rank high in their ability to convert feed into food products. Such high efficiency has increased progressively in recent decades. The nutrient requirement figures published in Nutrient Requirements of Poultry (National Academy of Sciences, 1994) are the most recent available and should be viewed as minimal nutrient needs for poultry. They are derived from experimentally determined levels after an extensive review of the published data. Criteria used to determine the adequacy of a given nutrient include growth, feed efficiency, health, productivity, and quality of poultry product. These requirements do not, however, include a margin of safety. Consequently, under practical conditions in which there may be different strains, energy content of the diets, environmental temperatures, type of floor, availability of nutrients from various feedstuffs, destruction or loss of nutrients in the gut, pro-oxidants, intestinal parasites, mycotoxins, diseases, and many other stresses, nutritionists should make the proper adjustment by adding a margin of safety to the nutrient requirements.
Water:
Many factors influence water intake, including environmental temperature, relative humidity, composition of the diet, birds’ productivity (rate of growth or egg production), and the individual bird’s ability to resorb water in the kidney. As a result, precise water requirements cannot be determined. However, water is of vital importance and is considered an essential nutrient. Water deprivation for ≥12 hr has an adverse effect on growth of young poultry and egg production of layers; water deprivation for ≥36 hr results in a marked increase in mortality of both young and mature poultry. Cool, clean water must be available at all times.
Energy, Protein, and Amino Acids:
The apparent metabolizable energy (AMEn) and the true metabolizable energy (TMEn) values are used for numerous feedstuffs in poultry rations. AMEn is the gross energy of the feed minus the gross energy of the excreta after a correction for the nitrogen retained in the body. Similarly, TMEn is the gross energy of the feed consumed minus the gross energy of the excreta of food origin after a correction for the nitrogen retained in the body. AMEn and TMEn are similar for many ingredients. However, the 2 values could differ substantially for some ingredients such as feather meal, rice bran, wheat middlings, and corn distiller’s grains with solubles. AMEn is the energy value used by most poultry nutritionists in feed formulation.
Because chickens and other fowl can adjust their feed intake over a considerable range of feed energy levels to meet their daily energy needs, dietary energy levels are used to set the levels of other nutrients, including protein and amino acids. As a result, the concept of the calorie to protein and amino acids ratio has been used extensively in poultry feed formulation. However, recent research indicated that changes in feed intake of both broilers and layers were not inversely proportional to changes in dietary energy levels. This is particularly true when birds were fed high-energy diets (layers) or moderate- to high-energy diets (broilers). Consequently, the use of these specific ratios must be carefully evaluated. Because factors other than dietary energy could also affect feed intake, including ambient temperature (which can have a considerable impact on feed consumption), nutrient density in the ration should be adjusted to provide appropriate nutrient intake based on requirements and the actual feed intake.
Vitamins:
One IU of vitamin A activity is equivalent to 1.3 µg of pure retinol (or 0.344 µg of retinyl acetate). In chickens, 0.6 µg of β-carotene is considered equivalent to 1 IU of vitamin A. However, young chicks are not efficient in using β-carotene. The vitamin A requirements currently recommended are based on use of stabilized vitamin A preparations and thus are somewhat lower than previously recommended levels.
Requirements for vitamin D are expressed in IU. Birds use vitamin D3 from fish oils and irradiated animal sterols quite effectively but cannot use vitamin D2 . Metabolic forms of vitamin D have been isolated and synthesized; these are 25-hydroxy vitamin D3, which is synthesized in the liver, and 1,25-dihydroxy vitamin D3, which is synthesized in the kidneys. One IU of vitamin D represents the vitamin D activity of 0.025 µg of pure vitamin D3 .
One IU of vitamin E is equivalent to 1 mg of synthetic dl-α-tocopherol acetate. Vitamin E requirements vary with the type and level of fat in the diet, the levels of selenium and trace minerals, and the presence or absence of other antioxidants.
Choline is required as an integral part of the body phospholipid, as a part of acetylcholine, and as a source of methyl groups. Growing chickens can use betaine as a methylating agent, but betaine cannot replace choline in preventing perosis. Betaine is widely distributed in practical feedstuffs and may be important in sparing choline. Adequate dietary vitamin B12 helps pullets develop the ability to biosynthesize choline. The choline requirement values apply to diets containing the specified levels of vitamin B12. [the merck]

Newcastle Disease (Avian pneumoencephalitis)

2007-08-21T09:51:00.000-07:00

Newcastle disease is an acute viral disease of domestic poultry and many other bird species. It is a worldwide problem that presents primarily as a respiratory disease, but depression, nervous manifestations, or diarrhea may be the predominant clinical form. Mortality is variable. Occurrence of a virulent form of the disease is reportable and may result in trade restrictions.
Etiology and Pathogenesis:
Newcastle disease is caused by an RNA virus, Newcastle disease virus (NDV), synonymous with avian paramyxovirus-1 which is in the genus Avulavirus , family Paramyxoviridae. Isolates are classified into 1 of 3 virulence groups by chicken embryo and chicken inoculation as virulent (velogenic), moderately virulent (mesogenic), or of low virulence (lentogenic). Lentogenic strains are used widely as live vaccines in healthy chickens. Clinical manifestations vary from high morbidity and mortality to asymptomatic infections. The severity of an infection is dependent on virus virulence and the age, immune status, and susceptibility of the host species. Chickens are the most and waterfowl the least susceptible of domestic poultry.
Epidemiology and Transmission:
Virulent NDV strains are endemic in poultry in most of Asia, Africa, and some countries of North, Central, and South America. Other countries, including the USA and Canada, are free of those strains and maintain that status with import restrictions and eradication by destroying diseased poultry. Cormorants, pigeons, and imported psittacine species have also been sources of virulent NDV infections of poultry. Low virulence NDV is prevalent in poultry and wild birds, especially waterfowl. Infection of domestic poultry with low virulence NDV contributes to lower productivity.
Infected birds shed virus in exhaled air, respiratory discharges, and feces. Virus is shed during incubation, during the clinical stage, and for a varying but limited period during convalescence. Virus may also be present in eggs laid during clinical disease and in all parts of the carcass during acute virulent infections. Chickens are readily infected by aerosols and by ingesting contaminated water or food. Infected chickens are the primary source of virus, but other domestic and wild birds may be sources of NDV. Transfer of virus, especially in infective feces, by the movement of people and contaminated equipment is the main method of spread between poultry flocks.

Chicken Anemia Virus Infection

2007-08-21T09:48:00.000-07:00

Chicken anemia virus (CAV), a 25 nm, nonenveloped, icosahedral virus with a single-stranded, circular DNA genome, is the only member of the genus Gyrovirus of the Circoviridae family. The genome codes for 3 viral proteins (VP). VP1 is the capsid protein, but VP2 may be needed as a scaffold protein to allow proper folding of VP1. VP3, or apoptin, is a nonstructural protein that induces apoptosis in infected cells. CAV infects only chickens, although antibodies have been detected in Japanese quail. The virus is present worldwide based on serology and virus isolation. The disease, chicken infectious anemia, has been described in most countries where chickens are raised commercially.
Horizontal transmission of CAV is by the fecal-oral route and perhaps by the respiratory route. Vertical transmission occurs when seronegative hens become infected and continues until neutralizing antibodies develop. Chicks hatched from these eggs are viremic, and CAV can rapidly spread horizontally from these chicks to susceptible, maternal antibody-negative hatchmates. Roosters shedding CAV in the semen are another source of vertical transmission. Vaccination of seronegative flocks prior to the onset of egg production is recommended to prevent vertical transmission.
Maternal antibody-negative chicks are susceptible to infection and disease until 1-2 wk of age. In contrast, maternal antibody-positive chicks are protected from disease and probably from infection. Age resistance to clinical disease, but not infection, begins at approximately 1 wk of age. The age resistance can be overcome by coinfection of CAV with immunosuppressive agents such as infectious bursal disease virus ( Infectious Bursal Disease: Introduction), Marek’s disease herpesvirus ( Marek’s Disease), and reticuloendotheliosis virus ( Reticuloendotheliosis).
Many SPF flocks developed antibodies to CAV during or after the onset of sexual development. Spread of infection by CAV-contaminated embryo- or cell-culture-derived vaccines is possible.
When day-old susceptible chicks are inoculated IM with CAV, viremia occurs within 24 hr. Virus can be recovered from most organs and rectal contents up to 35 days after inoculation. The principal sites of CAV replication are hemocytoblasts in the bone marrow, precursor T cells in the cortex of the thymus, and CD8 cells in the spleen. Replication in the first leads to anemia, while replication in the latter two causes immunosuppression. Neutralizing antibodies are detectable 21 days after infection and clinical, hematologic, and pathologic parameters return to normal ~35 days after infection. CAV infection has adverse effects on proliferative responses of spleen lymphocytes and on the production of interleukin-2 and interferons by splenocytes. Infection can cause a marked decrease in generation of antigen-specific cytotoxic T cells directed against other pathogens. In addition to T-cell defects, macrophage functions such as Fc-receptor expression, phagocytosis, and antimicrobial activity may be impaired. Subclinical, horizontally acquired infection with CAV in broiler progeny of seropositive parent flocks may be associated with impaired economic performance. [the merck]

Behavioral Medicine

2007-08-12T17:09:00.000-07:00

An animal’s “behavior” is the product of its genetic composition, the environment in which the animal functions, and the animal’s experience (ie, what it has learned given its previous genetic × environment interaction). While this section focuses primarily on abnormal behavior of domestic animals, the extent to which an animal’s behavior is abnormal is defined by its deviation from “normal.” For each group of domestic animals, normal social and group behavior is outlined and followed by a listing of the common behavioral disorders and treatment approaches.
In behavioral medicine, diagnoses are not diseases; correlation is not causality. Behavioral conditions for which there is putative etiologic and pathophysiologic heterogeneity (multifactorial disorders) are complex.
Phenotypic (functional, phenomenologic) diagnoses are open to various mechanistic bases of all subsequent levels. Some of these more reductionistic levels can be tested using treatment (eg, specific pharmacologic agents), but few phenotypic diagnoses can be specifically tested using behavior modification. Most of the behavioral diagnoses for farm animals are descriptive and relatively nonspecific. Behavioral diagnoses for dogs and cats have been more fully developed and are discussed in the context of the “necessary and sufficient” conditions (or criteria) for diagnosis. The use of “necessary and sufficient” conditions, using the terms as they are used in logical and mathematical applications, is a refinement over descriptive definitions. These conditions act as qualitative, and potentially quantitative, exclusion criteria, allowing for uniform and unambiguous assessment of aberrant, abnormal, and undesirable behaviors.
A necessary condition is one that must be present for the listed diagnosis to be made. A sufficient condition is one that can stand alone to singularly identify the condition. Sufficiency is an outcome of knowledge: as more becomes known about the genetics, molecular response, neurochemistry, and neuroanatomy of any condition and its behavioral correlates, a sufficient condition can be defined more succinctly and accurately. Definition of necessary and sufficient conditions is not synonymous with a compendium of signs associated with the behavior. The number of signs present and their intensity may be a gauge for the severity of the condition, or act as a flag when there can be variable, nonoverlapping presentations of the same condition. [the merck]

Blood Groups and Blood Transfusions

2007-08-12T17:03:00.001-07:00

Blood groups are determined by genetically controlled, polymorphic, antigenic components of the RBC membrane. The allelic products of a particular genetic locus are classified as a blood group system. Some of these systems are highly complex with many alleles defined at a locus; others consist of a single defined antigen. Blood group systems, in general, are independent of each other, and their inheritance conforms to Mendelian dominance. For polymorphic blood group systems, an animal usually inherits 1 allele from each parent and thus expresses no more than 2 blood group antigens of a system. An exception is in cattle, in which multiple alleles or “phenogroups” are inherited. Normally, an individual does not have antibodies against any of the antigens present on its own RBC or against other blood group antigens of that species’ systems unless they have been induced by transfusion, pregnancy, or immunization. In some species (human, sheep, cow, pig, horse, cat, and dog), so-called “naturally occurring” isoantibodies, not induced by transfusion or pregnancy, may be present in variable but detectable titers. For example, Group B cats have naturally occurring anti-A antibody. Also, circulating antibodies to animal blood group antigens may be induced by transfusion. With random blood transfusions in dogs, there is a 30-40% chance of sensitization of the recipient, primarily to blood group antigen DEA 1. In horses, transplacental immunization of the mare by an incompatible fetal antigen inherited from the sire may occur. Immunization also may result when some homologous blood products are used as vaccines (eg, anaplasmosis in cattle).
The number of major recognized blood group systems, varies among domestic species, with cattle being the most complex and cats the simplest. Animal blood groups are typed to aid in the matching of donors and recipients and to identify breeding pairs potentially at risk of causing hemolytic disease in their offspring. Because expression of blood group antigens is genetically controlled and the modes of inheritance are understood, these systems also have been used to substantiate pedigrees in cattle and horses; however in most cases, DNA testing has replaced blood typing for paternity testing. [The Merck]

Blood Groups Definition

2007-08-12T16:50:00.000-07:00

Neurohypophysis

2007-08-02T20:48:00.001-07:00

The neurohypophysis (pars nervosa, posterior lobe) has 3 anatomic subdivisions. Secretion granules that contain the neurohypophyseal hormones, ie, antidiuretic hormone (ADH, vasopressin) and oxytocin, are synthesized in the hypothalamus but are released into the bloodstream in the pars nervosa. The infundibular stalk joins the pars nervosa to the overlying hypothalamus.
ADH, an octapeptide synthesized in the hypothalamus, is packaged into membrane-limited granules with a corresponding binding protein (neurophysin) and transported to the pars nervosa, where it is released into the circulation. ADH binds to specific receptors in the distal part of the nephron and collecting duct of the kidney; it increases the renal tubular reabsorption of water from the glomerular filtrate.
The output of ADH is directly related to the degree of hydration of the body. Hydration of the body inhibits release of ADH, while dehydration or injection of hypertonic electrolyte solutions favors release of ADH, which in turn causes increased water resorption from the glomerular filtrate, resulting in dilution and decreased osmolarity of body fluids. Barbiturates, ether, chloroform, morphine, acetylcholine, nicotine, and pain increase ADH release, which leads to less urine formation. Ethanol inhibits ADH release, which leads to diuresis.
The pressor effect of ADH is less prominent than the antidiuretic effect. At a dosage several hundred times larger than the antidiuretic dosage, ADH has a pronounced pressor effect, which may also lead to coronary constriction. The contractile mechanism of the capillaries, as well as GI and uterine muscle, is stimulated, and a prolonged increase in blood pressure follows.
Oxytocin has specific effects on the smooth muscle of the uterus and the myoepithelial cells of the mammary gland. It has no established physiologic function in the male, although an effect on sperm transport has been suggested.

Adenohypophysis

2007-08-02T20:37:00.000-07:00

The adenohypophysis, which surrounds the pars nervosa of the neurohypophyseal system to varying degrees in different species, consists of the pars distalis, the pars tuberalis, and the pars intermedia. The pars distalis is the largest part and contains multiple populations of endocrine cells. The pars tuberalis functions primarily as a scaffold for the capillary network of the hypophyseal portal system. The pars intermedia forms the junction between the pars distalis and pars nervosa. It contains 2 populations of cells in dogs, one of which synthesizes adrenocorticotropic hormone (ACTH).
A specific population of endocrine cells in the pars distalis (and in the pars intermedia for ACTH in dogs) synthesizes and secretes each of the pituitary trophic hormones. Pituitary cells have a secretory cycle and enter an actively synthesizing phase in response to increased demand for a particular hormone. Secretory cells in the adenohypophysis are often subdivided into chromophils (acidophils, basophils) and chromophobes based on interaction of the secretory granules with pH-dependent histochemical stains.
Acidophils are further subdivided into somatotrophs that secrete growth hormone (GH, somatotropin) and lactotrophs that secrete prolactin. Basophils include gonadotrophs that secrete both luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and thyrotrophs that secrete thyrotropic hormone (thyroid-stimulating hormone [TSH]). Chromophobes include the endocrine cells involved in the synthesis of ACTH and melanocyte-stimulating hormone (MSH), nonsecretory follicular cells, and undifferentiated stem cells.
Endocrine cells in the adenohypophysis are under the control of corresponding hypothalamic-releasing hormones. These releasing hormones are conveyed by the hypophyseal portal system to specific cells in the adenohypophysis, where they stimulate the rapid release of preformed trophic hormones.
Separate hypothalamic-releasing hormones regulate the rate of secretion of each trophic hormone from the adenohypophysis. For most pituitary trophic hormones, negative feedback control is accomplished by a feedback loop involving the blood concentration of the hormone produced by the target endocrine gland (eg, thyroid gland, adrenal cortex, ovary, and testis). Hormones such as prolactin, GH, and MSH have more complex feedback mechanisms. For example, prolactin affects primarily the mammary gland, and GH has its principal effect on the liver—both nonendocrine tissues. The negative feedback in such cases includes metabolites and other messengers (eg, insulin-like growth factor I produced by the liver). In the case of GH, there is an inhibitory (somatostatin) as well as stimulatory (GH-releasing hormone) hypothalamic regulator.

Coccidiosis in Chickens

2007-08-02T20:35:00.000-07:00

Coccidiosis is caused by protozoa of the phylum Apicomplexa, family Eimeriidae. In poultry, most species belong to the genus Eimeria and infect various sites in the intestine. The infectious process is rapid (4-7 days) and is characterized by parasite replication in host cells with extensive damage to the intestinal mucosa. Poultry coccidia are strictly host-specific, and the different species parasitize specific parts of the intestine. Coccidia are distributed worldwide in poultry and wild birds.
Etiology:
Coccidia are almost universally present in poultry-raising operations, but clinical disease occurs only after ingestion of relatively large numbers of sporulated oocysts by susceptible birds. Both clinically infected and recovered birds shed oocysts in their droppings, which contaminate feed, dust, water, litter, and soil. Oocysts may be transmitted by mechanical carriers (eg, equipment, clothing, insects, and other animals). Fresh oocysts are not infective until they sporulate; under optimal conditions (70-90°F [21-32°C] with adequate moisture and oxygen), this requires 1-2 days. The prepatent period is 4-7 days. Sporulated oocysts may survive for long periods, depending on environmental factors. Oocysts are resistant to some disinfectants commonly used around livestock but are killed by freezing or high environmental temperatures.
Pathogenicity is influenced by host genetics, nutritional factors, concurrent diseases, and species of the coccidium. Eimeria necatrix and E tenella are the most pathogenic in chickens because schizogony occurs in the lamina propria and crypts of Lieberkühn of the small intestine and ceca, respectively, and causes extensive hemorrhage. Most species develop in epithelial cells lining the villi. Protective immunity usually develops in response to moderate and continuing infection. True age-immunity does not occur, but older birds are usually more resistant than young birds because of earlier exposure to infection.
Clinical Findings:
Signs range from decreased growth rate to a high percentage of visibly sick birds, severe diarrhea, and high mortality. Feed and water consumption are depressed. Weight loss, development of culls, decreased egg production, and increased mortality may accompany outbreaks. Mild infections of intestinal species, which would otherwise be classed as subclinical, may cause depigmentation. Survivors of severe infections recover in 10-14 days but may never recover lost performance.

Behavioral Problems Associated with Canine Aggression

2007-07-18T10:08:00.001-07:00

An attempt has been made to specify definitional criteria for behavioral diagnoses. The advantage to these is that they do not rely on nonspecific signs, so conditions that share signs are not confused, and conditions that show an atypical form are not ruled out because a nonspecific sign appears discordant. Clusters of nonspecific signs within a diagnosis or those shared in comorbid diagnoses may help to identify treatment and pathological groups. While this system is frequently used, it is not universal. It may be helpful to view these diagnostic categories as guidelines that will continue to be redefined, given that behavioral medicine is a quickly growing and evolving field. Some of these problems, in feline-specific form, also occur in cats; these include fear aggression, idiopathic aggression, interanimal aggression, pain aggression, play aggression, predatory aggression, redirected aggression, and territorial aggression.
Dominance/impulse control aggression has the following necessary condition: abnormal, inappropriate, out-of-context aggression (threat, challenge, or attack) consistently exhibited by dogs toward people under any circumstance involving passive or active control of the dog’s behavior or the dog’s access to the behavior. The following condition is sufficient (eg, if it is met there is little doubt that the diagnosis is valid): intensification of any aggressive response from the dog upon any passive or active correction or interruption of the dog’s behavior or the dog’s access to the behavior. The key is assessment of the dog’s need to control for the sake of maintaining control. The behaviors exhibited by dogs with this diagnosis are actually a rule structure that allows the dogs to learn how to act in situations that are potentially unclear, uncertain, and anxiety-provoking to them.

This definition of dominance/impulse control aggression is discrete and does not couple the challenge to food (food-related aggression), toys (possessive aggression), or space (territorial aggression). These aggressions can all be correlates of dominance/impulse control aggression and, when associated with it, may be indicative of a more severe situation. Control and access are key—most of the problems with diagnoses arise from human misunderstanding of canine social systems, canine signaling, and canine anxieties associated with endogenous uncertainty about contextually appropriate responses. Diagnosis cannot be made on the basis of a single event. The behavior, once it begins, will become more visible and consistent, but data on early signs, patterns of change with experience, and changes in intensity are lacking.

The necessary and sufficient conditions are different from the common descriptions of dominance/impulse control aggression that specify that the dog will often react to being pushed on, to being corrected with a leash, or to being pushed from a sofa by a person. The number of situations in which the dog reacts inappropriately, or the intensity with which he or she reacts, do not affect the necessary and sufficient conditions, although these factors may affect the ability to treat the condition, the prognosis, and the risk to people. These dogs are not fearful, and they exhibit none of the behavioral or physiologic signs associated with fear. All canine aggressions are likely based to some degree in anxiety, and the uncertainty associated with anxiety is not equivalent to fear.
Fear aggression has the following necessary condition: aggression that consistently occurs concomitant with behavioral and physiologic signs of fear as identified by withdrawal, passive, and avoidance behaviors associated with the sympathetic nervous system. The following condition is sufficient: as above and the aggression is accompanied by urination or defecation, or when the aggression is only active (beyond just posturing) when the target of the aggression is not interacting with the subject.

The actual behaviors associated with fear, fear aggression, and any other aggression that is primarily driven by anxiety are poorly qualified and quantified. However, in contrast to dominance/impulse control aggression, the dog relinquishes control and withdraws. Only when the dog can no longer avoid or withdraw does frank aggression occur. Also, unlike dominance/impulse control aggression, these dogs never deliberately provoke a situation or initially and voluntarily contribute to its escalation.

In extreme cases, the sufficient conditions are clear; in less clear situations, which could be due to uncertainty on the animal’s part, caution is urged in ruling out all other aggressions. The most likely diagnosis is the one that is most consistent with all signs and criteria. Fear aggression does not have to occur consistently, although identification of the fearful stimuli will permit assessment of the extent to which the behaviors are consistent and pose a predictable risk. Fear aggression is also seen in cats, in which it is one of the most common types of aggression, both toward other cats and people. (The Merck)

Face flies, Musca autumnalis

2007-07-13T11:50:00.000-07:00

Face flies, Musca autumnalis , are so named because they gather around the eyes and muzzles of livestock, particularly cattle. They may also be found on the withers, neck, brisket, and sides. Their mouthparts are adapted for sponging up saliva, tears, and mucus. Face flies are usually not considered blood feeders because their mouthparts are not piercing or bayonet-like. However, they follow blood-feeding flies, disturb them during the feeding process, and then lap up the blood and body fluids that accumulate on the host’s skin. Face flies are found on animals that are outdoors and usually do not follow animals into barns.
Face flies are found on rangeland cattle throughout southern Canada and most of the USA. The mouthparts consist of sponging labellae, and there are 4 longitudinal stripes on the abdomen. Although similar in appearance to the common house fly, face flies can be differentiated by the closeness and angles of the interior margins of the eyes and by the distinctive coloration of the face and abdomen. Speciation requires the skills of a trained entomologist.

Cattle are the principal host of the face fly in the USA, but face flies will also feed on horses and probably sheep and goats. The face fly is a pest of range cattle; it does not develop in feedlot situations and thus is not a parasite of confined cattle. The eggs are laid in fresh cattle feces in rangeland situations and hatch in ~1 day. The yellowish larvae develop in 2-4 days and, when mature, leave the manure to pupate in the surrounding soil. The complete life cycle from egg to adult requires 12-20 days, depending on climatic conditions. The diapausing adult overwinters within buildings and other protective places.

Pathology:

Face flies annoy the host and ultimately interfere with the host’s productivity. Females feed on facial secretions, such as tear fluid, nasal mucus, and saliva, to obtain protein for egg development. The irritation around the host’s eyes stimulates the flow of tears, which attracts even more flies.

Face flies also feed on other fluid sources, such as blood from wounds and milk on calves’ faces. Because face flies have small, rough spines (prestomal teeth) on their sponging mouthparts, only a few flies can cause irritation and mechanical damage to the eye tissue of the host. The feeding activity of face flies enhances transmission of Moraxella bovis

Diagnosis:

Adult face flies are morphologically similar to house flies. These 2 species can be differentiated only by minor differences in eye position and color of the abdomen. Speciation requires the skills of a trained entomologist. In general, if a medium-sized fly is found feeding around the eyes and nostrils of a cow or horse, it is most probably a face fly.

Treatment and Control:

Control of face flies is difficult. Much effort has been made using various insecticides and application techniques, such as dust bags, mist sprays, and wipe-on formulations. Also, insecticides and insect growth regulators are used as feed additives. However, results are usually less than satisfactory. The introduction of insecticide-impregnated ear tags has provided somewhat better control, but generally, seasonal face fly reduction of only 70-80% has been achieved, even with 2 tags (1 in each ear) per animal. (The Merck)

Reproductive System Introduction

2007-07-10T09:56:00.000-07:00

All functions of the reproductive system must be considered when resolving reproductive problems. The differences in the reproductive system between the sexes and among species are complex. In both sexes, there are primary sex organs and primary regulatory centers. Gonads and function-adapted, tubular, genital organs constitute primary sex organs in both sexes. The pituitary gland and the hypothalamus are the primary regulatory centers; thus, the regulatory function is, in part, neuroendocrine in nature. In pregnant females, the fetoplacental unit has a significant role in maintaining and terminating pregnancy. The temporal and physiologic features of the reproductive cycle vary greatly among species.
Both sexes have a pair of gonads (ovaries or testes), the main functions of which are gametogenesis and steroidogenesis. Both functions are regulated primarily by gonadotropins released by the anterior pituitary gland under the influence of the hypothalamus. The latter is mediated by a peptide, gonadotropin-releasing hormone (GnRH); the secretion and release of GnRH are governed by CNS stimuli and, through a feedback mechanism, by hormones produced by other endocrine organs such as the gonads, pituitary, thyroid, and adrenal glands.
The Ovaries: The size and location of the ovaries vary with the species. The ovaries can be directly examined by rectal palpation only in cows and mares. Once puberty is reached and an animal starts cycling, the size and form of the ovaries are altered by cyclic functional structures, namely corpora lutea (CL) and follicles. Follicle-stimulating hormone (FSH) is responsible for development of follicle(s) and synthesis of estrogens by the theca cells. Once a certain estrogen level is attained, luteinizing hormone (LH) is released from the anterior pituitary gland in spontaneously ovulating species. This LH peak triggers ovulation, which is followed by development of a new CL. The increase of luteal cells parallels an increase in progesterone output. In nonpregnant polyestrous and seasonally polyestrous females, the functional and morphologic life of the CL is terminated by endogenous prostaglandin (PG) F₂ _α from the uterus. As the CL regresses, a new ovulatory follicle(s) develops, which completes the estrous cycle. The hormonal changes during the estrous cycle can be monitored by radioimmunoassay and ELISA of hormones in blood, milk, or other body fluids. Estrual cycling is continuous after puberty unless interrupted by pregnancy and, in some species, by season or lactation during the immediate postpartum period. Cycling is also blocked by pathologic conditions of the ovaries (eg, nutritional and stress atrophy, ovarian cysts) and by uterine disease (eg, pyometra, severe endometritis), which may result in persistent CL. Estrogens and progesterone act locally, affecting target organs such as the tubular genital tract, and distally, regulating gonadotropin release by a feedback mechanism on both the hypothalamus and anterior pituitary. In addition, they are responsible for sex characteristics, behavior, and lactation. (The Merck)

Mastitis in Cattle

2007-07-10T09:48:00.001-07:00

Mastitis—inflammation of the mammary gland—is almost always due to the effects of infection by bacterial or mycotic pathogens. Pathologic changes to milk-secreting epithelial cells from the inflammatory process often bring about a decrease in functional capacity. Depending on the pathogen, functional losses may continue into further lactations, which impairs productivity and potential weight gain for offspring. Although most infections result in relatively mild clinical or subclinical local inflammation, more severe cases can lead to agalactia or even profound systemic involvement resulting in death. Mastitis has been reported in almost all domestic mammals, as well as humans, and has a worldwide geographic distribution. Climatic conditions, seasonal variation, density and housing of livestock populations, and husbandry practices may affect the incidence and etiology. However, it is of greatest frequency and economic importance in species that primarily function as producers of milk for dairy products, particularly dairy cattle.
Almost any bacterial or mycotic organism that can opportunistically invade tissue and cause infection can cause mastitis. However, most infections are caused by various species of streptococci, staphylococci, and gram-negative rods, especially lactose-fermenting organisms of enteric origin, commonly termed coliforms. From an epidemiologic standpoint, the source of infection may be regarded as contagious or environmental. Except for Mycoplasma spp , which may spread from cow to cow through aerosol transmission and invade the udder subsequent to bacteremia, contagious pathogens are spread during milking by milkers’ hands or the liners of the milking unit. Species that utilize this mode of transmission include Staphylococcus aureus , Streptococcus agalactiae , and Corynebacterium bovis . Most other species are opportunistic invaders from the cow’s environment, although some other streptococci and staphylococci may also have a contagious component. The bedding used for housing cattle is the primary source of environmental pathogens, but contaminated teat dips, intramammary infusions, water hoses used for udder preparation during milking, water ponds or mud holes, skin lesions, teat trauma, and flies have all been incriminated as sources of infection.

Intramammary infections are often described as subclinical or clinical mastitis. Subclinical mastitis is the presence of an infection without apparent signs of local inflammation or systemic involvement. Although transient episodes of abnormal milk or udder inflammation may appear, these infections are for the most part asymptomatic and, if the infection persists for at least 2 mo, are termed chronic. Once established, many of these infections persist for entire lactations or the life of the cow. Detection is best done by examination of milk for somatic cell counts (predominantly neutrophils) using either the California Mastitis Test or automated methods provided by dairy herd improvement organizations. Somatic cell counts are positively correlated with the presence of infection. Although variable (especially if determined on a single analysis), cows with a somatic cell count of ≥ 280,000 cells/mL (≥ a linear score of 5) have a >80% chance of being infected. Likewise, the higher the somatic cell count in a herd bulk tank, the higher the prevalence of infection in the herd. Causative agents must be identified by bacterial culture of milk.

Clinical mastitis is an inflammatory response to infection causing visibly abnormal milk (eg, color, fibrin clots). As the extent of the inflammation increases, changes in the udder (swelling, heat, pain, redness) may also be apparent. Clinical cases that include local signs only are referred to as mild or moderate. If the inflammatory response includes systemic involvement (fever, anorexia, shock), the case is termed severe. If the onset is very rapid, as often occurs with severe clinical cases, it is termed an acute case of severe mastitis. More severely affected cows tend to have more serous secretions in the affected quarter. Although any number of quarters can be infected simultaneously in subclinical mastitis, typically only one quarter at a time will display clinical mastitis. However, it is not uncommon for clinical episodes caused by Mycoplasma to affect multiple quarters. Gangrenous mastitis can also occur, particularly when subclinical, chronic infections of S aureus become severe at times of immunosuppression (eg, at parturition). As with subclinical mastitis, culture of milk samples collected from affected quarters is the only reliable method to determine the etiology of clinical cases. (The Merck)

Tumors of the Ear Canal in Dogs and Cats

2007-07-10T09:40:00.000-07:00

Ear canal tumors may develop from any of the structures lining or supporting the ear canal, including the squamous epithelium, the ceruminous or sebaceous glands, or the mesenchymal tissues. Tumors arising from the external ear canal and pinna are more common than tumors originating from the middle or inner ear. Ear canal tumors are more common in cats than in dogs. These tumors are relatively uncommon compared with cutaneous tumors elsewhere on the body.

Although the precise cause of ear canal tumors is unknown, several theories have been postulated. Chronic inflammation of the ear canal may lead to tissue hyperplasia, followed by dysplasia, and finally neoplasia. Inspissated apocrine secretions from hyperplastic ceruminous glands during otitis externa episodes may stimulate carcinogenesis in the ear canal. Feline nasal-pharyngeal polyps may be congenital or due to viral (calicivirus) or bacterial respiratory infections.

Cocker Spaniels have an increased incidence of benign and malignant ear canal tumors when compared with other breeds. Middle-aged to older dogs and cats are predisposed to benign and malignant ear canal tumors, while young cats (3 mo-5 yr) are more likely to develop nasopharyngeal polyps. Clinical signs of ear canal tumors include usually unilateral chronic otic discharge (ceruminous, purulent, or hemorrhagic) and necrotic odor, head shaking and ear scratching, swelling or draining abscesses in the parotid region below the affected ear, deafness, and vestibular signs if there is middle or inner ear involvement, including head tilt, ataxia, nystagmus, and Horner’s syndrome. In any case of medically refractory unilateral otitis, a neoplasm of the ear canal should be suspected.

Ear canal tumors are more likely to be malignant than benign in both dogs and cats, although cats have a higher incidence of malignant tumors. The most common pinnal neoplasms in dogs are sebaceous gland tumors, histiocytomas, and mast cell tumors. In cats, common pinnal neoplasms include squamous cell carcinoma, basal cell tumors, hemangiosarcomas, and melanocytic tumors. The most common external ear canal tumors reported in dogs are ceruminous gland adenomas and ceruminous gland adenocarcinomas. Other tumors reported in the external ear canal of dogs include inflammatory polyps, papillomas, sebaceous gland adenomas, histiocytomas, plasmacytomas, melanomas, fibromas, squamous cell carcinomas, and hemangiosarcomas. The most common external ear canal masses reported in cats are nasopharyngeal polyps, squamous cell carcinomas, and ceruminous gland adenocarcinomas. Lymphoma, fibrosarcoma, and squamous cell carcinoma are rarely seen in the middle or inner ear of dogs and cats. (the Merck)

Anemia

2007-07-03T11:20:00.000-07:00

Anemia is defined as an absolute decrease in the red cell mass as measured by RBC count, hemoglobin concentration, and PCV. It can develop from loss, destruction, or lack of production of RBC. Anemia is classified as regenerative or nonregenerative. In a regenerative anemia, the bone marrow responds appropriately to the decreased red cell mass by increasing RBC production and releasing reticulocytes. In a nonregenerative anemia, the bone marrow responds inadequately to the increased need for RBC. Anemias due to hemorrhage or hemolysis are usually regenerative. Anemias that are caused by decreased erythropoietin or an abnormality in the bone marrow are nonregenerative.

Clinical Findings:

Clinical signs in anemic animals depend on the degree of anemia, the duration (acute or chronic), and the underlying cause. Acute anemia can result in shock and even death if more than a third of the blood volume is lost rapidly and not replaced. In acute blood loss, the animal usually presents with tachycardia, pale mucous membranes, bounding or weak pulses, and hypotension. The cause of the blood loss may be obvious, eg, trauma. If no evidence of external bleeding is found, a source of internal or occult blood loss must be sought, eg, a ruptured splenic tumor, coagulopathy, GI ulceration or parasites, or other neoplasia. If hemolysis is present, the patient may be icteric. Patients with chronic anemia have had time to adjust, and their clinical presentation is usually more indolent with vague signs of lethargy, weakness, and anorexia. These patients will have similar physical examination findings, pale mucous membranes, tachycardia, and possibly splenomegaly or a new heart murmur, or both.

Diagnosis:

A complete history is an important part of the work-up of an anemic animal. Questions might include duration of clinical signs, history of exposure to toxins (eg, rodenticides, heavy metals, toxic plants), drug treatments, vaccinations, travel history, and any prior illnesses.

A CBC, including a platelet and a reticulocyte count, will provide information on the severity of anemia and degree of bone marrow response, and also allow for evaluation of other cell lines. A blood smear should be evaluated for abnormalities in RBC morphology or size and for RBC parasites. The RBC indices (measures of size and hemoglobin concentration) are calculated by automated cell counters calibrated for the species in question. RBC size is expressed by the mean corpuscular volume (MCV) in femtoliters and usually reflects the degree of regeneration. Macrocytosis (an increase in the MCV) usually correlates with a regenerative anemia. Macrocytosis can be a heritable condition in poodles without anemia and may occur in anemic cats infected with feline leukemia virus. Microcytic RBC are the hallmark of iron-deficiency anemia. The hemoglobin concentration of each RBC, measured in g/dL, is defined as the mean corpuscular hemoglobin concentration. Abnormalities in RBC morphology, such as basophilic stippling, can indicate lead intoxication. Heinz body formation indicates oxidant injury to RBC, secondary to toxin exposure (see Table:Toxic Causes of Anemia). Cats are more susceptible to Heinz body formation than other species, and even cats without anemia can have a small number of Heinz bodies.
A serum chemistry panel and urinalysis evaluate organ function. If GI blood loss is suspected, an examination of the feces for occult blood and parasites can be useful. Radiographs can help identify occult disease, such as a penny (zinc toxicity) in the stomach of a puppy with hemolytic anemia. Bruising or bleeding may be signs of a coagulopathy and indicate the need for a coagulation profile. If hemolytic disease is suspected, blood can be evaluated for autoagglutination and a direct Coombs test might be indicated. A test for autoagglutination can be done by placing a drop of saline on a slide with a fresh drop of the patient’s blood; the slide should be gently rotated to mix the drops together, then evaluated grossly and microscopically for macro- and microagglutination. Serology for infectious agents like feline leukemia virus, Ehrlichia , equine infectious anemia virus, and Babesia may also be helpful in defining the cause of anemia (see Table: Infectious Causes of Anemia). Bone marrow evaluation by aspiration and/or biopsy is indicated in any animal with an unexplained, nonregenerative anemia. If the CBC reveals a decrease in more than one cell line, possibly indicating a hypoplastic marrow, a biopsy would be indicated along with an aspirate. Biopsies and aspirates are complementary: biopsies are better for evaluating the architecture and degree of cellularity of the marrow, and aspirates allow for better evaluation of cellular morphology. Aspirates also allow for an evaluation of orderly maturation of the red and white blood cell lines, the ratio of red to white blood cell precursors (M:E ratio), and the number of platelet precursors. Iron store can also be evaluated by Prussian blue staining. An M:E ratio of <1>1 the opposite is likely. The M:E ratio is always interpreted in light of a recent CBC, because changes in the ratio could also be due to suppression of one cell line compared to the other.

Food Allergy

2007-07-03T10:58:00.000-07:00

Food allergy is ~10% as common as atopy in dogs and about as common as atopy in cats. The history is that of a nonseasonal pruritus, with little variation in the intensity of pruritus from one season to another in most cases. Most reports do not suggest a breed predilection; however, one report indicated an increased relative risk in Labrador Retrievers, West Highland White Terriers, and Cocker Spaniels. Food hypersensitivities have been reported in Soft Coated Wheaten Terriers in association with protein-losing enteropathy and nephropathy. The age of onset is variable, from 2 mo to 14 yr old. One report indicated that most food allergies begin at <12>

The distribution of pruritus and lesions varies markedly between animals. Ear canal disease that manifests as pruritus and secondary infection with bacteria (usually Staphylococcus intermedius , Pseudomonas spp , Proteus spp , or Escherichia coli ) or yeast ( Malassezia pachydermatis ) are common and may be the only presenting complaint. Other patterns seen include blepharitis, generalized pruritus, generalized seborrhea, a papular eruption, or a distribution pattern that may mimic that of atopy (feet, face, and ventrum) or flea allergy dermatitis (dorsal lumbosacrum and hindlegs). The most common areas of involvement include the ears, feet, inguinal region, axillary area, proximal anterior forelegs, periorbital region, and muzzle. The degree of pruritus is usually moderate to severe. Response to glucocorticoids varies from poor to excellent.

There is no reliable diagnostic test other than a strict food elimination diet. Serologic testing and intradermal testing for food allergens have proved unreliable. The ideal food elimination diet should be balanced and nutritionally complete and not contain any ingredients that have been fed previously to the animal. Many diets contain novel protein or carbohydrate sources (eg, lamb and rice). However, it is often misunderstood that if any previously fed ingredient is present in the elimination diet, the animal may be allergic to the novel ingredient and the diet trial will be a failure. The key point in any food elimination diet trial is that only novel food ingredients can be fed.

The trial diet should be fed for up to 3 mo. If marked or complete resolution in the pruritus and clinical signs occurs during the elimination diet trial, food allergy can be suspected. To confirm that a food allergy exists and that the clinical improvement was not just coincidental, the animal must be challenged with the previously fed food ingredients and a relapse of clinical signs must occur. The return of clinical signs after challenge is usually between 1 hr and 14 days, although it is sometimes within 3 days. Once a food allergy is confirmed, the elimination diet should be reinstituted until clinical signs resolve, which usually takes <14>

The number of offending food allergens varies from 1-5 ingredients. The most frequently identified causative allergens in canine food allergy include beef, chicken, eggs, corn, wheat, soy, and milk. Once the offending allergens are identified, control of the food allergy is by strict avoidance. Concurrent diseases (such as atopy or flea allergy) may complicate the identification of underlying food allergies. Infrequently, a dog will react to new food allergens as it ages.

Clinical presentations of food allergy in cats include miliary dermatitis, feline symmetric alopecia, eosinophilic granuloma complex ( primarily the eosinophilic plaque), and severe head and neck pruritus. No breed, sex, or age predilection is seen. Age of onset varies from 3 mo to 11 yr. In one study, however, 46% of affected cats became symptomatic at ≤2 yr of age, and Siamese cats represented 30% of the cases.

Response to steroids is variable, but about two-thirds of cats show excellent response initially. Many cats develop a poor response to steroids with repeated treatments. As with canine food allergy, an elimination diet should be fed for up to 3 mo. The elimination diet should not contain any previously fed ingredients. Food elimination diets can be difficult in cats because many cats are reluctant to change diets. Cats should not be starved or forced into eating a new elimination diet due to the serious nature of hepatic lipidosis that may be induced by prolonged anorexia.

Response time to the elimination diets varies from 1-9 wk. Time until relapse of pruritus after challenge with the offending food varies from 15 min to 10 days. The most frequently identified food allergens in cats include fish, beef, and chicken. Avoidance of the offending allergens will control the clinical signs associated with the food allergy.

The Merck Vet Manual

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2007-03-31T01:52:00.000-07:00

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Chihuahua, the Longest Lived Dog Breed

2007-01-12T03:58:00.000-08:00

Dogs have been selectively bred for thousands of years, sometimes by inbreeding dogs from the same ancestral lines, sometimes by mixing dogs from very different lines. The process continues today, resulting in a tremendous variety of dog breeds. Dog breeds are group of dogs, represented by a sufficient number of individuals to be interbred without forced inbreeding to stably transfer its specific characteristics over generations.
Chihuahua is one of the longest lived breeds. There are very few health problems that exist and it is not uncommon to see Chihuahuas live to its late teens. Being aware of all breed related health problems from the day before you own your Chihuahua and you and your Chihuahuas will have a long and happy life together.
The Chihuahua is also one of the most popular toy breeds because of its saucy personality and its devotion to its owner. This breed is usually reserved with strangers and can at times become jealous, but it is generally good with other dogs and pets in the home. It should be socialized at an early age to prevent aggressiveness with other dogs and timidity with strangers.

Aspiration pneumonia

2007-01-11T16:25:00.000-08:00

Aspiration pneumonia is a pulmonary infection characterized by inflammation and necrosis caused by inhalation of foreign material. The severity of the inflammatory response depends on the material aspirated, the type of bacteria aspirated, and the distribution of aspirated material in the lungs.
Etiology:
Faulty administration of medicines is a common cause of aspiration pneumonia. Liquids administered by drench or dose syringe should not be given faster than the animal can swallow. Drenching is particularly dangerous when the animal’s tongue is drawn out, when the head is held high, or when the animal is coughing or bellowing. Administration of liquids by nasal intubation is not without risk, and careful technique is especially necessary in debilitated animals.
Inhalation of irritant gases or smoke is an infrequent cause. Aspiration of vomitus or attempts by animals to eat or drink while partially choked can result in aspiration pneumonia as well. Disturbances of deglutition, as in anesthetized or comatose animals (eg, mature cattle under general anesthesia or cows in lateral recumbency), vagal paralysis, acute pharyngitis, abscesses or tumors of the pharyngeal region, esophageal diverticula, cleft palate, megaesophagus, or encephalitis, are frequent predisposing causes.
Cats are particularly susceptible to pneumonia caused by aspiration of tasteless products such as mineral oil. In sheep, poor dipping technique may cause aspiration of fluid. Calves and lambs may inhale inflammatory debris if affected with diphtheritic laryngitis. Inhalation of milk by pail-fed calves can cause an acute necrotizing pneumonia due to the diffuse distribution of foreign material. The muscles of deglutition may be affected in lambs with nutritional myopathy. Pigs fed fine particulate food in dry environments may inhale feed granules. Aspiration pneumonia in cattle following delayed treatment for milk fever is highly fatal. In dogs with myasthenia gravis, aspiration pneumonia is the leading cause of death.

Dog Distemper

2006-12-22T10:56:00.000-08:00

Canine distemper is a paramyxovirus, which appear very similar to the paramyxovirus causing human measles. The virus in the canine can affect a wide range of organs including the skin, brain, eyes, intestinal and respiratory tracts. The virus is transmitted through the air in addition to body secretions such as urine. Dogs of any age can be affected, however, most are puppies less than 6 months of age. What are the symptoms?

Distemper virus can affect many systems of the body. The most common signs are nasal and eye discharge, coughing, diarrhea, vomiting, and seizures. Mildly affected dogs may only cough and be misdiagnosed as "kennel cough." Others may develop pneumonia. Puppies that recover may have severe enamel damage. The nose and foot pads of the young dog may become thickened, hence the nickname "hardpad disease."

What are the risks?

Distemper is serious and can spread rapidly through a kennel, especially if unvaccinated individuals are present. Not all patients will die, however, a significant number may. Dogs of every age are susceptible, however, the very young and old have the highest death rate. Death rates may be as high as 75%. It is erroneously believed by some that all older dogs have a natural immunity. Although some may have immunity, many do not. Patients that recover from distemper may suffer permanent damage to vision as well as the nervous system. Puppies which recover can have severely mottled teeth due to abnormalities of the developing enamel.

How is canine distemper treated and prevented?

There is no specific treatment for canine distemper. Therapy is largely supportive. Intravenous fluids are administered to prevent dehydration. Anti-seizure medications can be used if neurologic signs develop.

Excellent vaccines have been developed to prevent distemper. The vaccines have been widely used for many years and have made significant strides in reducing the frequency of this disease. In the past, vaccines comprised of the human measles virus were occasionally utilized as a preventive. Using measles vaccines is a seldom practiced procedure today. Excellent vaccines with minimal side effects are available to give to puppies and dogs of every age. It must be emphasized that many older dogs do not develop a life long immunity to distemper. The vaccinations should be given yearly for life.

taken from peteducation.com

Parvovirus

2006-12-22T08:52:00.000-08:00

Canine parvovirus disease is currently the most common infectious disorder of dogs in the United States.

'Parvo' is a highly contagious disease characterized by diarrhea that is often bloody and is caused by a pathogen called canine parvovirus, Type 2 (CPV-2). In 1980, the original strain of CPV-2 was replaced by CPV-2A and in 1986, another variation called CPV-2B appeared. Today, CPV-2B has largely replaced the previous strains as the most common isolate. Since all of these strains are similar, we will lump them together and refer to them as CPV-2 (parvo). There is currently some discussion that there may be other strains that are beginning to emerge and have yet to be formally identified. Current vaccinations have helped to control the spread of this disease but despite being vaccinated, some dogs still contract and die from parvo. There is much that we do not know about the virus or the best way to control the disease, but we are learning new information daily. Misinformation about the disease, its spread, and vaccination is widespread in both breeding and veterinary circles. We hope that with a better understanding of the disease, pet owners will be able to make good husbandry decisions that will help prevent and reduce the spread of this disease.

How is parvo spread?

CPV-2 is known to survive on inanimate objects - such as clothing, food pans, and cage floors - for 5 months and longer in the right conditions. Insects and rodents may also serve as vectors playing an important role in the transmission of the disease. All parvoviruses are extremely stable and are resistant to adverse environmental influences such as low pH and high heat. Exposure to ultraviolet light and sodium hypochlorite (a 1:32 dilution of household bleach - ½ cup bleach to 1 gallon of water) can inactivate parvovirus. The bleach solution can be impaired by organic matter and needs to have adequate exposure time and proper concentrations to work effectively. The normal incubation period (time from exposure to the virus to the time when signs of disease appear) is from 7-14 days. Active excretion of the virus in the feces can begin the third day after exposure, often before clinical signs appear, and may last for one to two weeks after the onset of the disease.

Symptoms

There is a broad range in the severity of symptoms shown by dogs that are infected with parvovirus. Many adult dogs exposed to the virus show very few if any symptoms. The majority of cases are seen in dogs less than 6 months of age, with the most severe cases seen in puppies younger than 12 weeks of age. There are also significant differences in response to CPV-2 infections and vaccines among different breeds of dogs, with Rottweilers, Doberman Pinschers, and Labrador Retrievers being more susceptible than other breeds.

Diagnosis

Not all cases of bloody diarrhea with or without vomiting are caused by Parvovirus and many sick puppies are misdiagnosed as having 'Parvo.' The only way to know if a dog has Parvovirus is through a positive diagnostic test. In addition to the more time consuming and expensive traditional testing of the blood for titers, a newer and simpler test of the fecal matter with an enzyme-linked immunosorbent assay antigen test (ELISA) are also available through most veterinary clinics. Testing of all suspect cases of Parvo is the only way to correctly diagnose and treat this disease.

Treatment

The treatment of Parvovirus is fairly straightforward and directed at supportive therapy. Replacing fluids lost through vomiting and diarrhea is probably the single most important treatment. Intravenous administration of a balanced electrolyte solution is preferred, but in less severe cases, subcutaneus or oral fluids may be used. Antibiotic therapy is usually given to help control secondary bacterial infections. In cases of severe vomiting, drugs to slow the vomiting may also be used. After the intestinal symptoms begin to subside, a broad spectrum de-worming agent is often used. Restricting the food during periods of vomiting is also necessary. Undertaking the treatment of affected dogs and puppies without professional veterinary care is very difficult. Even with the best available care, the mortality of severely infected animals is high. Without the correct amount of properly balanced intravenous fluids, the chance of recovery in a severely stricken animal is very small.

taken from peteducation.com

Campylobacteriosis

2006-12-21T07:57:00.000-08:00

Gastrointestinal campylobacteriosis, caused by Campylobacter jejuni or C coli , is associated with diarrhea in various animal hosts, including dogs, cats, calves, sheep, ferrets, mink, several species of laboratory animals, zoo animals, and humans. In humans, it is a leading cause of diarrhea. C jejuni and C coli are also recovered from feces of asymptomatic carriers. (See also bovine genital campylobacteriosis, Bovine Genital Campylobacteriosis: Introduction). Animals, including dogs and cats (especially those recently purchased from shelters), and wild animals maintained in captivity can serve as sources of human infection. The agents also are isolated frequently from the feces of chickens, turkeys, pigs, and other species. The organism commonly contaminates poultry meat, which serves as one of the major vehicles of spread of C jejuni to humans.

The disease is found worldwide; its prevalence appears to be increasing as proper culture techniques for C jejuni and C coli are refined and updated. Clinical manifestations may be more severe in younger animals. In studies using monoclonal and polyclonal antibodies, Campylobacter spp (including C jejuni ) have been associated with proliferative ileitis in hamsters and proliferative colitis in ferrets. A cause and effect relationship has not been proved experimentally, however. Proliferative bowel disease in these animals is now known to be caused by Lawsonia intracellularis .

Etiology:

Campylobacter is a gram-negative, microaerophilic, slender, curved, motile bacterium with a polar flagellum. C jejuni is routinely associated with diarrheal disease; however, C coli , distinguished from C jejuni on the basis of hippurate hydrolysis, is occasionally isolated from diarrheic animals and is routinely recovered from asymptomatic pigs. Other intestinal, catalase-negative campylobacters, C upsaliensis and C helveticus , have been isolated from diarrheic dogs and cats as well as asymptomatic dogs and cats. Campylobacter was once associated with swine dysentery ( Swine Dysentery), but this is now recognized as being caused by Treponema hyodysenteriae . Most believe that Campylobacter spp do not produce porcine proliferative enteritis ( Porcine Proliferative Enteritis), even though a new organism, C hyoilei , isolated from swine in Australia, has been associated with porcine proliferative enteritis. Its role in this disease, however, is not clearly established. C mucosalis and C hyointestinalis have also been isolated from swine but are not considered enteric pathogens.

Because of slow growth and microaerobic requirements, standard culture methods require selective media that incorporate various antibiotics to suppress competing fecal microflora. C jejuni and C coli grow well at 42°C in an atmosphere of 5-10% carbon dioxide and an equal amount of oxygen. Cultures are incubated 48-72 hr; colonies are round, raised, translucent, and sometimes mucoid. The organism can be identified by a series of biochemical tests readily available in any diagnostic laboratory. Recently, PCR assays have been used to identify Campylobacter spp . Identification is important to distinguish campylobacters from the growing number of novel enterohepatic helicobacters being isolated from a variety of animals.

Transmission and Epidemiology:

As with most intestinal pathogens, fecal-oral spread and food- or waterborne transmission appear to be the principal avenues of infection. One suspected source of infection for pets, as well as mink and ferrets raised for commercial purposes, is ingestion of undercooked poultry and other raw meat products. Asymptomatic carriers can shed the organism in their feces for prolonged periods and contaminate food, water, milk, and fresh processed meats (including pork, beef, and poultry products). The organism can survive in vitro at 41°F (5°C) for 2 mo and can survive in feces, milk, water, and urine. Wild birds also may be important sources of water contamination. Unpasteurized milk has been cited as a principal source of infection in several human outbreaks. Strain identification to study the epizootiology of C jejuni and C coli , in addition to Penner serotyping, is now done using molecular techniques such as restriction fragment length polymorphism and ribotyping.

The diarrhea appears to be most severe in young animals. Typical signs in dogs include mucus-laden, watery, and/or bile-streaked diarrhea (with or without blood) that lasts 3-7 days; reduced appetite; and occasional vomiting. Fever and leukocytosis may also be present. In certain cases, intermittent diarrhea may persist >2 wk; in some, it may be present for months. Gnotobiotic puppies inoculated with C jejuni developed malaise, loose feces, and tenesmus within 3 days of inoculation.

In calves, signs vary from mild to moderate. The diarrhea is thick and mucoid with occasionally visible blood flecks; body temperature may be normal. Diarrhea with mucus and blood also has been observed in primates, ferrets, mink, and cats. Organisms with ultrastructure similar to that of Campylobacter spp have been seen in hyperplastic ileal epithelial mucosa of hamsters with proliferative ileitis; C jejuni has been isolated from these lesions but has failed to reproduce the syndrome. Organisms with Campylobacter -like morphology also have been associated with proliferative colitis in ferrets and with hyperplastic intestinal lesions in guinea pigs and rats. Campylobacter -like organisms have been described in young rabbits with acute typhlitis. It is now known that these organisms are Lawsonia intracellularis , an organism closely related to Desulfovibrio spp .

Lesions:

In 3-day-old chickens infected with C jejuni , the organisms were detected within epithelial cells and mononuclear cells of the lamina propria; the jejunum and ileum were the most severely affected. Congested and edematous colons were found in dogs 43 hr after inoculation; microscopically, epithelial height, brush border, and numbers of goblet cells in the colon and cecum were all reduced. Hyperplastic epithelial glands resulted in a thickened mucosa. Histologic changes in calves primarily involve the jejunum but also can involve the ileum and colon. The lesions vary from mild changes to severe hemorrhagic enteritis. The mesenteric lymph nodes are edematous. Experimentally, some strains of C jejuni produce a hepatitis in mice, and the organism has been isolated from inflamed livers of dogs. A cytotoxin, referred to as cytolethal distending toxin, has been identified in C jejuni ; however, its role in production of intestinal disease is not known. In vitro, the cytotoxin causes distention of cell lines and cell cycle arrest in the G2M1 phase of the cell cycle.

Diagnosis:

The standard method for diagnosis is microaerobic culture of feces at 42°C; a special medium is commercially available. Diagnosis is also possible by using darkfield or phase-contrast microscopy, by which fresh fecal samples are examined for the characteristic darting motility of C jejuni . This method is especially useful during the acute stage of diarrhea when large numbers of organisms are more likely to be shed in the feces. Various techniques can detect serum antibodies to various antigens of Campylobacter spp . Heat-stable or heat-labile antigen schemes are used routinely to serotype various strains. Serial serum samples to demonstrate rising antibody titers are helpful in diagnosis. Intestinal viruses and other intestinal bacterial pathogens must be ruled out as primary or copathogens in animals with Campylobacter -associated diarrhea.

Treatment and Control:

Isolation of C jejuni or C coli from diarrheic feces is not, in itself, an indication for antibiotic therapy. Because C jejuni and C coli are not routinely cited as potential intestinal pathogens in animals (except for diarrhea in young cats and dogs and in several species of primates), efficacy of antibiotic therapy has been reported infrequently. In certain cases in which animals are severely affected or are a zoonotic threat, antibiotic treatment may be indicated. In general, C jejuni and C coli isolates from animals are similar to isolates obtained from human populations. Erythromycin, the drug of choice for Campylobacter diarrhea in humans, is also effective in other animals, although erythromycin-resistant strains of Campylobacter spp have been recovered from swine. Gentamicin, furazolidone, and doxycycline also can be used. Ampicillin is relatively inactive against most strains of Campylobacter , and most strains are also resistant to penicillin. Tetracycline and kanamycin resistance in certain C jejuni strains is reported to be plasmid-mediated and transmissible within C jejuni serotypes. Efficacy of sulfadimethoxine and sulfa combinations is variable. Before therapy is instituted, isolation and sensitivity tests should be done. Some animals continue to shed the organism despite antibiotic therapy. Quinolone antibiotics may be useful in eliminating C jejuni and C coli in asymptomatic carriers, but drug resistance may develop.

taken from themerckvetmanual

Aspergillosis in Chicken

2006-12-21T07:27:00.000-08:00

Aspergillosis is a disease, usually of the respiratory system, of chickens, turkeys, and less frequently ducklings, pigeons, canaries, geese, and many other wild and pet birds. In chickens and turkeys, the disease may be endemic on some farms; in wild birds, it appears to be sporadic, frequently affecting only an individual bird. It is usually seen in birds 7-40 days old. (See also aspergillosis in mammals, Aspergillosis, and caged birds, Caged Birds: Introduction.)

Etiology and Epidemiology:

Aspergillus fumigatus is a common cause of the disease. However, several other Aspergillus spp may be incriminated.

Chicks and poults may become infected during hatching as a result of inhaling large numbers of spores in heavily contaminated hatching machines or from contaminated litter. In older birds, infection is caused primarily by inhalation of spore-laden dust from contaminated litter or feed or dusty range areas.

Dyspnea, hyperpnea, somnolence, and other signs of nervous system involvement, inappetence, emaciation, and increased thirst may be seen. The encephalitic form is most common in turkeys. In chicks or poults up to 6 wk, the lungs are most frequently involved. Pulmonary lesions are characterized by cream-colored plaques a few mm to several cm in diameter; occasionally, mycelial masses may be seen within the air passages on gross examination. The plaques also may be found in the syrinx, air sacs, liver, intestines, and occasionally the brain. An ocular form, in which large plaques may be expressed from the medial canthus, has been seen in chickens and turkeys.

Diagnosis:

The fungus can be demonstrated by culture or by microscopic examination of fresh preparations. One of the plaques is teased apart and placed on a suitable medium, usually resulting in a pure culture of the organism. Histopathologic examination using a special fungus stain reveals granulomas containing mycelia. Pathogenicity of the isolate is confirmed by injecting it into the air sacs of susceptible 3-wk-old chicks.

Differential diagnoses include infectious bronchitis, Newcastle disease, infectious laryngotracheitis, Dactylaria infection, and nutritional encephalomalacia.

Treatment and Control:

Treatment of affected birds is considered useless. Strict adherence to sanitation procedures in the hatchery minimizes early outbreaks. Grossly contaminated eggs should not be set for incubation because they may explode and disseminate spores throughout the hatching machine. Contaminated hatchers should be fumigated with formaldehyde or thiabendazole (120-360 g/m3). Avoiding moldy litter or ranges serves to prevent outbreaks in older birds. Pens should be sprayed with nystatin, and all equipment cleaned and disinfected.

taken from themerckvetmanual

Hepatitis in Dogs

2006-12-15T17:40:00.000-08:00

As with most liver diseases, the symptoms of hepatitis in dogs are nearly always aspecific: the dogs eat less, are apathetic, sometimes have polyuria/polydipsia, and sometimes have diarrhoea. Hepatoencephalopathy and ascites only occur with these symptoms in very advanced stages of chronic hepatitis. Only a part of the dogs have jaundice. Because of these aspecific symptoms, the diagnosis hepatitis is often not taken into consideration, even though the presence of a liver disease can be easily detected by measuring plasma concentrations of alkaline phosphatase and bile acids, one or both of which are elevated. The diagnosis is confirmed by histological examination of a liver biopsy sample. The most common forms of hepatitis are non-specific reactive hepatitis, acute hepatitis, and chronic hepatitis. Non-specific reactive hepatitis is a reaction against endotoxin as a result of sepsis or an increased gastrointestinal absorption. Treatment is directed to the primary process. Leptospirosis also causes non-specific reactive hepatitis, but then renal insufficiency is the most prominent feature. The diagnosis is made not on the basis of a liver biopsy but on the basis of increased IgM titres against Leptospira. Immediate treatment with antibiotics and infusions at the first signs (jaundice and uraemia) can save the animal's life. Acute hepatitis can develop as a result of infection, toxins, or liver hypoxia. There is no specific treatment, but adequate recovery often occurs with supportive treatment. Corticosteroids are contraindicated. Chronic hepatitis, which can lead to cirrhosis, is the most common form of hepatitis. It is an autoimmune inflammatory reaction that is usually caused by a virus infection but sometimes by poisoning (intoxication). Long treatment with prednisolone or azathioprine is usually successful, but early recognition of the disease increases the likelihood of success. Nowadays, chronic hepatitis due to hepatic copper accumulation in Beddlington terriers can be detected by DNA tests. Such tests make it possible to distinguish between carriers and non-carriers. Affected animals can be kept symptom-free by life-long treatment with zinc gluconate or penicillamine.

taken from pubmed

Chlamydiosis

2006-12-15T01:12:00.000-08:00

Chlamydiosis, a disease caused by the intracellular bacterium Chlamydia psittaci, is commonly seem in wild and pet birds. The infectious particles of Chlamydia psittaci, called elementary bodies, are shed in feather dust,feces, and lacrimal and nasal secretions. Elementary bodies are approximately 0.3 um in size and survive for long periods outside the body. If aerosolized elementary bodies are inhaled or ingested, they will attach to and penetrate host cells. Once inside the cell, elementary bodies transform into non-infectious reticulate bodies that grow and divide by binary fission. Often micro-colonies will form and can be seen microscopically as cellular inclusions, called LCL(Levinthal-Cole-Lillie) bodies.
As the reticulate bodies mature, they transform into the infectious elementary bodies which are released when the cell is lysed.Clinical signs in birds range from inapparent infections to severe disease and death. Young birds are most susceptible and often appear sick, while adult birds tend only to show clinical disease after periods of stress. Latent infections are possible with clinically normal birds shedding the organism.
The clinical signs caused by Chlamydia psittaci
The gross lesions of chlamydiosis vary and are nonspecific. Hepatomegaly, splenomegaly, and pneumonia are common findings. Fibrinous air sacculitis, serofibrinouspericarditis, and fibrinous peritonitis may be prominent. Histopathologic lesions are also nonspecific, unless the causative agent is seen. LCL bodies, which stain with Giemsa are pathognomonic if seen. Impression smears of liver, spleen, or air sac can be stained to observe LCL bodies. If LCL bodies are present, the diagnosis can be made; but, further diagnostics are necessary if LCL bodies are not observed.Two diagnostic serology tests are currently available. A Chlamydia-blocking antibody ELISA(BELISA) identifies serum antibodies to the Chlamydia organism. The antibodies deleted by this method are independent of the bird's shedding status; however, the assay only detects the patient's exposure to the organism, not necessarily a current infection. False negative test results are frequent in acute infections. An antigen ELISA test for Chlamydia trachomatis of humans is used to detect Chlamydia psittaci in birds. Cloacalswabs can be analyzed by this test. False negatives are possible in samples that contain low numbers of elementary bodies and in samples from birds with latent infections or irregular shedding. False positives are possible if high numbers of cross-reacting bacteria, such as Staphylococcusaureus. depend on the age, condition, and species of the bird combined with the dose, strain, and virulence of the bacteria. Respiratory and/or gastrointestinal signs are common along with ocular and nasal discharge, conjunctivitis, sinusitis, dyspnea, greenish diarrhea, and emaciation. Occasionally neurological signs are seen: tremors, seizures, torticollis, and/or opisthotonus. Hepatosplenomegaly may be observed on radiographs. Clinical pathology data may reveal a leukocytosis and elevated liver enzymes.

taken from addl.perdue.edu

Toxoplasmosis

2006-12-15T00:25:00.000-08:00

A single-celled parasite called Toxoplasma gondii causes a disease known as toxoplasmosis. While the parasite is found throughout the world, more than 60 million people in the United States may be infected with the Toxoplasma parasite. Of those who are infected, very few have symptoms because a healthy person's immune system usually keeps the parasite from causing illness. However, pregnant women and individuals who have compromised immune systems should be cautious; for them, a Toxoplasma infection could cause serious health problems.

A Toxoplasma infection occurs by:

Accidentally swallowing cat feces from a Toxoplasma-infected cat that is shedding the organism in its feces. This might happen if you were to accidentally touch your hands to your mouth after gardening, cleaning a cat's litter box, or touching anything that has come into contact with cat feces. Eating contaminated raw or partly cooked meat, especially pork, lamb, or venison; by touching your hands to your mouth after handling undercooked meat.
Contaminating food with knives, utensils, cutting boards and other foods that have had contact with raw meat.
Drinking water contaminated with Toxoplasma.
Receiving an infected organ transplant or blood transfusion, though this is rare.

Symptoms of the infection vary.

Most people who become infected with Toxoplasma are not aware of it.

Some people who have toxoplasmosis may feel as if they have the "flu" with swollen lymph glands or muscle aches and pains that last for a month or more.

Severe toxoplasmosis, causing damage to the brain, eyes, or other organs, can develop from an acute Toxoplasma infection or one that had occurred earlier in life and is now reactivated. Severe cases are more likely in individuals who have weak immune systems, though occasionally, even persons with healthy immune systems may experience eye damage from toxoplasmosis.

Most infants who are infected while still in the womb have no symptoms at birth, but they may develop symptoms later in life. A small percentage of infected newborns have serious eye or brain damage at birth.

People who are most likely to develop severe toxoplasmosis include:

Infants born to mothers who became infected with Toxoplasma for the first time during or just before pregnancy.

Persons with severely weakened immune systems, such as individuals with HIV/AIDS, those taking certain types of chemotherapy, and those who have recently received an organ transplant.

If you are planning to become pregnant, your health care provider may test you for Toxoplasma. If the test is positive it means you have already been infected sometime in your life. There usually is little need to worry about passing the infection to your baby. If the test is negative, take necessary precautions to avoid infection.

If you are already pregnant, you and your health care provider should discuss your risk for toxoplasmosis. Your health care provider may order a blood sample for testing.

If you have a weakened immune system, ask your doctor about having your blood tested for Toxoplasma. If your test is positive, your doctor can tell you if and when you need to take medicine to prevent the infection from reactivating. If your test is negative, it means you have never been infected and you need to take precautions to avoid infection.

Treatment

Once a diagnosis of toxoplasmosis is confirmed, you and your health care provider can discuss whether treatment is necessary. In an otherwise healthy person who is not pregnant, treatment usually is not needed. If symptoms occur, they typically go away within a few weeks to months. For pregnant women or persons who have weakened immune systems, medications are available to treat toxoplasmosis.

Prevent

There are several general sanitation and food safety steps you can take to reduce your chances of becoming infected with Toxoplasma.

Wear gloves when you garden or do anything outdoors that involves handling soil. Cats, which may pass the parasite in their feces, often use gardens and sandboxes as litter boxes. Wash your hands well with soap and water after outdoor activities, especially before you eat or prepare any food.

When preparing raw meat, wash any cutting boards, sinks, knives, and other utensils that might have touched the raw meat thoroughly with soap and hot water to avoid cross-contaminating other foods. Wash your hands well with soap and water after handling raw meat.

Cook all meat thoroughly; that is, to an internal temperature of 160° F and until it is no longer pink in the center or until the juices become colorless. Do not taste meat before it is fully cooked.

taken from cdc.gov