Canine Distemper

The disease is seen in animals like dogs, foxes, wolves, ferret, mink, skunk, raccoon, etc.

Canine distemper is caused by a paramyxovirus closely related to the viruses of measles and rinderpest. The enveloped virus is sensitive to lipid solvents and most disinfectants and is relatively unstable outside the host.

The main route of infection is via aerosol droplet secretions from infected animals. Some infected dogs may shed virus for several months. Virus initially replicates in the lymphatic tissue of the respiratory tract. A cell-associated viremia results in infection of all lymphatic tissues, which is followed by infection of respiratory, GI, and urogenital epithelium, as well as the CNS and optic nerves. Disease follows virus replication in these tissues. The degree of viremia and extent of spread of virus to various tissues is moderated by the level of specific humoral immunity in the host during the viremic period.

A transient fever usually occurs 3-6 days after infection, and there may be a leukopenia (especially lymphopenia); these signs may go unnoticed or be accompanied by anorexia. The fever subsides for several days before a second fever occurs, which lasts <1 wk. This may be accompanied by serous nasal discharge, mucopurulent ocular and anorexia. GI respiratory signs follow are usually complicated secondary bacterial infections. An acute encephalomyelitis occur in association with or following the systemic disease, absence of manifestations. Hyperkeratosis footpads (“hardpad” disease) epithelium plane seen. Neurologic frequently seen those dogs hyperkeratosis. CNS include following: 1) localized involuntary twitching a muscle group muscles, such as leg facial muscles; 2) paresis paralysis, hindlimbs ataxia, followed tetraparesis tetraparalysis; 3) convulsions characterized salivation often chewing movements jaw (“chewing-gum fits”).[>Canine Parvo virus

The origin of the canine parvovirus has not been established. The virus is very stable in the environment, able to withstand wide pH ranges and high temperatures. It is resistant to a number of common disinfectants and may survive for several months in contaminated areas.

Rottweilers, American Pit Bull Terriers, Doberman Pinschers and German Shepherds are at increased risk of disease. Toy Poodles and Cocker Spaniels appear at decreased risk for developing the disease. Mortality associated with canine parvovirus infection is variably reported to be 16-48%.

The virus is transmitted by direct contact with infected dogs. Indirect transmission, eg, from fecal-contaminated fomites, is also an important source of infection. The virus is shed in the feces of infected dogs for up to 3 wk after infection. Recovered dogs may serve as carriers and shed the virus periodically.

After ingestion, the virus replicates in lymphoid tissue of the oropharynx; from there, it spreads to the bloodstream. It attacks cells in the bone marrow, lymphopoietic tissue, and the crypt epithelium of the jejunum and ileum. Early lymphatic infection is accompanied by lymphopenia and precedes intestinal infection and GI signs. Replication in the bone marrow and lymphopoietic tissue causes neutropenia and lymphopenia, respectively. By 3 days after infection, rapidly dividing intestinal crypt cells are infected. Viral shedding in the feces begins 3-4 days after infection and peaks when clinical signs appear. Viral shedding decreases rapidly and may no longer be detected 10-14 days after initial infection. Replication of the virus in the crypt epithelium of the gut causes collapse of intestinal villi, epithelial necrosis, and hemorrhagic diarrhea. Normal enteric bacteria, eg, Clostridium perfringens and Escherichia coli enter the denuded mucosa and may gain entry to the bloodstream, resulting in bacteremia.

Are any differences between puppies and adolescent dogs in catching the infection?
When Parvo first appeared, no dogs had immunity to it. So it infects the young and the old in equal frequency. Today, it is puppies between the age of 6 weeks and 6 months that are most at risk. Puppies under 6-8 weeks of age are usually protected by their mother’s residual immunity that lingers in their bodies; so they are less likely to catch it as well.

Very often the dogs won’t show any symptoms. Stressful conditions like boarding will trigger the clinical disease and clinical signs may be exacerbated by concurrent infection with opportunistic enteric pathogens and various parasites. The dose of virus required to cause clinical disease may also be a factor. Prolonged contact with a dog shedding high levels of virus increases the likelihood of disease. The incubation period is 3-8 days. Viral shedding may begin on day 3, before the onset of clinical signs.

Initially, 2 common clinical forms of the disease were recognized-myocarditis and gastroenteritis. Myocarditis was seen in young pups, especially in the early neonatal period. However, myocarditis is rarely seen because effective immunization of bitches protects pups during the early period of life.

Gastroenteritis is most common in pups 6-20 wk old, ie, the period when maternal antibody protection falls and vaccination has not yet adequately protected the pup against infection. Most affected dogs (~85%) are <1 yr old. In dogs>6 mo old, males are more likely to develop enteritis than intact females, reflecting the tendency of male dogs to roam. Dogs with the enteric form suffer from an acute onset of lethargy, anorexia, fever, vomiting, and diarrhea. The feces are loose and may contain mucus or blood. Most dogs (80%) recover within a few days with appropriate supportive care; others can die within hours of the onset of clinical signs.

Diagnosis is based on history and clinical signs and confirmed by a positive fecal ELISA or hemagglutination test. Decreased white blood cell count (Leukopenia or lymphopenia) is seen in most infected dogs during the course of illness. Neutropenia is suggestive of the disease. Hypoalbuminemia, hyponatremia, hypokalemia, and hypochloremia may be seen. Diagnosis may also be confirmed by a 4-fold increase in serum IgG titer over 7-14 days.

There is no specific treatment to eliminate the virus. Most dogs recover with appropriate supportive care directed to restoration of fluid balance. Oral electrolyte solutions may be used in mildly dehydrated dogs without a history of vomiting. More severely affected dogs should receive IV fluid therapy to counter dehydration and maintain fluid balance. Most dogs that survive the first 2-3 days of disease recover. Persistent vomiting can be controlled with metoclopramide. More severe cases with infection a combination of either ampicillin or a first- or second-generation cephalosporin, plus an aminoglycoside or enrofloxacin, provide broad-spectrum coverage.

Food and water should be withheld until vomiting has subsided. After this, small amounts of a bland diet should be offered frequently. A small volume of warm, salted meat broth should be given concurrently.

Contaminated areas should be thoroughly cleaned and disinfected with Household bleach (1:30 dilution) or commercial products labeled for use against parvovirus are potent inactivators of the virus. The same solutions may be used as footbaths to disinfect footwear. Pups should be kept isolated from adult dogs returning from shows or field trials.

Vaccination is very important in the control of the disease. Currently available vaccines protect dogs against all strains of the virus. Vaccines containing live attenuated canine parvovirus generally induce more effective immunity and combined vaccines containing different components also works well.

Infectious canine hepatitis (ICH) is a contagious disease of dogs found worldwide, with signs that vary from a mild fever and congestion of the mucous membranes to severe depression, marked leukopenia, and prolonged bleeding time.

Along with Dogs, it also is seen in foxes, wolves, coyotes, and bears; other carnivores may become infected without developing clinical illness.

What causes ICH and how the disease occurs in dogs?

ICH is caused by canine adenovirus 1 (CAV-1), which is antigenically related only to CAV-2 (one of the causes of Infectious Tracheobronchitis of Dogs). CAV-1 is resistant to lipid solvents and survives outside the host for weeks or months, but a 1-3% solution of household bleach is an effective disinfectant. Ingestion of urine, feces, or saliva of infected dogs is the main route of infection. Recovered dogs shed virus in their urine for =6 months. Initial infection occurs in the tonsillar crypts and Peyer’s patches, followed by viremia and infection of endothelial cells in many tissues. Liver, kidneys, spleen, and lungs are the main target organs. Chronic kidney lesions and corneal clouding (“blue eye”) result from immune-complex reactions after recovery from acute or subclinical disease.

Signs vary from a slight fever to death. The mortality rate is highest in very young dogs. The incubation period is 4-9 days. The first sign is a fever of >104°F (40°C), which lasts 1-6 days and is usually biphasic. Clinical signs most commonly include lack of appetite, fever, pale gums, conjunctivitis, coughing, abdominal pain, vomiting and diarrhoea. Sometimes, the dog may later develop jaundice. In some dogs that recover, a clouding of the cornea occurs, known as ‘blue eye’ which usually resolves itself over time. Occasionally the disease is so severe as to cause sudden death before any signs have developed.

A characteristic early sign of ICH is leukopenia, or low white blood cell count, but this alone is not enough for a definitive diagnosis. Urine analysis and blood tests may be performed in an attempt to detect viral antibodies. Similarly, viral antibodies can be detected using immunofluorescent techniques. In addition, the ELISA test may be used to look for the presence of viral particles in the feces of a sick animal.

What are the treatment options for dogs with ICH?

Treatment for dogs suffering from ICH is mainly supportive and can be extremely variable depending upon the specific symptoms being exhibited by an individual animal. Blood transfusions may be necessary in severely ill dogs. In addition, 5% dextrose in isotonic saline should be given, preferably IV. A broad-spectrum antibiotic should be given. Dogs with corneal clouding should be protected against bright light.

Modified-live virus vaccines are available and are often combined with other vaccines. Vaccination against ICH is recommended at the time of canine distemper vaccinations. Attenuated CAV-1 vaccines have produced transient unilateral or bilateral opacities of the cornea, and the virus may be shed in urine. CAV-2 attenuated live virus strains, which provide cross protection against CAV-1, are preferentially used because they have very little tendency to produce corneal opacities or uveitis, and the virus is not shed in urine.
Leptospirosis

Leptospirosis is a disease that affects many kinds of animals besides dogs. It occurs throughout the World. Leptospirosis is a worldwide zoonotic disease of domestic animals and wildlife. It is caused by a spirochete bacteria classified under the Leptospira, of which there are ~17 species are important.

They are divided into strains (or serovars), based on the characteristic of their surface proteins. Eight of these are known to cause disease in dogs and cats. They are: Leptospira icterohaemorrhagiae, L. canicola, L. grippotyphosa, L. pomona, L. bratislava, L. automnalis, L. bataviae, L. hardjo, and L. grippotyphosa . The first four are the most common ones that infect dogs. Dogs are considered the reservoir host for serovar canicola. Based on studies that focused on urban populations of dogs, serovars canicola and icterohemorrhagiae were considered the most prevalent serovars infecting dogs.

Most of the infected wild animals and domestic animals that spread leptospirosis do not appear ill. In these animals, the leptospira have taken up residence in their kidneys. The type of infected reservoir animals varies from area to area. In some areas it is raccoons, in others, skunks, in some, rats. When reservoir animals void urine, they contaminate their environment with living leptospira. These carrier wildlife shed leptospira intermittently. Sometimes they shed for months and sometimes for life. Pets can become infected by sniffing this urine. More often, the leptospira are washed by rains into standing water. Then pets wading, swimming or drinking the contaminated water develop the disease.

Each species of wildlife has serovars (strains) of leptospira that live in relative harmony with it. We call these their “primary reservoirs hosts”.

Early in infection, these, leptospira are found throughout the carrier animal’s body. This includes their liver, spleen, kidneys, eyes and genital tract. As the animal produces antibodies, these spirochetes are cleared from most organs. However, within the kidneys, of carrier species (vectors), these leptospira are hidden from the animal’s antibody and continue to live in the microscopic tubes that carry urine out to the bladder (the proximal renal tubules).

All breeds of dogs will be affected irrespective of age or gender differences, although German Shepherds may be at increased risk compared with other breeds. The incubation period is 4-12 days but may be as short as 2 days. Acute renal failure occurs in 80-90% of dogs that develop clinically significant disease.

Early findings are nonspecific and include fever, depression, lethargy, anorexia, arthralgia or myalgia, and oculonasal discharge. Later the clinical signs are characterized by vomiting, dehydration, lumbar pain from renomegaly and nephritis, and tongue-tip ulceration and necrosis. Icterus and bilirubinuria, suggestive of cholestasis and/or hepatic necrosis, develop in ~20% of these cases and may be present without renal failure. A mild anemia is seen in 25-35% of cases and thrombocytopenia occurs in 10-20% of dogs.

Serological studies are the most useful and frequently used diagnostic tests for dogs. Acute and convalescent titers may be necessary to confirm a diagnosis. Other diagnostic tests, such as darkfield microscopy, fluorescent antibody, PCR, culture, and histopathology can be used. Demonstration of leptospires in tissues with silver staining or fluorescent antibody testing are done postmortem.

The most common ways people contract leptospirosis is from primary or secondary exposure to infected dog or rat urine. Because recovered pets can shed lepto in their urine for months, you need to continue to observe strict hygiene even after your pet has recovered.

Commercial vaccines for dogs are available for many serovars. There does not appear to be good cross-immunity between serovars, and vaccinated dogs may still be susceptible to infections with other serovars. Vaccination is recommended at yearly intervals but may be needed more frequently in enzootic areas.

Excellent vaccines are now available to protect dogs from canine distemper, parvo, adeno virus and Leptospira infection together. There are Single and Multicomponent Canine vaccines available.

There is multi component vaccine available for the active immunization against Canine Distemper, Canine Contagious Hepatitis, Canine Parvovirus disease, Leptospirosis.

The multi component vaccine comprises of two components:

Feeze Dried Vaccines: They contain (> 103 TCID50) live attenuated strains of following diseases
Canine Distemper, Canine Contagious Hepatitis canine adenovirus type-2 (CAV-2) virus and Canine Parvovirus

Aqueous Vaccines – They contain inactivated agents of

Canine contagious Hepatitis (canine adenovirus type-1), Leptospirosis: Leptospira canicola and Leptospira icterohaemorrhagiae (contains > 2 x 108 bacteria each).

1 ml intramuscularly or subcutaneously for the vaccine. Freeze dried vaccines may be reconstituted with either aqueous vaccines just before use.

Vaccination Regimen:

First vaccination: 6 -8 weeks of age

Second vaccination: one month from first dose

Revaccination: Two doses each after second and third dose

Adequate immunity is established approximately 10 to 15 days after last vaccination in case of seronegative dogs.