Canine distemper is caused by a single stranded RNA containing Paramyxovirus virus.

Canine distemper virus (CDV) is acquired from infective aerosol respiratory secretions.

The virus attaches to the upper respiratory epithelium. Local replication occurs in mononuclear cells and spreads to local lymph nodes and tonsils, and then to other lymphoid containing organs and epithelial tissues. Hematogenous dissemination results in infection of other epithelial organs and the CNS. Animals that mount an adequate humoral and cell-mediated response clear the virus. If immunity of the dog is inadequate, then spread of the virus to other tissues, skin, glandular tissue, epithelium of the gastrointestinal tract, and respiratory and urinary system occurs and clinical signs become evident. Shedding of virus from infected dogs may be of short or long duration, depending on the dog’s immunologic status and response.

Major clinical signs develop in young animals usually younger than 16 weeks. The most common systems affected by canine distemper include respiratory, gastrointestinal, skin and nervous systems.

Ocular and nasal discharges are present in early stages of the disease, and are usually associated with concomitant constitutional signs such as fever, lethargy, and anorexia. If the dog’s immunity is inadequate, secondary bacterial infections result in purulent ocular and nasal discharges and cough. Respiratory distress may be observed in severely infected animals.

Gastrointestinal signs such as vomiting and diarrhea may be observed because of the local replication of virus in these tissues. Enamel hypoplasia can be noted in young animals that were previously infected with canine distemper and subsequently develop neurologic signs.

Dermatologic signs such as impetiginous dermatitis in young dogs, or nasal and footpad hyperkeratosis may be noted. Pustular dermatitis is reported to be a good prognostic indicator but is not a consistent observation.

Neurologic signs in dogs are due to acute or chronic encephalitis. Manifestations include seizures, cerebellar and vestibular signs, paraparesis, tetraparesis, and myoclonus. Myoclonus and the classical “chewing gum fits” are features that are almost pathognomonic for this disease, but other CNS disease can produce similar clinical manifestations. However, if these signs are observed in a susceptible, unvaccinated young dog, it would lend more credence to canine distemper infection. Ocular manifestations associated with canine distemper infection include conjunctivitis, keratitis, optic neuritis, and keratoconjunctivitis sicca.

Leukopenia may be observed early in the disease and may persist in dogs with progressive disease and early neurologic manifestations. A mild anemia and thrombocytopenia have also been reported in the early stages of infection. Leukocytosis and neutrophilia result when secondary opportunistic infections are present.

Viral inclusions can be observed in erythrocytes, lymphocytes, and other mononuclear cells. These appear as round to oval gray/blue intracytoplasmic bodies. No major biochemical abnormalities are consistently noted.

A compatible history and clinical signs are usually supportive of a diagnosis of acute canine distemper. Lack of proper vaccination in a young animal should also increase the clinical suspicion. Chronic neurologic disease from canine distemper infection is difficult to differentiate from other causes of acquired seizures and paresis, based solely on historical and physical findings.

CSF analysis in dogs with acute encephalitis usually shows increases in protein concentration and increased mononuclear cells, predominately lymphocytes. Detection of anti-CDV antibody in the CSF is the most definitive evidence of distemper encephalitis, provided that blood contamination is minimal during collection. If blood contamination is present in CSF, serum, and CSF antibody titers for CDV and canine parvovirus can be measured and their corresponding CSF to serum ratios computed. If the ratio for CDV antibodies exceeds that of parvovirus, then a diagnosis of CDV infection is plausible (see Chapter 4). Immunocytology and immunohistochemistry can be used to detect viral antigen in tissue samples. Conjunctival, tonsillar, and respiratory samples may reveal a positive fluorescence test early in the course of disease before antibody titers increase. This technique may also be applied to tissue samples obtained at the time of biopsy or necropsy.

Serum titers can be detected by ELISA methodology. Immunoglobulin (Ig)M antibodies can be detected in both acute and chronic encephalopathies from canine distemper and is more definitive than IgG antibodies. IgG antibodies only denote that the animal has been exposed to the virus, either naturally or through vaccination.

A seminested reverse transcriptase PCR has also been used to detect viral antigen in fresh and formalin fixed tissues to aid in the detection of canine distemper.

There is no known effective antiviral therapy that moderates the disease. Supportive therapies consist of control of opportunistic infections and include, antibacterial therapy, and antiprotozoal therapy. Opportunistic infections reported include Bordetella spp., Salmonella spp., Toxoplasma gondii, and Neospora caninum.

Attention to general hygiene, fluid balance, and nutrition is also important. Cleaning of ocular and nasal discharges, application of ophthalmic preparations to prevent exposure keratitis, and a good high protein and caloric diet are all beneficial.

Vaccination is typically started at approximately 6 weeks to avoid lapse in protection in puppies with maternal antibody titers that are waning. Boosters are administered every 2 to 3 weeks until the dog is 16 weeks of age. The decline of maternal antibodies is predictable based on the maternal antibody titers by use of nomogram that shows the rate of antibody decline and the expected time for optimal vaccination. At least two vaccines should be administered to all dogs in the initial preventative program.

Several different vaccines are available that provide active immunization of animals. These include modified live, inactivated whole virus, subunit products, and recombinant vector–based vaccine. Use of heterologous vaccination with measles virus can provide temporary immunity in animals younger than 6 weeks.

Postinfection immunity from canine distemper infection is reported to last at least 7 years.

This virus is susceptible to most common disinfectants including sodium hypochlorite and the quandary ammonium compounds.

There are two different and distinct adenoviruses that infect dogs. CAV-1 causes infectious hepatitis and upper respiratory disease, whereas CAV-2 predominately results in an acute upper respiratory disease. CAV-2 is one viral agent incriminated in the canine “kennel cough” complex.

These viruses are shed in most body secretions from acutely infected dogs. Contact of susceptible dogs with contaminated fomites results in oronasal exposure. The virus replicates in tonsils and lymphoid tissues of the oral cavity and then disseminates hematogenously to other tissues and organs.

CAV-1 infections can be commonly asymptomatic infections, based on serologic surveys, or cause acute or chronic disease syndromes. These syndromes are related to organ injuries of the liver, kidneys, eyes, and respiratory tract. The predominant organ injury with CAV-1 is the liver, where it causes hepatic necrosis. Clinical signs related to hepatic injury include fever, vomiting, diarrhea, hepatic enlargement, and abdominal pain. If the dog mounts an effective immune response early in the disease, hepatic injury may be limited. In dogs with severe hepatic necrosis, disseminated intravascular coagulation (DIC) may result and cause a hemorrhagic diathesis. Partial immune responses in infected CAV-1–infected dogs can result in a chronic hepatopathy, characterized by persistent hepatic inflammation.

Renal injury also occurs in CAV-1 infection but is subclinical. The virus localizes in the glomerular vasculature and later leads to immune complex deposition and proteinuria. Virus persists in the renal tubular epithelium and a mild interstitial nephritis can develop. Clinical signs of renal involvement are not usually significant.

Ophthalmologic signs occur in some naturally infected dogs. Keratitis and uveitis develop from virus replication and antibody production within this tissue. Mild to severe corneal edema can develop. CAV-1 can eventually result in secondary glaucoma from obstruction of the ocular drainage angle from inflammatory debris. Ocular changes may be the only clinical sign noted in mild cases of CAV-1 infection. These ocular lesions are not always reversible in the dog on its recovery.

Respiratory involvement with CAV-1 and CAV-2 infections result in mild to moderate respiratory signs and produce a dry hacking cough and abnormal lung sounds. Interstitial pneumonia may be complicated with secondary bacterial infection in severely infected, susceptible dogs.

Severe CAV-1 infection can produce neurologic signs from hemorrhage and activation of the clotting system associated with vasculitis and from hepatic failure (hepatoencephalopathy).

Laboratory abnormalities depend on the severity of injury to the liver, kidneys, eye, and vascular endothelium. Hemogram changes include leukopenia and thrombocytopenia. In severe infections, DIC and associated coagulation abnormalities can be observed with increases in activated partial thromboplastin time, one-stage prothrombin time, fibrin degradation products, and d-dimer concentrations.

Hepatic enzyme elevations depend on the severity of infection and the host immune response to infection. Increases in alanine aminotransferase (ALT) and alkaline phosphatase (ALP) are usually present, with ALT concentrations being greater than ALP concentrations. Hyperbilirubinemia is not a feature of the acute hepatic syndrome because most dogs that recover do so rapidly. In animals with viral persistence causing chronic hepatic inflammation, this finding may be present along with other biochemical abnormalities associated with a chronic hepatopathy (decreased serum urea nitrogen, albumin and glucose, increased ALT, ALP, and total bilirubin).

Dogs infected with CAV-2 infections do not have any consistent laboratory abnormalities, except in cases of secondary respiratory bacterial infection in which an inflammatory leukogram may be present.

A clinical diagnosis of CAV-1 infection is difficult, but should be suspected when young, unvaccinated dogs are presented with an acute onset of gastrointestinal signs and elevated liver enzymes. Dogs presenting with this compatible history are often suspected of having toxicosis. Evidence of a hemorrhagic diathesis in dogs with the aforementioned signs and laboratory abnormalities consistent of DIC lend additional support for an acute hepatopathy with activation of the clotting pathways. CAV-1 can be isolated by viral isolation from oropharyngeal swabs, but this is not a viable diagnostic test for most clinical cases.

Histologic examination of the liver reveals an acute centrilobular to panlobular necrosis. Evidence of hemorrhage may be widespread in dogs that exhibit signs compatible with DIC. Intranuclear, acidophilic inclusion bodies can be identified in dogs that die from CAV-1 infection.

Vaccination with CAV-1 and CAV-2 modified live vaccines are highly effective in preventing disease. CAV-1 modified live virus (MLV) may result in ocular and renal lesions; therefore, a CAV-2 MLV is used to provide a heterotypic antibody response that is protective. Administration of two doses of MLV vaccine beginning at 8 to 9 weeks of age is recommended. Because of the duration of immunity with MLV, booster vaccination is not always required.

Pseudorabies, also known as Aujeszky’s disease or mad itch, is caused by an α-herpesvirus.

Infection is acquired when the dog ingests infected tissues. Whereas other mammals can be transient reservoirs of the virus, pigs are the predominant reservoirs of the disease and can have subclinical infections. Dogs can also contract pseudorabies by biting infected pigs or eating raw infected meat. Dogs are not a source of infection for other dogs. After ingestion, the virus ascends nerve fibers in the area of inoculation in a retrograde fashion, ultimately infecting the brain stem and cranial nerve nuclei.

Pseudorabies is found worldwide but is more common in areas with a high population of pigs.

Ptyalism was the most common clinical sign of pseudorabies in dogs and was reported in 100% of cases in one retrospective study. In the same report, all dogs had exposure to pigs. Restlessness, anorexia, ataxia, wandering aimlessly, tachypnea, dyspnea, vocalizing, and pruritus were associated with the disease in more than 50% of dogs with pseudorabies. Muscle spasms, vomiting, aggressiveness, trismus, dysphagia, and abnormal papillary light responses can also be seen. Death routinely occurs within a short period after the first clinical signs become apparent.

Hematologic or biochemical abnormalities are not consistently identified in dogs with pseudorabies infection.

Clinical signs and a history of exposure to pigs should raise a degree of suspicion of the disease. Antemortem diagnosis is uncommon as the disease is rapidly fatal. Postmortem diagnosis is accomplished with fluorescent antibody testing or virus isolation from affected tissues.

There is no effective treatment for pseudorabies.

Animals should not be allowed exposure to pigs or access to uncooked pork tissues. There are no available vaccines for dogs or cats in the United States.

This is a viral disease of mammals. The virus belongs to the genus Lyssavirus in the family Rhabdoviridae.

The disease is transmitted from the bite of an infected animal through its saliva to a susceptible animal. Domestic dogs are considered to have moderate susceptibility to this viral infection.

After the virus is injected into tissue, the virus replicates within tissues myocytes and then enters surrounding nervous tissue. The virus spreads in motor and sensory neurons by axonal spread to the central nervous system. After the central nervous system is infected, the virus disseminates to other body tissues via peripheral, sensory, and motor neurons. Salivary glands eventually become infected; from there, the viral disease can then be transmitted to other susceptible animals. Not all animals infected with rabies are efficient in the transmittal of this disease through their saliva.

Depending on the region of the country, skunks, foxes (gray, Arctic, and red), raccoons, and bats account for most of the wildlife species reported with rabies. The number of cases reported in 2001 increased among bats, cats, skunks, rodents/lagomorphs, and swine and decreased among dogs, cattle, foxes, horses/mules, raccoons, and sheep/goats. The relative contributions of the major groups of animals were as follows: raccoons (37.2%; 2767 cases), skunks (30.7%; 2282), bats (17.2%; 1281), foxes (5.9%; 437), cats (3.6%; 270), dogs (1.2%; 89), and cattle (1.1%; 82).

Clinical signs vary and are mainly neurologic in nature. Ptyalism, dysphagia, and an inability to swallow may suggest pharyngeal, esophageal, or a gastrointestinal disorder, but these are the result of neurologic dysfunction. In the early states of rabies, behavioral changes are present. These changes are subtle and are not always noticed by the owner or veterinarian.

Furious and paralytic forms of the disease are described in dogs. These clinical manifestations are arbitrary and are used to describe changes in the dog’s behavior during progression of the disease. The furious form of the disease in dogs is characterized by aggression to people, animals, or inanimate objects. Dogs may appear excitable, bark, or attack imaginary objects. Ataxia or incoordination precedes the more dramatic clinical neurologic signs. Seizures, coma, and paralysis are evident before the animal succumbs of the disease.

On the basis of current methods, the most rapid and sensitive test for detecting rabies is the direct fluorescent test on brain tissue. The head from the suspected dog should be cooled and maintained on ice and not frozen. Specimens of the medulla, cerebellum, and hippocampus are used for the direct FA test.

Conventional histopathologic examination of brain tissue does not always provide confirmation of the disease because changes are mild. Acute polioencephalitis is observed early in the course of the disease, with a necrotizing encephalitis in progressive infections. Presence of intracytoplasmic inclusions, or Negri bodies, may be observed in the hippocampus and Purkinje cells of affected dogs. Special stains may be required to demonstrate these structures more readily.

The first step is to prevent contact of dogs with wildlife reservoirs such as skunks, foxes, and raccoons. Vaccination of dogs is highly effective and should be performed based on current recommendations by the National Association of State Public Health Veterinarians.

Vaccination is recommended with a vaccination approved by the Food and Drug Administration at 3 months of age and 1 year later. Booster vaccinations after the initial two vaccinations should be performed in accordance with local public health laws with an approved product, either annually or every 3 years.

Procedures vary slightly and depend on local public health laws. Contact with local health officials should be established before any action of suspected animals.

The taxonomy of the Ehrlichia species has recently changed and is based on an objective classification scheme of the sequences of 16S ribosomal genes. The genus Ehrlichia belongs in the family Anaplasmataceae, which contains three other genera: Anaplasma, Neorickettsia, and Wolbachia. The Ehrlichia genus contains Ehrlichia canis, Ehrlichia chaffeensis, and Ehrlichia ewingii. Ehrlichia phagocytophila, Ehrlichia equi, and Ehrlichia platys are now classified in the genus Anaplasma, along with the agent of human granulocytic ehrlichiosis. These latter three Ehrlichia species have similar nucleotides and are considered by some to be the same organism.

The genus Neorickettsia now contains the organisms formally named Ehrlichia sennetsu and Ehrlichia risticii, along with the agent of that causes salmon poisoning in dogs, N. helminthoeca.