viral and chlamydial diseases in dogs
viral and chlamydial diseases in dogsa. Canine Parvovirus
Clinical signs. Clinical signs of canine parvovirus usually appear 5 days after inoculation by the fecal-oral route and are characterized by anorexia, fever, depression, and vomiting. Profuse, intractable diarrhea ensues, which may become hemorrhagic. Approximately 85% of affected dogs develop severe leukopenia, with a total granulocyte/lymphocyte count ranging from 500-2000 WBC/~d or less. Repeated hemograms may provide prognostic value because rebounds in leukocyte counts are indicative of impending recovery. Terminally ill dogs may develop hypothermia, icterus, or disseminated intravascular coagulation due to endotoxemia.
Epizootiology and transmission. Parvovirus can infect dogs of any age, but puppies between 6 and 20 weeks of age appear to be particularly susceptible. Puppies less than 6 weeks of age
are generally protected from infection by passive maternal antibody. Adult dogs probably incur mild or inapparent infections that result in seroconversion.
Pathogenesis. Canine parvovirus has an affinity for rapidly dividing cells of the intestine and causes an acute, highly contagious enteritis with intestinal crypt necrosis and villous atrophy.
The virus also has tropism for the bone marrow and lymphoid tissues; thus leukopenia and lymphoid depletion accompany the intestinal destruction.
Diagnosis and differential diagnosis. Parvovirus can be detected in fecal samples with a commercially available ELISA from CITE. At necropsy, diagnosis is based on gross and histopathologic evidence of necrosis and dilatation of intestinal crypt cells with secondary villous collapse. Other lesions include myeloid degeneration and widespread lymphoid depletion. Parvovirus can also be demonstrated in frozen sections by fluorescent antibody techniques. Differential diagnoses should include other viral enteritides, salmonellosis, and small intestinal obstruction.
Prevention and control. Prevention of transmission begins with the isolation of affected animals and quarantine for 1 week after full recovery. Disinfection of potentially infected kennel and
diagnostic areas with diluted bleach (1:30) or commercially prepared disinfectant (such as Kennesol, available from AlphaTech, Lexington, Massachusetts) is essential for the elimination of the virus. Six-week-old puppies should be vaccinated every 2-4 weeks with a commercially available modified live vaccine until 16-18 weeks of age. Young Rottweilers and Doberman pinschers appear to be predisposed to parvoviral enteritis and should be vaccinated every 3 weeks (5 times) from 6-18 weeks of age.
Treatment. Treatment is largely supportive and is aimed primarily at restoring fluid and electrolyte balance.
Research complications. Infection with parvovirus obviously precludes the use of a particular dog in an experimental protocol. Given the potential for significant discomfort of the affected animal, and the cost of therapy, humane euthanasia is usually the option chosen in a research setting.
b. Canine Coronavirus
Canine coronavirus infection is usually inapparent or causes minimal illness. This epitheliotropic virus preferentially invades the enterocytes of the villous tips, resulting in destruction, atrophy, and fusion and subsequent diarrhea of varying severity. Subclinical infections are most common, but abrupt gastrointestinal upset accompanied by soft to watery, yellow-orange feces is possible. Definitive diagnosis by virus isolation or paired sera is usually not made, because of supportive therapy generally results in rapid resolution of diarrhea. Inactivated coronavirus is present in commercially available combination vaccines, which are administered immunopro phylactically at 6 - 8, 10 - 12, and 12-14 weeks of age and then annually thereafter. The role of these vaccines in protection from coronaviral infection is unknown because the virus typically causes an inapparent or mild illness (Hoskins, 1998).
c. Canine Distemper
Etiology. Canine distemper virus (CDV) belongs to the family Paramyxoviridae, within the genus Morbillivirus, which includes human measles virus and rinderpest virus of ruminants.
Clinical signs. Although there is only one serotype of CDV, there is a wide difference in strain virulence and tissue tropism.
Some strains produce mild clinical signs that are similar to tracheobronchitis, whereas other strains cause generalized infections of the gastrointestinal tract, integument, and central nervous system, resulting in enteritis, digital hyperkeratosis, and
encephalitis, respectively. Other factors contributing to the severity and progression of clinical signs include environmental conditions, immune status, and age of the host.
A transient subclinical fever and leukopenia occur 4-7 days after exposure, with a subsequent fever spike 7-14 days later, accompanied by conjunctivitis and rhinitis. Other clinical signs associated with acute distemper include coughing, diarrhea, vomiting, anorexia, dehydration, and weight loss. Secondary bacterial infections can cause progression to mucopurulent oculonasal discharge and pneumonia. An immune-mediated pustular dermatitis may develop on the abdomen; this is usually a favorable prognostic sign (Greene and Appel, 1998), because dogs that develop skin lesions often recover.
Neurologic complications of distemper infection may occur weeks to months after recovery from an acute infection.
Dogs that develop the late-onset disease are usually immunocompetent hosts, suggesting that the virus may have escaped complete elimination by the immune system, possibly because of protective effects by the blood-brain barrier. Classic neurologic signs that may occur in acute or chronic CDV infection include ataxia, incoordination, vocalization, "chewing gum" seizures, and myoclonus with or without paresis of the affected limb. Canine distemper is the most common cause of seizures in dogs less than 6 months of age. Dogs with extensive neurologic involvement often have residual clinical deficits, including flexor spasm and olfactory dysfunction. CDV has also been associated with two forms of chronic encephalitis in mature dogs: multifocal encephalitis and "old dog encephalitis."
Epizootiology and transmission. The virus is highly prevalent and contagious to dogs and other carnivores, especially at the age of 3-6 months, coincident with the waning of maternal antibody. Transmission is primarily by aerosolization of infective droplets from body secretions of infected animals.
The predominant histopathologic lesion in neurologic forms of distemper is demyelination, which may be accompanied by gliosis, necrosis, edema, and macrophage infiltration. Acidophilic cytoplasmic inclusions can be found in epithelial cells of mucous membranes, reticulum cells, leukocytes, glia, and neurons, while intranuclear inclusions are often present in the lining or glandular epithelium and ganglion cells.
Diagnosis and differential diagnosis. Diagnosis Of CDV Young dogs who have not received routine immunoprophylaxis (or similarly, mature dogs with a questionable vaccination history) and
present with rhinitis, mucopurulent oculonasal discharge, plus or minus hyperkeratosis of the footpads and neurologic signs, are highly likely to have CDV. The ophthalmologic examination may reveal chorioretinitis with acute disease or retinal atrophy in chronic cases. Definitive diagnosis of acute infection can be made by fluorescent antibody testing of intact epithelial cells from conjunctival and mucous membranes. Attenuated strains of CDV, found in modified live vaccines, are not disseminated from lymphoid tissue to epithelial cells and thus are not detected by the fluorescent antibody. Serologic testing is usually not useful, because dogs frequently fail to mount a measurable immunologic response. Because of the variety of clinical signs, there are many differential diagnoses for canine distemper.
An important differential diagnosis for respiratory illness is infectious tracheobronchitis (a kennel cough). Bacterial, viral, and protozoal causes of gastroenteritis must be considered for cases presenting with vomiting and diarrhea, and rabies, pseudorabies, bacterial meningitis, and poisonings are differential diagnoses for dogs with central nervous system disorder.
Prevention and treatment. A series of three immunizations from 6 to 14 weeks of age, followed by yearly boosters, is a recommended preventative. Treatment is largely supportive, but because of the profound immunologic effects and significant morbidity of CDV, humane euthanasia is usually undertaken in the research setting.