Canine herpesvirus is best known as a severe viral infection of puppies worldwide, which often has a 100% mortality rate in affected litters. Increasingly sensitive molecular diagnostics have enabled its recognition in adult dogs with upper respiratory infection, ocular disease, vesicular vaginitis or posthitis, and in dogs with no clinical signs. As is typical of herpesviruses, recovery from clinical disease is associated with lifelong latent infection. Only canids (dogs, wolves, coyotes) are known to be susceptible. The seroprevalence in dog populations worldwide ranges from 20% to 98% depending on the region. Because latently infected animals may transiently convert to seronegative status, any seroprevalence study likely underestimates the true rate of exposure and carriage.
The disease is caused by an enveloped DNA canine herpesvirus (CHV) that is sensitive to lipid solvents (such as ether and chloroform) and most disinfectants. CHV is relatively unstable outside the host, so close contact is required for transmission.
Transmission usually occurs by contact between susceptible individuals and the infected oral, nasal, or vaginal secretions of shedding dogs. Many dogs shedding virus exhibit no clinical signs. Immunologically naive pregnant bitches are at risk of acute infection, which may be transmitted to fetuses or neonatal pups; previously infected bitches are unlikely to transmit infection. The most significant systemic disease occurs in fetal or neonatal puppies from in utero infection, or infection in the first 3 wk of life. After this time, natural resistance to infection improves as puppies mature and maintain a higher body temperature.
Infection of susceptible animals results in replication of CHV in the surface cells of the nasal mucosa, pharynx, and tonsils. In the case of newborn susceptible pups or other dogs with compromised immune response, viremia and invasion of diverse visceral organs occur. Primary systemic infection is associated with a high degree of viral shedding; shedding by latently infected animals after clinical or subclinical recrudesence is of lesser severity and duration.
Deaths due to CHV infection usually occur in puppies 1–3 wk old, occasionally in puppies up to 1 mo old, and rarely in pups as old as 6 mo. Typically, onset is sudden, and death occurs after an illness of ≤24 hr. If clinical signs are observed, they may include lethargy, decreased suckling, diarrhea, nasal discharge, conjunctivitis, corneal edema, erythematous rash, rarely oral or genital vesicles, and the notable absence of fever. Thoracic radiographs show a diffuse unstructured interstitial pattern that is typical of viral pneumonia, but, in contrast to other viral diseases of puppies, leukocytosis may be present.
Older dogs exposed to or experimentally inoculated with CHV may develop a mild rhinitis, which may be part of the “kennel cough” syndrome (infectious tracheobronchitis, see Infectious Tracheobronchitis of Dogs) or a vesicular vaginitis or posthitis. There are also reports of conjunctivitis and dendritic corneal ulcers in the absence of other upper respiratory signs. Acutely infected pregnant bitches may abort a litter, or deliver a partially stillborn litter; however, they seldom exhibit other clinical signs, and future breedings are likely to be successful.
The characteristic gross lesions at necropsy consist of disseminated focal necrosis and hemorrhages. The most pronounced lesions are seen in the lungs, cortical portion of the kidneys, adrenal glands, liver, and GI tract. All lymph nodes are enlarged and hyperemic, and the spleen is swollen. Lesions may also be found in the eyes and CNS. The basic histologic lesion is necrosis with hemorrhage in the adjacent parenchyma. The inflammatory reaction in many organs may be limited, but marked neutrophilic and mononuclear infiltration is seen in ocular lesions. Single, small, basophilic, intranuclear inclusion bodies are most common in areas of necrosis in the lung, liver, and kidneys; occasionally, they are seen as faintly acidophilic bodies located within the nuclear space.
In systemically affected puppies, CHV infection may be confused with infectious canine hepatitis (see Infectious Canine Hepatitis), but it is not accompanied by the thickened, edematous gallbladder often associated with the latter. The focal areas of necrosis and hemorrhage, especially those that are seen in the kidneys, distinguish it from hepatitis and neosporosis (see Neosporosis). CHV causes serious disease only in very young puppies. The rapid death and characteristic lesions distinguish it from canine distemper (see Canine Distemper).
Hemagglutination, ELISA, and immunofluorescence antibody tests are available, and PCR is highly sensitive and specific when used on fresh tissue and fluid samples. In cases of neonatal mortality, the diagnosis typically is made postmortem with virus isolation from fresh lung, liver, kidney, and spleen by cell culture techniques and subsequent identification by PCR and sequencing, transmission electron microscopy, immunofluorescence, or fluorescence in situ hybridization. The tissues should be submitted to the laboratory refrigerated but not frozen.
Therapy is typically unrewarding in systemically affected puppies, and the prognosis for puppies that do survive is guarded because damage to lymphoid organs, brain, kidneys, and liver may be irreparable. Before onset of clinical signs in littermates or other nearby puppies, rearing in incubators at an increased temperature (95°F [35°C], 50% relative humidity), and/or passive immunization with intraperitoneal serum may reduce losses within an exposed litter. Limited studies with antiviral agents such as vidarabine are inconclusive, but immediate recognition and treatment would be needed to have any possibility of success.
Adult dogs with ocular, respiratory, or genital disease often experience mild and self-limiting signs. Ophthalmic antiviral cidofovir (0.5% bid) has been used successfully in one reported case of primary ocular infection in an adult dog and may be useful for persistent or painful ocular lesions.
No vaccine is available in the USA. Infected bitches develop antibodies, and litters subsequent to the first infected litter receive maternal antibodies in the colostrum. Puppies that receive maternal antibodies may be infected with the virus, but disease does not result. Isolation of pregnant bitches from other dogs during the last 3 wk of gestation and first 3 wk postpartum, with excellent hygiene by human handlers, is the most effective way to minimize risk to puppies. Because of the high seroprevalence among adult dogs and because virus may be shed by asymptomatic individuals, complete avoidance of exposure is not a reasonable management strategy for most dogs.