Canine herpesvirus is a severe viral infection of puppies worldwide, which often has a 100% mortality rate in affected litters. It also may be associated with upper respiratory infection or a vesicular vaginitis or posthitis in adult dogs. 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.
Etiology and Pathogenesis
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.
Puppies are most susceptible in the first week of life, when they maintain a body temperature less than 37°C, because the virus replicates more successfully at this temperature. Transmission usually occurs by contact between susceptible puppies and the infected oral, nasal, or vaginal secretions of their dam or other dogs allowed to commingle with puppies during the first 3 wk of life. After this time, natural resistance to infection improves as puppies maintain a higher body temperature. In utero transmission may also occur.
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 that become hypothermic, viremia and invasion of visceral organs occur.
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, erythematous rash, rarely oral or genital vesicles, and the notable absence of fever. Thoracic radiographs show a diffuse unstructured interstitial pattern, 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 Respiratory Diseases of Small Animals: Infectious Tracheobronchitis of Dogs) or a vesicular vaginitis or posthitis. There are also reports of corneal ulcers in the absence of other upper respiratory signs. In utero infections may be associated with abortions, stillbirths, and infertility.
The characteristic gross lesions 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 CNS. The basic histologic lesion is necrosis with hemorrhage in the adjacent parenchyma. Most often there is no inflammatory reaction. 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.
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 occur 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 can identify viral DNA in fresh tissue and fluid samples. However, 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.
Prior to onset of clinical signs in littermates or other nearby puppies, rearing in incubators at an elevated 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 would require immediate recognition and immediate treatment to have any possibility of success.
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.
Removing puppies from affected bitches by cesarean section and rearing them in isolation has prevented deaths under experimental conditions. However, infections have been noted even in puppies delivered by cesarean section, likely due to in utero transmission. In the natural setting, subsequent litters of infected dams are likely protected by maternal antibodies, so cesarean section in a bitch with a history of herpesvirus infection in a prior litter is not necessary.
Last full review/revision March 2012 by Kate E. Creevy, DVM, MS, DACVIM