DVM NEWSMAGAZINE MAY, 2005

Herpesrpesvirus: DVMs must manage infected litters

ByJohnnyD.Hoskins

Dr. Hoskins is owner ofDocuTech Services. He is a dipbmate of the American College of Veterinary Internal Medicine with specialities in small animal pediatrics. He can be reached at (225) 955-3252,fax (214)242-2200, ore-mail: jdhoskins@mindspring.com.

I recently lost three litters of high-profile show dogs to herpesvirus shortly following c-sections. The litters were of separate breeds and unrelated breeders. The puppies fade and die, despite aggressive treatment within 48 hours of delivery. The show dogs seem to be the only one's affected because other c-sections do fine. What can I do to prevent these fading puppies from dying?
Some relevant points about canine herpesvirus infection are provided in this column.
Canine herpesvirus, an enveloped DNA virus, primarily causes severe illness and death in puppies less than 3 weeks old. Infections in dogs older than a few weeks are usually mfld or inapparent Older puppies (3-5 weeks old) may show mild respiratory signs with subsequent recovery. Puppies that recover usually have ktent canine herpesvirus infections, and some may develop neurologic signs, such as ataxia and blindness. Canine herpesvirus is not infectious for man, and only dogs are known to be susceptible. The virus is very labile and is rapidly inactivated by lipid solvents, such as ether or chloroform, and by heat, alcohol and aqueous solvents with a pH below 6.5. Virus infectivity is destroyed overnight at a temperature of 37 degrees C and within a week at room temperature (20 degrees C).
Canine herpesvirus infection occurs in the United States, Canada, Australia, Japan, England and Germany. Serologic surveys of large breeding kennels in the eastern and southeastern United States indicate that the virus is widespread. Although the incidence within kennels has varied from 20 percent to 90 percent, there has been no apparent relationship between the presence of antibody to this virus and incidence of clinical infection. In one large breeding kennel under close surveillance for more than five years, more than 90 percent of dogs older than 6 months of age possessed serum antibody to the virus. Only three known episodes of puppy deaths due to this virus occurred during this period.
The herpesvirus does not appear to spread by airborne routes, but rather by direct contact between infected and susceptible dogs. Infected adult dogs may shed virus in oral and nasal secretions for as long as two weeks following infection. Virus has been isolated from the urine of infected adult dogs and from young puppies. Because of the suckling behavior of puppies, a single infected puppy in a litter may transfer the infection readily via saliva, feces and urine to susceptible litter mates. Fetuses may be infected in-utero during primary infection of the bitch and probably more commonly during passage through the birth canal of a bitch exposed to the virus. The virus also can be transferred manually when infected and susceptible dogs are handled. Virus can be isolated from the diseased fetuses and from the kidneys of apparently healthy puppies.
Illness in young puppies usually commences between the 5th and 18th days after birth. A soft, odorless, yellow-green stool is the initial sign. Difficulty in breathing, anorexia, abdominal pain, retching or vomiting, and incessant crying are evident. Fever usually is not detected. Effected puppies usually die shortly (within 24 to 48 hours) after the onset of such signs. Regardless of the route of infection or the dose of virus, the incubation period varies between three days to eight days.
hi natural outbreaks, the entire litter typically is infected and dies after birth. Recovery has not been observed in puppies infected during the first week of life. The inability of puppies to regulate their body temperatures is thought to be an important factor in the pathogenesis of the disease because experimental elevation of body temperature to 102 degrees F has resulted in a remarkable conversion of the highly lethal infection to a mild or moderate one. Although generalized infections occurred in puppies reared at elevated temperatures, those kept at temperatures ranging from 99 degrees F to 100 degrees F survived the usually fatal infection; some recovered completely.
In older dogs, mild rhinitis and pharyngitis have been the only signs seen. Such dogs may shed virus in nasal and salivary secretions for as long as two weeks. Susceptible bitches inoculated intravaginally can develop mild vaginitis that can go unnoticed.
In young puppies naturally or experimentally infected, lesions consist of widespread focal necrosis and hemorrhages that involve not only parenchymal and stromal cells but also blood vessels. These lesions are found in virtually all tissues. Changes in the kidneys are especially severe. They consist of cortical necrosis and hemorrhages that appear as circumscribed red areas on a dull-gray background.
Renal hemorrhages varying in size and distribution have been consistently present in effected puppies. The lungs are involved extensively and appear mottled. The pulmonary changes vary from diffuse congestion to necrosis of alveolar walls and hemorrhages. The spleen usually is enlarged greatly. Focal necrosis and hemorrhages also are common in the liver, intestinal tract and lymph
nodes. There are extensive foci of coagulation necrosis in the adrenal glands. The meninges are commonly congested and are infiltrated by lymphocytes and macrophages. There are occasional hemorrhages in the cerebral cortex, and microscopically, perivascular foci of macrophages and lymphocytes are evident. Within these foci, there are necrotic and disintegrating neurons.
With the fluorescent antibody technique, virus can be demonstrated in virtually every tissue of the body. Infected cells are focal in distribution.
The determination of canine herpesvirus infection in puppies usually depends on the information obtained from clinical history and physical examination.