Hantaviral Infection

Craig E. Greene and Bruno B. Chomel

Foot-And-Mouth Disease

Craig E. Greene

Foot-and-mouth disease is a highly contagious illness of wild and domestic cloven-hoofed animals and is caused by strains of an Aphthovirus organism in the family Picornaviridae. It occurs worldwide; however, eradication has been variably successful in Australia, New Zealand, Japan, the British Isles, and North America. Carnivorous animals are relatively resistant to infection and do not play a major role in spreading or harboring the disease under conditions of natural exposure. The virus has been propagated in canine cell cultures.⁹⁵ Dogs and cats can be experimentally infected³⁶; however, no epizootics have been found among carnivores. These animals may become incidentally infected during outbreaks in herbivores by contacting these animals or their offal. Reports have been made of dogs that became infected by scavenging remains of dead animals.^46,87

As a result of epizootics, guidelines have been established for dog owners in areas known to have infected animals.³ Dogs must be kept under control—on a leash or within an enclosure—at all times. Dogs should not be walked across farmland and should have minimal contact with livestock and wild animals. Certain sporting activities involving dogs should not be allowed in quarantined areas. Minimal restrictions have been placed on cats, although they should be kept indoors as much as possible. Disinfectants suitable for inactivating the virus are 4% sodium carbonate, 0.5% citric acid, 2% formalin, or 2% sodium hydroxide.⁸⁴ Phenolic disinfectants, quaternary ammonium compounds, and biguanides are not effective. Halogens such as sodium hypochlorite or iodine are less effective because of inactivation by organic matter.

Vesicular Exanthema

Craig E. Greene

A calicivirus that causes vesicular exanthema of swine produces lesions on the mouth, lips, snout, and feet and is often confused with foot-and-mouth disease. Dogs have developed clinical signs of illness characterized by vesicular eruptions when outbreaks of vesicular exanthema virus infection have occurred in swine.⁵ Virus was not definitely isolated in these cases. However, in other studies, experimentally infected dogs developed fever within 24 hours after inoculation and vesicular eruptions on their tongues and in their oral cavities.⁵ These lesions healed within a few days. Virus was isolated from the spleen of a dog that became febrile after inoculation.

Hepatitis E Virus Infection

Craig E. Greene

Hepatitis E virus (HEV) is an unclassified virus that causes an acute self-limiting hepatitis in people, pigs, and chickens in tropical and subtropical countries. Pigs may be important reservoirs for human infection.¹¹¹ HEV infection is the most common form of acute hepatitis in human adults in regions of Asia. It has been reported in developing countries in southeast and central Asia, the Middle East, and North Africa. More sporadic outbreaks have occurred in Mexico and the United States and other countries in the Western Hemisphere. The virus is spherical and nonenveloped, ranging from 30 to 32 nm in diameter, with its nucleic acid in a single-stranded positive-sense RNA molecule. Although its structure resembles that of a calicivirus, its genome is closest to that of rubella virus, a member of the Togaviridae family. The strains found worldwide can be classified into three major genotypes. The virus is shed in feces with fecal–oral contact as the means of transmission.

There has been concern, but no documented proof, that dogs and cats develop clinical illness from infection with HEV or transmit infection to people.4,55,103,109 Anti-HEV globulins have been detected in species of wild and domestic animals.⁹⁷ Experimentally the virus has a broad host range. Chimpanzees, Old World and New World monkeys, pigs, rodents, and sheep have been experimentally infected. One swine isolate has been shown to have the broadest host range. Evidence of zoonotic transmission of infection occurred between a domestic pig and its owners.⁸⁶ In one report, a person from Japan with hepatitis E who had not traveled was suspected to have become infected in the home environment.⁵⁵ Fever, malaise, icterus, and brown-colored urine were observed in the family members. They were seronegative; however, the patient’s cat had a high HEV IgG titer. Although cats and dogs from Japan had antibodies to HEV in their sera, no virus could be detected by PCR of fecal specimens.⁶⁸ A high percentage (33%) of pet cats in Japan were shown to have an increased serum antibody titer to HEV⁸¹; however, HEV DNA was not detected in the cats⁸¹ or in the livers of 98 dogs with a variety of forms of hepatitis.¹⁷

The epidemics of HEV infection in humans have generally been foodborne or waterborne. For prevention in endemic areas, animal feces must be handled with care. General sanitation helps prevent the infection.

Rabbit Hemorrhagic Disease

Craig E. Greene

Rabbit hemorrhagic disease (RHD) is an acute fatal disease of European rabbits (Oryctolagus cuniculus) caused by an RHD virus of the family Caliciviridae. The disease has been reported in Asia, Europe, Africa, and the Americas. Feral cats in New Zealand have antibodies to RHD virus, and nested reverse transcriptase (RT)-PCR has identified virus in the liver of one seropositive cat.¹¹³ Cats fed rabbit livers infected with RHD virus developed serologic titers to the virus, and RHD viral RNA was detected in the tonsils, mesenteric lymph nodes, spleen, and liver. Even though large amounts of virus were found, clinical disease was not observed. Active replication of RHD virus was not demonstrated.

Lymphocytic Choriomeningitis

Craig E. Greene

As a group, the arenaviruses contain a number of geographically and genetically distinct members, some of which cause severe disease in people. Each arenavirus species is usually associated with a particular rodent reservoir host.⁴⁷ Lymphocytic choriomeningitis virus is a ubiquitous zoonotic arenavirus of house mice (Mus musculus) that is transmitted in utero or at birth and persists for life in high concentrations in various tissues. Several outbreaks have been associated to pet hamsters, including accidental transmission of the infection in organ recipients.²³ Outbreaks of rodent lymphocytic choriomeningitis infections have prompted concern that domestic dogs or cats might serve as reservoirs or vectors of the virus for human exposure. Puppies (8 to 12 weeks old) did not develop clinical illness after parenteral or cerebral inoculation.²⁷ Challenged animals had increased neutralizing antibody titers to the virus, and infection was transmitted from infected to noninfected puppies. Except for intranuclear inclusions in the adrenal cortex, pathologic changes were not observed in the animals, indicating that the infection was subclinical. It is unlikely that dogs or cats become infected or spread the virus by natural exposure, because most human infections have resulted from direct contact with rodents. Immunocompromised people are most susceptible; postnatal infections cause acute aseptic meningoencephalitis, whereas congenital infections produce central nervous system (CNS) and ocular malformations.