The re-excretion of feline viral rhinotracheitis (FVR) virus (feline herpesvirus I) by FVR-recovered cats is recorded both spontaneously and following a variety of stimuli, namely, corticosteroid administration, change of housing, and parturition and lactation. At least 27 of 33 (82%) FVR-recovered cats studied were shown to be viral carriers. The carrier state was characterised by periods of viral latency interspersed with episodes of viral shedding. Administration of 0-75 mg dexamethasone trimethylacetate and 2-25 mg prednisolone on days 0,2 and 4 resulted in re-excretion after a mean lag period of 7-2 days in 22 of 32 (69%) FVR-recovered cats on a total of 31 of 57 (54%) occasions. Rehousing resulted in virus re-excretion after a mean lag period of 7-2 days in four of 22 (18%) cats tested on a total of six of 40 (15%) occasions. Apparently spontaneous shedding occurred on a total of 10 occasions in nine of 31 (29%) cats during a mean observation period of 8-8 months. Four of six FVR-recovered queens in a total of four of 10 litters (40%) shed virus within two to 10 weeks of parturition. Serum neutralising antibody titres were generally boosted at the time of first re-infection but afterwards remained essentially constant. Although 82% of cats in these studies were shown to be viral carriers, only 45% of cats shed virus spontaneously or as a result of the natural stress situations and it is postulted that these naturally excreting cats are of most significance epidemiologically.
Recently, in the USA, virulent mutants of feline calicivirus (FCV) have been identified as the cause of a severe and acute virulent systemic disease, characterised by jaundice, oedema and high mortality in groups of cats. This severe manifestation of FCV disease has so far only been reported in the USA. However, in 2003, an outbreak of disease affected a household of four adult cats and an adult cat from a neighbouring household in the UK. Three of the adult cats in the household and the neighbouring cat developed clinical signs including pyrexia (39.5 to 40.5 degrees C), lameness, voice loss, inappetence and jaundice. One cat was euthanased in extremis, two died and one recovered. A postmortem examination of one of the cats revealed focal cellulitis around the right hock and right elbow joints. The principal finding of histopathological examinations of selected organs from two of the cats was disseminated hepatocellular necrosis with mild inflammatory infiltration. Immunohistology identified FCV antigen in parenchymal and Kupffer cells in the liver of both animals and in alveolar macrophages of one of them. In addition, calicivirus-like particles were observed by electron microscopy within the hepatocytes of one cat. FCV was isolated from two of the dead cats and from the two surviving cats. Sequence analysis showed that they were all infected with the same strain of virus, but that it was different from strains of FCV associated with the virulent systemic disease in cats in the USA. The outbreak was successfully controlled by quarantine in the owner's house.
The reservoir host of cowpox virus in Western Europe is not known, but epidemiological evidence from human and feline infections indicates that the virus is probably endemic in small wild rodents. Therefore, serum and tissue samples were collected from a variety of wild British mammals and some birds, and tested for evidence of Orthopoxvirus infection. Antibody reacting with cowpox virus was detected in 9/44 (20%) bank voles (Clethrionomys glareolus), 8/24 (33%) field voles (Microtus agrestis), 17/86 (20%) wood mice (Apodemus sylvaticus) and 1/44 house mice (Mus musculus), but in no other animal species tested. Although virus was not isolated from any animal, this serological survey, together with other evidence, suggests that bank and field voles and wood mice are the main reservoir hosts of cowpox virus in Great Britain.
The seroprevalence and, or, incidence of canine coronavirus infection was determined in several dog populations in the UK. Seroprevalence ranged from 76 per cent for a rescue kennel to 100 per cent in a commercial breeding colony. In the rescue kennel there was no difference in seroprevalence of the virus between dogs less than or more than four months of age. In the breeding colony, subclinical seroconversion occurred between six and 10 weeks of age. The virus was isolated from faecal samples from 45 of 100 dogs in the rescue kennel; it was isolated from 73 per cent of the dogs with diarrhoea and from 43 per cent of those which did not have diarrhoea. In field cases of acute, mainly haemorrhagic diarrhoea in pet dogs, eight of 32 were positive for canine coronavirus. No canine coronavirus was isolated from either clinically healthy pet dogs in a boarding kennel or from non-diarrhoeic pet dogs examined at the University of Liverpool Small Animal Hospital. It would appear that although canine coronavirus is widespread, the role of the virus in canine enteritis is still equivocal.
The domestic cat is now the most commonly recognised host of cowpox virus in Great Britain and several recent cases of human cowpox have been traced to contact with infected cats. This review brings together some of the recent developments in our understanding of the natural history of cowpox virus and cowpox in cats.
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