Transmissible spongiform encephalopathies related to bovine spongiform encephalopathy in other domestic and captive wild species

Transmissible spongiform encephalopathies related to bovine spongiform encephalopathy in other domestic and captive wild species



Excluding human transmissible spongiform encephalopathies (TSE) and scrapie, the only naturally occurring animal TSE known in 1985 before the advent of bovine spongiform encephalopathy (BSE) were transmissible mink encephalopathy of farmed mink (Mutela vison) (restricted to North America and northern continental Europe), and chronic wasting disease of mule deer (Odocoileus hemionus), Rocky Mountain elk (Alces alces) and white-tailed deer (Odocoileus virginianus) and various crosses (restricted to North America). These diseases have been reviewed.6, 7, 18

In 1986, just before the first case of BSE was confirmed, a spongiform encephalopathy in a captive nyala (Tragelaphus angasi) in the UK was confirmed by microscopic examination of the brain.14 This was a prelude to other cases in captive wild Bovidae, all in the UK.15 All these are believed to have been caused by exposure to TSE-infected meat and bonemeal (MBM) in precisely the same way as domestic cattle. These are reviewed by Bradley.6

In 1990 a naturally occurring TSE in a domestic cat was reported for the first time26 and this was soon followed by several other reports. Feline spongiform encephalopathy (FSE) cases have been mainly restricted to the UK (total number of confirmed cases to November 2001 was 89 with, in addition, one case in Norway and one in Liechtenstein without any clear connection with the UK8 ). The origin of infection in all cases appears most likely to be feed, but the precise source is unknown and difficult to determine because of the varied diets of domestic cats. However, an origin from TSE-infected MBM seems a likely, if unproven, source. A review of FSE in domestic cats has been published.19

The concurrent appearance of a case of conventional sporadic Creutzfeldt-Jakob disease (CJD) in a human in Italy and of FSE in his pet cat have recently been reported.27 At present it is unclear whether this is merely an unusual coincidence of each host acquiring infection from separate sources, or of one host contracting infection from the other, or whether each was infected from a common source.

The immunohistochemical findings of PrPSc in the tissues of several domestic cats with FSE have been reported.21 Although PrPSc in the brains of up to 14 cats was consistent, it was rarely found in lymphoreticular tissues, including the spleen and the intestine (Peyer’s patches and/or myenteric plexus), and then only in a small amount. However, PrPSc was found in the glomeruli of the kidney of 13 cats (100 per cent of those examined).

The peak occurrence of reported cases of FSE in domestic cats in the UK was in 1994 (16 cases). Since then the prevalence of reported cases has diminished regularly with just one case in 2000 and none in 2001. Only 7 of the 89 cats with FSE were born after the specified bovine offals (SBO) ban was in place to protect animals. This supports the view that the specified risk materials (SRM) ban (previously the SBO ban) is effective in preventing new exposures.

Feline symmetrical encephalopathy has also been reported in a number of captive wild felids in the UK including several species naturally resident in Africa.15 The origin of infection in most of these cases seems likely to be from TSE infected, uncooked carcass material from cattle that contained central nervous tissue. Similar to the situation in domestic cats, most of the total of 17 cases of FSE in captive wild felids were born before the SBO ban was in place, although one cheetah (Acinomyx jubatus) and one ocelot (Felis pardalis) were born in 1991, and one cheetah in 1992.

The epidemiological, clinical and pathological features of a case of FSE in a cheetah exported from the UK to France have been reported.2

The temporal and geographical coincidence of these newly reported TSE of domestic cats and wild Bovidae and Felidae with BSE in the UK, suggests that a cattle origin is possible and likely. Isolates from a nyala, a greater kudu (Tragelaphus strepsiceros) and three domestic cats all have the same biological strain characteristics of the BSE agent when tested in mice.9 It is assumed that the TSE in all the affected species have an origin from cattle with BSE and this is supported on geographical, epidemiological and temporal grounds, but has not been formally proved.

In France, captive primates (a single rhesus monkey (Macaca mulatta), 5 macaque monkeys (Macaca sp.) and lemurs (Eulemus spp.),4 have developed TSE naturally and it is suggested that this has occurred as a result of dietary exposure to TSE infection in feed imported from the UK before controls were in place.4 Experimental transmission of BSE to some of these primates has also been achieved with similar clinical signs and distribution of PrPSc in the brain. However, no natural TSE has been reported in any captive primate in the UK despite at least some of them being fed on feed containing high inclusion rates of MBM derived from UK abattoir waste.20 Bovine symmetrical encephalopathy and scrapie were experimentally successfully transmitted toeach of two marmosets (Callithrix jacchus) by parenteral inoculation.1 The incubation period for scrapie was 38 and 42 months and for BSE 46 and 47 months. Bovine spongiform encephalopathy has also been...

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