Can you catch the feline form of mad cow disease (FSE) from your cat?

Cats are the only pets that are known to have feline spongiform encephalopathy. It has been found in a small number of cats — about 100 — in the United Kingdom, as well as a handful in other European countries. Larger zoo felines that fed directly off infected carcasses also died from the disease.

Feline spongiform encephalopathy (FSE) is considered to be related to bovine spongiform encephalopathy (BSE) and has been reported in domestic cats as well as in captive wild cats including cheetahs, first in the United Kingdom (UK) and then in other European countries. In France, several cases were described in cheetahs either imported from UK or born in France.

Researchers have reported details of two other FSE cases in captive cheetah including a 2nd case of FSE in a cheetah born in France, most likely due to maternal transmission. Complete prion protein immunohistochemical study on both brains and peripheral organs showed the close likeness between the two cases. In addition, transmission studies to the TgOvPrP4 mouse line were also performed, for comparison with the transmission of cattle BSE.

The TgOvPrP4 mouse brains infected with cattle BSE and cheetah FSE revealed similar vacuolar lesion profiles, PrPd brain mapping with occurrence of typical florid plaques. Collectively, these data indicate that they harbor the same strain of agent as the cattle BSE agent. This new observation may have some impact on our knowledge of vertical transmission of BSE agent-linked TSEs such as in FSE.

For more information, see the medical journal article: Bencsik A, Debeer S, Petit T, Baron T (2009) Possible Case of Maternal Transmission of Feline Spongiform Encephalopathy in a Captive Cheetah. PLoS ONE 4(9): e6929. doi:10.1371/journal.pone.0006929. Editor: Neil Mabbott, University of Edinburgh, United Kingdom. Published: September 7, 2009.

In France, until now and in total, five FSE cases have been identified in cheetahs, from imported animals born and fed in the UK and more recently in the case of an animal born in France [12], [13]. The present article describes two of these cases of FSE (mother and offspring) that, interestingly, may very well represent the first case of maternal transmission of the FSE agent. this mouse model offers the great advantage that it allows easy recognition of the BSE agent by another signature: the occurrence of typical florid plaques, an histopathological feature previously described in humans with vCJD or in BSE-infected macaques [19], [20].

The results of first and second passage experiments indicate that BSE agent is the most probable source of contamination of the mother. The first case was diagnosed in an imported cheetah (born in Whipsnade Wild Animal Park in UK and kept in captivity in the French zoo of Peaugres). This FSE-affected female cheetah had given birth to young during the last period of the disease's progress.

After 5 weeks of disease development she was euthanized on humanitarian grounds. Because she was rearing three young she was left to raise the litter for as long as possible. During this period she continued to suckle the youngsters that were subsequently fed with 40% freshly-killed rabbit or hens and 60% beef. The second case reported in the present article was found among her offspring. This one was indeed diagnosed as affected with FSE at the age of 7 and interestingly may represent the first known case of maternal transmission of the FSE agent.

For FSE cases in domestic cats only, a link between BSE and FSE agent was demonstrated by the similarity of mean incubation periods and lesion profiles in FSE and BSE cases transmitted to wild-type mice [3], [23]. Here we report the transmission of the FSE case 1 (the mother of case 2) into the Tg(OvPrP4) mouse model that has been demonstrated as sensitive to and efficient at detecting the BSE strain of agent [2], [15], [16].

When BSE agent is transmitted in this model, at first passage the mean incubation periods may vary depending on the species of the host harboring the BSE agent (cattle, sheep etc.), and was reported to be from 300 d.p.i. +/−50 (mean +/− standard error) to 475 +/−69 d.p.i. (and even up to 500 d.p.i. +/−110 for an experimental ovine BSE in an ARR/ARR genotype sheep) [2], [15], [17].

The researchers concluded in the study that: "In summary, although oral contamination by the BSE agent could not be totally excluded, the elements reported in the present article indicate collectively that the 2nd case of cheetah FSE, concerning an animal born in France, is most likely due to maternal transmission from a cheetah harboring the same strain of agent as the cattle BSE agent."

So how did the mother feline catch it? The scientists report, "This question is still a current issue and a recent article underlines the caveats and difficulties in excluding this possibility, principally due to the limited availability of data concerning children in vCJD cases and a relatively short period of observation [35]. In this context, our article should bring additional elements for consideration in the hypothesis of a vertical transmission of the human disease linked to the BSE agent."

References/Resources on Cats and other animals with the Feline and other Forms of Mad Cow Disease

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