Re: Further response to James Parker FeLV Horizontal Transmission 5 April 2004
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Parker James E,
Retired Paediatrician
289 McCallum Rd ,Abbotsford B.C. CANADA v2s 8a1

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Re: Re: Further response to James Parker FeLV Horizontal Transmission

In the second paragraph of my submission of Mar 16 I should have written 'infectivity' rather than 'Koch's postulates'. I apologise. As Eleni Papadopulos-Eliopulos is well aware the application of Koch to viral as distinc from bacterial infections is unsatisfactory.

A response to her April 1st submission follows.

Having commented on test and removal of FeLV infected cats in paragraph three as reported in 1977 by Jarrett, Hardy and Essex, she dismisses this in paragraph four. 'Since the disease may be caused by other factors, it means that either decreasing or increasing the incidence of disease in a household by either removal or addition of cats is not proof that the disease is caused by FeLV............' What other factors ?.

FeLV appears to produce a spectrum of reaction in cats which varies from the development of natural immunity with the development of feline oncarnovirus membrane associated antigen (FOCMA )antibodies to anaemia, runting syndrome, immunodeficiency,thymic atrophy,infectious peritonitis, panleukopoenia leukaemia and lymphosarcoma etc. In Hardy et al's paper in Nature ( Sept 23 1976 263 326-328 ) 'Prevention of the contagious spread of feline leukaemia virus and the development of leukaemia in pet cats' all the FeLV associated conditions were removed from the 51 households under study. Also all the FeLV associated conditions remained in the 25 control households. This point is worthy of emphasis.

When Jarrett wrote in 1975 ' in the Glasgow urban area between 10% and 40% of normal cats have antibody titres to FeLV whereas the leukaemia incidence is only 0.05%', he did not conclude that no proof exists that FeLV causes the disease (these are Perth inferences). He had induced disease experimentally by inoculation of FeLV as far back as 1964 and also by the introduction of diseased animals in uninfected households.

The appearance of new objective signs after an incident suggests relationship. Thus ,if after exposure to a sick animal or inoculation of infective material there appears antibody to gs antigens, EM (Electron Microscopy) virus positive platelets or antibodies to FOCMA,this is significant. One would consider this evidence of FeLV infection. Not so says Eleni Papadopulos-Eliopulos. Antibodies to gs antigen not proven to be specific, EM particles commonplace and not proven to be infectious and since the FOCMA antigens are cellular and not viral (Essex et al), finding antibodies to them cannot be considered proof for FeLV infection (Perth opinion).

FOCMA -Feline oncarnovirus ASSOCIATED membrane antigen. As Eleni Papadopulos-Eliopulos is probably well aware, there is an inverse correlation between antibody to this antigen and the development of FeLV related disease and elaboration of a vaccine based on this has been available for over 20 years.

Eleni Papadopulos-Eliopulos reporting on Jarrett et al's paper in J Nat Cancer Inst(1973 51 833-841) is critical of lack of proper controls. In discussing Experiment 6 ,in which a seriously ill cat in the terminal stages of alimentary lymphoblastic lymphosarcoma was put in a house with 4 healthy unrelated adult cats (FeLV negative), three of the cats developed positive EM for virus at week 3 and the fourth a positive FOCMA antibody titre (0.16) at week 4. She denies the claim of horizontal transmission because the seriously ill cat was not reported to be FeLV infected. On reviewing the paper in question I cannot find any evidence that this cat was or was not tested for FeLV. It was obviously presumed to be infected. If this experiment were repeated and the index cat appropriately tested positive would Eleni Papadopulos-Eliopulos then accept this as evidence of horizontal transmission of FeLV ?.

James E Parker

Competing interests: None declared