Rabbit pox: An experimental study of the pathways of infection in rabbits

Bedson, H. S.; Duckworth, Marjorie J.

doi:10.1002/path.1700850102

Cited by 55 publications

(47 citation statements)

References 15 publications

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“…However, rinderpest obviously differs from pox-virus infections, which have been the subject of many previous studies on the pathogenesis of generalized virus diseases and in which proliferation at the initial site of virus penetration is readily demonstrable. (See Fenner (1948a, b) for ectromelia; Fenner & Woodroofe (1953) for myxomatosis; Hahon & Wilson (1960) for monkey small-pox; Bedson & Duckworth (1963) for rabbit pox.) Grist (1950), reviewing the position with respect to human measles, suggested that in this disease there may sometimes be a transient 'illness of infection', associated possibly with the production of a 'primary complex'.…”

Section: Discussionmentioning

confidence: 99%

Studies on the pathogenesis of rinderpest in experimental cattle II. Proliferation of the virus in different tissues following intranasal infection

Plowright

1964

J. Hyg.

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The pathogenesis of rinderpest virus was studied in twenty-nine grade cattle, which were infected by the intranasal route with a virulent strain of virus recently isolated in East Africa (RGK/1). These animals were killed or died at intervals of 1–16 days after infection and a number of tissues from each of them (usually 21) was titrated for virus infectivity in monolayer cultures of primary bovine kidney cells.Temperature reactions were first detected on the 3rd to 5th days (mean 4·1), mouth lesions on the 6th to 9th and diarrhoea on the 8th or 9th days, following infection. The course of the disease was divided into four phases, viz. incubation (days 1–4), prodromal (days 5–7), mucosal (days 8–12) and early convalescence (days 13–16). Virus proliferation in different tissues was related to these clinical phases, detailed results being presented in tabular and graphical form.No primary multiplication was detected in the nasal mucosa but virus was demonstrable within 48 hr. in its associated lymph nodes. Low-level viraemia began on the 2nd or 3rd days after infection and generalization had occurred by the end of the incubation period. The virus had established itself at this time throughout the alimentary tract and, sometimes, in the lungs.The prodromal phase was characterized by plateaux of high virus titres in the lymphopoietic and lympho-epithelial tissues; there was a descending gradient from the cephalic nodes to the superficial lymph and haemolymph nodes of the body, to the visceral lymph nodes and spleen. There was a similar gradient in the titre of virus in the mucosae of the gastro-intestinal tract—from caecum to colon, to ileum and pylorus. Virus first appeared in the turbinate mucosa on the 5th day, post-infection and lung titres were high towards the end of this period. Some virus proliferation may have occurred in the liver, but none was certainly demonstrable in the kidney, myocardium or brain.The mucosal phase began with continuing high titres of virus in all the major sites of proliferation, but a decline set in from the 9th day onwards. This at first involved the cephalic lymph nodes but soon extended to the spleen and other lymphopoietic tissues. It was most delayed in lympho-epithelial structures such as the tonsil, lung and gastro-intestinal mucosae. It was suggested that the decline in virus titres was due to the destruction of susceptible cells, accompanied by the local production and later circulation of antibody. Neutralizing antibody was present in the serum on and after the 9th day.During the early convalescent period virus had disappeared from four animals, with the exception of one recovery from the lung tissue. Antibody titres were high during this time.These results were discussed with reference to previously existing information on the distribution of rinderpest virus in infected cattle. An attempt was made to correlate them with published information on the pathogenesis of human measles and canine distemper. The data were also used to explain some previously reported observations on the excretion of rinderpest virus by experimentally infected cattle.This study would not have been possible without the enthusiastic co-operation of Messrs C. S. Rampton, A.I.M.L.T., R. F. Staple, A.I.M.L.T., and R. Pillinger, F.I.M.L.T., in organizing and carrying out a very considerable number of laborious titrations. Dr B. Liess helped with some of the animals killed at earlier stages of the infection. Our junior African staff gave invaluable assistance with their careful and efficient handling of many thousands of tissue cultures; amongst them we should particularly like to mention Mr Francis Ngugi and Mr Harrison Agili.This paper is published with the permission of the Director, E.A.V.R.O., Mr H. R. Binns, C.M.G., O.B.E.

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Section: Discussionmentioning

confidence: 99%

Studies on the pathogenesis of rinderpest in experimental cattle II. Proliferation of the virus in different tissues following intranasal infection

Plowright

1964

J. Hyg.

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“…The lethal dose of vaccinia or cowpox viruses in a single intradermal injection is very large, and probably infinite, while that of rabbitpox is small, 0.1-1.0 pfu (Bedson & Duckworth, 1963), and it was felt that challenge with this virus would be a test of lifeprotecting immunity.…”

Section: Challenge With Rabbitpox Virusmentioning

confidence: 99%

“…It was intended to give enough antigen to ensure a maximal response, and the nature of the antibody produced was examined in detail. Finally, these results were related to the rabbits' ability to withstand intradermal challenge with vaccinia, cowpox or the more lethal rabbitpox, an infection similar in several respects to human smallpox (Bedson & Duckworth, 1963).…”

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confidence: 99%

The immunogenicity of heat-inactivated vaccinia virus in rabbits

Madeley

1968

J. Hyg.

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SUMMARYRabbits were immunized by multiple intradermal injections followed by six intravenous doses of vaccinia virus inactivated by heating to 65° C. Particular attention was paid to confirming that the virus used was fully inactivated and incapable of reactivation. The immunized rabbits developed neutralizing and other antibodies to a titre comparable with those developed in response to live virus, but multiple intravenous injections were required to elicit a maximum titre. A qualitatively different response was seen only in immunodiffusion tests in agar gel where two or three fewer lines developed with antisera to heated virus than with those to live virus. The rabbits were subsequently challenged intradermally either with vaccinia and cowpox or with rabbitpox. They showed some immunity to vaccinia and cowpox, compared with normal controls, but less than that elicited by live virus. Their resistance to lethal doses of rabbitpox was life-saving though some rabbits did develop lesions. Later rechallenge of the rabbits showed that they had not developed further immunity, in distinction from the normal controls. The implications of these findings are discussed.I wish to thank the National Fund for Research into Poliomyelitis and Other Crippling Diseases for their generous support in providing a Research Fellowship during which this work was done. I wish to thank also Professor A. W. Downie F.R.S. and the Staff of the Department of Bacteriology, University of Liverpool, for their encouragement and assistance respectively.

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“…So far as we are aware, the only comparable experimental study of naturally acquired cases of a viral exanthem is that of Bedson & Duckworth (1963), who f-a04…”

Section: V P Taylor and Othersmentioning

confidence: 99%

“…However, in their experiments there was a tendency for rabbits killed later after exposure to show a wider dissemination and higher titres of virus than those killed earlier; this, surprisingly, was not our experience with naturally acquired rinderpest. Bedson & Duckworth (1963) encountered cases of both upper and lower respiratory tract infection, but in many instances a complete 'primary complex' was established, with virus proliferation both at the presumed surface of entry and in the regional lymph node.…”

Section: V P Taylor and Othersmentioning

confidence: 99%

Studies on the pathogenesis of rinderpest in experimental cattle: IV. Proliferation of the virus following contact infection

et al. 1965

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Cattle were infected with rinderpest virus by housing them for 24 hr. in stalls containing donor animals which had been reacting to the disease for 3–5 days. They were then transferred to individual clean stalls and killed on the 2nd to 10th days following first exposure. Various tissues were collected, particularly those of the upper and lower respiratory tracts, and their virus content was estimated in calf-kidney tissue cultures.Virus was recovered from 15 of 35 animals tested and in eight of these generalization had occurred, although only two had begun to show a pyrexial response. The stage of the infection could not be predicted from the time that had elapsed following exposure, since early, limited proliferation was encountered on the 3rd to the 10th days.It was considered that seven animals gave indications of the pathways by which natural infection had occurred. In each of these virus proliferation was established very early in the pharyngeal lymph node; in three the submaxillary lymph node was similarly involved and in four the palatal tonsil. It was suggested that these data probably indicated that infection always occurred via the upper respiratory tract.In three cases virus titres were highest in the bronchial or costocervical lymph nodes; this was construed as evidence for the additional involvement of the lower respiratory tract in primary infection.No infectivity could be demonstrated in the mucosae or lung parenchyma associated with the above-mentioned lymph nodes and this, together with previously published data, was accepted as strong presumptive evidence that the infecting virus passes through the mucosae without producing a local lesion or proliferating there. These results were compared briefly with those of Bedson & Duckworth (1963) for rabbit pox.

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Rabbit pox: An experimental study of the pathways of infection in rabbits

Cited by 55 publications

References 15 publications

Studies on the pathogenesis of rinderpest in experimental cattle II. Proliferation of the virus in different tissues following intranasal infection

Studies on the pathogenesis of rinderpest in experimental cattle II. Proliferation of the virus in different tissues following intranasal infection

The immunogenicity of heat-inactivated vaccinia virus in rabbits

Studies on the pathogenesis of rinderpest in experimental cattle: IV. Proliferation of the virus following contact infection

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