foot-and-mouth disease in man

1
994 were unsatisfactory for this purpose, and in Holland the production of effective high-titre anti-D serum could be achieved only by using male volunteers. D. Lehane has confirmed this finding and shown that the yield of serum can be increased by plasmapheresis. These donors at present run the risk of serum hepatitis from the repeated injections of Rh-positive red cells required to produce a high-titre antiserum; and they will continue to do so until a synthetic Rh antigen can be prepared. This risk can be made very small by always immunising from a donor whose blood has never been known to produce jaundice in the recipient of a transfusion. Further developments will depend on the criteria eventually adopted for the use of anti-D serum, on the titre of the antiserum produced, and on the results of studies of the efficacy of various quantities of anti-D y-globulin needed to ensure elimination of the foetal cells from the maternal circulation. Present opinion is that the provision of sufficient antiserum is possible. A method for preventing rhesus immunisation is now available: the indications for its use and the question of supplying antiserum on a large scale have still to be settled. FOOT-AND-MOUTH DISEASE IN MAN IN July and August, 1966, an outbreak of foot-and- mouth disease in Northumberland affected a man as well as a great many cattle. Apart from the extreme rarity of a human infection,! the events of the outbreak created interest and controversy, because the suggestion was made that the human patient might have played an important part in spreading the disease to animals. This issue became all the more lively because the patient suffered what was taken to be a relapse of his foot-and-mouth infection three weeks after he was first infected at the end of July, 1966. Moreover, he had another similar clinical illness in December and January. From vesicles on the patient’s hands during his first attack (July, 1966) foot-and-mouth virus of type 0 was isolated. Titration of the amount of virus in the tissue examined showed a quantity greater than could be accounted for by mere contamination of the skin, although less than that normally found in lesions from susceptible animals. There was a striking rise in the amount of the patient’s serum-antibody neutralising virus type 0 from 1 in 178 on July 31 to 1 in 708 on Aug. 24. Thereafter the antibody titre fell steadily to 1 in 355 on Sept. 3, and 1 in 80 on Feb. 6. The titre of complement-fixing antibody followed a corresponding course at the usual much lower levels. In July and August virus was present in the patient’s lesions for less than one week. It was not isolated from the lesions of the second and third attacks; and these attacks did not interrupt the steady decline in the level of antibody. What ought we to learn from this episode ? Dr. J. W. Howie and Sir William Weipers, who were asked by the Minister of Agriculture, Fisheries and Food and the Minister of Health to investigate and report on the matters concluded that the extreme rarity of human foot-and-mouth infection is well established. Moreover, the few authenticated cases in humans have been mild and transient, as was true also in the present event. The Animal Virus Research Institute at Pirbright, which deals 1. Pilz, W., Garbe, H. G. Zentbl. Bakt. Parasitkde, 1966, 198 S, 154. 2. Hansard (House of Commons), April 19, 1967, col. 491. See Lancet, April 29, 1967, p. 961. with all foot-and-mouth problems in Great Britain, and which has also much experience of fundamental and applied research and of overseas outbreaks, has no evidence, during the forty years of his history, of any- thing resembling foot-and-mouth disease in any of the staff employed there. Routine sampling of workers at the Institute, since the appropriate methods became available, have shown only one person with a slight rise of serum-antibody titre-this despite the heavy exposures to virus which many of the workers inevitably experience. The patient in the 1966 Northumberland outbreak was infected in the sense that virus multiplied in his tissues, although for a period not longer than one week. His " relapses ", which presented a similar clinical picture to the original illness, were not infections with foot-and- mouth virus. What they were is not known. They were not " hand, foot and mouth disease " 3- ’-a different disease altogether, associated with entirely different viruses. They might have been due to herpes, to hyper- sensitivity of some sort, or to one of the other causes of tongue ulceration. Tongue ulcers are not at all infrequent in humans, and their causation is often obscure. A pos- sible interpretation of the facts of this case might well be that foot-and-mouth virus, which was present in abund- ance during the outbreak at the patient’s place of resi- dence, first contaminated and then colonised a lesion of unknown causation affecting his tongue and hands. This lesion, whatever it may have been, was recurrent; but the negative results of investigations for virus and antibody in the suspected relapses show that they at any rate were not caused by foot-and-mouth virus. This may also raise doubts whether foot-and-mouth virus actually caused the first illness, although the virus certainly multiplied in the lesions. Obviously systematic searches for cases of human foot-and-mouth disease are not required, or indeed desirable. They would create misunderstandings, and possibly even panic, and they would be most unlikely to be in any sense rewarding. Laboratory examination of material from suspected cases is quite correctly restricted to Pirbright, both because of that Institute’s unique experience and because the disease is so highly com- municable that the risks of escape of virus must be mini- mised by having all laboratory work done at one centre. If that Institute were to be asked to accept more material than is either necessary or desirable, its resources would not be available to carry out the extensive work it is required to undertake whenever the disease is found or suspected in farm animals. The susceptibility of animals is the problem. We need not add to the difficulties of containing the disease by regularly looking for non-existent human cases. Where such are found it is enough to admit the patient to hos- pital-where he will not infect animals. Nature will see to his recovery. To enable the appropriate public- health measures to be taken and to offer a chance of rational discussion of the event, the medical officer of health and the Ministry of Health should be informed whenever the virus is isolated from a human or if such an infection is strongly suspected on good grounds. 3. Robinson, C. R., Doane, F. W., Rhodes, A. J. Can. med. Ass. J. 1958, 79, 615. 4. Magoffin, R. L., Jackson, E. W., Lennette, E. H. J. Am. med. Ass. 1961, 175, 441. 5. Alsop, J., Flewett, T. H., Foster, J. R. Br. med. J. 1960, ii, 1708. 6. Flewett, T. H., Warin, R. P., Clarke, S. K. R. J. clin. Path. 1963, 16, 53. 7. Higgins, P. G., Ellis, E. M., Boston, D. G., Calnan, W. L. Mon. Bull. Minist. Hlth, 1965, 24, 38.

Upload: dangkhuong

Post on 30-Dec-2016

212 views

Category:

Documents


0 download

TRANSCRIPT

Page 1: FOOT-AND-MOUTH DISEASE IN MAN

994

were unsatisfactory for this purpose, and in Holland theproduction of effective high-titre anti-D serum could beachieved only by using male volunteers. D. Lehane hasconfirmed this finding and shown that the yield of serumcan be increased by plasmapheresis. These donors at

present run the risk of serum hepatitis from the repeatedinjections of Rh-positive red cells required to produce ahigh-titre antiserum; and they will continue to do sountil a synthetic Rh antigen can be prepared. This riskcan be made very small by always immunising from adonor whose blood has never been known to producejaundice in the recipient of a transfusion.

Further developments will depend on the criteria

eventually adopted for the use of anti-D serum, on thetitre of the antiserum produced, and on the results ofstudies of the efficacy of various quantities of anti-Dy-globulin needed to ensure elimination of the foetal cellsfrom the maternal circulation. Present opinion is that theprovision of sufficient antiserum is possible. A method forpreventing rhesus immunisation is now available: theindications for its use and the question of supplyingantiserum on a large scale have still to be settled.

FOOT-AND-MOUTH DISEASE IN MAN

IN July and August, 1966, an outbreak of foot-and-mouth disease in Northumberland affected a man as wellas a great many cattle. Apart from the extreme rarityof a human infection,! the events of the outbreak createdinterest and controversy, because the suggestion was madethat the human patient might have played an importantpart in spreading the disease to animals. This issue becameall the more lively because the patient suffered what wastaken to be a relapse of his foot-and-mouth infectionthree weeks after he was first infected at the end of July,1966. Moreover, he had another similar clinical illness inDecember and January.From vesicles on the patient’s hands during his first

attack (July, 1966) foot-and-mouth virus of type 0 wasisolated. Titration of the amount of virus in the tissueexamined showed a quantity greater than could beaccounted for by mere contamination of the skin, althoughless than that normally found in lesions from susceptibleanimals. There was a striking rise in the amount of thepatient’s serum-antibody neutralising virus type 0 from1 in 178 on July 31 to 1 in 708 on Aug. 24. Thereafterthe antibody titre fell steadily to 1 in 355 on Sept. 3,and 1 in 80 on Feb. 6. The titre of complement-fixingantibody followed a corresponding course at the usualmuch lower levels.

In July and August virus was present in the patient’slesions for less than one week. It was not isolated fromthe lesions of the second and third attacks; and theseattacks did not interrupt the steady decline in the levelof antibody. What ought we to learn from this episode ?Dr. J. W. Howie and Sir William Weipers, who wereasked by the Minister of Agriculture, Fisheries and Foodand the Minister of Health to investigate and report onthe matters concluded that the extreme rarity of humanfoot-and-mouth infection is well established. Moreover,the few authenticated cases in humans have been mildand transient, as was true also in the present event. TheAnimal Virus Research Institute at Pirbright, which deals1. Pilz, W., Garbe, H. G. Zentbl. Bakt. Parasitkde, 1966, 198 S, 154.2. Hansard (House of Commons), April 19, 1967, col. 491. See Lancet,

April 29, 1967, p. 961.

with all foot-and-mouth problems in Great Britain, andwhich has also much experience of fundamental andapplied research and of overseas outbreaks, has no

evidence, during the forty years of his history, of any-thing resembling foot-and-mouth disease in any of thestaff employed there. Routine sampling of workers at

the Institute, since the appropriate methods became

available, have shown only one person with a slight riseof serum-antibody titre-this despite the heavy exposuresto virus which many of the workers inevitably experience.The patient in the 1966 Northumberland outbreak was

infected in the sense that virus multiplied in his tissues,although for a period not longer than one week. His"

relapses ", which presented a similar clinical picture tothe original illness, were not infections with foot-and-mouth virus. What they were is not known. They werenot " hand, foot and mouth disease " 3- ’-a differentdisease altogether, associated with entirely differentviruses. They might have been due to herpes, to hyper-sensitivity of some sort, or to one of the other causes oftongue ulceration. Tongue ulcers are not at all infrequentin humans, and their causation is often obscure. A pos-sible interpretation of the facts of this case might well bethat foot-and-mouth virus, which was present in abund-ance during the outbreak at the patient’s place of resi-dence, first contaminated and then colonised a lesion ofunknown causation affecting his tongue and hands. Thislesion, whatever it may have been, was recurrent; but thenegative results of investigations for virus and antibody inthe suspected relapses show that they at any rate were notcaused by foot-and-mouth virus. This may also raisedoubts whether foot-and-mouth virus actually causedthe first illness, although the virus certainly multipliedin the lesions.

Obviously systematic searches for cases of humanfoot-and-mouth disease are not required, or indeeddesirable. They would create misunderstandings, andpossibly even panic, and they would be most unlikely tobe in any sense rewarding. Laboratory examination ofmaterial from suspected cases is quite correctly restrictedto Pirbright, both because of that Institute’s uniqueexperience and because the disease is so highly com-municable that the risks of escape of virus must be mini-mised by having all laboratory work done at one centre.If that Institute were to be asked to accept more materialthan is either necessary or desirable, its resources wouldnot be available to carry out the extensive work it is

required to undertake whenever the disease is found or

suspected in farm animals.The susceptibility of animals is the problem. We need

not add to the difficulties of containing the disease byregularly looking for non-existent human cases. Wheresuch are found it is enough to admit the patient to hos-pital-where he will not infect animals. Nature will seeto his recovery. To enable the appropriate public-health measures to be taken and to offer a chance ofrational discussion of the event, the medical officer ofhealth and the Ministry of Health should be informedwhenever the virus is isolated from a human or if such aninfection is strongly suspected on good grounds.3. Robinson, C. R., Doane, F. W., Rhodes, A. J. Can. med. Ass. J. 1958,

79, 615.4. Magoffin, R. L., Jackson, E. W., Lennette, E. H. J. Am. med. Ass.

1961, 175, 441.5. Alsop, J., Flewett, T. H., Foster, J. R. Br. med. J. 1960, ii, 1708.6. Flewett, T. H., Warin, R. P., Clarke, S. K. R. J. clin. Path. 1963, 16, 53.7. Higgins, P. G., Ellis, E. M., Boston, D. G., Calnan, W. L. Mon. Bull.

Minist. Hlth, 1965, 24, 38.