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POLIOMYELITIS: THE PORT OF ENTRY

THE LANCET

LONDON: SATURDAY, NOVEMBER 13, 1937

INCREASED incidence of acute poliomyelitis hasrecently been causing anxiety in this country aswell as in Australia and the U.S.A., and the searchfor a remedy goes on. The problem of immunityto the virus has been studied continuously eversince its discovery in 1909, but the mechanism ofits production still eludes us. At one time itwas thought that the principal factor ensuringthis immunity was specific antibody, and it wason this assumption that the treatment of polio-myelitis in the preparalytic stage by means ofconvalescent serum was advocated and practised.A more critical attitude to the evaluation of this

therapeutic measure showed that the earlier

reports of its value were, to say the least, toooptimistic, and a better understanding of the routeof infection followed by the virus has furnishedthe reason. Although most authorities hold thatthe route by which it invades the body is the

nasopharyngeal mucosa, this thesis is not uni-

versally accepted. There are some who believethat the virus may be absorbed from the intestinaltract, reaching the central nervous system via thelymph and blood streams. Some four or five yearsback KLING and LEVADITI, in conjunction withtheir colleagues LBPiNE and HoRNUS, advancedexperimental evidence in support of the alimentaryroute. More recently J. A. TooMEY in Americahas published a summary of data questioning thenasopharynx as a port of entry. S. FLEXNER,2a pioneer in this field who has recently returned tothe investigation of problems connected with

poliomyelitis, has however failed to confirm anyof this work. He shows that monkeys do notdevelop poliomyelitis when virus is introducedinto the stomach provided contamination of thebuccal and nasal mucosa is avoided. He pointsout further that in the type of experiment wherevirus is injected direct into the small intestine,infection, when it does occur, is most probablythe result of virus passing into the intestinal walland making contact with nerve-fibres there.FLEXNER gives his entire supportto the view that themucosa of the nasopharynx is the only establishedportal of entry of poliomyelitis virus-a conclusionwhich is shared by most workers. Obviouslythis has a direct bearing on the mechanism ofimmunity to poliomyelitis, for were the alimentaryroute of infection the usual one, with distributionof the virus by the blood stream, neutralisingantibody would play a more important r6le in

preventing infection than it could do if the nasalroute was substantially the only one by whichvirus entered.

1J. Amer. med. Ass. August 7th, 1937, p. 402.2 J. exp. Med. 1936, 63, 209.

FLEXNER has also studied the response of

monkeys to nasal instillation of the virus of

poliomyelitis. This animal is relatively resistentto infection by the nasal route unless, as E. W.SCHULTZ has shown, the mucosa is prepared bytreatment with a buffer solution of acid reaction.But FLEXNER has found that even when the monkeydoes not develop poliomyelitis as the result ofnasal instillation, it does not remain indifferentto this treatment. Quite constantly a reactionoccurs in the cerebro-spinal fluid consisting of alymphocytic pleocytosis and associated increase ofcells ; less constant is the appearance of detectableamounts of globulin. Often there is a concomitantrise of temperature and although these changes aresimilar to, though of less degree than, those occurr-ing in the monkey which develops manifest infectionthey are not associated with the development ofimmunity. This inapparent infection in the

monkey gives rise to no production df specificantibody ; the animal may develop paralyticdisease when given a further course of nasalinstillationof virus and it is as susceptible to cerebralinoculation as the normal monkey. Apparentlyfrank infection is necessary for development of

immunity in the monkey, and if our belief is truethat man commonly acquires immunity to polio-myelitis as the result of symptomless infectionthen one must conclude that the two species differmarkedly in their ability to develop immunity.FLEXNER further shows that when immune monkeysare given virus by the nasal route some two yearsafter recovery, not only will they react with

changes in the cerebro-spinal fluid and pyrexia,but a considerable proportion of them will developfrank and even severe second attacks. This mayoccur whether the homologous or a heterologousstrain of virus is used to reinfect and even when the

monkey has been hyperimmunised after the firstattack of poliomyelitis. Admittedly the amount ofvirus instilled into the nares in these experimentsis enormously greater than man is likely to receivein the natural course of events ; but second attacksof poliomyelitis are known to occur in man,

possibly with greater frequency than we at presentimagine. This lack of durability in acquiredimmunity to poliomyelitis is an aspect of the

subject which must be borne in mind when consider-ing the mechanism of immunity to poliomyelitisand the prophylaxis of the disease.

THE OUT-PATIENT

ON another page some account is given of howthe British Hospitals Association is facing thefirst three recommendations made by the VoluntaryHospitals Commission appointed at its annual

- conference in June, 1935. The question of theareal distribution of hospital facilities is funda-mental, but when that has been dealt with therewill remain the problem of overcrowded out-

patient departments about which the Commissionhad something trenchant to say in its report lastApril. The gravamen of this complaint is that the

3 Ibid, 1935, 62, 787.4 Ibid, 1937, 65, 497.