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BRITISH MEDICAL JOURNAL LONDON: SATURDAY, -JULY 11th, 1936 EPIDEMIC POLIOMYELITIS EPIDEMIOLOGY, CAUSES, AND PREVENTION * BY SIR ARTHUR S. MAcNALTY, K.C.B., M.A., M.D., F.R.C.P. CHIEF MEDICAL OFFICER OF THE MINISTRY OF HEALTH Poliomyelitis has been described by Simon Flexner as Wickman (1901 and 1905), Strauss (1910), and Peabody, " one of the saddest of diseases," and Dr. Thomas Buzzard Draper and Dochez (1912). characterized it as being " peculiarly cruel " to its hapless Striimpell gave the first complete account of the ceretral victims. Apart from the fact that the majority of the type of poliomyelitis (polio-encephalitis) in 1884. The first adult case of poliomyelitis was described by Vogt in 1859. sufferers are young children, it leaves a considerable pro- portion of the survivors permanently paralysed, and so crippled as to constitute for them a life-long handicap in Pathology the struggle for existence. The studies of Flexner and Lewis, Leiner and von and and others have The has been described by somewhat cumbrous Wiesner, Landsteiner Levaditi, malady shown that the disease is due to a virus which passes names. It is scientifically known as acute poliomyelitis through the finest filter and that the filtrate is capable of (including polio-encephalitis and polio-encephalo-myelitis). reproducing the disease in monkeys. The virus attacks " infantile It has long been known under the name of the nervous system, causing inflammation of- the grey paralysis," but the term is inisleading, for the disease may rmatter, especially of the anterior cornua of the spinal cord. occur in adults, though not so frequently as in children, Most I'he histological lesions are hyperaemia, exudation of and paralysis does not always supervene. lymphocytes round the blood vessels, and degeneration of as epidemiologists prefer to speak of the disease simply the motor cells. Occasionally the whole thickness of " large epidemic poliomyelitis." the cord may become involved and a transverse myelitis result. The brain may be primarily or secondarily History affected (polio-encephalitis a-nd polio-encephalo-myelitis) Acute poliomyelitis appears to have existed from very and the meninges implicated. Widespread visceral lesions early times. are found, such as hyperplasia of the tonsils, the spleen and " Since the days of Mephibosheth," wrote Osler, " parents the lymphatic glands, together with cloudy swelling of the have been inclined to attribute this form of paralysis to the kidney and liver. carelessness of nurses in letting the children fall, but very rarely is the disease induced by traumatism." Sir Walter Clinical Features Scott was attacked in 1773 when 18 moilths old. He describes Acute poliomyelitis is best described as an acute it as " the fever which often accompanies the cutting of large infectious fever which may or may not proceed to invasion teeth " (Lockhart's Life of Sir Walter Scott). Scott's right of the nervous system. Walshe' submits that a precise leg was paralysed and permanent lameness resulted. and practical conception of poliomyelitis is obtained by The first medical description of poliomyelitis appears to recognizing the existence of three clinically and pathologi- have been given by an English practitioner, Michael in Underwood, in the first-edition of his treatise on the Diseases cally distinct stages its evolution: one of general infection of Children in 1784. He devotes two pages in his book to during which the virus obtains lodgment in the liver, spleen, the disease under the title of " Debility of the Lower lymphatic glands and bone-marrow, in all of which tissues Extremities." In 1822 Shaw-reported a few cases. Dr. John Iesions are found; one of invasion of the subarachnoid Badham, of Worksop, Notts, in 1835 described four cases, space, when the virus gives rise to- a characteristic and for the first time drew attention to the cerebral symptoms meningeal reaction as revealed by examination of the of the disease. Jacob Heine in 1840 wrote an instructive cerebro-spinal fluid; and a third of invasion of the grey monograph and is regarded generally as the pioneer contributor matter of the central nervous system, where the virus to modern knowledge of poliomyelifis. Some thirty years later, Medin of Stockholm called attention to the fact that produces inflammatory lesions. Walshe's classification is the disease occurred occasionally in epidemics; hence the adopted in the following description of the clinical features, term " Heine-Medin disease," which is commonly used in but it must be emphasized that the three stages- often Germany and Scandinavia to include the various clinical forms overlap or synchronize. of acute epidemic poliomyelitis. From the writings of Underwood in 1784 up to 1863, the Clinical Character clinical side of poliomyelitis was chiefly studied and there was 1. Initial Stage.-This stage is variable in duration; it little or no knowledge of the pathological processes involved. may last only a few hours and be unrecognized, or on the But in 1863 von Reinecker and von Recklinghausen in other hand it may extend to five or even ten days. The Germanv, and Cornil in France, described the lesions in the be those associated with anterior horns and the lateral columns of the spinal cord. initial symptoms may commonly Then followed a long procession of workers. Rissler first the pre-eruptive period of the exanthemata-headache, investigated the histology of the acute cases and his work has pyrexia (102°-103°), malaise, sore throat, tonsillitis, been completed by the studies of Harbitz and Scheel (1907), coryza, nasal- discharge and irritability of temper. Epistaxis may occur and, in some epidemics, vomiting and * A Chadwick Lecture delivered at the Royal United Services Institution on March 19th, 1936. diarrhcea are leadilig symptoms. There is no typical skin [3940] Tux BRIMTIW 58 JULY 11, 1936 EPIDEMIC POLIOMYELITIS MEDICAL JOURNAL 2 eruption; herpes and herpes zoster have been noted; After-effects erythematous or morbilliform rashes may occur, and cases In the poliomyelitic form the paralysis may persist and have been erroneously diagnosed as scarlet fever or the patient is to a degree corresponding with the measles. The condition may clear up rapidly and complete crippled extent of the damage to the spinal cord. In the recovery ensue (mild or abortive cases). On the other encephalitic form, though the risk of fatality is greater, hand, the initial stage may merge into a second phase. Ex- there are commonly no after-effects on recovery. ceptionally therc may be a remission period of some hours, or even days, between these phases in which the temperature falls to normal, the child appears to have recovered and Diagnosis perhaps is allowed to go about on the assumption that he The initial symptoms of poliomyelitis are indistinguish- has had a slight febrile ailment. But there comes a able from those of the onset of other infectious diseases, recrudescence of temperature and an accentuation of the but it must be remembered that in poliomyelitis this stage disease. may pass very rapidly into that of involvement of the 2. The preparalytic stage indicates subarachnoid or central nervous system, and, if there be any cause for meningeal invasion. It varies in intensity and duration, suspicion of poliomyelitis, the patient should be kept under being at times so slight and transient as to be unnoticeable, close medical supervision so that the physician may detect and at others of great severity. On the whole its duration the earliest signs of meningeal invasion. is short and it ends either in speedy recovery or passes into As regards the polio-encephalitic form, the implication the paralytic stage within a few hours. The chief signs of the brain, medulla, meninges or spinal nerves may give are continuation (or renewal) of the pyrexia and headache, rise to varying symptoms (for example, in bulbar paralysis onset of pains in the back and limbs with tenderness speech disturbances are noted). There may be confusion in over the upper dorsal vertebrae, stiffness of the neck and the differential diagnosis between polio-encephalitis and spine with resistance to passive flexion, muscular twitch- cerebro-spinal meningitis, encephalitis lethargica, tubercu- ings (often indicating the site of future paralysis), lous meningitis or septic meningitis. The previous history hyperaesthesia, retention of urine, drowsiness and some- of the patient and the presence of similar cases in the times deep stupor, occasionally even opisthotonos. vicinity, together with the examination of the cerebro- Diminution or disappearance of the superficial or some of spinal fluid, will assist in the determination of the the deep tendon reflexes may be the first indication of the diagnosis. nature of the case. Kernig's sign is frequently present. The Cerebro-spinal Fluid 3. Paralytic Stage (stage of invasion of the central Examination of the cerebro spinal fluid is often of value nervous system).-Once the virus is established in the in the diagnosis of poliomyelitis. central nervous system paralytic phenomena may appear, In the initial stage the cerebro-spinal fluid is normal with their character being dependent on the localization and a cell count of from 0 to 10 c.mm. In the preparalytic stage intensity of the lesions. (subarachnoid or meningeal invasion) the fluid is usually under (a) Poliomyelitic Form.-In this form the lesions moderately increased pressure (aggravated by anaesthesia) and involve the lower motor neurons, giving rise to flaccid appears to be clear, though when viewed by transmitted light " " it presents a faint haziness or ground glass appearance. paralysis affecting one or two muscles, or a group of There is an increase in the number of cells (mononuclear and muscles, or one or more limbs. The paralysis comes on polymorphonuclear), the count usually being between 50 and as a rule three or four days after the onset of illness, but 250 per c.mm., but occasionally it may be as high as 700 to it may be the first sign of the disease detected.