914

of tuberculosis, which may be partly explained by theirvery hard life ; besides housework, and perhaps mindingthe garden, they help with fishing, preparing baits, andmending nets.The diet of many of the islanders is glaringly deficient

in fresh fruit and vegetables, and in milk,2 and could beimproved by such means as home preparation of vitamin Cfrom local berries, and by keeping goats for milk (cowsare a rarity, and bovine tuberculosis does not play animportant part). Houses are bad only in St. John’s,but the general standard of living is low : in 1937 athird of the population was on relief and the allowancesare wholly inadequate, sometimes " forcing a tuberculoushousehold into the most abject poverty." It is suggestedthat special allowances be made to tuberculous patientsand their families, and that industries should be obligedto take a proportion of those recovering from the disease.There is at present only one sanatorium for the wholeisland, and hospitals and dispensaries are needed. Train-

ing will be required for the doctors and nurses staffingthese institutions, and Dr. Garland and Dr. Hart wantto see more mass radiography, using the miniature

film, and tuberculin-testing of children to act as a pointerto open cases.

LOUSE-BORNE TYPHUS

COMPLICATION and simplincation seem to alternate inthe classification of the typhus group of fevers. Thisstatement applies equally to tick-borne, mite-borne, andlouse-borne typhus.! Up to about forty years ago onlyone form of louse-borne typhus was recognised-thatnow called epidemic exanthematous typhus, caused byRickettsia prowazeki, and conveyed by Pediculus humanics-but about that time Wolhynian fever, caused byR. 2uothyziccc, was described as a specific entity in Poland.In the war of 1914-18 a third entity, trench fever orfive-day fever, was recognised and attributed to 7<*. quin-tana. In the interval between that war and 1939 verylittle was heard of trench fever ; but a fourth formof louse-borne typhus, in laboratory workers, was

described by Mosing,2 who named the causal organismR. weigli. Weigl’s prophylactic vaccine against typhus- exanthematicus is prepared by injecting suspensions ofR. prowazeki into lice per rectum and after an intervalremoving their intestines and grinding them up informol-saline. For this method very large numbers oflice are needed and these have to be fed on laboratoryworkers ; it was these workers who contracted the disease.A few years later, however, it was considered thatR. q1tintana and R. wolhynica, the causal organisms of trenchfever and wolhynian fever respectively, were identical, andthat R. weigli was probably the same organism.An outbreak similar to that described by Mosing took

place at Addis Ababa in 1941-42, soon after the occupa-tion by British troops. It involved seven laboratoryworkers engaged in feeding lice for Weigl’s method ofmaking prophylactic vaccine, and is described byCodeleoncini,3 who details the isolation of a rickettsiafrom such cases, the laboratory findings, and experi-mental work on guineapigs and monkeys (Papio doeep),all of which convince him that trench fever, the diseasedescribed by Mosing, and the Ethiopian disease are

identical and due to one and the same rickettsia, whichis the common louse rickettsia, R. pediculi. Codeleoncinifurther suggests that the disease develops only whenenormous numbers of lice are present-e.g., in trenchwarfare and in laboratory feeding of lice for makingWeigl’s vaccine-and that probably an endemic focusin Russia acts as a reservoir between outbreaks.

2. Sec Lancet, 1945, i, 760.1. See Lancet, Oct. 12, p. 531.2. Mosing, H. Med. dosw. spol. 1936, 21, 218 (abstr. in Arch. Inst.

Pasteur, Tunis, 1936, 25, 373).3. Codeleoncini, E. Boll. Soc. ital. Med. Igiene trop. (see Eritrea),

1946, 6, 129.

CAUSE OF NUTRITIONAL &OElig;DEMA

NUTRITIONAL oedema is usually thought to be dueto hypoproteinsemia, especially a deficiency of serum-albumin, which normally maintains the osmotic pressureof the plasma, thus preventing the escape of fluid fromthe blood-stream. This view was put forward in 1896by Starling, who did not, however, postulate that

hypoproteinsemia was the sole cause of the cedema.

Bayliss later showed that a second factor was a highvenous pressure. When the hydrostatic pressure inthe venous capillaries is raised fluid filters from the

plasma through the vessel walls to swell the intercellularfluid of the tissues-e.g., in the oedema of chronicheart-failure.

There is yet a third possible cause of nutritionaloedema. Peters has emphasised the importance of thecell membrane as a physiological boundary separatingthe cells and intracellular fluid from the intercellularfluid. Consequently it is imaginable that cedema canalso be produced by leakage from intracellular to inter-cellular fluid. This supposition is supported by Bachet,2who found that 17 cases of early oedema among 120 casesof nutritional oedema had a normal serum-albumin level,and estimations of serum-albumin in non-oedematouspatients who subsequently developed oedema showed nohypoproteinaemia anticipating the oedema. Further, hefound that signs of heart-failure were rare in the early stagesof nutritional cedema. These findings militate against thetheories that nutritional oedema is caused, in the firstinstance, by hypoproteinaemia or by high venous pressure,though both of these mechanisms come into play in thelater stages and increase the existing oedema. Bachettherefore argues that nutritional cedema starts in thecells, and that it is only later that the serum-albuminlevel falls-in other words, that nutritional oedema, isdue to an insufficiency of proteins in the diet, leadingto a deficiency of albumin in the tissues. On the otherhand, the occurrence of cedema with a normal serum-protein may be due to some factor which interferes withthe function of the vascular endothelium-vitamindeficiencies, for example-rather than to actual proteinlack within the cells. For the present the verdict onBachet’s hypothesis must be

" not proven."Lamy and his co-workers,3 in a study of 38 prisoners-

of-war, have confirmed the lack of correlation betweenserum-protein levels and cedema and have carried theinvestigation a step further. They measured the serum-protein levels and the osmotic pressure of the serum in8 prisoners-of-war suffering from malnutrition, 2 withno oedema, 2 with slight malleolar cedema, and 4 withsevere oedema, and found that a lowering of the osmoticpressure of the serum was clearly correlated with anincrease in oedema, though the serum-protein level wasnormal in all cases. They conclude that the serum ofthe patients with oedema contains an abnormal proteinof low osmotic pressure, and that this protein is derivedfrom muscle. They do not, however, believe that thelow osmotic pressure alone is responsible for the onsetof oedema in malnutrition, and support the view that themain factor is an increased permeability of the capillarywalls.

Sir WILLIAM COLLINS, K.C.V.O., F.R..C.S., who died onDec. 11 at the age of 87, will be remembered as the creatorof the London Ambulance Service. As chairman of theLondon County Council, as Member of Parliament, andas ophthalmic surgeon to several London hospitals, heserved medicine both inside and outside his profession.He was also British plenipotentiary at conferences on thecontrol of dangerous druas.

1. Peters, J. P. Body Water, London, 1935 (see also Lancet,1940, i, 794).

2. Bachet, M. Etude des troubles caus&eacute;s par la d&eacute;nutrition dansun asile d’ali&eacute;n&eacute;s, Paris, 1943, and Bull. m&eacute;d. 1945, 59, 1.

3. Lamy, M., Lamotte, M., Lamotte-Barillon. Pr. m&eacute;d. Dec. 7, 1946,p. 814.