Outbreaks of sprue during the Burma Campaign

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Abstract
Three outbreaks of sprue in epidemic proportions are described. The affected personnel were British and Indian troops in Burma Campaign 1943–44. Including all degrees of severity, approximately 3,000 were affected. The majority suffered from a mild or moderate form, conforming to that recently described as para-sprue; but as cases from the same units and areas developed severe symptoms clinically indistinguishable from true sprue, the disease is believed to have been, aetiologically and pathogenically, the same throughout, i.e., sprue. There was no discernible fundamental difference between British and Indian cases. The clinical features in general were identical with those traditionally associated with sprue. The noteworthy variants were the watery, more frequent and less bulky stools, and their lower fat content as compared with “typical” sprue. Factors responsible for these variations are considered to have included the duration of the disease, the amount and nature of fats (fatty acids) and carbohydrates ingested, rapidity of passage of the intestinal contents, and lack of available minerals, especially calcium. Ample soap-formation yields more solid stools, and the lesser-irritant calcium soaps decrease diarrhoea. The traditional massive, pultaceous “sprue-stool” is probably the expression of megacolon rather than of sprue per se, and should be regarded as a later (though not inevitable) development rather than as an essential diagnostic feature in the early phases of sprue. Varying stages in the development of sprue were recognizable from prodromata only, to mild, moderate and severe forms. Not all cases showed the same combination of features or severity of individual symptoms. The commonest features, in average order of development, were lethargy, muscular weakness, anorexia, flatulent dyspepsia, pale diarrhoea, glossitis, anaemia and loss of weight.Even in the early phases an abnormal fat excretion was evidenced in the pale, greasy nature of the stools, excess of fat globules and fatty-acid crystals microscopically, and a total faecal fat of over 25 per cent. with excessive splitting in the majority of those analysed. The stools were additionally fermentative and contained excess of carbohydrate debris. Such stools are considered to be as truly indicative of an abnormal fat (and carbohydrate) metabolism and excretion as those of advanced sprue in which extremely high faecal fat percentages may be found. Aetiologically, the primary causal factor was considered to have been a prolonged dietary inadequacy of one or more of the components of vitamin B2 complex. There was a calculable deficiency of riboflavin and nicotinic acid in the rations issued which were also poor in pyridoxin values. This evidence is considered to be presumptive of a general deficiency of vitamin B2 complex components which are closely associated in nature. Further support for the deficiency-nature of the disease is found in the known association of certain individual clinical features with deficiencies of specific fractions of the complex, the reported association of a deficiency of vitamin B2 complex foods with para-sprue, the excretion of subnormal amounts of nicotinic acid, and the therapeutic response to parenteral and oral crude liver extract and other vitamin B2 complex preparations.In addition, troops subsisting on rations richer in fresh foods containing this complex did not contract the disease. British and Indian troops suffered considerably from the syndrome in the same area when their diets, though widely different in general composition, had a common inadequacy of vitamin B2 complex. Secondary aetiological factors including the increased metabolic demands of a rigorous campaign—malaria, dysentery, antecedent malnutrition and anaemia, progressive deterioration of appetite and, hypothetically, dietetic imbalances of which the high carbohydrate intake in Indian cases and excess of (unwholesome) fats in British cases—are stressed. The possible dual role in pathogeny of these excesses is discussed both in terms of gastro-intestinal irritation (as applied to fats) with malabsorption and diarrhoea, and also with reference to Stannus's hypothesis that sprue is the expression of a failure of phosphorylation of glucose and fatty acids through lack of co-enzymes which catalyse the process, these including certain and as yet unspecified fractions of the vitamin B2 complex. The vitamin B2 complex: fatty acid/carbohydrate ratio in the cases described lends support to the theory of such a mechanism. There was no evidence that the development of sprue was dependent on an infective agent, antecedent intestinal disease or “inherent metabolic errors.” Therapeutic response to modern sprue therapy was pronounced and supported the diagnosis. The heightened response to crude liver extract given parenterally supports the view that sprue is associated with a deficiency of one or more substances present in liver, presumably fractions of the vitamin B2 complex. That these outbreaks occurred in epidemic proportions is not a cogent argument against a sprue diagnosis in view of the factors involved. The observations made support the view that tropical sprue is a disease of malnutrition and indicate means to its prevention.