A classic work on the synergistic association of malnutrition and infection was published in 1968 (Scrimshaw, Taylor, and Gordon 1968). In the case of PEM, the condition predisposes to other diseases, but diseases can also bring on the condition. For example, children with PEM are particularly susceptible to respiratory and gastrointestinal infections, whereas measles frequently precipitates severe PEM. An intriguing question is whether PEM interferes specifically with the protective immune responses or whether the generally poor environmental conditions associated with PEM (which implies frequent exposure to infection) means the child with PEM has less metabolic reserve to resist infection. For example, although exposure to measles will infect a well-nourished child and a child with PEM equally, the well-nourished child will survive with some weight loss, whereas the child with PEM, already underweight, becomes severely ill and frequently dies.
The various and complex ways in which immunity to infection can be impaired by PEM has been recently reviewed (Waterlow 1992: 290-324). Although in some communities the relationship between PEM and infection is linear, in others there is a much weaker association. But what is clear is that a child with severe PEM is seriously at risk of infection in any community. An early observer of reduction of cell-mediated immunity in PEM (Smythe et al. 1971) also noted reduction in the weight of the thymus gland as well as a reduced size of the spleen, lymph nodes, tonsils, appendix, and Peyer’s patches.
Much interest has also been shown recently in the role of vitamin A deficiency in the susceptibility of PEM victims to infection, especially respiratory disease and diarrhea (Sommer, Katz, and Tarwotjo 1984). Earlier, it was demonstrated that some patients with kwashiorkor had dangerously low levels of plasma vitamin A (Konno et al. 1968), and treatment of measles with large doses of vitamin A has given good results (Hussey and Klein 1990), which, in conjunction with widespread immunization, means that measles is no longer the threat to the life of PEM victims that it was in 1969 (Morley 1969).
Diarrhea has always been a clinical characteristic of kwashiorkor and marasmus, both as a precipitating factor in a marginally malnourished child and as a continuing recovery-retarding drain of electrolytes, energy, and protein. The organisms and viruses responsible have been well defined (Waterlow 1992: 297), but in the case of PEM victims, frequently no pathogens are isolated. Balance studies on patients recovering from kwashiorkor have revealed a remarkably high daily fecal loss (500 to 1,000 grams [g] per day compared with a normal figure of 100-150 g/day), part of which was found to have been caused by lactose intolerance as a result of secondary lactase deficiency in the duodenum (Bowie, Brinkman, and Hansen 1965; Bowie, Barbezat, and Hansen 1967).
At the time, this discovery was thought to be a breakthrough in the cause of the diarrhea in PEM; further experience, however, revealed that lactose intolerance is not universal in PEM, although it can explain the severe diarrhea that frequently occurs when PEM cases are treated with milk. Diarrhea also occurs in PEM because the gastrointestinal tract atrophies and becomes paper-thin and almost transparent. The mucosa of the intestine has a reduced absorptive surface, and electron microscopy reveals considerable disorganization of the intracellular architecture (Shiner, Redmond, and Hansen 1973). Marked improvement occurs within a few days of treatment.
Looking back on the last 50 years of research on diarrhea in PEM, it is apparent that infection, intestinal atrophy, lactose intolerance, and immunological deficiencies all play their part. Recently, the advent of AIDS has particularly affected the immunological defenses in infected children, resulting in diarrhea, severe wasting, and marasmus or kwashiorkor. In a summing up of all the recent evidence, it can be said that there is a causal relationship between a state of malnutrition (PEM) and diarrhea morbidity and mortality (Waterlow 1992: 313, 339). The same may be said for respiratory disease (pneumonia) and measles, but not for malaria, which has little or no relation to the state of nutrition (Waterlow 1992: 333). Confounding factors in morbidity and mortality are vitamin A deficiency, breast feeding, sanitary facilities, and the mother’s education, caring capacity, and availability.
World History
