The series of articles that follow in this volume deals with specific aspects of how parasites might influence nutrient utilization by their human hosts. To put these aspects of parasitic disease in context, this contribution is intended to provide an overview of human nutritional needs and to introduce concepts of how nutritional consequences of parasitic infection might be viewed. Although parasitic diseases are often considered to be those caused by protozoa and helminths, the principles considered here can be applied to any infectious agent, including bacteria and viruses.

Gastrointestinal pathogens are of three varieties, those that can, and often do, take the life of the host, those that infect transiently and rarely are life-threatening, and those (parasites) that establish a relatively prolonged residence or colonization of the host's alimentary tract. In the case of the second form, if infections are recurrent, both catabolic effects during the episode and failure to digest foods and/or absorb nutrients result. Similarly, catabolic wastage through activation of the acute phase response, and interference with the host's acquisition of nutrients by maldigestion, malabsorption, intestinal losses and competition with the parasite burden can impair growth and nutrition with helminthic infections. Growth and nutrition with respect to all of the macronutrients and virtually all of the micronutrients have been documented to be adversely affected by gastrointestinal pathogens. For its burgeoning importance as a worldwide health problem, both with the HIV virus as a direct intestinal pathogen and with the opportunistic gut infections occurring in the immunocompromised host, AIDS represents the emerging context of the impairment of nutritional status by intestinal pathogens.

In the Freetown area of Sierra Leone, the proportion of children under five years of age dying from diarrhoea-associated conditions has decreased since the 1970s from 4% to 3%. This reduction relates to children between 12 months and 5 years; deaths associated with diarrhoeal disease in infancy do not appear to have decreased significantly. Currently, 2% of children die in infancy and a further 1% before their fifth birthday from diarrhoeal diseases. Thirty-one percent of short-term growth-faltering in children under five years of age is attributed to diarrhoeal disease. Reasons for improvement in mortality may include the implementation of a National Diarrhoeal Diseases Control Programme and improved case management; some 55% of cases of acute diarrhoea in Freetown now receive oral rehydration therapy. Morbidity and mortality are influenced by the seasons. This is likely to be related to the fact that the nutritional status of children shows a significant deterioration in the early rainy season. At this time incidence of severe diarrhoea warranting hospital admission and diarrhoea mortality rates in hospital and at a Rehydration Center increased significantly. On the other hand, the presentation of dehydrating diarrhoea is greatest in the driest months of the year. Progress in the rural areas of Sierra Leone may not have been so evident although 60% of the population now have access to primary health units within 4 miles and efforts to increase host resistance have included the measles immunization programme which currently protects 60% of under-fives nation-wide. Efforts to reduce the transmission of pathogens have meant increasing access to safe water to 22% and to improved sanitation to 35% in rural areas of Sierra Leone. The sustainable prevention and control of diarrhoeal diseases in developing countries depends also upon increasing levels of adult literacy especially of women.

Nutritional support of patients with HIV or acquired immune deficiency syndrome (AIDS) has many similarities to other disease states in that the same nutritional products and techniques are used. Some patients with HIV, and many with AIDS without secondary infection, experience a metabolic milieu similar to patients with cancer cachexia. In providing dietary counselling to the HIV patient, we encounter many of the obstacles that must be overcome to improve nutrition in cancer: anorexia, gastrointestinal discomfort, lethargy, and poor nutrient utilization, which limit the ability for nutritional repletion. When a secondary infection is superimposed on HIV, patients resemble more highly catabolic trauma patients or patients in the intensive care unit (ICU), where, despite aggressive efforts to feed, there is usually a net nitrogen wasting leading to the more rapid development of cachexia. However, even in this setting, feeding will limit substantially net catabolism when compared to total starvation. Because the nutritional needs of HIV patients vary greatly, individual strategies have to be designed as the patient moves through the stages of disease. Patients are generally able to consume adequate nutrition either as regular food or dietary supplements during the latency period of viral replication. Once secondary infections become prevalent, artificial diets administered by tube or by vein may be required during the period of active secondary infections, with dietary supplements often helpful during more quiescent periods. Patients with HIV are among the most challenging for clinicians providing nutritional support. Knowledge from treatment of patients with other diseases may be useful, but more data must be gathered on the unique aspects of aetiology and treatment of the anorexia, malabsorption, and ultimate wasting associated with AIDS.

A murine AIDS model with many similarities to human AIDS, LP-BM5 Murine Leukaemia, suppresses T and B cell numbers and functions in the intestine. This permits chronic colonization by Giardia and Cryptosporidium. Cocaine and the nutrient alcohol, which are immunosuppressive, further reduce resistance to intestinal parasites and intestinal lymphocyte numbers. Protein undernutrition, vitamin E supplementation, and alcohol use further modify immune dysfunction induced by the murine retrovirus infection. This suggests that both undernutrition and nutrient supplementation could affect parasite resistance during AIDS. Thus this murine model of human AIDS has great potential to accelerate studies of the role of nutrients in immune dysfunction and resistance to intestinal parasites.

The number of episodes of diseases caused by bacterial contamination of food has shown a real increase by about threefold in the last decade in the U.K. The numbers for 1992 are estimated to be 2 million. The causes are multifactorial and complex, and 4 representative pathogens are reviewed. The main increase in diseases due to salmonella has been caused by Salmonella enteritidis, especially from eggs. The commonest bacterial food pathogen is Campylobacter, which causes an illness with specific season peaks in May and June. This may be related to the activities of birds and mammals. Both these bacteria cause common diseases that are rarely fatal. In contrast, Listeria and E. coli are ubiquitous but rarely produce disease; however, the consequences of any such illness are often dire. Procedures and techniques are available for the control of most of these diseases, but society does not seem determined to implement them.

Susceptibility to oxidative stress is a well-established feature of the malarial parasite. Pharmacologists have taken advantage of this property to design highly effective pro-oxidant antimalarial drugs. Less well appreciated is the fact that nutritional manipulation of host oxidative stress status by dietary means can have a profound effect on the growth of the parasite. In particular, rapid induction of vitamin E deficiency in mice by feeding highly unsaturated fatty acids (fish oil) strongly suppresses plasmodial growth. Likewise, the status of other antioxidant nutrients (e.g., riboflavin or vitamin C) may also influence the course of malarial infection under certain conditions. A combined nutritional pharmacology approach may offer some promise in controlling malaria.

This article reviews studies that examine the negative effects of urinary and intestinal schistosomiasis on the following nutritional parameters in humans: urinary and faecal blood and iron loss, anaemia and haemoglobin levels, proteinuria, child growth and adult protein-energy status, physical fitness, physical activity, appetite and symptomatology. The conclusions reached are (1) that community-level treatment and control of schistosomiasis in areas where the infection, protein-energy malnutrition, and anaemia are common are to be encouraged and are likely to improve child growth, appetite, physical fitness and activity levels and to decrease anaemia and symptoms of the infection, and (2) that further studies are needed to determine how much and by what means decreases in and treatment of schistosomal infection may improve nutritional status, cognitive and school performance and attendance, and work capacity and productivity in communities with different amounts of parasitism and malnutrition.

The present review will examine epidemiological perspectives and be confined mainly to the results of those field studies published since 1975 in order to provide concrete scientific evidence of the effect of ascariasis on childhood malnutrition, particularly on growth. The field studies were done in many developing countries from Africa, Asia and Latin America, using cross-sectional and intervention studies in which anthelmintics were employed, with different dosing frequency and follow-up periods ranging from 33 days to 2 years. In general, a better nutritional status in terms of growth, lactose tolerance, vitamins A and C, and albumin levels were observed among Ascaris–free or treated than among Ascaris–infected or untreated children even in cross-sectional or non-randomized studies. More importantly, the improvement in weight or height after chemotherapeutic treatment was found to be significant particularly in those randomized controlled studies with an initially high prevalence of ascariasis and malnutrition, a low prevalence of other intestinal parasites, repetitive and regular treatments of children with tetramisole, levamisole or pyrantel, within a period of 12 or 24 months. Reasons for failures to detect improved growth in some studies are provided. This review strongly indicates that A. lumbricoides infection definitely retards childhood growth.

Ancylostoma duodenale and Necator americanus are extremely common species of soil-transmitted helminth which flourish where poverty and malnutrition prevail. Hookworms contribute significantly to iron-deficiency anaemia, which remains one of the world's major nutritional problems, through the feeding activities of intestinal stages leading to chronic blood loss into the gut. In this article, a mathematical model is proposed to explain how human iron metabolism may respond to hookworm infection of varying intensity. The model draws attention to the importance of the regulation of stored iron levels in the process. The results from the model are presented for the effects of hookworm infection on the iron metabolism of a healthy adult male. Calculations are also presented in which the effects of hookworms on the iron metabolism of a non-pregnant woman are compared with those of a pregnant woman. Use of the model may help develop a better understanding of the pathology of hookworm disease.

Vector-borne nematodes of the Order Filarioidea produce chronic, debilitating human infections which are usually non-fatal but are associated with a high degree of severe morbidity. Weight loss often accompanies infection and is probably a consequence of the increased energy cost associated with filarial fever, lymphangitis and lymphadenitis. In onchocerciasis, weight loss is associated with heavy worm loads as assessed by abundant nodules and large numbers of skin microfilariae. Experimental infections using rodent filariae have confirmed these observations and have also shown that low protein diets render hosts more susceptible to infection; nevertheless, parasite growth and embryogenesis is retarded in stunted female worms from protein deficient animals. In the absence of appropriate evidence, studies of experimental filariasis suggest that human protein-energy malnutrition may delay the development of stage-specific acquired immunity with a corresponding prolongation of patency. Epidemiological and experimental evidence shows that filarial nematodes acquire certain nutrients directly from their hosts. Of major importance in this respect is vitamin A which is taken up preferentially by human and rodent filariae; in humans, symptoms of hypovitaminosis A often accompany infection and could be an aggravating factor in onchocerciasis. Filariae also appear to require other specific nutrients such as iodine, thiamine and pyridoxine; dietary levels of these nutrients affect the host-parasite relationships in filariasis and pyridoxine seems to be of particular importance in this respect. Filarial parasites obviously compete with their hosts for available nutrients and, in the real world, human filariasis is often associated with a deterioration in the plane of nutrition of infected individuals.

Interactions between infection and nutrition have been well recognized for several years now since they contribute directly to the health of individuals and communities. Malnourished individuals are specially prone to developing infections while infections themselves can lead to profound changes in the nutritional status of the individual. Health workers in developing countries in the tropics have long recognized the mutually aggravating interactions of malnutrition and infection. The importance of this synergistic relationship between infection and nu-tritional status has been studied extensively in the case of young children. The nutritional status of a young child is a critical determinant of both c morbidity and mortality resulting from a wide range of infections: bacterial, viral, or parasitic. Chandra (1983), in his review on the relationship of nutrition, immunity and infection has categorized the wide range of infectious agents (bacterial, viral, fungal and parasitic) into those that are definitely, variably or minimally influenced by the nutritional status of the child.

The energy requirement of pregnancy reflects a problem which contains a great deal of uncertainty. To supply the theoretical energy needs for the increases in maternal and foetal tissues and to cover the elevated basal metabolic rate involves an amount equivalent to an extra 250–300 kcal/day on average, but in real-life situations there is seldom a rise in dietary energy of a comparable quantity. Data from co-ordinated longitudinal studies in four countries, together with results from other published papers, show energy intakes increasing by only 100–150 kcal/day, and only in the third trimester. Although it is difficult to demonstrate, the probability is that there are energy savings in reduced physical activity which compensate for the larger energy needs.

A frequent characteristic of many malignant tumours is an increase in anaerobic glycolysis, that is the conversion of glucose to lactate, when compared to normal tissues. The causes of this intensification involve changes in enzyme and glucose transporter levels, shifts of the isoenzyme patterns in the cancer cells to those similar to foetal tissues and a breakdown in the normal control mechanisms, most notably the Pasteur effect. The host must adapt, with a corresponding increase in gluconeogenesis. This change, along with other adaptations made by the host, eventually results in the syndrome known as cancer cachexia, which is characterized by anorexia and depletion and redistribution of the host energy stores. In some ways many malignant tumours behave much like parasites, drawing upon the host for nutrients such as glucose and returning waste products such as lactate to the host for recycling or disposal. This cycling of glucose and lactate between host and tumour has been the target for a number of proposed and tested treatments, with regard to the possible inhibition of tumour growth and/or possible prevention of some or all of the cachectic effects. Some of these suggested treatments have reached the point of clinical testing and show promise for continued research.

The paper considers briefly the nature of cognition and its relationship to intelligence. The information processing model of human cognition is outlined and IQ and DQ are explained. The literature dealing with the effects of malnutrition and parasitic infection on cognitive performance and development in children is selectively reviewed. A speculative hypothesis concerning the psychological effects of parasitic infection is sketched and brief consideration is given to models and measures in research on development.

According to Carpenter (1993), the first problem for nutritional science, to identify the chemicals required in a diet to support human growth and maintenance, has been solved. Enough information has been amassed from the study of many populations to enable nutritionists to offer safe recommendations about daily intakes of energy and nutrients for all stages of the human life cycle (see reviews by Nesheim and by Solomons, this volume). Adoption of these recommendations would generally correct deficiency diseases and would reduce the incidence of health complications which are linked to excessive intakes of fat, sodium, alcohol and other substances. Carpenter also drew attention to malnutrition, the solution of which he believed to have become largely political and economic although the fact remains that very many people still do not receive or grow enough food. In the context of this volume, Carpenter's most interesting point was his view that our understanding of the complex relationship between nutrition and disease was still at an early stage.