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close this bookMalnutrition and Infection - A review - Nutrition policy discussion paper No. 5 (UNSSCN, 1989, 144 p.)
close this folderMALNUTRITION AND INFECTION - by Andrew Tomkins and Fiona Watson1
close this folder3. INFECTION AND RISK OF MALNUTRITION
View the document3.1 MECHANISMS OF NUTRITIONAL CHANGES DURING INFECTION
View the document3.2 GENERAL INFECTIONS
View the document3.3 DIARRHOEA
View the document3.4 MEASLES
View the document3.5 MALARIA
View the document3.6 RESPIRATORY INFECTIONS
View the document3.7 INTESTINAL PARASITES
View the document3.8 AIDS

3.1 MECHANISMS OF NUTRITIONAL CHANGES DURING INFECTION

Most infections are associated with a reduced food intake. In some illnesses such as gastroenteritis, vomiting and abdominal pain are obvious causes. In others there appears to be a centrally controlled anorexia. Infection by endotoxin in experimental animals causes pronounced anorexia. Current studies suggest that this is mediated by Interleukin-1 which is released by infected macrophages. There are many other metabolic effects of Interleukin-1 which are reviewed by Keusch and Farthing (1986). A particularly interesting action is the release of lactoferrin from o9o5 neutrophil-specific granules. The lactoferrin binds iron thus causing a reduction in plasma iron. Similarly, Interleukin-1 stimulates the synthesis of metallothionine causing a reduction of plasma zinc, and stimulates caeruloplasmin production which is reflected in the increase of bound serum copper during infection.

It is well recognised that microbial growth is stimulated by the presence of zinc and iron. Perhaps the reduction of plasma zinc and iron may be a protective mechanism during the early stages of infection. An explanation of the pathophysiology of kwashiorkor in terms of the action of free radicals has been put forward by Golden & Ramdath (1987). The body’s defence against invading organisms is to produce free radicals in sufficient quantities to kill the organisms. Free radicals are chemical compounds such as superoxide and hydrogen peroxide capable of damaging tissues through their action on lipid membranes. Toxins and stimulated leucocytes produce large quantities of free radicals. A major catalyst of free radical reactions is iron. This is because of the ease with which the valency state can be changed between the ferrous and ferric forms through redox cycling. Thus the presence of abundant storage iron enhances the damaging effects of free radicals.

A reduction in dietary intake of iron and possibly other ions could therefore be regarded as a primitive defence mechanism against infection. In many traditional societies there has been a practice of ‘starving a fever’. Although this has obvious nutritional implications it may be that this is a cultural ‘infection control strategy’ which supplements the biological ‘infection control strategy’.

Anorexia may be compounded by withholding of certain foods by parents - the patterns of foods allowed in febrile disease vary considerably between cultures. In addition there may be reasons for poor intake related to the mouth and throat. Dehydration during severe diarrhoea may cause a very dry buccal mucosa. Monilia infection of the tongue and measles lesions of the lips may combine to reduce dietary intake.

In such cases solid foods are less easily swallowed than liquids. To an infant receiving most of his dietary energy in the form of breast milk an infection may have little nutritional impact whereas in older children, accustomed to receiving more than half their energy as solids, a considerable reduction in energy intake during infection may result. The physiology of intestinal absorption is relatively well understood and many mechanisms of nutrient malabsorption are described. Destruction of villi, leading to a decrease in surface area and reduction in brush border enzymes are of considerable importance. In addition, deconjugation of bile salts and reduction of their concentration in luminal fluid can lead to steatorrhoea. The secretory response in the intestinal mucosa which is stimulated by bacterial toxins can also result in malabsorption.

A variety of metabolic responses occur during infection which have profound effects on utilisation of diet and endogenous nutrient stores. There is increased energy expenditure, ranging from 10 to 15% increase per 1 degree C rise in body temperature. Although this has nutritional implications for an anorexic individual who is not being offered much food, there are immunological advantages of fever. Most of the immune systems are more active at 39.0 degrees C than 37.0 degrees C. The metabolic changes during infection are reviewed elsewhere but it is now clear that carbohydrate stores for fuel are rapidly depleted, there is o9o5 inhibition of the effective use of fat and obligatory gluconeogenesis and mobilisation of skeletal muscle are needed to provide substrate for the synthesis of acute phase proteins necessary during the various phases of infection. Many of these processes appear to be under the control of Interleukin-1.

Recent studies have also identified cachectin as an important control factor. It has been isolated from endotoxin activated macrophages and has similar molecular properties to Interleukin-1. Among its actions, depression of lipoprotein lipase leading to abnormal clearance of triglyceride from the circulation is important. During infection, Interleukin stimulates the pancreatic cells to release insulin. This probably explains the development of hyperglycaemia and hyperinsulinaemia during systemic infection. It is claimed that Interleukin and cachectin are responsible for the weight loss in chronic infection but the evidence is not established.

The intestinal mucosa is made up of cells that are produced and, usually within a few days, shed into the lumen where they are broken down and nutrients are released. Thus there is a continual enteral-systemic circulation of endogenous nutrients. In health, these nutrients are well absorbed and faecal losses are minimal. During infection, however, there may be increased losses and/or poor absorption. Any cause of intestinal damage is likely to lead to increased rates of shedding. Furthermore there may be increased permeability of the intestinal mucosa allowing leakage of endogenous nutrients between the intestinal cells. In addition certain parasites may cause macroscopic blood loss. If the absorptive mechanisms are intact and the damage is in the upper intestine much of this nutrient leakage will be re-absorbed. If the damage is below the maximally absorptive area of the intestine, however, there will be considerable nutrient loss in the faeces.