The Effect of Infection on Nutritional Status

Infection triggers several processes that lead to the deterioration of nutritional status (Figure 2). The innate response to an acute infection induces a cata-bolic response that increases basal metabolism (therefore increasing energy expenditure), places individuals in negative nitrogen balance (as a result of amino acid mobilization from peripheral muscle for gluconeogenesis), and leads to loss of body weight. This primarily occurs in the febrile stage of an infection during which the increase in body temperature is accompanied by an increase in basal energy requirements. This energy is required to fuel the increased rates of enzymatic reactions that occur when body temperature is elevated and to provide energy for the synthesis of proteins involved in the response to infection, e.g., acute phase proteins and immunoglobulins. The latter explains why energy metabolism can also be increased in subclinical nonfebrile infections.

The acute phase reaction is mainly driven by cyto-kines produced by infected leucocytes. Interleukin-1 (IL-1) is the primary mediator of the acute phase response and stimulates endocrine changes that lead to amino acid mobilization as well as the initiation of anorexia (loss of appetite). This can be compounded by physical discomfort associated with eating or swallowing that can occur in certain infections. For example, dehydration due to diarrhea can lead to mouth dryness, and opportunistic oral infections may occur following acute infections. Nutritional intake can be further reduced as a result of the cultural practice of withdrawal of food from individuals with signs of infection (such as fever or diarrhea).

Amino acid mobilization during the acute phase response to infection is also accompanied by redistribution of other nutrients among tissues as well as vitamin (e.g., retinol, folate, riboflavin, ascorbic acid) and mineral (e.g., potassium, zinc, copper) losses from the body. These changes reflect a shift in the transport of nutrients by nutrient transport proteins, the synthesis of which is reduced in response to infection, in order to prioritize the synthesis of acute phase proteins by the liver. Consequently, plasma nutrient concentrations fall due to reduced circulating levels of nutrient transport proteins.

Reductions in circulating levels of iron also occur through the sequestration of iron by the reticuloendothelial system as well as the release of the iron-binding protein lactoferrin by neutrophils, increased storage of iron as ferritin in the liver and spleen, and reduced intestinal iron absorption. This is

Figure 2 The effect of infection on nutritional status.

a protective mechanism that deprives microorganisms of the iron required for microbial growth and replication, therefore restricting further spread of infection.

Serum retinol levels are also reduced in a range of infections including acute respiratory infections, gastroenteritis, measles, malaria, pneumonia, and hookworm infection. Retinol depletion in measles infection has been shown to be closely related to the severity of infection.

Direct nutrient losses also occur in infection through diarrhea and nutrient malabsorption. Various infections of the gastrointestinal (GI) tract can cause diarrhea including viral, bacterial, protozoan, and helminthic infections, although non-GI infections such as malaria may also precipitate diarrheal episodes. GI infections can damage the gastrointestinal epithelium leading to flattening of microvilli, this decreases the absorptive surface area of the intestine resulting in malabsorption and electrolyte imbalance.

Table 1 lists examples of major infections, how they affect nutritional status, and the ways in which these infections may be modulated by certain nutrients.

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