Infection not only causes local damage but also has important generalized effects.
Body temperature is controlled by the thermoregulatory centre in the anterior hypothalamus in the floor of the third ventricle. This centre is sensitive to endogenouspyrogen (IL-1) which is released from a variety of cells involved in host defence, primarily blood monocytes and phagocytes, under the influence of microbial exogenous yrogens. IL-l is thought to act on the thermoregulatory centre by increasing prostaglandin synthesis. The ntipyretic effect of salicylates is brought about, at least in part,
through its inhibitory effects on prostaglandin synthetase.
production is thought to have a positive effecton the course of nfection. However, for every 1°C risein temperature, there is a 13% increase in basal metabolicrate and oxygen consumption. Fever therefore leads to increased energy requirements at a time when anorexia leads to decreased food intake. The normal compensatory
mechanisms in starvation, e.g. mobilization of fat stores, are nhibited in acute infections. This leads to an increasein skeletal muscle breakdown, releasing amino acids,which, via gluconeogenesis, are used to provide energy. In chronic infection there is time for adaptation and the body is able to utilize fat stores more effectively and thus weight loss is much slower.
Protein metabolism During acute infection three major changes occur in protein metabolism:
1 There is a diversion of synthesis away from somatic and circulating proteins such as albumin towards acute-phase proteins such as C-reactive protein, haptoglobin, aI-antitrypsin, caeruloplasmin and fibrinogen.
2 Protein synthesis is also directed towards immunoglobulin production and there is production of lymphocytes, neutrophils and other phagocytic cells.
3 There is a marked increase in nitrogen losses, which may reach 10-15 g per day.
Mineral metabolism and acid-base balance Mineral metabolism and acid-base balance are disturbed during acute infection. In general, sodium and water are retained, principally owing to the effects of increased levels of aldosterone and inappropriate secretion of antidiuretic hormone. During the convalescent period after a cute infection, a diuresis may occur. Acid-base balance disturbance is common, and includes respiratory alkalosis following tachypnoea related to fever, respiratory acidosis and hypoxaemia associated with pneumonia, and metabolic acidosis associated with septicaemia. In acute infection these changes are mild and resolve
promptly without specific intervention. However, in situations where infections are prolonged and resolution is slow, supportive care may be necessary, particularly with respect to managing nutritional deficits and electrolyte and acid-base disturbances.
Interaction between nutrition and infection
Undernutrition impairs host defence. Natural resistance to infection is lowered by alterations in the integrity of body surfaces, the reduced ability to repair epithelia, and the reduction in gastric acid production. In addition, immunological abnormalities are found:
MACROPHAGE FUNCTION. Tissue and circulating macrophage function is impaired.
T LYMPHOCYTE FUNCTION is depressed.
TOTAL LYMPHOCYTE COUNT is below 1 x 109 cells/litre, which is indicative of a relatively immunocompromised
CELL-MEDIATED IMMUNITY is in a state of anergy, i.e. the body fails to respond to a recall antigen such as the Mantoux test.
ANTIBODY PRODUCTION is less sensitive to undernutrition, but in severe malnutrition depression in both circulating and secretory immunity are detectable. This is of importance clinically in that vaccination (e.g. against polio) may have to be more aggressive in malnutrition before protective immunity is achieved.
COMPLEMENT LEVELS fall rapidly in severe acute malnutrition and remain low during long periods of established. suboptimal nutritional status. Complement
levels have been used as a biochemical marker of nutritional status.
Host defence and susceptibility