Malnutrition and infection

The issues of starvation and malnutrition are raised again in Chapter 8, where foods rich in energy but poor in protein are discussed. Malnutrition is discussed under Sodium, Potassium, and Water in Chapter 10, w here the problem of infant diarrhea is outlined. This problem often occurs with weaning in underdeveloped countries, when pathogenic bacteria and parasites are inadvertently introduced into the infant s diet. The problem is compounded when basic supplies, such as firewood for boiling drinking water, are missing. Malnutrition and infection are also discussed under Vitamin A in Chapter. ... 

Furst et al. reported on the separation of middle molecules that they contended were peptides (FI 2). Using high-speed gel filtration and ultraviolet absorption at 254 and 206 nm, they separated normal and uremic plasma into 10 and 11 peaks. One of these peaks, peak 7, was present in uremia but not in normal serum. Using ion-exchange chromatography, Furst and Bergstrom further separated peak 7 into seven or eight subpeaks (7a, 7b, 7c, etc.) peak 7 was prominent in uremic patients with symptoms such as malnutrition and infection (F13). Amino acid analysis indicated that peak 7c consisted of a small peptide chain with 8-10 amino acids (B17). 

We had to acknowledge that we could not specify the degree to which radiation had been responsible for the morbidity and mortality, These women had suffered extensive trauma, burns, malnutrition, and infection, each of which could have had a role in the negative pregnancy outcomes. 

A decaying of the flesh around the mouth, due to a combination of malnutrition and infection. However, the infectious organism responsible for this condition has not been isolated. 

Conditions which predispose to infection include those which decrease gastric acidity, antibiotic use, malnutrition, and immunodeficiency states. Contaminated food or water is implicated in most cases. 

A pressure sore is also called a decubitus ulcer and bed sore. A classification system for pressure sores is presented in Table 47-5. Many factors are thought to predispose patients to the formation of pressure ulcers paralysis, paresis, immobilization, malnutrition, anemia, infection, and advanced age. Four factors thought to be most critical to their formation are pressure, shearing forces, friction, and moisture however, there is still debate as to the exact pathophysiology of pressure sore formation. The areas of highest pressure are generated over the bony prominences. 

It is generally accepted that malnutrition decreases the effectiveness of the immune system so that it increases the incidence of infections. Thus famine and infections are always considered together since it is assumed that the former exacerbate the latter. The influenza pandemic in 1918-19 in Europe led to the deaths of more than 20 million people. Poor nutrition caused by the First World War may well have impaired the immune system in many people, thus contributing to the large number of deaths. This topic is discussed in Chapter 18. 

Even when a disease has been effectively treated in a conntry, retention of the disease in small isolated pockets can act as a source for future infection. This can readily occnr when movement of even a small nnmber of infected people into a population in which the immnne system is impaired can lead to the spread of this new disease to areas that were previously free of it. Chronic illness due to malnutrition can weaken the immune system which then facilitates the spread of an infection. This is a particular problem if malnutrition is accompanied by a chronic illness. Althongh malnutrition and accompanying diseases are associated with developing countries, the phenomenon also occurs in developed countries, for example, in the very poor, the homeless, drug abusers and the elderly. It is now considered to be a major factor in the increased incidence of tuberculosis in these gronps. 

The higher than normal serum IgA in many children with protein calorie malnutrition may be related to increased synthesis of IgA by the intestinal lamina propria in resjionse to increased antigenic stimuli from bacteria and virus. This is probably supported by the observation that children with kwashiorkor were found to maintain their polio antibodies during malnutrition, and their immune mechanism seemed to be quite capable of inhibiting poliovirus infection, indicating that the intestinal receptor cell for poliovirus operates normally in kwashiorkor (B8). It is now known that polio antiliodies are mainly associated with IgA. 

Simtharasamai, P., and Marsden, P. D., Studies of splenomegaly in rodent malaria. Ill Protein-calorie malnutrition and splenomegaly in mice infected with Plasmodium berghei yoeii. Trans. Roy. Soc. Trop. Med. Hyg. 66, 214-221 (1972). 

There are also immunodeficiency states that are primary and can be caused by phagocytic cell defects, deficiencies in the complement system, B- and T-cell deficiency, and other causes. Secondary immunodeficiency disorders can result from malnutrition, cytotoxic drugs, infections with pyrogenic bacteria, and infections with an RNA retrovirus, as in the acquired immunodeficiency syndrome (AIDS). 

Interpretation of plasma concentrations of retinol is confounded by the fact that both RBP and transthyretin are negative acute phase proteins, and their synthesis falls, and hence the plasma concentration of retinol fall, in response to infection. Similarly, both protein-energy malnutrition and zinc deficiency result in a low plasma concentration, despite possibly adequate liver reserves as a result of impaired synthesis of RBP. 

Studies in underdeveloped countries have shown that xerophthalmia results in the blindness of a quarter million children per year in Asia alone. Attempts have been made to detect a relationship between the occurrences of xerophthalmia and respiratory or diarrheal infections. Some studies have found an association others have not, Generally, the populations suffering from malnutrition and chronic diarrheal iiifections are those afflicted with xerophthalmia. 

The concept of schizophrenia as a neurode- velopmental disorder has inspired attempts to create adverse and early postnatal events in, animals to model the psychopathological processes underlying the disorder (109, 110). These neurodevelopmental models include prenatal malnutrition, viral infection and hypoxia, disrupted neurogenesis by X-ray irradiation or neurotoxins in utero, adverse postnatal experiential factors such as maternal deprivation and social isolation, and postnatal brain damage created by hippocampal, neocor-tical, or thalamic lesions (109-111). With the possible exception of maternal deprivation and social isolation, these models have not been sufficiently characterized pharmacologically to be used for antipsychotic drug screening. 

Akingbemi, B. T., Ogwuegbu, S. O., Onwuka, S. K., Oke, B. O., and Aire, T. A. (1995). The effects of protein malnutrition and experimental infection with Trypanosoma brucei on gossypol treatment in the rat Haematological and serum biochemical changes. J. Comp. Pathol. 112, 361-371. 

Patients with alcoholic CP usually present with an initial acute attack followed by successive attacks that are slower to resolve. Continued alcohol use leads to chronic abdominal pain and progressive exocrine and endocrine insufficiency. In about 50% of patients, the pain diminishes 5 to 10 years after the onset of symptoms. Steatorrhea, calcification, and diabetes usually develop after 10 to 20 years of heavy ethanol ingestion. Most patients present with varying degrees of pain, malnutrition, and glucose intolerance. The mortality rate of CP is approximately 50% within 20 to 25 years of the diagnosis. About 15% to 20% actually die of complications associated with acute attacks. Most deaths occur as a consequence of malnutrition, infection, or ethanol, narcotic, and tobacco nse. The clinical course of idiopathic CP is more favorable than that of alcoholic pancreatitis. ... 

Iron deficiency is the most common cause of resistance to erythropoietic therapy. Evaluation and treatment of iron deficiency should occur prior to initiation of erythropoietic therapy as previously discussed (see Figs. 44—1 and 44—2). Inflammation (localized or systemic infection, active inflammatory disease, or surgical trauma) is associated with defective iron utilization known as reticuloendothelial block. Reticuloendothelial block is characterized by a reduction in iron delivery from body stores to the bone marrow, and is generally refractory to iron therapy. Failure to respond to erythropoietic therapy requires evaluation of other factors causing resistance, such as infection, inflammation, chronic blood loss, aluminum toxicity, hemoglobinopathies, malnutrition, and hyperparathyroidism. Erythropoietic therapy may be continued in the infected or postoperative patient, although increased doses are often required to maintain or slow the rate of decline in Hgb/Hct. Deficiencies in folate and vitamin Bi2 should also be considered as potential causes of resistance to erythropoietic therapy, as both are essential for optimal erythropoiesis. Patients on hemodialysis or peritoneal dialysis should be routinely... 

Table 45-8 hsts the numerous medical comphcations of PD. An average PD patient absorbs up to 60% of the dextrose in each exchange. This continuous supply of calories leads to increased adipose tissue deposition, decreased appetite, malnutrition, and altered requirements for insulin in diabetic patients. Fibrin formation in dialysate is common and can lead to obstruction of catheter outflow. Infectious comphcations of PD are a major cause of morbidity and mortality and are the leading cause of technique failure and transfer from PD to hemodialysis. The two predominant infectious complications are peritonitis and catheter-related infections, which include both exit-site and tunnel infections. 

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