Chronic infection

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Infection causes metabolic disturbance that leads to short-term shifts in circulating levels of certain nutrients in association with the acute-phase response. In the presence of underlying malnutrition, infection may not be resolved, and a vicious cycle may be established. Although chronic infectious diseases are less prevalent in industrialized countries, infections with HIV, Mycobacterium tuberculosis (MTB), and hepatitis C virus (HCV) are significant problems that interact with nutritional status and immune response. Where there are recent immigrant populations, otherwise highly unusual parasitic infections must be considered in seeking the cause of metabolic disturbances in children living in industrialized countries [131, 132].

The role of malnutrition in pediatric HIV disease was appreciated as a significant cause of stunting and delayed maturation before the availability of effective anti-retroviral treatment and continues to be a significant area of investigation. Oral candidiasis and lower respiratory tract infections are more common than in children with non-HIV-associated immune deficiency [133]. Malnutrition, intestinal dysfunction, and immune impairment have been shown to increase the progression of HIV disease in children, and nutritional intervention in the form of total parenteral or enteral feeding can improve both nutritional status and CD4 count [134]. Children with HIV-associated FTT have similar levels of energy expenditure compared to HIV-positive children who have normal growth but show more advanced disease, severe immune suppression, increased viral burden, increased IL-6 activity, decreased total serum protein, and decreased IGF-1 levels [135].

Deficiencies of micronutrients are common in HIV-infected persons. Micronutrient impairment is causally associated with the course of HIV infection and immune dysfunction. This occurs due to malabsorption, altered metabolism, gut infection, and altered gut barrier function. Selenium deficiency increases the virulence of HIV and enhancing disease progression, while supplementation reduces high levels of IL-8 and TNF-a [136]. Vitamin A may increase the risk of HIV-1 transmission through breast milk [137]. In contrast, multivitamin supplementation of breastfeeding mothers with B, C, and E reduces child mortality and HIV-1 transmission through breastfeeding among immunologically and nutritionally compromised women. Supplementation in children with HIV-1 improves overall health.

Generally, declining rates of MTB in industrialized countries have lead to less rigorous surveillance. In countries such as Canada, where BCG immunization has been used for selected indigenous population with higher risk of MTB, greater emphasis is placed on adverse reactions to BCG. However, MTB is an important opportunistic pathogen and can lead to significant infection in persons with nutritional insufficiency such as AN [138]. International adoptees are at high risk for acquisition of MTB and progression to active TB infection [139]. Many children have been vaccinated with BCG and, due to the mistaken belief that this always results in a positive Mantoux test and should be ignored, adds to the complexity of evaluation. Current studies indicate that less than 50% of infants given BCG shortly after birth have reactive Mantoux test results at 12 months of age and almost all vaccinated infants have nonreactive skin test results by 5 years of age [140]. The natural history and clinical manifestations are different in children and are associated with the age at infection and the host immune status.

Vitamin D deficiency is associated with an increased risk for TB infection. Studies using in vitro systems indicate that 1,25-dihydroxyvitamin, the most active form of the vitamin, enhances mycobacterial killing by increasing NO production. Aerosol-challenge with Mycobacterium bovis in the NO synthase 2 deficient (NOS2-/) mouse leads to increased myco-bacterial colonization and lesion formation compared to wild-type mouse.

Infected NOS2-/- mice developed severe necrotizing pyogranulomatous inflammation [141]. In these studies, lung colonization and lesion area of vitamin D-deficient mice exceeded that of vitamin D-replete mice, regardless of NOS2 phenotype, demonstrating a fundamental role for vitamin D. However, effects of vitamin D on colonization, but not lesion area, were more pronounced in NOS2+/+ mice than in NOS2-/- mice, suggesting NO-independent effects of vitamin D as well.

Primary malnutrition increases the incidence and exacerbates clinical manifestations of MTB infection. Experimental studies in the mouse have shown that PCM reduces production of IFN-y, TNF-a and NO after MTB infection, leading to a decreased granulomatous reaction, higher lung bacil-lary load, and a more fatal TB course than in well-nourished control mice, and that this can be reversed by restoring a diet with normal protein content [142, 143].

One study of US immigrants reported that the most common pathogens were Trichuris trichiura, Giardia lamblia, and Ascaris lumbricoides. Giardia lamblia was more prevalent in the younger than 5-year-old age group, and helminths were more prevalent in the 6- to 10-year-old age group. No helminths were found in immigrants who had been in the US for more than 3 years. Infection caused by intestinal parasites irritate the GI tract, cause pain, anorexia, flatulence, tenderness, and affect the host nutrition directly as a result of inflammatory and non-inflammatory diarrhea. Host response mechanisms include accelerated epithelial cell turnover [144]. Trace element deficiencies affect the host pathogen interaction. Examples include the exacerbating effect of selenium deficiency on Trypanosoma cruzi, which is responsible for Chagas disease [145]. Malnutrition can cause an imbalance in T cell subpopulations that may lead to a defective T cell maturation and a decreased specific anti-Ascaris IgE response and worsens infection with A. lumbricoides [146]. Malaria causes the most serious nutritional consequences of any major parasite. It infects the placenta and compromises blood flow to the fetus, causing low birth weight. It also causes PCM in pregnant and lactating women and young children. Anemia, recurrent fever with acute-phase cytokine responses, vomiting and anorexia all produce adverse nutritional consequences in an already fragile child or pregnant women. Recent investigation suggests that micronutrients such as vitamin A, vitamin E, and zinc, may improve the morbidity of malaria through immune modulation and alteration of oxidative stress [147].

The lack of an effective HCV vaccine and the risk of mother-to-child transmission may increase the number of children with vertically acquired HCV that ultimately go on to develop liver fibrosis or cirrhosis [148]. There appear to be no direct effects of HCV on growth in the first 5 years [149]. Chronic HCV infection is usually asymptomatic, although viremia and liver enzyme increases are found in children [150], but significant liver disease may occur [151]. In patients with liver cirrhosis, PEM is a frequent finding and a risk factor influencing survival [152].

The overall impact of chronic subclinical malnutrition in children may determine the quality and duration of immune response to vaccines and may be an important topic for future research.

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Breaking Bulimia

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