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Nutrition and Infection AJ Rodriguez-Morales, Universidad Tecnológica de Pereira, Pereira, Risaralda, Colombia A Bolivar-Mejı́a, Clı́nica FOSCAL Internacional, Floridablanca, Santander, Colombia C Alarcón-Olave, Universidad Autónoma de Bucaramanga, Bucaramanga, Santander, Colombia LS Calvo-Betancourt, Fundación Cardiovascular de Colombia, Floridablanca, Santander, Colombia ã 2016 Elsevier Ltd. All rights reserved. Introduction Nutrition is a fundamental aspect of life, and it is linked to multiple components, systems, and processes, including those occurring during diseases, such as infection. In this context, nutrition has a close relationship with infection. For example, malnutrition is considered to be an important cause of immunodeficiency worldwide, predisposing the malnourished to multiple infections. All forms of immunodeficiency predispose to malnutrition, particularly those opportunistic, related to those altered states of immunity. Malnutrition is a condition that, by itself, increases the host’s susceptibility to infectious diseases, and these infections, in turn, have negative repercussions on the metabolism of the host, worsening the nutritional state. In other words, malnutrition alters the host’s response to infections, and infections increase malnutrition. This malnutrition–infection complex is associated with significant morbidity and mortality worldwide, particularly in developing countries, where food insecurity and undernutrition primarily affect children. Accordingly, children constitute one of the most vulnerable populations, and infectious diseases cause over half of the total deaths in children under 5 years of age. As stated, the relationship between malnutrition and infection is bidirectional, because infectious diseases can be associated with malnutrition (e.g., giardiasis can compromise intestinal absorption). In regard to parasitoses, many epidemiological studies have found significant connections between helminthic diseases (e.g., ascariasis, trichuriasis, hookworm, and strongyloidiasis, etc.) and protozoan infections (e.g., giardiasis, amebiasis, etc.). Micronutrient deficiencies and infections are intricately linked, with deficiencies being related to poor growth, impaired intellectual performance, and predisposition to infections (mainly bacterial, viral, and parasitic). In fact, poor nutrition may drive the enormous worldwide impact of parasitic infections. Foodborne infection, in particular, represents a major burden on public health and even the political and economic development of many countries and regions, and this phenomenon should be the subject of ever more focused investigation. This article describes the relationship between nutrition and infection, with a focus on how malnutrition affects susceptibility to infection and the burden that infections, especially foodborne infections, place on public health. Food and Infections Foodborne diseases are considered to be a major public health problem, being an important cause of morbidity and mortality worldwide, with the highest rates in low- and middle-income 98 countries. Foodborne infections are related to unsafe food, and their global burden and economic costs are considered to be a threat to public health and development. According to the U.S. Centers of Disease Control and Prevention (CDC), around 76 million cases of foodborne illnesses occur in each year in the United States, leading to 325 000 hospitalizations and 5000 deaths. The resulting economic burden is estimated to be $10–83 billion USD per year. Australia and New Zealand have estimated costs up to $86 million per year, and across Europe, the annual cost has been estimated to be $71 million. However, there are no comprehensive global assessments of foodborne disease, and, as a result, the real total burden remains unclear, especially in the tropical, developing countries where these infections are most prevalent. A foodborne disease occurs as the result of the ingestion of contaminated food products, and it includes a huge number of illnesses caused by different pathogens (e.g., bacteria, fungus, viruses, parasite, and even prions). Chemicals in foods can also produce illness, but this type of illness is not infectious in nature, and it will not be considered here. The World Health Organization (WHO), United Nations Food and Agriculture Organization (FAO), and CDC, as well as other international health organization, have identified risk factors crucial to foodborne outbreaks, including the use of unsafe water sources, inadequate cooking processes, contaminated equipment, and poor personal hygiene, especially as it applies to the food handler. Recently, the FAO and WHO investigated the ten foodborne parasites with the greatest global impact, developing a joint report, ‘Multicriteria-based ranking for risk management of food-borne parasites,’ based on the parasites’ burden on human health and other factors, including the geographical ranges of the organisms. According to the report, the top ten parasites are as follows: 1. Taenia solium (pork tapeworm): in pork 2. Echinococcus granulosus (hydatid worm or dog tapeworm): in fresh produce 3. Echinococcus multilocularis (a type of tapeworm): in fresh produce 4. Toxoplasma gondii (protozoa): in meat from small ruminants, pork, beef, game meat (red meat and organs) 5. Cryptosporidium spp.(protozoa): in fresh produce, fruit juice, milk 6. Entamoeba histolytica (protozoa): in fresh produce 7. Trichinella spiralis (pork worm): in pork 8. Opisthorchiidae (family of flatworms): in freshwater fish 9. Ascaris spp. (small intestinal roundworms): in fresh produce 10. Trypanosoma cruzi (protozoa): in fruit juices Although the report looked at the problem of parasites on a global scale, individual parasites can have greater relevance to Encyclopedia of Food and Health http://dx.doi.org/10.1016/B978-0-12-384947-2.00491-8 Nutrition and Infection different countries and regions. For instance, T. cruzi is commonly encountered in rural Brazil, where Opisthorchiidae is unknown, while the latter is prevalent in Southeast Asia, which has no presence of the former. The different pathogens can be transmitted to food by many ways. T. cruzi, which causes Chagas disease, is most commonly associated with household insect vectors (bed bugs), but it can also be orally transmitted. However, hand hygiene plays the most important role as a vehicle for transfering pathogens to food. That is why the food handlers, defined as the persons who manipulate the food in process, are considered to be crucial as vectors of foodborne infections. All of these factors remain of utmost importance, leading to the necessity for strict hygiene practices among food handlers, in order to prevent foodborne illness. Fecal–oral transmission tends to be to most common cause of food contamination, and it involves the fecally contaminated hands of food workers. Bacterial, viral, and parasitic infections have been connected to this way of transmission, including Salmonella spp., hepatitis A viris, Giardia intestinalis, and Yersinia spp., among many others. The only effective strategy for preventing of fecal–oral transmission is strict personal hygiene. Another important point to consider is that the presence of infected skin lesions in the food handler has been closely related with staphylococcal and streptococcal infections. Regarding the different types of food implicated in foodborne diseases, there appears to be a relationship between hand contact time during the preparation of the food and the transmission of pathogens, with sandwiches, salads, and cooked meals being the most important vehicles of transmission. In addition to hands, nasopharyngeal secretions can cause the transmission of a pathogen into the food supply. Foodborne illness via staphylococcal and streptococcal infections has also been related to nasopharyngeal secretions, as shown by the development of streptococcal pharyngitis and its connection to the presence of the bacteria in the pharynx of the food handler. Aerosolization, fomites (infectious media adhering to solid objects), and insects are also different ways for pathogens to be transmitted, outside of the contamination of food. Aerosolization transmits the norovirus. Fomites can also spread the norovirus, as well as hepatitis A. Finally, insects, such as flies, cockroaches, and triatomine bugs, are the vectors for assorted bacteria and protozoans. hospitalizations and fatalities. Comparing in these populations for the period 2006–08 with the year 2012, infection rates increased for Campylobacter (by 14%) and Vibrio (by 43%). Vibrio infection was also related to a high percentage of mortality in persons over 65 years. For different infections, the incidence rates, per 100 000 people, were as follows: Salmonella: 7800; Campylobacter: 6793; Shigella: 2138; Cryptosporidium: 1234; non-Shiga toxinproducing E. coli (nSTEC): 551; STEC: 531; Vibrio: 193; Yersinia: 155; Listeria: 121; and Cyclospora: 15. In children under 5 years of age, there was a high incidence of Cryptosporidium, and in adults over 65 years, there were more cases of Listeria and Vibrio infection. Malnutrition and the Infection Cycle The complex interaction between infection and malnutrition creates a hostile environment that perpetuates a vicious circle that leads to the two entities benefiting from each other. Some of the phenomenon involved during different parts of the cycle include decreases in the activity of macrophages, diminishment of the inflammatory response, and a reduction in the capacity to create specific antibodies. However, there are two effects that can occur in the presence of both malnutrition and infection. The first one is the synergistic effect, and it happens when an infection worsens the malnutrition or when the malnutrition contributes to decreasing the immune response to infection. The second effect is an antagonist mechanism, which occurs less frequently than the synergistic effect. The antagonistic mechanism happens when malnutrition decreases the multiplication of the agent. Malnutrition can make a person more susceptible to infection, and infection contributes to malnutrition, which causes a vicious cycle (Figure 1). -Appetite loss -Nutrient loss -Malabsorption Malnutrition -Altered metabolism Incidence and Trends The Foodborne Diseases Active Surveillance Network (FoodNet) has been describing the incidence and trends of foodborne disease in the United States since 1996, and the 2012 FoodNet report shows that there was a total of 19 531 infections, leading to 4563 hospitalizations and 68 deaths (for a overall case fatality rate of 3.4%). Another two recent reports from FoodNet show that Salmonella, Campylobacter, Shigella, Cryptosporidium, and Shiga toxin Escherichia coli (STEC) remain the main causes of laboratory-confirmed foodborne diseases in the United States. Age is an important factor in foodborne illnes, with most cases in children under 5 years of age. In people older than 65 years, there has also been a high incidence, including 99 Nutrition and Infection Cycle -Lowered immunity -Epithelial barrier Infection damage -Weight loss -Growth faltering Figure 1 Nutrition and infection cycle. 100 Nutrition and Infection Worldwide, severe malnutrition is the most prevalent cause of immunodeficiency, affecting as much as 50% of the population in some impoverished communities. Severe protein energy malnutrition (PEM) in children is clinically defined as a weight-to-height ratio below 70% and/or the appearance of pitting edema on both feet, and it is categorized as either marasmus, a chronic wasting condition, or kwashiorkor, which is characterized by edema and anemia. PEM causes susceptibility to the infections described in the following section. During childhood, severe malnutrition affects thymic development, which, in turn, compromises immunity in children through a long-term reduction of peripheral lymphocyte counts, causing susceptibility to infections and nutritionally acquired immunodeficiency syndrome. Thymus atrophy has been observed in children with malnutrition, and the patent atrophic condition appears to result from a decrease in T-cell proliferation and increased depletion by apoptosis, affecting mainly immature T CD4 þ and T CD8 þ cells. This has been, at least partially, attributed to lower leptin levels during starvation or malnutrition. Malnutrition clearly affects hematopoiesis, determining anemia, leucopenia, and severe reduction in bone marrow. The production of IL-6 and TNF-a by bone marrow cells is also significantly lower in malnourished animals. The capacity of malnourished hematopoietic stroma to support the growth of hematopoietic stem cells (CD34 þ) in vitro is also decreased. This finding relates to disease formation, because CD34þ cells are able to generate multiple lymphohematopoietic lineages, including myeloid, erythroid, and lymphoid (B and T) types. In malnourished children, both acquired and innate immunity is affected, making them more susceptible to opportunistic pathogens such as Pneumocystis jirovecii. In addition, PEM impairs the linear growth of children; it has been suggested that acute-phase response and proinflammatory cytokines directly affect the bone remodeling required for longitudinal growth. Specific Immunological Alterations in Undernutrition A series of specific immune responses and their alteration during undernutrition have been described and characterized. Cell-mediated immune response alterations As previously mentioned, severe malnutrition in newborns and small children causes atrophy of the thymus, with reduced cell numbers and, subsequently, ill-developed peripheral lymphoid organs (e.g., lymph nodes and spleen). This leads to long-lasting immune defects characterized by leucopenia, depressed serum complement activity, decreased CD4 to CD8 ratio, and increased numbers of CD4/CD8 double-negative T cells, contributing to the appearance of immature T cells in the periphery. The biological function of different cell types (macrophages and Kupffer cells) is clearly decreased during nutritional deficiencies. There is also impaired activation of T cells, which has been clearly associated with deficits of cytokine production, which are the main molecular mediators of immunity. This was evident from a study of malnourished children who showed reduced production of type 1 cytokines (IL-2 and IFN-g). Epithelial barrier alterations Immune defense at the epithelial barrier of the undernourished host is compromised because of the altered architecture of the gut mucosa, with structural effects including the flattening of the hypotrophic microvilli, reductions in lymphocyte counts in Peyer’s patches, and reductions in immunoglobulin A (IgA) secretion, all of which are characteristics of environmental enteric dysfunction. Complement alterations The availability of complement components and phagocyte function are compromised during malnutrition, directly affecting pathogen elimination. This happens because the complement system by itself can destroy bacteria or viruses or because complement receptors present on the phagocyte surface mediate the capture of pathogens. Significantly lower levels of complement, especially C3, which is the main opsonic component, were described by Sakamoto and coworkers. In addition, the ability of phagocytes to ingest and kill pathogens was also reduced. The restriction of complement components affects the capacity of professional phagocytes to engulf and eliminate pathogens. Antibody alterations In regard to antibody production, malnourished children are deficient in IgE antibodies that protect against Ascaris lumbricoides, even though they have high concentrations of total IgE; the IgE antibodies that these children do have are neither worm-specific nor protective, and their memory T cells do not recognize helminthes antigens. Malnutrition Increases Risk of Infection Malnourished children suffer more frequently from respiratory infections, infectious diarrhea, measles, and malaria, with each condition characterized by a protracted course and exacerbated disease. Tuberculosis is an infection that is particularly influenced by undernutrition, and it is a major cause of morbidity and mortality in developing countries. Approximately onethird of the world’s population is infected with Mycobacterium tuberculosis, generally in a subclinical form. Similarly, undernutrition may also affect the clinical outcome of tuberculosis. A recent meta-analysis suggested that low serum vitamin D levels are associated with higher risk of tuberculosis activation. It has also been suggested that malnutrition may contribute to the appearance of M. tuberculosis strains that are multiply resistant to antituberculosis medications. Another disease that is associated with malnutrition is measles; even though effective vaccines for measles exist, it continues to cause severe disease and death in children worldwide. Among other factors, malnutrition and vitamin A deficiency increase complication rates. There is experimental evidence that vitamin A supplementation in children is associated with an average reduction of 23% in mortality risk, as well as an attenuation in disease severity. For this reason, the WHO recommends the administration of two oral doses of 200 000 IU of vitamin A to children with measles who live in vitamin A deficiency areas. Malnutrition and intestinal parasitism share a similar geographic distributions, with the same individuals experiencing Nutrition and Infection both diseases simultaneously. The coexistence of undernutrition and nematode infection involves two causal pathways: (1) malnutrition augments susceptibility to infection, and (2) the infection itself leads to a more accentuated undernutrition. Parasites that clearly affect the nutritional status are soiltransmitted helminths, G. intestinalis, E. histolytica, coccidian protozoans, and Schistosoma spp. Noma is an opportunistic infection promoted by extreme poverty, which evolves rapidly from a gingival inflammation to mutilating orofacial gangrene. Even though it can be observed worldwide, noma is much more common in sub-Saharan Africa. It results from very complex interactions between malnutrition, infection, and compromised immunity, and it is very frequently preceded by malaria, measles, and severe necrotizing ulcerative gingivitis. As mentioned previously, undernourished hosts are more susceptible to infections and to developing a severe course of infection due to impaired immune function. However, current works suggest that nutritional status can also increase the pathogenicity of the infecting agent or even change an avirulent virus into a virulent one. Animal models, particularly mice models, have provided the foundation of this theory. In a mouse model with selenium and vitamin E deficiency, a benign strain of Coxsackie virus B3 became virulent and caused myocarditis, as the result of a mutation in the viral genome caused by a decrease in dietary nutritional antioxidants; in other words, nutritional deficiencies changed an avirulent virus into a virulent one. Additionally, deficiencies of lycopene, vitamin E, and the B group vitamins have been serologically related to both CVB4 and CVA9, which were responsible for an epidemic of optic and peripheral neuropathy in Cuba in the early 1990s. These studies suggest that host nutritional status has influence beyond the host itself, altering the genome of viruses present in the host community. 101 riboflavin, iron, zinc, and selenium, have immunomodulating functions and thus influence susceptibility to infections, as well as the course and outcome of the illness. The effects of micronutrient deficiency have been evaluated by several experimental models (Table 1). Vitamin A has been termed the ‘anti-infective nutrient,’ although there is little evidence that it prevents the incidence of new infections. The one area in which the administration of this vitamin has actually been effective is in the prevention of neonatal infections. It has also been demonstrated that children with infectious diseases such as pneumonia and rheumatic fever tend to have low levels of vitamin A. In addition, adequate vitamin A stores are related to faster growth and better appetite. Similarly, although iron supports components of the hostdefense system, such as phagocytosis, there is no evidence that iron itself prevents infections. In fact, rich stores of iron and the high-dose administration of the nutrient have been associated with increased susceptibility to or morbidity from certain intracellular pathogens such as the plasmodium of malaria and the protozoa E. histolytica, among others. By contrast, zinc is emerging as a nutrient that can reduce the risk of infections and reinfection through supplementation. Recent trials of zinc supplementation have shown substantial benefits to children at risk of deficiency. Zinc supplementation also appears to reduce the duration and severity of acute diarrhea in India, as well as to improve outcomes in subsets of patients with persistent diarrhea in Peru. Zinc supplementation may not be safe and advantageous for everyone, however. In children with severe PEM, a three-armed trial in Bangladesh comparing a placebo to two doses of zinc supplementation found a higher mortality rate among those receiving a very high zinc dose. Finally, vitamin D has recently emerged as a nutrient of interest with promise for prophylactic application in epidemic viral diseases such as influenza and diverse microbial infections. Micronutrients in the Prevention of Infections Obesity and Infection Ensuring adequate micronutrient status is important for the prevention of certain infections. Several micronutrients, such as vitamin A, beta-carotene, folic acid, vitamin B12, vitamin C, Table 1 Obesity is an increasing problem in public health, clearly associated with a high risk of multiple pathological conditions, Effects of malnutrition on the immune system in some experimental models Experimental model Diet restriction Effect Human reconstituted SCID mice SD rats Total vitamin A restriction; 7-day gestation period Total Zn restriction; 34 weeks Impaired antibody production after tetanus toxoid immunization BALB/c mice C57BL/6 mice Total vitamin A restriction; 2–5 weeks Total dietary restriction (70%); 52 weeks Thymus atrophy, oligospermia, testicular atrophy, and loss of sperm cells and spermatocytes Increased Th2 and T regulatory cells, decreased Th1 Decreased humoral response to hepatitis B virus Source: Molrine, D. C., Polk, D. B., Ciamarra, A., Phillips, N. and Ambrosino, D. M. (1995). Impaired human responses to tetanus toxoid in vitamin A-deficient SCID mice reconstituted with human peripheral blood lymphocytes. Infection and Immunity 63(8), 2867–2872; Anstead, G. M., Chandrasekar, B., Zhao, W., Yang, J., Perez, L. E. and Melby, P. C. (2001). Malnutrition alters the innate immune response and increases early visceralization following Leishmania donovani infection. Infection and Immunity 69(8), 4709–4718; Rivadeneira, D. E., Grobmyer, S. R., Naama, H. A., Mackrell, P. J., Mestre, J. R., Stapleton, P. P., et al. (2001). Malnutrition-induced macrophage apoptosis. Surgery 129, 617–625; Nodera, M., Yanagisawa, H. and Wada, O. (2001). Increased apoptosis in a variety of tissues of zinc-deficient rats. Life Sciences 69, 1639–1649; Anstead, G. M., Chandrasekar, B., Zhang, Q. and Melby, P. C. (2003). Multinutrient undernutrition dysregulates the resident macrophage proinflammatory cytokine network, nuclear factor-kappa-B activation, and nitric oxide production. Journal of Leukocyte Biology 74(6), 982–991; Sakai, T., Mitsuya, K., Kogiso, M., Ono, K., Komatsu, T. and Yamamoto, S. (2006). Protein deficiency impairs DNA vaccine-induced antigen-specific T cell but not B cell response in C57BL/6 mice. Journal of Nutritional Science and Vitaminology 52(5), 376–382. 102 Nutrition and Infection including cardiovascular and metabolic diseases. Likewise, obesity affects different organs and systems, generating an environment susceptible to an increased risk of infection, and there is evidence of immune system impairment, indicated by alteration in cell differentiation, cytokine production, and thus chemotaxis during the immune response. In terms of cardiorespiratory function, overweight states produce mechanical ventilation disorders, causing pulmonary restriction and affecting the immune response at this level; this is analogous to infections at the skin level, because of altered tissue perfusion. There has been developing research interest on the relationship between obesity and infection, with a focus on the bidirectional interaction between the two: obesity has been linked to increased risk of infection with different pathogens, and some pathogens have been associated with an increased risk for developing obesity. For example, Taenia infection has been associated with decreased levels of leptin, a hormone associated with signaling satiety after food intake. Also, an association has been found between seropositivity for T. gondii and obesity, although the causal mechanism of this interaction has not been identified. As a matter of speculation, it may be mediated by complex mechanisms through which T. gondii influences different neurological centers involved in motivation and survival. Finally, it has been shown that obesity is an independent risk factor for the development of Clostridium difficile infection, but the mechanisms underlying this relationship are still unknown. Given this evidence, future research should be directed toward clarifying the mechanisms involved in the relationship between obesity and the risk of infection, as well as the clinical significance of this interaction, in order to define the relevance and potential benefit of early therapeutic interventions for patients predisposed to acquiring potentially dangerous pathogens. From Infection to Malnutrition Multiple mechanisms have been associated with nutritional impairment during infection, including factors related to the decreased intake of nutrients and increased nutrient loss. Although initially representing a host-defense strategy, some of these mechanisms can ultimately have a negative impact on nutritional status. Many infectious diseases that compromise the nutritional status directly affect the gastrointestinal tract. Hyporexia, poor appetite, or frank anorexia is frequent when the food intake is associated with vomiting or diarrhea. The symptomatic manifestations can evolve from a variety of associated mechanisms, however; these include the decreased intake of solids due to xerostomia (dry mouth) secondary to diarrheal dehydration; changes in the absorption surface of the gastrointestinal lumen, with destruction of the intestinal villi, induced by bacterial toxins; and nutrient loss through hypersecretion across the mucosa. These mechanisms directly affect the absorption or retention capacity of a nutrient. Not only the nutrients acquired through diet are lost, though. Endogenous nutrients that are generated during the normal cell turnover of the gastrointestinal epithelium can also be lost, when, under normal conditions, they would be largely reabsorbed. Similarly, respiratory diseases can affect undernutrition. Delay in growth has been documented in children with recurrent lower respiratory infections, as compared to unaffected children. Although the mechanisms behind this relationship have not been clearly elucidated, it has been suggested that fever and hyporexia are the main associated factors. There are also chronic infectious diseases whose characteristics of chronicity lead to a state of cachexia, as occurs with tuberculosis and HIV infection. In fact, in children with HIV, alterations in nutritional status can often represent the first clinical sign of the condition, and wasting syndrome is considered to be a feature of AIDS. In HIV patients with more severely disrupted nutritional status, the CD4 lymphocyte count is general substantially reduced, emphasizing the important role of immunological alterations in the pathogenesis of malnutrition. Conclusions The activation and maintenance of the immune response requires adequate energy consumption. PEM is a critical – but underestimated – factor contributing to susceptibility to infection, causing impaired immune function, as well as alterations in the normal development of children. Once the infection is established, it, in turn, contributes to further malnutrition, therefore perpetuating a vicious cycle. An adequate micronutrient status is important for the prevention of certain infections; therefore, in impoverished countries where malnutrition represents a great burden, mainly in children, strategies must be implemented in order to reduce the morbidity and mortality caused by malnutrition and, more particularly, chronic undernourishment. See also: Food and Agriculture Organization of the United Nations; Food Poisoning: Epidemiology; Foodborne Pathogens; HIV Disease and Nutrition; Malnutrition: Concept, Classification and Magnitude; Malnutrition: Prevention and Management; Nutritional Epidemiology; Parasites in Food: Occurrence and Detection. Further Reading Centers for Disease Control and Prevention (2013) Incidence and trends of infection with pathogens transmitted commonly through food – foodborne diseases active surveillance network, 10 U.S. sites, 1996–2012. Morbidity and Mortality Weekly Report 62: 283–287. Chandra RK (2002) Nutrition and the immune system from birth to old age. European Journal of Clinical Nutrition 56: S73–S76. Field CJ, Johnson IR, and Schley PD (2002) Nutrients and their role in host resistance to infection. Journal of Leukocyte Biology 71: 16–32. Fock RA, Vinolo MA, de Moura Sá Rocha V, de Sá Rocha LC, and Borelli P (2007) Protein-energy malnutrition decreases the expression of TLR-4/MD-2 and CD14 receptors in peritoneal macrophages and reduces the synthesis of TNF-alpha in response to lipopolysaccharide (LPS) in mice. Cytokine 40: 105–114. França T, Ishikawa LLW, and Zorzella-Pezavento SFG (2009) Impact of malnutrition on immunity and infection. Journal of Venomous Animals and Toxins Including Tropical Diseases 15: 374–390. Henao OL, Scallan E, Mahon B, and Hoekstra RM (2010) Methods for monitoring trends in the incidence of foodborne diseases: Foodborne Diseases Active Surveillance Network 1996–2008. Foodborne Pathogens and Disease 7: 1421–1426. Nutrition and Infection Henao OL, Crim SM, and Hoekstra RM (2012) Calculating a measure of overall change in the incidence of selected laboratory-confirmed infections with pathogens transmitted commonly through food in the Foodborne Diseases Active Surveillance Network (FoodNet), 1996–2010. Clinical Infectious Diseases 54: S418–S420. Huttunen R and Syrjanen H (2013) Obesity and the risk and outcome of infection. International Journal of Obesity 37: 333–340. McLinden T, Sargeant JM, Thomas MK, Papadopoulos A, and Fazil A (2014) Component costs of foodborne illness: a scoping review. BMC Public Health 26: 509. Savino W (2002) The thymus gland is a target in malnutrition. European Journal of Clinical Nutrition 56: S46–S49. Schaible U and Kaufmann S (2007) Malnutrition and infection: complex mechanisms and global impacts. PLoS Medicine 4: 806–812. Scrimshaw NS, Taylor CE, and Gordon JE (1968) Interaction of nutrition and infection. World Health Organization monograph series. vol. 57. Geneva: WHO. Solomons NW (2007) Malnutrition and infection: an update. British Journal of Nutrition 98: 5–10. View publication stats 103 Tomkins, A and Watson, F. (1989). Malnutrition and Infection – a review – nutrition policy discussion paper No. 5. United Nations and Nations Unies Government of the Netherlands. World Health Organization (2014) Multicriteria-based ranking for risk management of food-born parasites. Geneva: World Health Organization. Relevant Websites http://www.fao.org/ – FAO. http://www.oie.int/ – OIE. http://www.promedmail.org/ – ProMEDMail. http://www.who.int/ – WHO. http://www.who.int/zoonoses/ – WHO Zoonoses and veterinary public health.
