Role of Animals in E Coli Infection - Case Study Example

?Role of animals in E. coli infection Shiga toxin-producing E. coli (STEC) is the principal cause of hemolytic uremic syndrome (HUS), manifesting as acute renal failure, hemolytic anemia and thrombocytopenia (Bentancor et al., 2012). One of the more common STEC is the bacterial strain O157. The intestines of ruminant animals such as cattle, sheep, goats, and cow act as the principal reservoir for the growth of E. coli O157 (Bentancor et al., 2012; Quilliam et al., 2011). Because of its fecal-oral route of exposure, these animals are constantly exposed to this strain because of their diet. When an infected animal defecates, the grasses around it become exposed to the bacteria as well. When other animals graze on the land, they become exposed to the bacteria as well, turning their intestinal tract as an incubator. The animals’ significant role in the epidemiology of E. coli infection is to be expected since the prevalence of STEC is more than half of the total number of sheep and goats, and more than a fifth of cattle population (Bentancor et al., 2012). True enough, it is clearly seen from the increase in reported cases of human infection, which coincides with the maximal strain O157 fecal excretion by the reservoir. Soil properties, climates, animal husbandry, and farm management thus explains the variations in E. coli infection prevalence that populations experience (Quilliam et al., 2011). This epidemiologic and exposure analysis looks into different populations to explain the E. coli infection occurrences in their area. Exposure of farmers to E. coli O157 Indeed, unsafe water, together with poor sanitation and poor personal hygiene, causes almost two million deaths per year due to infectious diarrhea. Because of exposure to these animals, farmers are understandably at risk of developing E. coli infection manifesting as HUS. However, frequent and direct exposure to domestic animals makes farmers more immune to strain O157 infection that other members of their community. This is because they develop antibodies from the zoonoses they are exposed to without acquiring any disease. Possibly, this occupational exposure does not have enough bacterial units to cause disease. These antibodies, in turn, protect these farmers from the pathogenic O157 that is related from the bacteria they were previously exposed to. Seroprevalence of O157 lipopolysaccharide-specific antibodies among sampled farmers are also associated with a private water supply and contact with child under 5 years old. Similarly, both of these factors independently expose the farmers to a limited number of bacterial units (Quilliam et al., 2011). Contamination of water influences E. coli infection prevalence When an animal releases fecal material, their manure can also become agricultural run-offs, exposing groundwater to infected material (Quilliam et al., 2011). That is why having a private water source is important in preventing infection. In contrast, drinking of non-pasteurized apple juice has been associated with cases of HUS in the United States. Also, exposure to recreational water, which may be contaminated, is found to increase the risk for HUS development. One of the reasons why children are more susceptible to E. coli infection is that they are more likely to engage in swimming activities and to intentionally or accidentally swallow contaminated water (Bentancor et al., 2012). Fecal-oral route of human exposure Similar to infected ruminants, human carriers can act as reservoir as well because of the fecal-oral route of human exposure and person-to-person transmission of infection. When they do not properly wash their hands after defecation, their fecal material can get to the food they prepare and the children they take care of. Indeed, food contamination can occur anywhere among processing, distribution and cooking, and infection from contaminated food products is highly likely since as little as 100 bacterial units per gram of food can establish STEC infection. Food handling has substantially been modified to increase production because of the increased number of frozen food consumers and subsequent growth in demand. Many prefer to buy such products because of its convenience, affordability, palatability and advertisement. Among the changes in processing include inadequate cooking, which allows survival of pathogens, especially of frozen ground meat, such as hamburgers (Quilliam et al., 2011). In addition, when humans fail to properly cook meat products to a temperature of at least 72°C, they allow the bacteria to survive and reach the gastrointestinal tract of those that will ingest the food. Such practice makes many people susceptible, since many eat meat. In Argentina, for example, meat consumption is more than 60/kg/person/day. True enough, one risk factor highly associated with HUS is consumption of ground meat, especially incompletely cooked hamburgers. A study among Argentinian children found that 94% of children consume hamburgers, and 80% of these subjects eat commercially prepared processed hamburgers. Children are thus susceptible to E. coli infection, because they depend on others to prepare their food and groom themselves. This can be seen statistically. Most cases of STEC infection are seen in children younger than 16 years old, especially those aged 0-5 years. In Argentina, there are over 450 sporadic cases reported per year. In fact, 20% of pediatric transplants in Argentina are directly caused by HUS (Bentancor et al., 2012). Effects of antibiotics to E. coli infection Surprisingly, patients treated empirically for O157 E. coli-caused diarrhea are found to be at greater risk for developing HUS. In contrast, fosfomycin treatment in the second day of illness decreased the risk for HUS. Based on this data, many infected individuals are susceptible to HUS, because, in 2008 and 2009 study in the United States and Scotland, 36% of HUS patients took in antibiotics even before diagnosis. The reason for this observation most possibly be the eradication of the natural gut flora and subsequent promotion of the growth of E. coli strain O157. This competitive advantage of this strain is observed in metronidazole (Wong et al., 2012). Similarly, the promoting effect of antibiotics, especially of floroquinolone, to bacterial growth has been seen in extended spectrum ?-lactamase (ESBL)-producing E. coli. Aside from antibiotics, previous exposure to healthcare-associated infections also increases susceptibility to ESBL E. coli. These strains that are resistant to antimicrobials are significant pathogens because they cause about 6.7% of all community acquired E. coli bacteremia (Kang et al., 2012). . References Bentancor, A. B., Ameal, L. A., Calvino, M .F., Martinez, M. C., Miccio, L., & Degregorio, O. J. (2012). Risk factors for Shiga toxin-producing Escherichia coli infections in preadolescent schoolchildren in Buenos Aires, Argentina. J Infect Dev Ctries, 6(5), 378-386. Kang, C., et al. (2012). Epidemiology and Risk Factors of Community Onset Infections Caused by Extended-Spectrum-Lactamase-Producing Escherichia coli Strains. J Clin Microbiol, 50(2), 312-317. Quilliam, R. S., et al. (2011). Seroprevalence and Risk Factors Associated with Escherichia coli O157 in a Farming Population. Zoonoses and Public Health, 59, 83-88. Wong, C. S., et al. (2012). Risk Factors for the Hemolytic Uremic Syndrome in Children Infected With Escherichia coli O157:H7: A Multivariable Analysis. CID, 2-9. Read More