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Figure 2-10. The rabbit ileal loop model of diarrheal disease. Shown are tied-off segments (loops) of rabbit ileal injected with culture filtrates from an E. coli strain producing cholera-like toxin that induces diarrhea. Loop 1 was injected with positive control solution of cholera toxin, loop 2 with negative control solution of phosphate-buffered saline, and loops 3 through 6 with increasing amounts of E. coli culture filtrates. After overnight exposure in the animal, the animal is sacrificed and the ileal loops are removed and examined for distension (swelling). Reproduced from Sack RB. 2011. Indian J Med Res 133:171–180, with permission.
Genetically engineered mice called transgenic mice or knockout mice are being increasingly used in experiments to probe the interaction of the normal microbiota and the intestinal mucosal cells because they have genes that have been altered or disrupted. Unexpectedly, some of the mice designed originally for studies of the immune system that were missing genes encoding the cytokines, interleukins IL-1 and IL-10 (see chapter 3), proved to be good models for a type of intestinal inflammation called inflammatory bowel disease (IBD). The presence of the normal bacterial microbiota of the colon seems to be responsible for the inflammatory bowel condition seen in some of these mice.
These examples are given to provide an introduction to the types of animal models that are available for studying the protective features of skin and mucosa and the consequences of breaching these barriers. Additional animal models used in connection with studying bacterial diseases, as well as alternatives to animal models such as mammalian host cells cultured in vitro in the laboratory, will be described in chapter 8 and other chapters covering specific types of infectious diseases.
SELECTED READINGS
Bik EM, Eckburg PB, Gill SR, Nelson KE, Purdom EA, Francois F, Perez-Perez G, Blaser MJ, Relman DA. 2006. Molecular analysis of the bacterial microbiota in the human stomach. Proc Natl Acad Sci USA 103:732–737.[PubMed][CrossRef]
Cooper GM, Hausman RE. 2007. The Cell—A Molecular Approach, 4th ed. ASM Press, Washington, DC.
Hooper LV. 2004. Bacterial contributions to mammalian gut development. Trends Microbiol 12:129–134.[PubMed][CrossRef]
Hooper LV, Wong MH, Thelin A, Hansson L, Falk PG, Gordon JI. 2001. Molecular analysis of commensal host-microbial relationships in the intestine. Science 291:881–884.[PubMed][CrossRef]
Mirmonsef P, Spear GT. 2014. The barrier to HIV transmission provided by genital tract Lactobacillus colonization. Am J Reprod Immunol 71:531–536.[PubMed][CrossRef]
Mukherjee S, Hooper LV. 2015. Antimicrobial defense of the intestine. Immunity 42:28–39.[PubMed][CrossRef]
Pronovost P, Needham D, Berenholtz S, Sinopoli D, Chu H, Cosgrove S, Sexton B, Hyzy R, Welsh R, Roth G, Bander J, Kepros J, Goeschel C. 2006. An intervention to decrease catheter-related bloodstream infections in the ICU. N Engl J Med 355:2725–2732.[PubMed][CrossRef]
Salemi C, Canola MT, Eck EK. 2002. Hand washing and physicians: how to get them together. Infect Control Hosp Epidemiol 23:32–35.[PubMed][CrossRef]
Servin AL. 2004. Antagonistic activities of lactobacilli and bifidobacteria against microbial pathogens. FEMS Microbiol Rev 28:405–440.[PubMed][CrossRef]
Strober W. 2006. Immunology. Unraveling gut inflammation. Science 313:1052–1054. [Review of an article in the same issue of the journal.][PubMed][CrossRef]
Toke O. 2005. Antimicrobial peptides: new candidates in the fight against bacterial infections. Biopolymers 80:717–735.[PubMed][CrossRef]
Winslow EH, Jacobson AF. 2000. Can a fashion statement harm the patient? Long and artificial nails may cause nosocomial infections. Am J Nurs 100:63–65.[PubMed]
Questions
1. In what sense are S. epidermidis infections an example of how changing human practices can provide new opportunities for bacterial pathogens? S. epidermidis is classified as an opportunist. Why is this the case?
2. Explain why infections of the skin occur more often in folds of the skin or under bandages than in regions of skin exposed to air.
3. How and why do the defenses of mucosal surfaces differ from those of the skin? How do they resemble each other?
4. Consider a bacterium that is ingested via contaminated water and locally colonizes the small intestine. What host defenses would hamper this type of colonization from occurring initially and from leading to an infection in an unimmunized person?
5. Resident microbiota are essential in preventing the colonization of pathogenic bacteria in certain parts of the body. Name the regions of the body where normal microbiota might be protective. Name some mechanisms by which they accomplish this protection. Name some organs that normally remain sterile to bacterial contamination and that do not contain a resident microbiota.
6. Why are people with indwelling catheters more susceptible to infection?
7. Explain the role that mucin plays in host defense.
8. Lysozyme is more effective against growing bacteria. Why might that be so? Why is lysozyme digestion often more effective against Gram-positive bacteria than Gram-negative bacteria?
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