Chapter 114. Molecular Mechanisms of Microbial Pathogenesis (Part 11)

Transmission to New HostsAs part of the pathogenic process, most microbes are shed from the host, often in a form infectious for susceptible individuals. However, the rate of transmissibility may not necessarily be high, even if the disease is severe in the infected individual, as transmissibility and virulence are not linked traits. Most pathogens exit via the same route by which they entered: respiratory pathogens by aerosols from sneezing or coughing or through salivary spread, gastrointestinal pathogens by fecal-oral spread, sexually transmitted diseases by venereal spread, and vector-borne organisms by either direct contact with the vector through a blood...
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Chapter 114. Molecular Mechanisms of Microbial Pathogenesis (Part 11) Chapter 114. Molecular Mechanisms of Microbial Pathogenesis (Part 11) Transmission to New Hosts As part of the pathogenic process, most microbes are shed from the host,often in a form infectious for susceptible individuals. However, the rate oftransmissibility may not necessarily be high, even if the disease is severe in theinfected individual, as transmissibility and virulence are not linked traits. Mostpathogens exit via the same route by which they entered: respiratory pathogens byaerosols from sneezing or coughing or through salivary spread, gastrointestinalpathogens by fecal-oral spread, sexually transmitted diseases by venereal spread,and vector-borne organisms by either direct contact with the vector through ablood meal or indirect contact with organisms shed into environmental sourcessuch as water. Microbial factors that specifically promote transmission are notwell characterized. Respiratory shedding is facilitated by overproduction ofmucous secretions, with consequently enhanced sneezing and coughing. Diarrhealtoxins such as cholera toxin, E. coli heat-labile toxins, and Shigella toxinsprobably facilitate fecal-oral spread of microbial cells in the high volumes ofdiarrheal fluid produced during infection. The ability to produce phenotypicvariants that resist hostile environmental factors (e.g., the highly resistant cysts ofE. histolytica shed in feces) represents another mechanism of pathogenesisrelevant to transmission. Blood parasites such as Plasmodium spp. changephenotype after ingestion by a mosquito—a prerequisite for the continuedtransmission of this pathogen. Venereally transmitted pathogens may undergophenotypic variation due to the production of specific factors to facilitatetransmission, but shedding of these pathogens into the environment does not resultin the formation of infectious foci. In summary, the molecular mechanisms used by pathogens to colonize,invade, infect, and disrupt the host are numerous and diverse. Each phase of theinfectious process involves a variety of microbial and host factors interacting in amanner that can result in disease. Recognition of the coordinated geneticregulation of virulence factor elaboration when organisms move from their naturalenvironment into the mammalian host emphasizes the complex nature of the host-parasite interaction. Fortunately, the need for diverse factors in successfulinfection and disease implies that a variety of therapeutic strategies may bedeveloped to interrupt this process and thereby prevent and treat microbialinfections Further Readings Camilli A, Bassler BL: Bacterial small-molecule signaling pathways.Science 311:1113, 2006 [PMID: 16497924] Finlay BB, McFadden G: Anti-immunology: Evasion of the host immunesystem by bacterial and viral pathogens. Cell 124:767, 2006 [PMID: 16497587] Han J, Ulevitch RJ: Limiting inflammatory responses during activation ofinnate immunity. Nat Immunol 6:1198, 2005 [PMID: 16369559] Kawai T, Akira S: Innate immune recognition of viral infection. NatImmunol 7:131, 2006 [PMID: 16424890] Knirel YA et al: Structural features and structural variability of thelipopolysaccharide of Yersinia pestis, the cause of plague. J Endotoxin Res 12:3,2006 [PMID: 16420739] Mendes-Giannini MJ et al: Interaction of pathogenic fungi with host cells:Molecular and cellular approaches. FEMS Immunol Med Microbiol 45:383, 2005[PMID: 16087326] Pizarro-Cerda J, Cossart P: Bacterial adhesion and entry into host cells.Cell 124:715, 2006 [PMID: 16497583] Spear PG et al: Different receptors binding to distinct interfaces on herpessimplex virus gD can trigger events leading to cell fusion and viral entry. Virology344:17, 2006 [PMID: 16364731] Takahashi K et al: The mannose-binding lectin: A prototypic patternrecognition molecule. Curr Opin Immunol 18:16, 2006 [PMID: 16368230] Bibliography Abe A et al: Type-III effectors: Sophisticated bacterial virulence factors. CR Biol 328:41, 2005 Kobasa D, Kawaoka Y: Emerging influenza viruses: Past and present. CurrMol Med 5:791, 2005 [PMID: 16375713] ODonnell RA, Blackman MJ: The role of malaria merozoite proteases inred blood cell invasion. Curr Opin Microbiol 8:422, 2005 [PMID: 16019257]