Waterborne transmission and the evolution of virulence among gastrointestinal bacteria

The two major disease-causing biotypes of Vibrio cholerae, classical and El Tor, exhibit differences in their epidemic nature. Their behavior in the laboratory also differs in that El Tor strains produce two major virulence factors, cholera toxin (CT) and the toxin coregulated pilus (TCP), only under very restricted growth conditions, whereas classical strains do so in standard laboratory medium. Expression of toxin and TCP is controlled by two activator proteins, ToxR and ToxT, that operate in cascade fashion with ToxR controlling the synthesis of ToxT. Both biotypes express equivalent levels of ToxR, but only classical strains appear to express ToxT when grown in standard medium. In this report we show that restrictive expression of CT and TCP can be overcome in El Tor strains by expressing toxT independently of ToxR. An El Tor strain lacking functional ToxT does not express CT or TCP, ruling out existence of a cryptic pathway for virulence regulation in this biotype. These results may have implications for understanding the evolution of El Tor strains toward reduced virulence with respect to classical strains.

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“…classical strains, suggesting that the pathogenicity of El Tor strains is reduced compared with that of classical strains (3). Ewald (25,26) …”

Section: Resultsmentioning

confidence: 99%

Differential expression of the ToxR regulon in classical and E1 Tor biotypes of Vibrio cholerae is due to biotype-specific control over toxT expression.

DiRita

Neely

Taylor

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

104

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“…2. Also in apparent support of the Associated model is a series of medical studies in which an initially benign Plasmodium was transferred serially from human to human (170 transfers), eventually evolving to virulence (reviewed by Ewald 1983Ewald , 1994. The increase in virulence was accompanied by a 500-fold increase in circulating parasite concentrations.…”

Section: Ila the Associated Modelmentioning

confidence: 99%

“…300-301) invoked this mechanism when suggesting that myxoma virus transmission would be favored by extensive skin lesions in a sick host that could not easily dislodge mosquitoes (the vector of transmission). In a similar vein, Ewald (1983) argued that host immobility induced by malaria enhances the chance that mosquitoes will bite the host and transmit the parasite. Many other obvious possibilities come to mind: coughing enhances transmission of respiratory pathogens, and open sores on genitalia enhance transmission of sexually transmitted diseases.…”

Section: Ia Direct Benefitsmentioning

confidence: 99%

“…Ewald has made extensive use of trade-off models. In a series of papers (Ewald 1983, 1987, 1991a, 1991b, Ewald and Schubert 1989) and a book (Ewald 1994), he compared published observations on the natural history ofhuman and other diseases with two predictions: (l) greater virulence should evolve with increased host-host transmission, and (2) vector-borne diseases should evolve higher virulence than diseases requiring direct person-to-person contact with the infected individual. Ewald has suggested that the evidence is largely supportive of the predictions.…”

Section: Ic2 Empiricalmentioning

confidence: 99%

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Virulence

1994

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Abstract. -Why do parasites harm their hosts? Intuition suggests that parasites should evolve to be benign whenever the host is needed for transmission. Yet a growing theoretical literature offers several models to explain why natural selection may favor virulent parasites over avirulent ones. This perspective first organizes these models into a simple framework and then evaluates the empirical evidence for and against the models. There is relatively scant evidence to support any of the models rigorously, and indeed, there are only a few unequivocal observations of virulence actually evolving in parasite populations. These shortcomings are surmountable, however, and empirical models of host-parasite interactions have been developed for many kinds of pathogens so that the relevant data could be acquired in the near future.Aside from academic interest, the evolution of virulence has potential medical and agricultural ramifications that may provide evolutionary biology with opportunities for contributions to human welfare. For example, understanding the evolution of parasite virulence may help us design better vaccines, prevent the emergence of highly virulent strains in the future, and diminish the virulence of present pathogens. These potential applications notwithstanding, the usefulness of an evolutionary theory of virulence to social problems has not been demonstrated and is even doubtful in some cases. One promising area for contributions from evolutionary theory is in designing live, attenuated vaccines.Key words.-Evolution, microparasite, population biology, virulence, virus.Received April 10, 1994. Accepted April 12, 1994 Evolutionary biologists are becoming increasingly enamored of the idea that evolutionary thinking may contribute substantially to the alleviation of human health problems. Much of the fanfare has centered on applications of natural selection to disease (the Darwinian Medicine school; Profet 1991Profet , 1993Williams and Nesse 1991; Ewald 1994) but these applications of evolutionary biology are so far without obvious success in penetrating the fields of medicine. In contrast, a far more visible impact from evolutionary biology is the use of phylogenetic reconstruction to trace routes and sources of in-I

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“…Dating as far back as 1933 there have been documented cases of deaths caused by shigellosis in the United States (Ewald, 1991). DuPont and Hornick, asserted that ingestion of only lo-100 Shigellu cells can lead to infection.…”

Section: Introductionmentioning

confidence: 99%

Prevalence of shigellosis in the U.S.: consistency with dose-response information

Crockett

Haas

Fazil

et al. 1996

International Journal of Food Microbiology

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Every year there are estimated 300000 cases of Shigella in the United States (Bennett et al., 1987, Am. J. Prev. Med. 3, 102-114). A beta-Poisson model was fit to human dose-response information on pathogenic Shigella using the Maximum Likelihood Estimation technique (Haas, 1983, Am. J. Epidemiol. 118, 573-582). Pooled and separate data sets for the Shigella species were fit to the beta-Poisson model and 95% confidence limits and regions were calculated. Shigella dysentariae and Shigella jlexneri confidence regions and limits overlapped with each other and with the pooled data set, suggesting that this model can describe Shigella in general. The pooled Shigella model as well as the upper and lower confidence limits of the three data sets showed average exposures based on the estimated U.S. caseload of pathogenic Shigella of 0.01 to 0.014 organisms (confidence limits O.OOl-0.05) for a 7-day per annum period of exposure and ranges from 0.07 to 0.1 organisms (confidence limits 0.006-0.4). for a l-day per annum period of exposure. The plausibility of the pooled dose-response model was then evaluated by comparison with two known cruise ship outbreaks. The pooled model estimated that the two outbreaks studied could have been due to ingestion of 344 (confidence limits 72-915) Shigella cells per meal and 10.5-12 (confidence limits l-44) Shigella cells per glass of water by passengers.

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Waterborne transmission and the evolution of virulence among gastrointestinal bacteria

Cited by 72 publications

References 182 publications

Differential expression of the ToxR regulon in classical and E1 Tor biotypes of Vibrio cholerae is due to biotype-specific control over toxT expression.

Differential expression of the ToxR regulon in classical and E1 Tor biotypes of Vibrio cholerae is due to biotype-specific control over toxT expression.

Virulence

Prevalence of shigellosis in the U.S.: consistency with dose-response information

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