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Journal of Clinical Microbiology, April 2002, p. 1565-1566, Vol. 40, No. 4
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.4.1565-1566.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

LETTER TO THE EDITOR

Prevalence of the sat Gene among Clinical Isolates of Shigella spp. Causing Travelers' Diarrhea: Geographical and Specific Differences

Top Letter References

 
In the last several years, developing countries have become popular tourist destinations. The large number of travelers to these areas has brought an increase in the so-called travelers' diseases (5). These diseases are due both to the sanitary conditions encountered in some of these places and to the irresponsible attitudes of the travelers themselves. In fact, travelers' diseases may be seen as a mirror of the reality of the sanitary conditions of the tourist destinations influenced by the conduct of the travelers. Thus, analysis of the prevalence and characteristics of travelers' diseases may be considered an indirect source of sanitary information for the visited areas. Among the aforementioned diseases, traveler's diarrhea is one of the most common pathologies found among those returning from developing countries (5).

Diarrhea associated with Shigella infections results in around 1,100,000 deaths each year, especially among children in developing countries (3). To study in depth the virulence determinants of this microorganism is a public health priority. Sequences homologous to Sat, a urovirulence factor of Escherichia coli, have been described for Shigella spp. (2). However, no extensive studies on the prevalence of this virulence factor among Shigella spp. have been performed.

The prevalence of the sat gene in 36 Shigella sonnei and 43 Shigella flexneri isolates causing traveler's diarrhea collected during the period of 1995 to 2000 has been established in this study.

The presence of the sat gene was determined by PCR amplification of 387 bp using the primers 5'-ACTGGCGGACTCATGCTGT-3' and 5'-AACCCTGTAAGAAGACTGAGC-3' under previously reported conditions (4). Some of the PCR products were sequenced, and all presented 100% homology to those described previously for E. coli.

Overall, 44 isolates (55.69% of the total) were positive; 11 were S. sonnei (25.58% of the total number of S. sonnei isolates analyzed), while 23 were S. flexneri (63.89% of the S. flexneri isolates analyzed). Independent of its exact geographical origin, the prevalence of the sat gene has always been found to be 30 to 40% higher in S. flexneri than in S. sonnei. In both species, the higher prevalence of sat (35.71 and 71.43% in S. sonnei and S. flexneri, respectively) was found in isolates obtained from travelers returning from Latin America (Tables 1 and 2). Using a chi-square test, such a proportion was found to be significant (P < 0.001). The results of the Mantel and Haensel stratified analysis by continent were still significant (P = 0.002).

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TABLE 1. Geographical distribution of the Shigella isolates

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TABLE 2. Geographical prevalence of the sat gene

Nineteen (48.72%) out of the 39 S. flexneri strains belonged to serotype 2a. This high prevalence of S. flexneri serotype 2a might be explained by the particularly enhanced virulence of this serotype (1). Furthermore, 15 (78.95%) out of these 19 S. flexneri 2a strains were positive for the sat gene. In contrast, among the remaining 20 S. flexneri strains belonging to other serotypes, only 4 (20%) contained it.

In summary, our results show a high incidence of the sat gene among clinical isolates of Shigella spp. of different intercontinental origins. Further studies are necessary to establish, with greater accuracy, the geographical distribution of this toxin, as well as its relevance as a diarrheagenic factor of Shigella spp.

 
This work was supported by grant FIS00/0997 from Fondo de Investigaciones Sanitarias.

The statistical support of John Jairo Aponte is greatly appreciated.

Top Letter References

 

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1. Al-Hasani, K., I. R. Henderson, H. Sakellaris, K. Rajakumar, T. Grant, J. P. Nataro, R. Robins-Browne, and B. Adler. 2000. The sigA gene which is borne on the she pathogenicity island of Shigella flexneri 2a encodes an exported cytopathic protease involved in intestinal fluid accumulation. Infect. Immun. 68:2457-2463.[Abstract/Free Full Text]
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2. Guyer, D. M., I. R. Henderson, J. P. Nataro, and H. L. Mobley. 2000. Identification of sat, an autotransporter toxin produced by uropathogenic Escherichia coli. Mol. Microbiol. 38:53-66.[CrossRef][Medline]
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3. Kotloff, K. L., J. P. Winickoff, B. Ivanoff, J. D. Clemens, D. L. Swerdlow, P. J. Sansonetti, G. K. Adak, and M. M. Levine. 1999. Global burden of Shigella infections: implications for vaccine development and implementation of control strategies. Bull. W. H. O. 77:651-666.[Medline]
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4. Vila, J., J. Ruiz, F. Marco, A. Barcelo, P. Goñi, E. Giralt, and T. Jimenez de Anta. 1994. Association between double mutation in gyrA gene of ciprofloxa-cin-resistant clinical isolates of Escherichia coli and MICs. Antimicrob. Agents Chemother. 38:2477-2479.[Abstract/Free Full Text]
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5. Virk, A. 2001. Medical advice for international travelers. Mayo Clin. Proc. 76: 831-840.[Abstract]

						Joaquim Ruiz* Margarita M. Navia Jordi Vila Servicio de Microbiologia, Institut Clinic d’Infeccions i Immunologia Joaquim Gascón Secció de Medicina Tropical Centre de Salut Internacional IDIBAPS Hospital Clínic Villarroel 170 08036-Barcelona, Spain
						* Phone: 34932275522, ext. 2361 Fax: 34932275454 E-mail: joruiz{at}clinic.ub.es

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Journal of Clinical Microbiology, April 2002, p. 1565-1566, Vol. 40, No. 4
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.4.1565-1566.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

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