Altwegg, Martin

Hinrikson, Hans Peter

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1602CORRESPONDENCEShigella boydii as Cause of Malacoplakia in aHuman Immunodeficiency Virus–Infected PatientSIR—We read with great interest the report by Raguin et al.[1] on Shigella boydii as a possible causative agent of colonicmalacoplakia in an HIV-infected patient. In the absence ofpositive cultures, S. boydii was identified by means of universalbacterial 16S rDNA–based amplification and sequencing. Sincemalacoplakia is usually caused by Escherichia coli, a close rel-ative of shigellae and genetically belonging to the same species(!), despite being classified in 2 separate genera for reasons ofdifferent clinical and epidemiological significance, the reliableseparation of these 2 organisms would be essential to acceptingthe conclusion made by the authors. On the basis of the datapresented (highest relatedness of the sequence detected to S.boydii, with 459 [98%] of 468 nucleotides being identical) andthe analysis shown below, this does not seem possible.When the fragment of the S. boydii 16S rRNA gene amplifiedwith primers 91E and 13B [2, 3] is compared with the corre-sponding sequences deposited in the EMBL/Genebank data-bases, no differences at all are found between it and severalother members of the family Enterobacteriaceae, including E.coli, Escherichia vulneris, Salmonella paratyphi A, Salmonellaweltevreden, Shigella sonnei, Shigella flexneri, and Hafnia alvei.Above the 98% identity level, there are also other organisms,such as Klebsiella planticola and Citrobacter diversus. Further-more, intraspecies variation of 16S sequences has been de-scribed for various organisms [4, 5].This illustrates that several species and genera within thefamily Enterobacteriaceae are so closely related to each otherthat their identification solely on the basis of partial sequencesof their 16S rRNA genes is certainly not conclusive, even if theamplified fragments are repeatedly sequenced in both direc-tions, thus resulting in absolutely reliable sequence data.On the basis of the above considerations, we think that it israther unlikely (though not impossible) that malacoplakia inthe patient described was indeed caused by S. boydii.Martin Altwegg and Hans Peter HinriksonDepartment of Medical Microbiology, University of Zurich,Zurich, SwitzerlandReferences1. Raguin G, Nemeth J, Wassef M, et al. Identification of Shigella boydii incolonic malacoplakia by universal bacterial 16S ribosomal DNA–basedamplification in a human immunodeficiency virus–infected patient. ClinInfect Dis 1999;28:142–3.2. Relman DA. Universal bacterial 16S rDNA amplification and sequencing. In:Persing DH, Smith TF, Tenover FC, White TJ, eds. Diagnostic molecularmicrobiology: principles and applications. Washington, DC: American So-ciety for Microbiology, 1993:489–95.3. Wang RF, Cao WW, Cerniglia CE. Phylogenetic analysis and identificationof Shigella spp. by molecular probes. Mol Cell Probes 1997;11:427–32.4. Stackebrandt E, Goebel BM. Taxonomic note: a place for DNA-DNA re-association and 16S rRNA sequence analysis in the present species defi-nition in bacteriology. Int J Syst Bacteriol 1994;44:846–9.5. Goldenberger D, Schmidheini T, Altwegg M. Detection of Bartonella henselaeand Bartonella quintana by a simple and rapid procedure using broad-rangePCR amplification and direct single-strand sequencing of part of the 16SrRNA gene. Clin Microbiol Infect 1997;3:240–5.Reprints or correspondence: Dr. Martin Altwegg, Gloriastrasse 30, 8028 Zu¨r-ich, Switzerland (altwegg@immv.unizh.ch).Clinical Infectious Diseases 1999;29:1602q 1999 by the Infectious Diseases Society of America. All rights reserved.1058-4838/1999/2906-0062$03.00ReplySIR—Altwegg and Hinrikson, in their letter, question the con-clusion in our report that Shigella boydii may be the causativeagent of malakoplakia. We agree that the fragment of the 16SrRNA gene amplified with primers 91E and 13B does not per-mit sequences of several members of the family Enterobacter-iaceae to be distinguished reliably.At the time of writing our report, the BLAST search versionwe used (BLASTN 1.4.9 MP 26 h1996) gave the highest scoreof homology for S. boydii, closely followed by Shigella sonnei,Shigella flexneri, Hafnia alvei, and Escherichia coli. We agreethat the subtle differences given by the alignment search toolshould have been interpreted more cautiously. However, sincethen, we have used the Microseq 16S rRNA Gene Kit (Perkin-Elmer, Applied Biosystems, Foster City, CA) to amplify thefirst 500 bp in the 5′ region of the bacterial 16S rDNA gene,which allows discrimination between S. boydii and E. coli. TheDNA extracted from the malakoplakia tissue was confirmedto contain a 16S rDNA sequence giving the highest geneticrelatedness with S. boydii 16S sequences and demonstrating 7bp of difference from E. coli 16S rDNA sequences in discrim-inant codons.On the basis of these data, we think that it is probable(though not certain) that malakoplakia in the patient describedwas caused by S. boydii.Gilles Raguin,1 Judith Nemeth,2 Michel Wassef,2Jean Aerts,1 Marcelo Salmeron,3 Nicole Desplaces,3and Laurent Belec31Hoˆpital de la Croix-Saint-Simon, 2Hoˆpital Lariboisie`re, and 3HoˆpitalBroussais, Paris, FranceReprints or correspondence: Dr. Gilles Raguin, Hopital de la Croix-Saint-Simon, 125 rue d’Avron, 75960 Paris Cedex 20, France (graguin@croix-saint-simon.org).Clinical Infectious Diseases 1999;29:1602q 1999 by the Infectious Diseases Society of America. All rights reserved.1058-4838/1999/2906-0063$03.00

Shigella boydii as Cause of Malacoplakia in a Human Immunodeficiency Virus-Infected Patient

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