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Journal of Clinical Microbiology, November 2002, p. 4397-4398, Vol. 40, No. 11
0095-1137/02/$04.00+0 DOI: 10.1128/JCM.40.11.4397-4398.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Antigenic and Genotypic Relationships between Bartonella henselae Strains

LETTER
The ubiquitous feline intraerythrocytic pathogen
Bartonella henselae causes a range of important human infections, and seroprevalence
in blood donors in Australia is around 5% (
6). Two antigenically
distinct subtypes have been described, named for the type strain
(Houston-1) and the more recently recognized Marseille strain
(
5), which have characteristic DNA sequences in the 16S rRNA
gene (rDNA) and the
gltA (citrate synthase) gene (
2,
3,
5).
Culture of this fastidious, gram-negative bacterium is difficult,
and serology is a primary diagnostic approach. A recent report
that Houston-like strains (including Houston-1, 90-615, and
SA-2) may be distinguished from serologically distinct Marseille-like
strains (including URBHLLY-8, URBHLIE-9, Fizz, and CAL-1) by
the faster migration of a characteristic band (ca. 29 kDa) on
sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE)
analysis and immunoblotting of whole-cell lysates is therefore
particularly noteworthy (
7).
However, the SDS-PAGE data appear to contrast with previous publications from the same laboratory (8, 9) and others (11). We therefore compared local human isolates with the Houston-1 and Marseille strains and also found two closely related genotypes with corresponding patterns on SDS-PAGE of whole-cell lysates (Fig. 1). All human strains appear to have either the 30-kDa band (Houston) or the 29-kDa band (Marseille), in agreement with earlier studies (10, 11). The agar-pitting colony phenotype and number of in vitro passages have no apparent influence (Fig. 1 and Table 1). However, a local feline strain of the type II (Marseille-like) 16S rDNA genotype has the faster-migrating (29-kDa) band and a gltA gene sequence typical of Houston strains, consistent with the considerable diversity known to exist in feline strains (1, 10) and illustrating a dissociation of the accepted genotype-phenotype relationships. The strains in the recent study (7) were all human isolates and were assigned to genotypes by individual sequencing of several genes, including groEL (12) and the 16S rDNA (3). While the 29- to 30-kDa antigen(s) may yet prove useful for serotyping of human isolates, it thus seems unlikely that reported inconsistencies in the data can be easily explained by phase variation or genotype. In addition, we have no reason to assume that the more diverse feline strains are all nonpathogenic in humans. For both of thesereasons, we therefore urge caution in adopting this promising target as a basis for serotype distinction until the picture is clearer.

ACKNOWLEDGMENTS
P.K. and D.B. are recipients of Australian Postgraduate Awards.

REFERENCES
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Jon Iredell* Josh McHattan Pierre Kyme Belinda Dillon Deborah Blanckenberg
Centre for Infectious Diseases and Microbiology Level 3, ICPMR Bldg. Westmead Hospital Hawkesbury Road Westmead, New South Wales 2145, Australia
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* Phone: 61-2-98456255 Fax: 61-2-98915317 E-mail: joni{at}icpmr.wsahs.nsw.gov.au. |
Journal of Clinical Microbiology, November 2002, p. 4397-4398, Vol. 40, No. 11
0095-1137/02/$04.00+0 DOI: 10.1128/JCM.40.11.4397-4398.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
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