Where is staphylococcus saprophyticus

The transmission chain of S lineage isolates appears to be different and to have no link to meat production. S lineage UTIs might originate from human gut or vaginal colonization; both have been reported as possible human niches 2 , 4.

The distinct genetic content and phenotypic features of lineages G and S further reflected the diverse selective pressures of the human and animal, slaughterhouse, and food environments and suggest different evolutionary strategies toward pathogenicity.

In particular, we found that tetracycline and antimicrobial resistance genes associated with colonization-contamination also were associated with isolates of the G lineage. Furthermore, genes encoding sugar metabolism, serine proteases, and a trimethoprim resistance associated with infection were also associated with isolates of the S lineage, implying distinctive specialization of the 2 lineages.

Our results also indicate a key role of setting-associated antimicrobial drug usage, especially for trimethoprim, macrolides, and tetracycline, in resistance development and pathogenicity. Subinhibitory concentrations of these drugs have been shown to promote virulence in bacteria through the induction of biofilm production 45 , quorum-sensing 45 , or phages 46 and might also increase S.

A similar phenomenon was observed for S. The recombination might have resulted from defects in repair of double stranded DNA breaks from oxidative stress induced by leukocytes during infection, as previously described However, the mechanism linking infection and recombination in S. Last, we identified factors associated with infection that could represent new S. In addition, phages have been described to transport pathogenicity islands in staphylococci Our study constitutes a deep-structured analysis of S.

His primary research interests include antimicrobial resistance, bacterial evolution and transmission dynamics of Staphylococcus saprophyticus. All authors read and approved the final manuscript. This work was partially supported by FCT project no. Table of Contents — Volume 27, Number 3—March Please use the form below to submit correspondence to the authors or contact them at the following address:.

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Table 1 Table 2. Article Metrics. Related Articles. Opeyemi U. Lawal, Maria J. Bartels, Maria L. Lawal, O. Bouchami, H. Worning, M. Bartels, H. Empel, M. Abstract Staphylococcus saprophyticus is a primary cause of community-acquired urinary tract infections UTIs in young women. Ethics Considerations The human isolates used in our study were recovered as part of routine clinical diagnostic testing; thus, ethics approval and informed consent were not required.

Bacterial Isolates The global S. Figure 4 Figure 4. Resistome and Virulome Analyses We screened genomes for resistance and virulence genes by using ResFinder version 2. Statistical Analyses We used Prism 6. Lineages of S. Figure 2 Figure 2. Figure 3 Figure 3. Figure 5 1 were considered statistically significant. Some genetic factors that were associated with infections and contamination also were associated with the lineages despite subjecting the GWAS to lineage correction.

Local and Global Spread of S. Genetic Relatedness of S. UTIs and S. Disease Signatures among S. Figure 6 Figure 6. Coagulase-negative staphylococci. Clin Microbiol Rev. Urinary tract infections in young adult women caused by Staphylococcus saprophyticus. Staphylococcus saprophyticus causing native valve endocarditis. Scand J Infect Dis. Colonization of the female genital tract with Staphylococcus saprophyticus. J Clin Microbiol. Staphylococcus saprophyticus recovered from humans, food, and recreational waters in Rio de Janeiro, Brazil.

Int J Microbiol. Staphylococcus saprophyticus found to be a common contaminant of food. J Infect. Genetic diversity and antibiotic resistance of Staphylococcus saprophyticus isolates from fermented foods and clinical samples. DOI Google Scholar. Adaptation in a fibronectin binding autolysin of Staphylococcus saprophyticus. Whole genome sequence of Staphylococcus saprophyticus reveals the pathogenesis of uncomplicated urinary tract infection.

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The gastrointestinal tract is the major reservoir of S. In an early study, Latham et al. Rupp et al. The urine sediment of a patient with UTI caused by S. Colonization is more frequent during the summer and fall. Hovelius et al. None of the women developed symptomatic UTI during the next 6 months. Further support for the existence of a rectal reservoir was the isolation of the same plasmid-identified clone from both urine and stool samples [ 22 ].

The remarkable selective susceptibility of young women to colonization by S. They isolated the microorganism from the genital tracts of 4.

These observations are in accord with numerous clinical reports [ 9—17 ] that UTI caused by S. The microorganisms colonize the human gastrointestinal tract, particularly during the gastroenteritis season in the summer and fall, and this is probably the reason for this seasonal variation in the incidence of UTI caused by S.

However, there was no seasonal variation in Western Australia and Israel [ 11 , 16 ]. There is a strong association between the use of condoms coated with nonoxynol 9 and the occurrence of UTI [ 23 ], which suggests that vaginal spermicides interfere with the normal vaginal flora and promote colonization by S.

Other associations include outdoor swimming prior to colonization and occupations related to meat processing and meat products [ 6 ]. The seasonal variation in the prevalence of colonization by S. The microorganism was found to contaminate Nevertheless, S.

However, recurrence of UTI due to S. In addition, single-dose therapy with quinolones is less effective than a 3-day course [ 27 ]. The virulence factors of S. The hemagglutinin appears to be more important than adherence factors in enabling colonization of kidney tissue in rats [ 29 ]. Hedman et al. Clinical features. Common symptoms of inflammation of the lower tract, such as hematuria and pyuria, were seen more often among patients with colonization of S.

In addition, S. In addition, Jellheden et al. These observations provide a framework for the sequence of events in the pathogenesis of infections caused by S. Humans acquire the microorganism from direct exposure to animals or inadequately cooked animal food products. Young women are more susceptible to genitourinary colonization than are others, and some people develop infection in association with hormonal influences that occur near or during menstruation.

Sexual intercourse promotes colonization and infection. Alterations in the genital flora effected by spermicides or candidal infection favor colonization by S. Anal intercourse may play a role in infection in homosexual men. Research questions. The following questions need to be answered: can the microorganism be transmitted by human-to-human contact? If so, is casual contact among family members sufficient, or is more intimate contact needed, such as vaginal or anal intercourse?

How long does the carrier state last? How often do carriers develop UTI? What triggers UTI in some carriers? Does long-term colonization protect against infection? Does infection result in immunity? Are some strains more urovirulent than others? Do the same or different clones cause recurrent infections? How many microorganisms need to be ingested to produce gastrointestinal colonization? Can more thorough cooking or irradiation of meat products reduce the incidence of infection?

Can genital colonization occur independently of gastrointestinal colonization? What is the role of vaginal pH and commensal microbes? What is the natural history of S. How often do such women acquire urolithiasis?

Is climate important? The answers to these and other questions should improve our understanding of this fascinating microorganism and hopefully lead to its control.

We would like to thank Ms. Frances Nachmani and Ms. Hana Edelstein for preparing the manuscript. Potential conflicts of interest. All authors: no conflicts. Google Scholar.

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