RESUMO
BACKGROUND: Healthcare-associated infections (HCAIs) continue to be a major cause of morbidity and mortality. Many HCAI pathogens, including multidrug-resistant organisms (MDROs), colonize the gastrointestinal tract. AIM: To determine the frequency of MDRO carriage in patients who do and do not harbour toxigenic Clostridioides difficile in their stools. METHODS: Stool specimens received from nine US laboratories were cultured using media selective for C. difficile, Staphylococcus aureus, vancomycin-resistant enterococci (VRE), and carbapenem-resistant Gram-negative organisms (CROs). Specimens and isolates were also tested by polymerase chain reaction (PCR). Bacterial isolates underwent susceptibility testing and genotyping. FINDINGS: Among 363 specimens, 175 yielded toxigenic C. difficile isolates spanning 27 PCR ribotypes. C. difficile (TCD+) stools harboured an additional 28 organisms, including six CROs (3.4%), of which two (1.1%) were carbapenemase-producing organisms (CPOs), 19 VRE (10.9%), and three meticillin-resistant S. aureus isolates (MRSA, 1.7 %). Stools that were culture negative for toxigenic C. difficile (TCD-) yielded 26 organisms, including four CROs (2.1%), 20 VRE (10.6), and two MRSA (1.1%). Excluding C. difficile, no significant differences were seen in the rates of the MDROs between TCD+ and TCD- specimens. CONCLUSION: Overall, 15.4% of the TCD+ stools and 11.2% of the TCD- stools carried at least one non-C. difficile MDRO pathogen, indicating that multiple MDROs may be present in the gastrointestinal tracts of patients, including those that harbour C. difficile.
Assuntos
Clostridioides difficile/isolamento & purificação , Infecção Hospitalar/epidemiologia , Infecção Hospitalar/microbiologia , Farmacorresistência Bacteriana Múltipla , Fezes/microbiologia , Clostridioides difficile/genética , Infecções por Clostridium/epidemiologia , Infecções por Enterobacteriaceae/epidemiologia , Infecções por Enterobacteriaceae/microbiologia , Trato Gastrointestinal/microbiologia , Hospitalização , Humanos , Staphylococcus aureus Resistente à Meticilina/genética , Staphylococcus aureus Resistente à Meticilina/isolamento & purificação , Estados Unidos/epidemiologia , Enterococos Resistentes à Vancomicina/genética , Enterococos Resistentes à Vancomicina/isolamento & purificaçãoRESUMO
BACKGROUND: The SELH/Bc mouse strain has 10-30% exencephaly and is an animal model for human neural tube closure defects. This study examined the number of causative genes, their dominance relationships, and linkage map positions. METHODS: The SELH/Bc strain (S) was crossed to the normal LM/Bc strain (L) and frequencies of exencephaly were observed in the F(1), BC(1), and F(2) generations. 102 F(2) males were individually testcrossed by SELH/Bc. The extremes, the 10 highest and 10 zero exencephaly-producing F(2) sires, were typed for 109 SSLP marker loci in a genome screen. Next, the resultant five provisional chromosomal regions were tested for linkage in 31 F(2) exencephalic embryos. Finally, 12 males, SS or LL for the Chr 13 region on an LM/Bc background, were testcrossed by SELH/Bc. RESULTS: The exencephaly frequencies in the F(1) (0.3%), BC(1) (4.4%), and F(2) (3.7%), and the distribution of F(2) males' testcross values (0-15.5%), indicated that the high risk of exencephaly in SELH/Bc is due to the cumulative effect of two or three loci. Linkage studies indicated the location of semidominant exencephaly-risk genes on Chr 13 near D13Mit13 (P < 0.001), Chr 5 near D5Mit168 (P < 0.025), and possibly Chr 11 near D11Mit10 (P < 0.07). The gene on Chr 13, Exen1, and the strong role of other loci were confirmed by the congenic males. CONCLUSIONS: The high risk of exencephaly in SELH/Bc mice is caused by the cumulative effect of two to three semidominant genes. Candidate genes include Msx2, Madh5, Ptch, and Irx1 (Chr 13) and Actb and Rac1 (Chr 5).
