Are Host Characteristics or Exposure Factors Mainly Involved in the Acquisition of ZoonoticSalmonellaandCampylobacterCoinfection in Humans?

Abstract

We hypothesized that patients coinfected with zoonotic Salmonella and Campylobacter were frailer than monoinfected Salmonella or Campylobacter patients. The study cohort included all first-time Salmonella/Campylobacter infections in Aarhus and North Jutland counties, Denmark, from 1991 through 2003. Data on comorbidity, hospitalization in relation to the Salmonella/Campylobacter infection, and 1-year mortality were obtained from electronic registries. Among 13,449 individuals, 114 (0.85%) had Salmonella/Campylobacter coinfection, 6567 (48.8%) had Salmonella monoinfection, and 6768 (50.3%) had Campylobacter monoinfection. There were no major differences in age, gender, comorbidity, hospitalization rates, 1-year mortality, or seasonal variation between coinfected patients on the one hand and each of the monoinfected patient groups on the other. The main difference was encountered between the Salmonella serotype distribution as 49.1% of coinfected patients versus 20.3% of monoinfected Salmonella patients had Salmonella serotypes other than Salmonella Enteritidis and Salmonella Typhimurium (odds ratio [95% confidence interval]: 4.07 [2.73-6.06]). In conclusion, Salmonella/Campylobacter coinfected patients were not frailer than monoinfected patients. The difference in Salmonella serotype distribution was compatible with a higher proportion of coinfections acquired during foreign travel.

Concurrent Conditions and Human Listeriosis, England, 1999–2009

“…Such method limitations might explain the high incidence associated with both diabetes and kidney disease and reinforce the need to consider these findings as highly refined hypotheses to be tested by other methods ( 12 ). …”

Plasmacytoid Dendritic Cells Are Crucial in Bifidobacterium adolescentis-Mediated Inhibition of Yersinia enterocolitica Infection

“…The secretion of Reg3γ could be restored via stimulation of intestinal TLR4 thereby boosting the innate immune resistance of antibiotic-treated mice against infections with VRE [13]. In addition, antibiotic-induced disruption of the intestinal microbiota enhances the susceptibility of human hosts to infections with nontyphoidal Salmonellae [14], and is a prerequisite for infection of mice with Salmonella typhimurium [15], [16].…”