• Pediatric Infection and Vaccine
• /
• v.26 no.3
• /
• pp.148-160
• /
• 2019

Purpose: This study aimed to investigate the molecular epidemiology of a methicillin-resistant Staphylococcus aureus (MRSA) outbreak at a newborn nursery and neonatal intensive care unit (NICU). Methods: During the outbreak, from August to September 2017, MRSA isolates collected from neonates and medical staff underwent genotyping and screened for virulence factors. Antibiotic susceptibilities were tested. Results: During the study period, 41 neonates were admitted at the nursery (n=27) and NICU (n=14). Of these, 7 had MRSA infections (skin infection [n=6] and sepsis [n=1]) and 4 were colonized with MRSA. Associated medical staff (n=32) were screened; three were nasal MRSA carriers. Staphylococcal chromosomal cassette mec (SCCmec) type II, sequence type (ST) 89, spa type t375 was found to be the skin infection outbreak causing strain, with multi-drug resistance including low-level mupirocin resistance. SCCmec type IVa, ST 72, and a novel spa type designated t17879, was the cause of MRSA sepsis. Many different types of MRSA were colonized on the neonates; however, SCCmec type IVa, ST 72, spa type t664 was colonized in both neonates and a NICU nurse. All MRSA isolates from colonized infants were positive for the Panton-Valentine leukocidin (PVL) toxin gene. Conclusions: The strain causing an outbreak of skin infections had multi-drug resistance. Also, MRSA colonized in the neonates were found to carry the PVL toxin gene. Because different strains are present during an outbreak, molecular epidemiologic studies are important to identify the outbreak strain and colonized strains which aid in effective control and prevention of future MRSA outbreaks.

• Korean Journal of Microbiology
• /
• v.48 no.2
• /
• pp.109-115
• /
• 2012

Helicobacter pylori is an important factor of chronic gastritis, digestive ulcer, and stomach cancer. CagL, a virulence factor of H. pylori, is well-known as a pilus protein which acts as adhesion to host cell and a component of Type 4 secretion system. In this study, we evaluated the protective response of recombinant CagL protein (rCagL) using Mongolian gerbil animal model for H. pylori infection. The cagL gene was cloned from 26695 H. pylori followed by over-expression and purification of the protein in E. coli. Mongolian gerbils were immunized with rCagL protein mixed with aluminum adjuvant via intramuscular injections once a week during 4 weeks. At a week after the last immunization, the Mongolian gerbils were administrated with H. pylori 7.13 strain into the stomach and sacrificed to measure antibody titer on rCagL by ELISA and bacterial colonization in the stomach, and to examine the histopathological changes and cytokine expression at 6 week after challenge. Antibody titers on recombinant protein were significantly increased from a week after the first immunization. There was no significant change of the number of bacterial colony between control group and immunized group. The relative stomach weight was significantly decreased in immunized group, but the significant change of histopathological assessment was not observed in the stomach. Cytokine expression such as IL-$1{\beta}$ and KC also was not significantly different between control and immunized groups. These results indicate that rCagL could effectively induce the formation of the specific IgG antibodies. However, bacterial colonization and histopathological lesions could not be inhibited by the immunization in the stomach, indicating not enough protection against H. pylori infection. We consider that along with CagL other adequate antigens could be needed stimulating immune response and inducing protective effects against gastric disease, and also a better adjuvant could be considered.