Antibiogram of nasal methicillin resistant Staphylococcus aureus (MRSA) from antenatal clinic attendees in a tertiary hospital, South-South Nigeria

The antibiogram of nasal methicillin resistant Staphylococcus aureus (MRSA) from pregnant women attending University of Uyo Teaching Hospital was investigated using standard microbiological procedures. Out of 772 women, 180(23.3%) harboured nasal MRSA while 592 (76.7%) had MSSA (Methicillin Sensitive Staphylococcus aureus). The highest frequency (33.3%) occured at week 16 while the lowest occured at week 36 of the pregnancy period. Evaluation by logistic regression showed no risk factor involvement for MRSA. The patients were evaluated on their first visit (booking) therefore the MRSA were likely community-acquired. Antibiogram of isolates showed sensitivity mostly to clindamycin (80%), amoxacillin-clavulanic acid (76.7%), ceftriazone (69.4%) and resistance to co-trimoxazole (51.7%). The asymptomatic nasal colonisation of MRSA in pregnant women may therefore be a risk factor for serious systemic infection after delivery

Cecum Lymph Node Dendritic Cells Harbor Slow-Growing Bacteria Phenotypically Tolerant to Antibiotic Treatment

<div><p>In vivo, antibiotics are often much less efficient than ex vivo and relapses can occur. The reasons for poor in vivo activity are still not completely understood. We have studied the fluoroquinolone antibiotic ciprofloxacin in an animal model for complicated Salmonellosis. High-dose ciprofloxacin treatment efficiently reduced pathogen loads in feces and most organs. However, the cecum draining lymph node (cLN), the gut tissue, and the spleen retained surviving bacteria. In cLN, approximately 10%–20% of the bacteria remained viable. These phenotypically tolerant bacteria lodged mostly within CD103⁺CX₃CR1⁻CD11c⁺ dendritic cells, remained genetically susceptible to ciprofloxacin, were sufficient to reinitiate infection after the end of the therapy, and displayed an extremely slow growth rate, as shown by mathematical analysis of infections with mixed inocula and segregative plasmid experiments. The slow growth was sufficient to explain recalcitrance to antibiotics treatment. Therefore, slow-growing antibiotic-tolerant bacteria lodged within dendritic cells can explain poor in vivo antibiotic activity and relapse. Administration of LPS or CpG, known elicitors of innate immune defense, reduced the loads of tolerant bacteria. Thus, manipulating innate immunity may augment the in vivo activity of antibiotics.</p></div