Multidrug-resistant Gram-negative bacterial infections and associated factors in a Kenyan intensive care unit: a cross-sectional study.

BACKGROUND: Patients admitted to intensive care units (ICU) are at risk of Gram-negative bacteria (GNB) infections, especially those caused by multidrug-resistant (MDR) isolates, increasing morbidity, mortality, and healthcare costs. However, epidemiological surveillance data on MDR bacteria to inform infection prevention and control (IPCs) interventions is limited in our study setting. Here we assessed the prevalence and factors associated with GNB infections in ICU- patients admitted in our study setting. METHODS: This was a hospital-based cross-sectional study among patients admitted to ICU at the Nairobi West Hospital, Kenya, between January and October 2022. Altogether, we recruited 162 patients, excluding those hospitalized for less than 48 h and declining consent, and collected demographics and clinical data by case report form. Blood, wound and throat swab, ascetic tap, stool, urine, tracheal aspirate, and sputum samples were collected cultured. Isolates identity and antimicrobial susceptibility were elucidated using the BD Phoenix system. RESULTS: The prevalence of GNB infections was 55.6%, predominated by urinary tract infections (UTIs). We recovered 13 GNB types, with Escherichia coli (33.3%) and Klebsiella pneumoniae (31.1%) as the most common isolates. Factors associated with GNB infections were a history of antibiotic use (aOR = 4.23, p = 0.001), nasogastric tube use (NGT, aOR = 3.04, p = 0.013), respiratory tract (RT, aOR = 5.3, p = 0.005) and cardiovascular (CV, aOR = 5.7, p = 0.024) conditions. 92% of the isolates were MDR,predominantly Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa. CONCLUSION: We report a high prevalence of MDR-GNB infections, predominated by UTI, in ICU, whereby patients with a history of antibiotic use, using the NGT, and having RT and CV conditions were at increased risk. To improve the management of ICU-admitted patients, continuous education, training, monitoring, evaluation and feedback on infection prevention and control are warranted in our study setting.

Coenzyme Q10 exhibits anti-inflammatory and immune-modulatory thereby decelerating the occurrence of experimental cerebral malaria.

Cerebral Malaria (CM) is associated with the complex neurological syndrome, whose pathology is mediated by severe inflammatory processes following infection with Plasmodium falciparum. Coenzyme-Q10 (Co-Q10) is a potent anti-inflammatory, anti-oxidant, and anti-apoptotic agent with numerous clinical applications. The aim of this study was to elucidate the role of oral administration of Co-Q10 on the initiation or regulation of inflammatory immune response during experimental cerebral malaria (ECM). For this purpose, the pre-clinical effect of Co-Q10 was evaluated in C57BL/6 J mice infected with Plasmodium berghei ANKA (PbA). Treatment with Co-Q10 resulted in the reduction of infiltrating parasite load, greatly improved the survival rate of PbA-infected mice that occurred independent of parasitaemia and prevented PbA-induced disruption of the blood-brain barrier (BBB) integrity. Exposure to Co-Q10 resulted in the reduction of infiltration of effector CD8 + T cells in the brain and secretion of cytolytic Granzyme B molecules. Notably, Co-Q10-treated mice had reduced levels of CD8 +T cell chemokines CXCR3, CCR2, and CCR5 in the brain following PbA-infection. Brain tissue analysis showed a reduction in the levels of inflammatory mediators TNF- α, CCL3, and RANTES in Co-Q10 administered mice. In addition, Co-Q10 modulated the differentiation and maturation of both splenic and brain dendritic cells and cross-presentation (CD8α+DCs) during ECM. Remarkably, Co-Q10 was very effective in decreasing levels of CD86, MHC-II, and CD40 in macrophages associated with ECM pathology. Exposure to Co-Q10 resulted in increased expression levels of Arginase-1 and Ym1/chitinase 3-like 3, which is linked to ECM protection. Furthermore, Co-Q10 supplementation prevented PbA-induced depletion of Arginase and CD206 mannose receptor levels. Co-Q10 abrogated PbA-driven elevation in pro-inflammatory cytokines IL-1ß, IL-18, and IL-6 levels. In conclusion, the oral supplementation with Co-Q10 decelerates the occurrence of ECM by preventing lethal inflammatory immune responses and dampening genes associated with inflammation and immune-pathology during ECM, and offers an inimitable opening for developing an anti-inflammatory agent against cerebral malaria.