Molecular Detection of Panton Valentine Leukocidin Toxin in Clinical Isolates of from Kiambu County, Kenya.

Panton-Valentine leukocidin gene is produced by , and methicillin-resistant isolates as a pore-forming toxin is largely responsible for skin and soft tissue illnesses. MRSA produces PVL toxins through S and F proteins causing tissue necrosis by damaging membrane of the defense cells. Presence of PVL toxin was tested from the 54 clinical isolates obtained from Thika and Kiambu Level 5 Hospitals, in Kiambu County, Kenya, by Geno Type® MRSA assay (Hain Life Science, Nehren, Germany).

Phenotypic analysis and antibiotic susceptibility of methicillin-resistant Staphylococcus aureus in Kiambu County, Kenya.

Introduction: Methicillin resistant Staphylococcus aureus (MRSA) causes illness to people and can be picked up from both healthcare facilities and the environment leading to high morbidity and mortality. The study was aimed at identifying phenotypic characteristics of Methicillin-Resistant Staphylococcus aureus and determine the antibiotic susceptibility pattern of clinical samples isolated from patients attending or admitted in two health facilities in Kiambu County, Kenya.

Methodology: One hundred and thirty-eight (138) clinical samples were collected from patients attending Thika and Kiambu Level-5 Hospitals.

Lipid metabolism and other metabolic changes in vervet monkeys experimentally infected with Trypanosoma brucei rhodesiense.

Background: Human African trypanosomiasis is associated with metabolic changes which have not been well characterized.

Methods: Chlorocebus aethiops were experimentally infected with Trypanosoma brucei rhodesiense and late-stage disease induced at 28 days post-infection. Ear prick blood for glucose determination and blood samples were obtained at weekly intervals for 56 days.

Endotoxin-like effects in acute phase response to Trypanosoma brucei brucei infection are not due to gastrointestinal leakage.

Trypanosomosis is mainly an immunological and inflammatory response mediated by increased levels of pro-inflammatory cytokines. Evidence suggests that pathological changes produced during infection with trypanosomes could be initiated by nonspecific endotoxin-like substances in trypanosomes and/or Gram-negative secondary bacterial infection. Studies in trypanosome-infected rats indicate damage to the gastrointestinal tract (GIT) accompanied by increased leakage of the GIT mucosa.

Calcium entry in Trypanosoma brucei is regulated by phospholipase A2 and arachidonic acid.

In contrast with mammalian cells, little is known about the control of Ca2+ entry into primitive protozoans. Here we report that Ca2+ influx in pathogenic Trypanosoma brucei can be regulated by phospholipase A2 (PLA2) and the subsequent release of arachidonic acid (AA). Several PLA2 inhibitors blocked Ca2+ entry; 3-(4-octadecyl)-benzoylacrylic acid (OBAA; IC50 0.