Background Bartonella bacilliformis is the etiological agent of Carrion’s disease, a neglected tropical poverty-linked illness. This infection is endemic of Andean regions and it is estimated that approximately 1.7 million of South Americans are at risk. This bacterium is a fastidious slow growing microorganism, which is difficult and cumbersome to isolate from clinical sources, thereby hindering the availability of phylogenetic relationship of clinical samples. The aim of this study was to perform Multi Locus Sequence Typing of B. bacilliformis directly in blood from patients diagnosed with Oroya fever during an outbreak in Northern Peru. Methodology/Principal Findings DNA extracted among blood samples from patients diagnosed with Oroya’s fever were analyzed with MLST, with the amplification of 7 genetic loci (ftsZ, flaA, ribC, rnpB, rpoB, bvrR and groEL) and a phylogenetic analysis of the different Sequence Types (ST) was performed. A total of 4 different ST were identified. The most frequently found was ST1 present in 66% of samples. Additionally, two samples presented a new allelic profile, belonging to new STs (ST 9 and ST 10), which were closely related to ST1. Conclusions/Significance The present data demonstrate that B. bacilliformis MLST studies may be possible directly from blood samples, being a promising approach for epidemiological studies. During the outbreak the STs of B. bacilliformis were found to be heterogeneous, albeit closely related, probably reflecting the evolution from a common ancestor colonizing the area. Additional studies including new samples and areas are needed, in order to obtain better knowledge of phylogenetic scenario B. bacilliformis

Faculty of Health Science School of Public Health 0418444d benido_impouma@yahoo.com / Study objectives The objective of this meta-analysis was to review the comparative efficacy and tolerance of sulfadoxine-pyrimethamine (SP) given alone or in combination with one (SPAS1) or three (SPAS3) doses of artesunate in children with uncomplicated P. falciparum malaria, aged 6 months to 10 years. Specifically, it assessed cure rate, fever and parasite clearance time, gametocyte carriage and tolerability. Methods The methodology used was a systematic review and a meta-analysis of four randomised controlled trials. The primary endpoint was the parasitological cure rate at day 28. Secondary endpoint included the parasitological cure rate at day 14, time to fever and parasite clearance, gametocyte carriage and occurrence of adverse events. Results Cure rate at day 28 corrected by PCR was 2.5 times higher in the combination of SPAS3 than in SP alone (pooled OR=2.55, 95% CI 1.93 to 3.37). There was no difference in cure rate at day 28 corrected by PCR between the combination of SPAS1 and SP alone (pooled OR=1.06 95% CI 0.98 to 1.15). Fever and parasite clearance times were significantly faster in both SPAS1 and SPAS3 compared to SP alone (p<0.001). By day 28 all children on the combination therapy were agametocytaemic as opposed to those on SP alone (p<0.001). All drug regimens were well tolerated and safe. Conclusion The combination of SPAS3 is more efficacious than SP alone in treatment of children with uncomplicated P. falciparum malaria. The combination is recommended for adoption as a replacement for SP alone in areas where malaria is endemic.

T V Gale

No description available.

Acute Q fever is the disease manifestation of Coxiella burnetii infection. This obligate intracellular bacterium is phagocytosed by innate immune cells, where it replicates within the usually bactericidal environment of the phagolysosome. As the immune response is activated, the resultant pro-inflammatory cytokines aid in pathogen clearance but also trigger an acute sickness response in the host. This thesis describes the natural history of acute Q fever in a prospective cohort ??? the Dubbo Infection Outcomes Study (DIOS). In these subjects, the acute febrile illness was characterised by severe headache, drenching sweats and fatigue. In approximately 10% of subjects, symptomatic illness marked by fatigue remained present for months, or occasionally years, after the acute illness. Subjects with more severe acute illness were more likely to develop this post Q fever fatigue syndrome (QFS). The aim of this thesis was to determine whether ongoing infection or aberrant immune activation drive the prolonged symptoms of QFS. Sensitive real time PCR detection of Coxiella DNA revealed a significant minority of subjects had very low copy numbers in circulating monocytes, with an increased prevalence in those with QFS. However, the detection was not consistently found within individual subjects and the copy number was at the threshold of reliable detection. C. burnetii was shown here to stimulate cytokine production in monocytic cells via interaction with Toll-like receptor (TLR)-2 and not TLR-4. Functional polymorphisms in these TLRs were identified in subjects with Q fever, but were not associated with Q fever susceptibility, severity or duration. Phase I-specific responses are believed to be critical in the generation of protective immunity to C. burnetii, yet the phase II-specific responses of innate and adaptive immune components were consistently of higher magnitude. Whole C. burnetii organisms induced antigen-non-specific T cell activation, presumably via the indirect activation of monocytes by C. burnetii LPS. No significant differences were found in the magnitude or kinetics of the host response to infection, or in the carriage of genetic polymorphisms, when comparing subjects who developed QFS with subjects who had promptly resolving illness. It remains unclear what factors mediate the progression of acute Q fever to QFS.

Caption title: An inaugural dissertation on yellow fever. / Dedicated to Dr. Wright Post, professor of anatomy and surgery in Columbia College, and also to Dr. Isaac Ledyard, health officer, Dr. James Tillary, resident physician, and Dr. Edward Miller, health commissioner.

Thesis equivalent (M.P.H.)--University of Michigan, 1947.

Thesis equivalent (M.P.H.)--University of Michigan, 1947.

Thesis (Ph. D.)--University of Hong Kong, 2000. / Includes bibliographical references (leaves 136-146).

Thesis (Ph. D.)--University of Wisconsin--Madison, 1949. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 113-121).