Search bioRxivSearch

bioRxiv · 10.1101/723379

Incidence of mortality and its predictors among adult Visceral Leishmaniasis patients at University of Gondar Comprehensive Specialized Hospital, Ethiopia

Abstract

BackgroundVisceral leishmaniasis (VL) is a neglected tropical disease resulting in a huge burden of mortality and impact on development of a country. Even though anti-leishmanial drugs reduce the incidence of mortality among VL patients, still there is a death of VL patients while on treatment. However, study on incidence of mortality and its predictors among these patients while on treatment is scarce in Ethiopia.\n\nObjectiveThe aim of this study was to determine incidence of mortality and its predictors among adult VL patients at University of Gondar Hospital.\n\nMethodsInstitution based retrospective follow up study was conducted from 2013 to 2018 at University of Gondar Hospital. Data were collected from patients chart and analyzed using Stata 14. Kaplan Meier failure curve and Log Rank test was used to compare survival probability of patients with categorical variables. Multivariable stratified Cox model was used to identify predictors of mortality among VL patients. P[≤] 0.05 was employed to declare statistically significant factors. Adjusted Hazard Ratio (AHR) and its 95% confidence interval (95% CI) was estimated for potential risk factors included in the multivariable model.\n\nResultsA total of 586 VL patients were included in the study. The median age of patients was 23 years. The incidence of mortality was 6.6 (95% CI: 5.2 - 8.4) per 1000 person-days of observation. Independent predictors of mortality were: presence of comorbidity (AHR=2.29 (95% CI: 1.27-4.11)), relapse VL (AHR=3.03 (95% CI: 1.25-7.35)), toxicity of treatment drug (AHR=5.87 (95% CI:3.30-10.44)), nasal bleeding (AHR=2.58 (95%CI: 1.48-4.51)), jaundice (AHR=2.84 (95% CI: 1.57-5.16)) and being bedridden (AHR=3.26 (95 % CI: 1.86-5.73)).\n\nConclusionThe incidence of mortality among VL patients was high. Mortality was higher among VL patients with concomitant disease, relapse, toxicity during treatment, nasal bleeding, jaundice, and bedridden patients. Therefore, strict follow up and treatment of VL patients who have comorbidity, relapse VL, toxicity, nasal bleeding and jaundice were crucial so as to reduce the risk of mortality.\n\nAuthors summaryVisceral leishmaniasis is a neglected tropical disease caused by a protozoa parasite. Over 90% of global burden of VL occurs in poor rural and suburban areas in seven countries including our country, Ethiopia. If not appropriately treated, over 95% of VL cases will eventually die. The emergence of VL in Ethiopia places a huge burden on society as it affects poor, young and productive age group of its population. However, there is scarcity of data about incidence of mortality and its predictors among adult VL patients in Ethiopia.\n\nIn this study, a registry of VL patients at Gondar University Hospital was taken to determine the incidence of VL mortality and its predictors. Mortality rate was higher among VL patients with concomitant disease, relapse, drug toxicity, nasal bleeding and jaundice. Therefore, strict follow up and treatment of VL patients who had comorbidity, relapse VL, drug toxicity, nasal bleeding and jaundice were crucial.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Yeshaw, Y., Tsegaye, A. T., Nigatu, S. G.. 2019-08-02. Incidence of mortality and its predictors among adult Visceral Leishmaniasis patients at University of Gondar Comprehensive Specialized Hospital, Ethiopia. https://doi.org/10.1101/723379

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

A conserved cysteine-histidine-glutamate metal site identifies DUF501 (Rv1025), an essential uncharacterised protein family of Mycobacterium tuberculosis, as a candidate metalloenzyme and drug target

A substantial fraction of the Mycobacterium tuberculosis proteome remains functionally uncharacterised. Rv1025, a 155-residue protein carrying the domain of unknown function DUF501 (Pfam PF04417), is essential by transposon mutagenesis and vulnerable by CRISPR interference, an attractive but neglected drug target, yet has never been functionally described. The family (4,370 proteins, no Gene Ontology term, no solved structure) is uncharacterised across all organisms and essential in three Actinobacterial genera. A Foldseek search of the AlphaFold model against complete structural databases finds no significant homolog, indicating a novel fold. The operon eno-divIC-Rv1025-ppx2 is conserved across the Actinobacteria phylum, yet AlphaFold-Multimer finds no direct complex between Rv1025 and its neighbour DivIC. Instead, conservation across 8,700 homologous sequences reveals a near-invariant Cys113-His115-Glu59 cluster forming a pocket. Holo AlphaFold3 predictions with Zn, Fe and Mn confidently place a divalent metal on this triad at 2.25-2.47 A; mutating the triad relocates the metal, and an independent backbone-geometry predictor recovers the same site, confirming specificity. The triad is universal across the family: present in all 1,472 near-complete bacterial sequences of the Pfam alignment, with no non-conservative substitution among the 2,228 sequences examined, a defining feature of bacterial DUF501 rather than a mycobacterial peculiarity. We propose that DUF501 is a metal-binding protein and candidate metalloenzyme, the first functional hypothesis for this family, whose conserved, essential metal pocket is a promising drug target. As the predictions build on a conservation-defined site within a fully computational study, they are supportive rather than proof of metal occupancy and warrant experimental validation.

microbiology

Mycoplasmal endosymbionts of Trichomonas vaginalis are associated with reduced risk for Chlamydia trachomatis endometrial infection in asymptomatic, coinfected, women.

Trichomonas vaginalis is a protozoan parasite that causes trichomoniasis, the most common curable non-viral sexually transmitted infection, and Chlamydia trachomatis is a bacterial pathogen that can ascend to the upper genital tract and cause pelvic inflammatory disease, infertility, and ectopic pregnancy. T. vaginalis harbors bacterial endosymbionts, including Candidatus Malacoplasma girerdii, an obligate symbiont, and Metamycoplasma hominis, which can live freely or symbiotically. In a 16S rRNA sequencing study of the cervicovaginal microbiome of women at high risk for chlamydial infection, Ca. M. girerdii abundance was one of 13 features predicting lack of chlamydial spread to the endometrium, despite no direct association between T. vaginalis infection and reduced chlamydial ascension. Investigating the relationship between these microorganisms further, we found that T. vaginalis vaginal abundance correlated positively with chlamydial burden in women whose infection was confined to the cervix, while a nonsignificant inverse relationship was seen in women with endometrial spread. Among participants with high chlamydial burden, Ca. M. girerdii was detected exclusively in women without endometrial infection. Both endosymbionts trended toward more frequent detection, and higher abundance, in coinfected women without endometrial spread, while M. hominis abundance correlated strongly with T. vaginalis burden in this group. These findings suggest that mycoplasmal endosymbionts of T. vaginalis, rather than T. vaginalis itself, are microbial factors limiting chlamydial ascension, and point to a three-way interaction between parasite, endosymbiont, and bacterial pathogen that shapes upper genital tract C. trachomatis infection risk.

microbiology

Understanding the physiological alterations of Vibrio cholerae upon exposure to L-ascorbic acid

The scourge of cholera remains a major global public health threat. It affects up to 4 million people worldwide and causes tens of thousands of deaths each year. The disease is experiencing a concerning resurgence in many parts of Africa, the Middle East, and Asia. To effectively tackle cholera and circumvent rising antimicrobial resistance, targeted biological and preventive approaches, complementing traditional rehydration, are urgently needed. In this regard, our group has demonstrated the efficacy of L-ascorbic acid in controlling the growth and pathogenesis of Vibrio cholerae in vitro. The present work further provides a mechanistic elucidation of the L-ascorbic acid-mediated physiological changes in V. cholerae and also bolsters such a non-antibiotic approach to control cholera.

microbiology