Journal of Pathogens最新文献

Our study aimed to describe the epidemiological, clinical, and diagnostic aspects of African histoplasmosis in Togo through a descriptive and cross-sectional study on histological diagnosed African histoplasmosis in Pathology Department of Lomé from 2002 to 2016 (15 years). A total of 17 cases of African histoplasmosis were diagnosed. The sex ratio (M/F) was 1.8. The annual incidence was 1.1 cases. The mean age of the patients was 27.2 ± 0.4 years. All our patients were of social categories with a low socioeconomic level. HIV infection was known in 3 patients and one patient contracted tuberculosis. The clinical manifestations were cutaneous in 7 cases, cutaneous and mucous in 3 cases, cutaneous and lymph node in 3 cases, cutaneous and bone in 2 cases, and disseminated in 2 cases. The samples examined consisted of 14 cutaneous biopsies measuring 2-3 cm and 3 ganglionic biopsies each measuring 4 cm of major axis. Histologically, all cases were of chronic form made of granulomatous reaction with ovoid yeasts measuring between 1 and 2 microns. Despite the low frequency of this disease in our country, it should be kept constantly in mind before any granulomatous lesions, especially in the context of the HIV pandemic.

Epstein-Barr virus (EBV) is a pathogen that infects more than 90% of global human population. EBV primarily targets B-lymphocytes and epithelial cells while some of them infect monocyte/macrophage, T-lymphocytes, and dendritic cells (DCs). EBV infection does not cause death by itself but the infection has been persistently associated with certain type of cancers such as nasopharyngeal carcinoma (NPC), Burkitt's lymphoma (BL), and Hodgkin's lymphoma (HL). Recent findings have shown promise on targeting EBV proteins for cancer therapy by immunotherapeutic approach. Some studies have also shown the success of adopting EBV-based therapeutic vaccines for the prevention of EBV-associated cancer particularly on NPC. In-depth investigations are in progress to refine the current therapeutic and vaccination strategies. In present review, we discuss the highly potential EBV targets for NPC immunotherapy and therapeutic vaccine development as well as addressing the underlying challenges in the process of bringing the therapy and vaccination from the bench to bedside.

Hepatitis E virus (HEV) remains a major public health concern in resource limited regions of the world. Yet data reporting is suboptimal and surveillance system is inadequate. In Nigeria, there is dearth of information on prevalence of acute HEV infection. This study was therefore designed to describe acute HEV infection among antenatal clinic attendees and community dwellers from two geographical regions in Nigeria. Seven hundred and fifty plasma samples were tested for HEV IgM by Enzyme Linked Immunosorbent Assay (ELISA) technique. The tested samples were randomly selected from a pool of 1,115 blood specimens previously collected for viral hepatitis studies among selected populations (pregnant women, 272; Oyo community dwellers, 438; Anambra community dwellers, 405) between September 2012 and August 2013. One (0.4%) pregnant woman in her 3rd trimester had detectable HEV IgM, while community dwellers from the two study locations had zero prevalence rates of HEV IgM. Detection of HEV IgM in a pregnant woman, especially in her 3rd trimester, is of clinical and epidemiological significance. The need therefore exists for establishment of a robust HEV surveillance system in Nigeria and especially amidst the pregnant population in a bid to improve maternal and child health.

The Xpert MTB/RIF assay can detect mutations in rpoB gene that confer rifampicin resistance (RR) using five overlapping probes (A, B, C, D, and E). In this study, we described our experience with the Xpert assay in a rural setting in India. During the study period, 3250 samples were processed. The result was unsuccessful in 5.7% of cases. For extrapulmonary specimens, the risk of unsuccessful result was higher in tissue biopsy and stool samples. Among samples positive for Mycobacterium tuberculosis, rifampicin resistance was indeterminate in 1.2% of them. Our results and a review of the literature showed that the most frequent mutations conferring RR were located in the region of Probe E (63.6%; 95% confidence interval [CI] 56.26-70.94), followed by Probe B (15.02%; 95% CI 11.94-18.10), Probe D (13.35%; 95% CI 10.01-16.69), Probe A (4.73%; 95% CI 1.92-7.54), and Probe C (1.61%; 95% CI 0.67-2.54). Although the high cost of the cartridges precluded using the Xpert assay for routine diagnosis of tuberculosis, our results demonstrate that the assay can be used to diagnose RR-tuberculosis in rural areas with limited laboratory infrastructure and could be a convenient tool to investigate the molecular epidemiology of RR in resource-limited settings.

Response of Nigerian indigenous (local) and broiler chickens to experimental Eimeria infections was investigated by measures of clinical signs, packed cell volume (PCV), body weights (BW), feed consumption, faecal oocyst counts (oocyst per gram), and microscopic intestinal lesions. Three-week-old chickens of each breed received single pulse infections with 2500, 5000, and 100.000 sporulated Eimeria oocysts. Infected birds were dull and passed bloody diarrhoea. OPG showed a dose related response but no significant difference between groups (P > 0.05). OPG was significantly higher in local chickens (P < 0.05) and varied significantly with time (P < 0.05). PCV declined significantly in infected birds within breeds and groups (P < 0.05); however, the decline in PCV was significantly greater in broilers (P < 0.05). Both breeds had significant BW gains (P < 0.05). BW gain varied between groups being significantly higher in the uninfected control broilers than in the infected broilers (P < 0.05). Comparatively, broilers gained significantly more BW than their local counterparts (P < 0.05). Feed intake increased significantly with time (P < 0.05) in both breeds. The Eimeria isolate was pathogenic to both breeds of chicken although clinical signs and lesions were more severe in indigenous chickens suggesting the breed's more susceptibility.

Fulminant hepatitis (FH) is a life-threatening liver disease characterised by intense immune attack and massive liver cell death. The common precore stop codon mutation of hepatitis B virus (HBV), A1896, is frequently associated with FH, but lacks specificity. This study attempts to uncover all possible viral nucleotides that are specifically associated with FH through a compiled sequence analysis of FH and non-FH cases from acute infection. We retrieved 67 FH and 280 acute non-FH cases of hepatitis B from GenBank and applied support vector machine (SVM) model to seek candidate nucleotides highly predictive of FH. Six best candidates with top predictive accuracy, 92.5%, were used to build a SVM model; they are C2129 (85.3%), T720 (83.0%), Y2131 (82.4%), T2013 (82.1%), K2048 (82.1%), and A2512 (82.1%). This model gave a high specificity (99.3%), positive predictive value (95.6%), and negative predictive value (92.1%), but only moderate sensitivity (64.2%). We successfully built a SVM model comprising six variants that are highly predictive and specific for FH: four in the core region and one each in the polymerase and the surface regions. These variants indicate that intracellular virion/core retention could play an important role in the progression to FH.

This study was designed to compare both the cell culture dependent and independent enterovirus detection algorithms recommended by the WHO and assess how either might impact our perception of the diversity of enterovirus types present in a sample. Sixteen paired samples (16 isolates from RD cell culture and their corresponding stool suspension, i.e., 32 samples) from AFP cases in Nigeria were analyzed in this study. All the samples were subjected to RNA extraction, cDNA synthesis, the WHO recommended RT-snPCR, and its modification. Amplicons were sequenced and strains identified. Enterovirus diversity was the same between the isolates and fecal suspension for the control and five of the samples. It was, however, different for the remaining 10 (62.5%) samples. Nine (CV-B4, E6, E7, E13, E14, E19, E29, EV-B75, and EV-B77) and five (CV-A1, CV-A11, CV-A13, EV-C99, and PV2) EV-B and EV-C types, respectively, were detected. Particularly, E19 and EV-B75 were only recovered from the isolates while E14, EV-B77, CV-A11, and CV-A13 were only recovered from fecal suspension. Both the cell culture dependent and independent protocols bias our perception of the diversity of enterovirus types present in a sample. Hence, effort should be directed at harmonizing both for increased sensitivity.

Enzymatic modification results in high-level resistance to aminoglycoside (HLAR), which eliminates the synergistic bactericidal effect of combined exposure to a cell wall-active agent and an aminoglycoside. So aim of the study was to determine prevalence of HLAR enterococcal isolate and to study distribution of aminoglycoside modifying enzyme genes in them. A total of 100 nonrepeat isolates of enterococci from various clinical samples were analyzed. As per Clinical and Laboratory Standards Institute guidelines enterococci were screened for HLAR by Kirby-Bauer disc diffusion method. Minimum inhibitory concentration of all isolates for gentamicin and streptomycin was determined by E-test. Multiplex polymerase chain reaction (PCR) was carried out for HLAR enterococcal isolates to identify aminoglycoside modifying enzymes genes responsible for resistance. 60% isolates were found to be high-level gentamicin resistant (HLGR) whereas 45% isolates were found to be high-level streptomycin resistant (HLSR). By multiplex PCR 80% HLGR isolates carried bifunctional aminoglycoside modifying enzyme gene aac(6')-Ie-aph(2'')-Ia whereas 18 out of 45 high-level streptomycin resistant, that is, 40%, isolates carried aph(3')-IIIa. However, aph(2'')-Ib, aph(2'')-Ic, aph(2'')-Id, and ant(4')-Ia genes which encode other aminoglycosides modifying enzymes were not detected. Bifunctional aminoglycoside modifying enzyme gene aac(6')-Ie-aph(2'')-Ia is the predominant gene responsible for HLAR.