Background Plasmodium vivax is considered to be absent from western Africa, where the prevalence of Duffy-negative red blood cell phenotype proves to be high. Several studies have, however, detected P. vivax infection cases in this part of Africa, raising the question of what is the actual prevalence of P. vivax in local populations. MethodsThe presence of P. vivax was investigated in a large population of healthy blood donors in Benin using microscopy, serology and molecular detection. The seroprevalence was measured with species-specific ELISA using two recombinant P. vivax proteins, namely rPvMSP1 and rPvCSP1. Specific molecular diagnosis of P. vivax infection was carried out using nested-PCR. The performances and cut-off values of both rPvCSP1 and rPvMSP1 ELISA were first assessed using sera from P. vivax-infected patients and from non-exposed subjects.ResultsAmong 1234 Beninese blood donors, no parasites were detected when using microscopy, whereas 28.7% (354/1234) of patients exhibited had antibodies against rPvMSP1, 21.6% (266/1234) against rPvCSP1, and 15.2% (187/1234) against both. Eighty-four samples were selected for nested-PCR analyses, of which 13 were positive for P. vivax nested-PCR and all Duffy negative. ConclusionThe results of the present study highlight an unexpectedly high exposure of Beninese subjects to P. vivax, resulting in sub-microscopic infections. This suggests a probably underestimated and insidious parasite presence in western Africa. While the vaccination campaigns and therapeutic efforts are all focused on Plasmodium falciparum, it is also essential to consider the epidemiological impact of P. vivax.Electronic supplementary materialThe online version of this article (doi:10.1186/s12936-016-1620-z) contains supplementary material, which is available to authorized users.

Gap junction-mediated communication helps synchronize interconnected Sertoli cell activities. Besides, coordination of germ cell and Sertoli cell activities depends on gap junction-mediated Sertoli cell-germ cell communication. This report assesses mechanisms underlying the regulation of connexin 46 (Cx46) and Cx50 in mouse testis and those accompanying a "natural" seasonal and a pathological arrest of spermatogenesis, resulting from autoimmune orchitis (AIO) in mink. Furthermore, the impact of deleting Cx46 or Cx50 on the expression, phosphorylation of junction proteins, and spermatogenesis is evaluated. Cx46 mRNA and protein expression increased, whereas Cx50 decreased with adulthood in normal mice and mink. Cx46 mRNA and protein expression increased, whereas Cx50 decreased with adulthood in normal mice and mink. During the mink active spermatogenic phase, Cx50 became phosphorylated and localized to the site of the blood-testis barrier. By contrast, Cx46 was dephosphorylated and associated with annular junctions, suggesting phosphorylation/dephosphorylation of Cx46 and Cx50 involvement in the barrier dynamics. Cx46-positive annular junctions in contact with lipid droplets were found. Cx46 and Cx50 expression and localization were altered in mink with AIO. The deletion of Cx46 or Cx50 impacted on other connexin expression and phosphorylation and differently affected tight and adhering junction protein expression. The level of apoptosis, determined by ELISA, and a number of Apostain-labeled spermatocytes and spermatids/tubules were higher in mice lacking Cx46 (Cx46-/-) than wild-type and Cx50-/- mice, arguing for life-sustaining Cx46 gap junction-mediated exchanges in late-stage germ cells secluded from the blood by the barrier. The data show that expression and phosphorylation of Cx46 and Cx50 are complementary in seminiferous tubules.

BackgroundMalaria Is A Life-Threatening Pathology In Africa. Plasmodium Falciparum And Plasmodium Vivax Attract The Most Focus Because Of Their High Prevalence And Mortality. Knowledge About The Prevalence Of The Cryptic Pathogens Plasmodium Ovale And Plasmodium Malariae Is Limited. Thanks To Recombinant Tools, Their Seroprevalence Was Measured For The First Time, As Well As The Prevalence Of Mixed Infections In A Malaria-Asymptomatic Population In Benin, A Malaria-Endemic Country.MethodsA Panel Of 1,235 Blood Donations Collected Over Ten Months In Benin Was Used For Validation Of The Recombinant Tools. Recombinant P. Falciparum, P. Malariae, P. Ovale MSP1, And P. Falciparum AMA1 Were Engineered And Validated On A Biobank With Malaria-Infected Patients (N = 144) Using A Species-Speific ELISA Test (Recelisa). Results Were Compared To An ELISA Using A Native P. Falciparum Antigen (NatELISA).ResultsAmong Microscopically Negative African Blood Donors, 85% (1,050/1,235) Present Antibodies Directed To Native P. Falciparum, 94.4% (1,166/1,235) To rPfMSP1 And rPfAMA1, 56.8% (702/1,235) To rPoMSP1, 67.5% (834/1235) To rPmMSP1 And 45.3% Of The Malaria Seropositive Population Had Antibodies Recognizing The Three Species.ConclusionA High Rate Of Antibodies Against P. Ovale And P. Malariae Was Found In Asymptomatic Blood Donors. The Proportion Of Mixed Infections Involving Three Species Was Also Unexpected. These Data Suggest That Determining Seroprevalence For These Cryptic Species Is An Appropriate Tool To Estimate Their Incidence, At The Eve Of Upcoming Anti-P. Falciparum Vaccination Campaigns.

Scavenger receptor class B type I (SR-BI) contributes to HDL-mediated cellular cholesterol efflux and is a phagocytosis-inducing phospholipid phosphatidylserine receptor in rat Sertoli cells, whereas the spliced variant of the SR-B gene, SR-BII, is implicated in the efflux of free cholesterol in macrophages. This study aimed to assess whether spontaneous autoimmune orchitis (AIO), which causes impaired clearance of apoptotic germ cells and spermatogenic arrest, involves SR-BI, SR-BII, and/or cholesterol. The levels measured during development and the annual reproductive cycle in normal mink were compared with those in mink with spontaneous AIO. Time periods with lowest tubular esterified cholesterol (EC) levels showed maximal SR-BI and SR-BII levels, and the periods when one or the other SR-BI isoform predominated showed increased EC levels and spermatogenic arrest in normal mink seminiferous tubules. In tubules with AIO, the predominance of only one or the other SR-BI isoform was the reverse of that measured in normal tubules, and it was associated with an increase in EC levels but not with apoptosis levels. SR-BI and SR-BII levels were not correlated with serum testosterone levels. SR-BI mainly localized to the Leydig cell, germ cell, and Sertoli cell surface, where its distribution was stage-specific. SR-BII was principally intracellular. Tubules from testes with AIO showed a deregulation of cholesterol homeostasis and SR-BI expression but relatively unchanged apoptosis levels. These results suggest that the expression of both SR-BI isoforms is required for the maintenance of low EC levels and that the predominance of only one isoform is associated with the accumulation of EC but not with apoptosis in the tubules.-Akpovi, C. D., S. R. Yoon, M. L. Vitale, and R-M. Pelletier. The predominance of one of the SR-BI isoforms is associated with increased esterified cholesterol levels and not with apoptosis in mink testis.

BackgroundBeta lactams are the most commonly used group of antimicrobials worldwide.The presence of extended-spectrum lactamases (ESBL) affects significantly the treatment of infections due to multidrug resistant strains of gram-negative bacilli. The aim of this study was to characterize the beta-lactamase resistance genes in Escherichia coli isolated from nosocomial infections in Cotonou, Benin.MethodsEscherichia coli strains were isolated from various biological samples such as urine, pus, vaginal swab, sperm, blood, spinal fluid and catheter. Isolated bacteria were submitted to eleven usual antibiotics, using disc diffusion method according to NCCLS criteria, for resistance analysis. Beta-lactamase production was determined by an acidimetric method with benzylpenicillin. Microbiological characterization of ESBL enzymes was done by double disc synergy test and the resistance genes TEM and SHV were screened by specific PCR.ResultsESBL phenotype was detected in 29 isolates (35.5%). The most active antibiotic was imipenem (96.4% as susceptibility rate) followed by ceftriaxone (58.3%) and gentamicin (54.8%). High resistance rates were observed with amoxicillin (92.8%), ampicillin (94%) and trimethoprim/sulfamethoxazole (85.7%). The genotype TEM was predominant in ESBL and non ESBL isolates with respectively 72.4% and 80%. SHV-type beta-lactamase genes occurred in 24.1% ESBL strains and in 18.1% of non ESBL isolates.ConclusionThis study revealed the presence of ESBL producing Eschericiha coli in Cotonou. It demonstrated also high resistance rate to antibiotics commonly used for infections treatment. Continuous monitoring and judicious antibiotic usage are required.

The anterior pituitary folliculostellate (FS) cells are key elements of the paracrine control of the pituitary function. These cells are the source and the target of growth factors and cytokines, and are connected to other pituitary cells via Cx43-mediated gap junctions. Here, we show that acute treatment of the FS TtT/GF cell line with TNF-alpha caused a transient cell uncoupling that was accompanied by the dephosphorylation of Cx43 in Ser368. These TNF-alpha-evoked effects were dependent on protein phosphatase 2A (PP2A) and protein kinase C (PKC) activities. TNF-alpha did not affect total cell Cx43-PP2A catalytic subunit interaction, but it did induce PP2A catalytic subunit recruitment to the Triton X-100 insoluble subcellular fraction, in which Cx43-gap junction plaques are recovered. This recruitment temporally coincided with Cx43 phosphorylated in Ser368-Cx43 dephosphorylation. Cx43 did not interact with the conventional PKC-alpha, but it did interact with the atypical PKC-zeta. Moreover, this interaction was weakened by TNF-alpha. Cx43 dephosphorylation in Ser368 was followed by the tyrosine phosphorylation of the protein. The temporary closure of gap junctions during acute TNF-alpha challenge may constitute a protective mechanism to limit or confine the spread of inflammatory signals among the FS cells.

We identified aberrations leading to spontaneous autoimmune orchitis (AIO) in mink, a seasonal breeder and natural model for autoimmunity. This study provides evidence favoring the view that a malfunction of the clearance mechanisms for apoptotic cell debris arising from imbalances in phagocyte receptors or cytokines acting on Sertoli cells constitutes a major factor leading to breakdown of self-tolerance during spontaneous AIO. Serum anti-sperm antibody titers measured by ELISA reflected spermatogenic activity without causing immune inflammatory responses. Orchitic mink showed excess antibody production accompanied by spermatogenic arrest, testicular leukocyte infiltration, and infertility. AIO serum labeled the postacrosomal region, the mid and end piece of mink sperm, whereas normal mink serum did not. Normal serum labeled plasma membranes, whereas AIO serum reacted with germ cell nuclei. Western blot analyses revealed that AIO serum reacted specifically to a 23- and 50-kDa protein. The number of apostain-labeled apoptotic cells was significantly higher in orchitic compared with normal tubules. However, apoptosis levels measured by ELISA in seminiferous tubular fractions (STf) were not significantly different in normal and orchitic tubules. The levels of CD36, TNF-alpha, TNF-alpha RI, IL-6, and Fas but not Fas-ligand (L), and ATP-binding cassette transporter ABCA1 were changed in AIO STf. TNF-alpha and IL-6 serum levels were increased during AIO. Fas localized to germ cells, Sertoli cells, and the lamina propria of the tubules and Fas-L, to germ cells. Fas colocalized with Fas-L in residual bodies in normal testis and in giant cells and infiltrating leukocytes in orchitic tubules.

Background: Malaria is a leading cause of mortality in southern Benin. The main causative agent, Plasmodium falciparum, poses a threat on critical transfusions in pregnant women and children. This study's objective was to compare the performance of different malaria screening methods in blood donors in southern Benin, a malaria-endemic country.