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Visceral leishmaniasis is a chronic parasitic disease associated with severe immune dysfunction. Treatment options are limited to relatively toxic drugs, and there is no vaccine for humans available. Hence, there is an urgent need to better understand immune responses following infection with Leishmania species by studying animal models of disease and clinical samples from patients. Here, we review recent discoveries in these areas and highlight shortcomings in our knowledge that need to be addressed if better treatment options are to be developed and effective vaccines designed.

Chikungunya virus (CHIKV) is a mosquito-borne pathogen that causes an acute febrile syndrome and severe, debilitating rheumatic disorders in humans that may persist for months. CHIKV’s presence in Asia dates from at least 1954, but its epidemiological profile in the region remains poorly understood. We systematically reviewed CHIKV emergence, epidemiology, clinical features, atypical manifestations and distribution of virus genotypes, in 47 countries from South East Asia (SEA) and the Western Pacific Region (WPR) during the period 1954–2017. Following the Cochrane Collaboration guidelines, Pubmed and Scopus databases, surveillance reports available in the World Health Organisation (WHO) and government websites were systematically reviewed. Of the 3504 records identified, 461 were retained for data extraction. Although CHIKV has been circulating in Asia almost continuously since the 1950s, it has significantly expanded its geographic reach in the region from 2005 onwards. Most reports identified in the review originated from India. Although all ages and both sexes can be affected, younger children and the elderly are more prone to severe and occasionally fatal forms of the disease, with child fatalities recorded since 1963 from India. The most frequent clinical features identified were arthralgia, rash, fever and headache. Both the Asian and East-Central-South African (ECSA) genotypes circulate in SEA and WPR, with ECSA genotype now predominant. Our findings indicate a substantial but poorly documented burden of CHIKV infection in the Asia-Pacific region. An evidence-based consensus on typical clinical features of chikungunya could aid in enhanced diagnosis and improved surveillance of the disease.

Extraction ofCell surface polypeptides of gram-positive bacteria may be divided into a number of classes on the basis of the way in which they are anchored to the cell envelope. In two such classes, the LPXTG-containing proteins and the lipoproteins, attachment is covalent. The former are anchored to cell wall peptidoglycan via the threonine residue in the C-terminally located LPXTG motif (20), while the latter are anchored to cytoplasmic membrane lipids via the cysteine residue in the N-terminally located LXXC motif (29). Many lipoproteins of gram-positive bacteria are homologs of periplasmic solutebinding proteins of gram-negative bacteria, and it is currently thought that lipid anchoring of these proteins is necessary in gram-positive bacteria because there is no outer membrane to prevent their loss to the environment (29).A number of other surface-located proteins are anchored via charge interactions. Examples include S-layer proteins which form regular arrays covering the cell surface and the protein monomers that constitute polymeric structures such as fimbriae and flagella. A characteristic of S-layer proteins from lactobacilli is that they can be extracted from the cell surface by charge-occupying agents such as concentrated salt or guanidine hydrochloride (17, 18).The cell surfaces of lactobacilli are poorly understood in comparison to those of the related streptococci. Only S-layer proteins and surface-located enzymes have been extensively characterized (2,4,11,12,33). We are currently investigating the surface of the guinea pig female genital tract isolate Lactobacillus fermentum BR11 (26). Here we report the sequence of BspA, a surface-located polypeptide of this organism. BspA is selectively removed by extraction with 5 M LiCl and is clearly homologous to family III of the bacterial solute-binding proteins (30). Unlike solute-binding proteins from gram-positive bacteria, BspA does not contain a lipoprotein consensus sequence. It has a highly alkaline isoelectric point, and it appears likely that it is anchored by electrostatic interaction with negatively charged groups on the cell surface. MATERIALS AND METHODSStrains and plasmids. L. fermentum BR11 is a guinea pig vaginal isolate that has been previously described (26). It was grown in liquid or solid MRS medium (Oxoid) for 18 to 24 h at 37°C in the presence of 5% CO 2 . Escherichia coli JM109 (36) and recombinant derivatives were grown at 37°C in Luria-Bertani medium (27) supplemented with ampicillin (100 g/ml), isopropyl-␤-D-thiogalactopyranoside (IPTG) (0.25 mM), and 5-bromo-4-chloro-3-indolyl-␤-D-galactopyranoside (X-Gal) (40 l of a 20-mg/ml solution) as appropriate. Plasmid pUC18 has been described previously (36), while plasmids pMFT1, pMFT2, and pMFT3 are pUC18 derivatives described more fully in Results.L. fermentum BR11 extractions. Cell surface extractions were made from 35-ml stationary-phase cultures. The cells were harvested by centrifugation (10,000 ϫ g, 5 min), washed once with an equal volume of 0.15 M NaCl, resuspended in 500 l of ...

Chlamydia trachomatis is the leading cause of bacterial sexually transmitted disease worldwide resulting in 4-5 million new cases of Chlamydia annually and an estimated 100 million cases per annum. Infections of the lower female genital tract (FGT) frequently are asymptomatic; thus, they often remain undiagnosed or untreated. If infections are either not resolved or left untreated, chlamydia can ascend to the upper FGT and infect the fallopian tubes (FTs) causing salpingitis that may lead to functional damage of the FTs and tubal factor infertility (TFI). Clinical observations and experimental data have indicated a role for antibodies against C. trachomatis proteins such as the 60-kDa heat shock protein 60 (cHSP60) in the immunopathogenesis of TFI. When released from infected cells, cHSP60 can induce proinflammatory immune responses that may functionally impair the FTs leading to fibrosis and luminal occlusion. Chlamydial pathogenesis of irreversible and permanent tubal damage is a consequence of innate and adaptive host immune responses to ongoing or repeated infections. The extracellular matrix that is regulated by metalloproteinases may also be modified by chlamydial infections of the FGT. This review will highlight protective and pathogenic immune responses to ongoing and repeated chlamydial infections of the FGT. It will also present two recent hypotheses to explain mechanisms that may contribute to FT damage during a C. trachomatis infection. If Chlamydia immunopathology can be controlled, it might yield a method of inducing fibrosis and thus provide a means of nonsurgical permanent contraception for women.