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The chikungunya virus (CHIKV) and scrub typhus infection has scattered worldwide creating human health hazards in India and Asia specific region. We aimed to identify chikungunya, scrub typhus, and their co-infection in dengue-negative samples having undifferentiated febrile illnesses. Enzyme linked immunosorbent assay (ELISA) methods were used to detect the chikungunya and scrub typhus specific IgM antibody by using chikungunya IgM capture ELISA kit and scrub typhus IgM Microlisa ELISA kit, respectively. OD value was measured with the help of BeneSphera (India) ELISA microplate reader. Among 490 suspected patients, 57 (11.63%) samples were tested positive for chikungunya IgM antibodies, while 43 (8.77%) came positive for scrub typhus IgM antibodies, but all samples tested negative for dengue IgM antibodies. Additionally, 5% of the total positive cases were positive for both chikungunya and scrub typhus infection. Our study offers a hypothesis regarding one of the possible causes of the decline in the frequency of scrub typhus and chikungunya cases reported in Kolkata and other districts of West Bengal. As an outcome, physicians treating undifferentiated febrile patients in endemic locations should look for chikungunya, scrub typhus, and existing coinfection between them to avoid delayed diagnosis and provide proper treatment against these infections.

Background: The incidence of diabetes mellitus (DM) throughout the world is increasing strikingly and is becoming a serious public health problem especially in the developing countries. Infections are important cause of death in diabetes and remain a very important cause of morbidity and mortality in people with diabetes. Most common type of diabetes in Indian population is type 2 DM. Most common infection associated with DM found to be urinary tract infections (UTI). Objective: The main objectives of this study were to isolate, identify and to determine antimicrobial susceptibility pattern of microbiological agents of UTI in type 2 DM patients and assess prognosis of these patients with prescribed antimicrobial treatment regimen. Results and Discussions: We conducted the study from December 2013 to December 2018 in the department of microbiology from the patients attending the outpatients department of a tertiary care hospital. In this study, total 774 non-repetitive patients’ samples were included but 14 samples were contaminated and lost from follow-up. Thus, available data for analysis were 760 samples. Total 254 samples showed significant growth (32.82%). Most common isolated pathogen was Escherichia coli. In our study, 17.82% patients were asymptomatic but culture positive. The asymptomatic patients with positive urine culture turn up with symptomatic UTI, often with complications. Conclusion: UTI with multidrug-resistant organism in outpatients has emerged; limiting the treatment options in the high-risk groups. The need for an antibiotic policy based on adequate and continuous monitoring of susceptibility patterns in the institutions is recommended.

Introduction: Dermatophytosis is one of the most prevalent cutaneous mycosis and a public health problem in West Bengal as well as in India. Its footprint spans far and wide across urban and rural Bengal, with a distribution that is determined by a multitude of factors like geography, environmental conditions, hygiene and sanitation. Despite its surging incidence, Dermatophytosis in Bengal remains a seldom studied topic. Aim: The present study was undertaken to assess the burden of dermatophytosis by clinico-mycological evaluation using standard laboratory protocol and its correlation with clinical parameters. Material and Methods: A cross sectional and observational study was conducted in 100 clinically diagnosed patients of dermatophytosis of skin attending the dermatology outpatient department of our tertiary care hospital. Skin scrapings, were collected from the active margins of the obvious new lesions and processed in the Mycology laboratory following standard protocol. All specimens were screened for presence of dermatophytes by direct microscopy using KOH DMSO preparation and were confirmed by fungal culture. Results: Among all clinical types, Tinea corporis (58.0%) was the predominant clinical condition. Males were affected more (60.0%) than females. The predominantly affected age group was found to be 21- 30 years (35.0%) followed by 31-40 years (24.0%). Fungi were demonstrated in 72.0% cases by direct microscopy in KOH mount while 51.0% cases were found as culture positive. However 02.0% cases were KOH negative but culture positive. Microsporum audouinii (20.0%) was the predominant species identified followed by Trichophyton rubrum (10%). Some rare species like Microsporum persicolor, Microsporum distortum, Microsporum fulvum were also isolated in our study which are rarely documented in the literature till date. Conclusions: In our study, males in the age group 21-40 years were most commonly affected. Tinea corporis was found to be the most common clinic

Clinical and mycological features of onychomycosis show variation with time and place. Onychomycosis is a major public health problem with high incidence, associated morbidity and long lasting treatment with anti-fungal agents. A study was carried out on 118 patients having clinical diagnosis of onychomycosis, attending the dermatology out-patient department of R. G. Kar Medical College, Kolkata. Nail clippings were subjected to direct microscopy and cultured on Sabouraud's Dextrose Agar with antibiotics. The commonest age group affected was 21-40 years with a female preponderance and housewives were most commonly affected group. Finger nail involvement were more frequent and distolateral subungal onychomycosis (DLSO) was the most common clinical type observed . Out of 118 cases total KOH positivity was in 72 (61.01%) and culture positivity was in 62 (52.54%). Total culture positive cases were 62 and total number of fungi identified were 66 as dual pathogen had been identified in four cases . Among 66 culture positive isolates dermatophytes were 30 ( 45.55%), candida 21(31.82%) and non-dermatophyte moulds (NDM) 15 ( 22.73%) . T. rubrum was the commonest etiological agent. Among dermatophytes, Trichophyton rubrum, and among NDM, Fusarium moniliforme, were the most common isolates identified in our study.

Isolated sulfite oxidase deficiency is a rare autosomal recessive inborn error of sulfur metabolism. Clinical features generally include devastating neurologic dysfunction, ectopia lentis, and increased urinary excretion of sulfite, thiosulfate, and S-sulfocysteine. Missed diagnosis is not unusual because of variability in the sensitivity of the urinary sulfite and thiosulfate screening test. We present clinical, biochemical, and molecular data on two unrelated patients with isolated sulfite oxidase deficiency. The two patients belong to an Indigenous genetic isolate in Manitoba, Canada. Both patients (one male and one female, both now deceased) developed neonatal seizures and demonstrated progressive neurodevelopmental delay. Based on increased urinary excretion of sulfite, thiosulfate, and S-sulfocysteine and normal serum uric acid levels, sulfite oxidase deficiency was suspected. Both patients have a homozygous 4-bp deletion, 1347–1350delTTGT in the sulfite oxidase gene (SUOX), predicting a premature termination of the sulfite oxidase protein leading to absence of the carboxy-terminal third portion of the protein. This domain contains most of the contact sites essential for enzyme dimerization. This deletion mutation resulted in sulfite oxidase deficiency with early-onset severe clinical phenotype.

Trisomy 9p is a well-described dysmorphic syndrome. The physical features include hypertelorism, down-slanting palpebral fissures, deep-set eyes, down-turned corners of the mouth, and mild skeletal anomalies including hypoplastic terminal phalanges. We report an infant born with some of the typical features of trisomy 9p syndrome, as well as additional features that include extreme joint hyperlaxity with subluxation of the knees and elbows, arachnodactyly, and total anomalous pulmonary venous return. The karyotype revealed an unbalanced chromosome complement. Specifically, a derivative chromosome from a de-novo unbalanced translocation of chromosomes 9 and 15 resulted in partial trisomy of 9pter to 9q13 and deletion of the long arm of chromosome 15 proximal to band q13. Fluorescence in-situ hybridization studies and methylation analysis by Southern blotting revealed deletion of the SNRPN locus on the paternally derived chromosome 15, consistent with Prader-Willi syndrome. This infant represents the first reported case of trisomy 9p syndrome with total anomalous pulmonary venous return and hypoplasia of the amygdala and hippocampus, with the additional finding of Prader-Willi syndrome resulting from a derivative chromosome arising from an unbalanced de-novo t(9;15) translocation.

Background:Chlamydia trachomatisis recognized as one of the most common sexually transmitted pathogen in the world. 50-80% of infected females are asymptomatic. These untreated women are at risk of developing chronic sequelae leading to tubal pathology causing infertility. Infertility is defined as 1 year of unprotected intercourse without pregnancy. It may be primary or secondary.Aim:To find out the association of genitalChlamydia trachomatisinfection with female infertility.Materials and Methodology:This case control study has been carried out in collaboration with R. G. Kar Medical College and Institute of Post Graduate Medical Education & Research, India, between July 2012 and June 2013. 40 infertile and 40 pregnant women were enrolled by purposive sampling as per inclusion and exclusion criteria. ELISA test was performed to detect serum IgG and IgA antibody against recombinant analogs of MOMP and 3 different PCR assays were done targeting MOMP and rRNA DNA from DNA extracted from first void urine.Results:IgG seropositivity was significantly higher (15%vs0%,P=.0255) in cases than controls, though there was no significant difference in the proportion of IgA seropositivity among 2 groups (12.5%vs2.5%,P=0.2007). Out of 80 samples 2 samples showed the production of amplicons with R1 – R2 primers. Only 1 sample gave positive result with production of amplicons with all the 3 primers used (R1 – R2, CT0005 – CT06 and JM15 – JM16).Conclusion:PersistentC. trachomatisinfection must be recognized as a risk factor of infertility in this region of India. The low PCR positivity in FVU sample helps to conclude the diagnostic utility of serological tests in screening of infertile women.

BNIP3 (formerly NIP3) is a pro-apoptotic, mitochondrial protein classified in the Bcl-2 family based on limited sequence homology to the Bcl-2 homology 3 (BH3) domain and COOH-terminal transmembrane (TM) domain. BNIP3 expressed in yeast and mammalian cells interacts with survival promoting proteins Bcl-2, Bcl-X(L), and CED-9. Typically, the BH3 domain of pro-apoptotic Bcl-2 homologues mediates Bcl-2/Bcl-X(L) heterodimerization and confers pro-apoptotic activity. Deletion mapping of BNIP3 excluded its BH3-like domain and identified the NH(2) terminus (residues 1-49) and TM domain as critical for Bcl-2 heterodimerization, and either region was sufficient for Bcl-X(L) interaction. Additionally, the removal of the BH3-like domain in BNIP3 did not diminish its killing activity. The TM domain of BNIP3 is critical for homodimerization, pro-apoptotic function, and mitochondrial targeting. Several TM domain mutants were found to disrupt SDS-resistant BNIP3 homodimerization but did not interfere with its killing activity or mitochondrial localization. Substitution of the BNIP3 TM domain with that of cytochrome b(5) directed protein expression to nonmitochondrial sites and still promoted apoptosis and heterodimerization with Bcl-2 and Bcl-X(L). We propose that BNIP3 represents a subfamily of Bcl-2-related proteins that functions without a typical BH3 domain to regulate apoptosis from both mitochondrial and nonmitochondrial sites by selective Bcl-2/Bcl-X(L) interactions.

Fusraium is a non-dermatophytic hyaline mould found as soil saprophytes and plant pathogens. Human infections are probably a result of various precipitating predisposing factors of impaired immune status. Immunocompetent individuals of older age group are also vulnerable to various unassuming saprophytic and plant pathogen. We report 5 cases with onychomycosis caused by a rare species of Fusarium , namely, Fusarium dimerum . Fusarium is known to cause a variety of infections like keratitis, eumycetoma, onychomycosis, skin lesions and sometimes disseminated infection in individuals with impaired immunity. Hence it is of utmost importance to identify this newly emerging fungal pathogen correctly and institute appropriate treatment to control human infections at the earliest so that disseminated infections can be avoided.

We have studied ceBNIP3, the orthologue of BNIP3 in C. elegans. Sequence analysis reveals that the different domains of BNIP3 have been conserved throughout evolution. ceBNIP3 contains a C-terminal transmembrane (TM) domain, a conserved domain (CD) of 19 amino acids, a BCL-2 homology-3 (BH3)-like domain and a PEST sequence. ceBNIP3 is expressed primarily as a 25 kDa monomer and a 50 kDa homodimer. After transfection, ceBNIP3 protein is rapidly degraded through a ubiquitin-dependent pathway by the proteasome. Like BNIP3, the TM domain of ceBNIP3 mediates the localization of the protein to mitochondria and is also necessary for homodimerization and cell death in mammalian cells. Neither the putative BH3 domain nor conserved domain is necessary for killing. ceBNIP3 protein interacts with CED-9 and BCL-XL, but unlike other pro-apoptotic BCL-2 family members, the BH3-like domain does not participate in dimerization. The ceBNIP3 TM domain mediates interaction with both CED-9 and BCL-XL. ceBNIP3 interacts with CED-3 but co-expression of CED-3 and ceBNIP3 does not significantly enhance induction of cell death in the presence or absence of CED-4. ceBNIP3 kills mammalian cells by a caspase-independent mechanism. In conclusion, we find that although ceBNIP3 interacts with CED-9 and CED-3 it kills by a BH3- and caspase-independent mechanism.