Biomedical subjects
Publications and source records attributed to A Chakrabarti.
Subcutaneous phaeohyphomycosis caused by dematiaceous fungi has rarely been described in immunocompromised patients. We report a case of subcutaneous infection caused by Phialophora parasitica in a renal transplant recipient. The role of early identification of the offending fungal species followed by a wide local excision in the management of such patients has been discussed.
Acid-reducing drugs can cause increased growth of microbes, including fungus, because of high gastric pH. Our purpose was to evaluate the occurrence of mycotic infection in patients with duodenal ulcer on anti-ulcer therapy and to compare the effects of cimetidine, famotidine, and omeprazole. Eighty patients with duodenal ulcer (62 males and 18 female patients, 16-65 years old) were evaluated for mycotic infection before and after 6 weeks of therapy (cimetidine, 20 patients; famotidine, 40 patients; omeprazole, 20 patients). Mycotic infection was diagnosed by endoscopic biopsy from the ulcer edge subjected to smear, culture, and histopathology and by endoscopic brush samples and gastric aspirate. On the basis of these studies, patients were categorized as having no fungal growth, saprophytic growth, or significant fungal growth. Thirty-five (43.8%) patients had evidence of fungus before ulcer therapy, and 16 of the 35 (20%) had significant fungal growth. The fungal isolation rate was higher in older patients (> and = 45 years of age) and in those with an ulcer size > and = 2 cm. While there was no significant increase in the total number of patients with evidence of fungus after therapy (n = 36), there was a significant increase in those with significant growth (n = 27, p < 0.05) compared with pretreatment status. We found that posttreatment gastric pH of > and = 4 was associated with a higher fungal positivity rate (59.4%) than pH values < 4 (32.4%, p < 0.05). However, neither the type of drug used nor the response in terms of ulcer healing correlated with the presence of fungus. Regardless of the type of drug used, acid-reducing therapy is associated with increased significant fungal growth.
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A marked increase in the incidence of patients of candidaemia is reported from a tertiary care hospital in north India over the last five years (15 patients in 1991 and 275 in 1995). The distribution of Candida species isolated from January 1991 through December 1995 was investigated. Antifungal susceptibility against amphotericin B, 5-fluorocytosine, ketoconazole and fluconazole of 100 randomly selected non-albicans Candida species isolated during 1995 was determined by an in-house standardized disc diffusion method and the standard broth dilution procedure recommended by the National Committee for Clinical Laboratory Standards (NCCLS, USA). The disc diffusion method correlated well with NCCLS method except for ketoconazole. Resistance against any antifungal was confirmed only by results of NCCLS method. A shift to higher isolation of non-albicans Candida species was observed during this period (52.6% in 1992 to 89.5% in 1995). Resistance was observed against 5-fluorocytosine in 3 per cent strains of C. krusei; and against fluconazole in 24.2 per cent of C. krusei, 15.4 per cent of C. guilliermondii and 5.7 per cent strains of C. tropicalis. No resistance was detected against amphotericin B and ketoconazole. Thus Candida species with fluconazole resistance have become more prominent in recent years.
The effect of augmentin alone and in combination with various beta-lactam antibiotics was studied against a pathogenic Mycobacterium, M. marinum. The in vitro studies did not reveal any additional advantage over that found with augmentin alone and this antibiotic seemed considerably inhibitory to M. marinum at < 1 microgram/ml concentration. In vivo, the effects of augmentin on experimentally produced lesions in the mouse foot pads (MFPs) showed a significant regression of the lesions, which was compatible with an early disappearance of M. marinum from the MFP, in contrast with those of the untreated, control animals.
Anxiogenic agents, yohimbine, pentylenetetrazole (PTZ), quinine, bufotenine, flumazenil and isatin were administered (ip) to rats at doses known to induce anxiety in this species. All the drugs exhibited anxiogenic response on the elevated plus-maze and induced a parallel increase in endogenous brain monoamine oxidase (MAO) inhibitory (tribulin) activity. The intensity of the drug-induced anxiety was fairly well correlated with the magnitude of increase in the MAO A inhibitory component of tribulin but not so with its MAO B inhibitory component. Thus, in the doses used, the degree of anxiogenic activity was PTZ > yohimbine > bufotenine > quinine > isatin > flumazenil, in terms of % entries on the open arms of the maze, whereas the magnitude of endogenous MAO A inhibition was PTZ > yohimbine > bufotenine > quinine > flumazenil > isatin. The results indicate that the MAO A inhibitory component of tribulin, rather than its MAO B inhibitory component, may be responsible for the postulated function of tribulin as an endogenous marker of anxiety.
The differential sensitivity following the administration of delta 9-THC to 3 mouse strains, C57BL/6, DBA/2 and ICR mice, indicated that some of the neurobehavioral changes may be attributable to genetic differences. The objective of this study was to determine the extent to which the cannabinoid (CB1) receptor is involved in the observed behavioral changes following delta 9-THC administration. This objective was addressed by experiments using: (1) DNA-PCR and reverse PCR; (2) systemic administration of delta 9-THC, and; (3) intracerebral microinjection of delta 9-THC. The site specificity of action of delta 9-THC in the brain was determined using stereotaxic surgical approaches. The intracerebral microinjection of delta 9-THC into the nucleus accumbens was found to induce catalepsy, while injection of delta 9-THC into the central nucleus of amygdala resulted in the production of an anxiogenic-like response. Although the DNA-PCR data indicated that the CB1 gene appeared to be identical and intronless in all 3 mouse strains, the reverse PCR data showed two additional distinct CB1 mRNAs in the C57BL/6 mouse which also differed in pain sensitivity and rectal temperature changes following the administration of delta 9-THC. It is suggested that the diverse neurobehavioral alterations induced by delta 9-THC may not be mediated solely by the CB1 receptors in the brain and that the CB1 genes may not be uniform in the mouse strains.
Morphine (10 mg/kg), ethanol (8% w/v, 2 ml/kg), nicotine (0.1 mg/kg), cannabis extract (200 mg/kg), lorazepam (10 mg/kg) and ondansetron (0.1 mg/kg) were each administered to rats twice daily i.p. for 14 days and the anxiogenic response following their withdrawal was monitored by the elevated plus-maze test 24 h later. Brains were removed and endogenous monoamine oxidase (MAO) A and B inhibitory activity (tribulin) levels measured on day 14 and 24 h after drug withdrawal in different groups of animals. Morphine, ethanol, lorazepam and nicotine withdrawal was associated with significant anxiety and corresponding increase in brain tribulin activity, particularly its MAO A inhibitory component. Cannabis and ondansetron withdrawal were neither associated with anxiety or change in tribulin levels. The investigation supports the postulated role of tribulin as an endogenous correlate of anxiety, its MAO A inhibitory component accounting for a major part of this effect.
Aureolic acid group of antibiotics inhibit transcription by reversible binding to DNA in presence of divalent magnesium. We for the first time report binding of the one of such antitumor antibiotic, mithramycin (MTR), to the major protein component of erythrocyte cytoskeleton, spectrin. A reasonably high apparent dissociation constant was estimated to be 1.5 microM. The binding of mithramycin in the absence of any divalent cation to the large cytoskeletal protein led to quenching in the tryptophan fluorescence of the protein. Stern-Volmer quenching of the tryptophan residues by acrylamide revealed conformational change in the MTR-bound spectrin. This preliminary study might be useful in understanding other possible sites of actions after translocation.
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Forty nine patients with mycologically confirmed Tinea cruris were investigated for the association of hypersensitivity to trichophytin and the isolation of dermatophytes from clinically normal sites with chronicity and recurrence of infection. At the end of six months following specific therapy, 24 patients returned for follow up and they were similarly studied. Dermatophytes were isolated from clinically asymptomatic sites in 46% patients before treatment and in 21% of the patients on follow up. Immediate weal reaction and increased concentration of IgE antibodies were seen in 73% and 80% of the patients respectively. However, the delayed hypersensitivity reaction was more associated with patients having lesions for more than 6 months (48%) in comparison with patients with a short history (17%). On follow up after 6 months, the different hypersensitivity reactions and IgE antibody concentration maintained more or less the same association. Therefore in persistent or recurrent Tinea cruris infection, besides potential carriage in clinically normal sites, hypersensitivity to antigens of dermatophytes possibly plays an important role in pathogenicity.
Western-blot immunoassay of cerebrospinal fluid (CSF) specimens of patients with central nervous system (CNS) aspergillosis (3), CNS candidosis (1) and bacterial meningitis (2) was carried out using pooled serum from histopathologically proven deep-seated aspergillosis cases to detect unique antigenic fractions for aspergillosis in CSF. No reactivity was observed in patients with non-fungal meningitis. Four cross-reactive bands (40, 90, 200 and > 200 KD) were detectable in CSF from patients with both aspergillosis and candidosis of the CNS. Four additional bands (90-200 KD) were consistently present only in patients with aspergillosis. One prominent band (110 KD) was found only in the patient with aspergillosis who had a fatal outcome and raised the possibility of being a poor prognostic marker.
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