ABSTRACT
Non-O1/non-O139 Vibrio cholerae, a comparably poorly studied pathogen is culpable of sporadic but serious infections. We report a case of non O1 non O139 Vibrio cholerae septicemia in a middle aged male recently diagnosed with carcinoma pancreas. He underwent biliary tract interventional procedure for hematemesis three weeks before the presentation. Now, he presented with fever, abdominal pain, hematemesis and melena. Endoscopy revealed severe portal hypertensive gastropathy and mild hemobilia. Blood culture grew Vibrio cholerae, identified as non O1 non O139 by serogrouping. He recovered successfully with timely diagnosis, appropriate antibiotics and supportive measures.
Subject(s)
Anti-Bacterial Agents , Pancreatic Neoplasms , Sepsis , Vibrio cholerae non-O1 , Humans , Male , Pancreatic Neoplasms/complications , Pancreatic Neoplasms/microbiology , Vibrio cholerae non-O1/isolation & purification , Vibrio cholerae non-O1/classification , Vibrio cholerae non-O1/pathogenicity , Vibrio cholerae non-O1/genetics , Sepsis/microbiology , Sepsis/diagnosis , Middle Aged , Anti-Bacterial Agents/therapeutic use , Cholera/microbiology , Cholera/diagnosis , Cholera/complications , Vibrio Infections/diagnosis , Vibrio Infections/microbiologyABSTRACT
PURPOSE: Cladophialophora bantiana is a wonted melanized fungus causing brain abscess. In past many cases were reported from Asia, particularly from India. Of late, there is a rise in cases in places besides Asia and hence a review of the cases is warranted. METHODS: We present a case of fatal cerebral phaeohyphomycosis caused by C. bantiana and conduct a systematic review of culture confirmed brain abscess due to C. bantiana reported between 2015 and 2022. RESULTS: Of the 39 cases found, majority (68%) were immunocompromised. The various clinical presentations were headache (53%), hemiparesis (34%), visual disturbance (25%), altered sensorium (18%), aphasia/dysarthria (12%) and seizures (9%). Isolated lesion was observed in 18 (60%) patients. In the sequence of occurrence, the lesions were in frontal (30%), temporal (27%) and parietal (20%) region. There were five cases with coinfections such as concurrent detection of Nocardia pneumonia in two cases, toxoplasma DNA in brain abscess, coexisting pulmonary Cryptococcus neoformans infection and coexisting Candida in a case of brain abscess in one case each. Surgical intervention was performed in 84% cases. Antifungal therapy included voriconazole (80%), liposomal amphotericin B (76%), 5-fluorocytosine (30%), posaconazole (10%), and amphotericin B deoxycholate (6%). The overall mortality was 50% with lower mortality (42%) in regions outside Asia compared to Asia (63.6%) though not statistically significant. CONCLUSIONS: C. bantiana brain abscess is an emerging infection worldwide. Next generation sequencing is an upcoming promising diagnostic test. Early complete excision of the lesion with effective antifungals may improve the outcome.
Subject(s)
Ascomycota , Brain Abscess , Cerebral Phaeohyphomycosis , Humans , Cerebral Phaeohyphomycosis/diagnosis , Cerebral Phaeohyphomycosis/drug therapy , Cerebral Phaeohyphomycosis/microbiology , Antifungal Agents/therapeutic use , Voriconazole/therapeutic use , Brain Abscess/diagnosis , Brain Abscess/drug therapy , Brain Abscess/microbiologyABSTRACT
Despite tuberculosis and melioidosis being endemic in many countries, coinfections are unusual. Only fourteen cases of tuberculosis melioidosis coinfections have been reported. To the best of our knowledge, this is the first case of coinfection of tuberculosis and neurologic melioidosis. We report a case of 48 year diabetic male presented with fever, headache and altered sensorium for two days. On examination, there was scalp abscess with subgaleal hematoma, pus culture of which grew B. pseudomallei. Sputum culture grew the same and sputum tuberculosis PCR was positive. Patient was concurrently treated for both the conditions and recovered.
Subject(s)
Burkholderia pseudomallei , Coinfection , Melioidosis , Tuberculosis, Pulmonary , Tuberculosis , Humans , Male , Melioidosis/complications , Melioidosis/diagnosis , Melioidosis/drug therapy , Coinfection/diagnosis , India , Tuberculosis, Pulmonary/complications , Tuberculosis, Pulmonary/diagnosis , Tuberculosis/diagnosisABSTRACT
In the present study about, 66 copepod parasites of Lernaeenicus hemiramphi of two Hemiramphus sp., H. far (17 copepod) and H. lutkei (49 copepod), and an isopod (Mothocya plagulophora) on the gill chamber were observed. H. lutkei was added as a new host for L. hemiramphi. The copepod infestation was almost on the ventral side of the hosts.
ABSTRACT
The effects of ornithine alpha-ketoglutarate (OKG) on ammonium acetate induced hepatotoxicity were studied biochemically in rats. The levels of urea, nonprotein nitrogen, and thiobarbituric acid reactive substances were significantly increased in ammonium acetate treated rats; these levels were significantly decreased in rats treated with ammonium acetate and OKG. Similar patterns of alterations were observed in the levels of free fatty acids, triglycerides, and phospholipids. Furthermore, nonenzymatic antioxidants (vitamins C and E) were significantly decreased in ammonium acetate treated rats, when compared with control rats, and increased in OKG and ammonium acetate treated rats. The biochemical alterations during OKG treatment could be (1) by detoxifying excess ammonia; (2) by participating in nonenzymatic oxidative decarboxylation in the hydrogen peroxide decomposition process, and (3) by enhancing the proper metabolism of fats which could suppress oxygen radical generation and thus prevent the lipid peroxidative damages in rats.
Subject(s)
Acetates/administration & dosage , Antioxidants/metabolism , Hyperammonemia/chemically induced , Lipid Peroxidation/drug effects , Liver/drug effects , Liver/physiopathology , Ornithine/analogs & derivatives , Ornithine/pharmacology , Analysis of Variance , Animals , Ascorbic Acid/blood , Lipids/blood , Nitrogen/blood , Rats , Rats, Wistar , Thiobarbituric Acid Reactive Substances/metabolism , Urea/blood , Vitamin E/bloodABSTRACT
The effects of ornithine alpha-ketoglutarate (OKG) on ammonium acetate induced hepatotoxicity were studied in experimental rats. The levels of urea, non-protein nitrogen and thiobarbituric acid reactive substances were significantly increased in ammonium acetate treated rats; but these levels were significantly decreased in ammonium acetate-OKG treated rats. Similar patterns were observed in the levels of free fatty acids, triglycerides and phospholipids. Furthermore, non-enzymatic (reduced glutathione) and enzymatic (glutathione peroxidase, superoxide dismutase and catalase) antioxidants were significantly decreased in ammonium acetate treated rats, when compared with control and were significantly increased in ammonium acetate-OKG treated rats compared to ammonium acetate treatment alone.
Subject(s)
Acetates/pharmacology , Antioxidants/metabolism , Gene Expression Regulation, Enzymologic , Lipid Peroxidation , Ornithine/analogs & derivatives , Acetates/chemistry , Animals , Fatty Acids, Nonesterified/metabolism , Free Radicals , Mitochondria/metabolism , Models, Biological , Ornithine/physiology , Rats , Rats, Wistar , Thiobarbituric Acid Reactive SubstancesABSTRACT
The effects of alpha-ketoglutarate on ammonium acetate induced hyperammonemia were studied biochemically in experimental rats. The levels of circulatory, non-protein nitrogen, serum transaminases and thiobarbituric acid reactive substances were significantly increased in ammonium acetate treated rats. These levels were significantly decreased in alpha-ketoglutarate and ammonium acetate treated rats. Similar patterns of alterations were observed in the levels of free fatty acids, triglycerides, phopholipids and cholesterol inbetween various groups. Further non-enzymatic (vitamins C and E) and enzymatic (superoxide dismutase and catalase) antioxidants were significantly decreased in ammonium acetate treated rats; and were significantly increased in alpha-ketoglutarate and ammonium acetate treated rats. The biochemical alterations during alpha-ketoglutarate treatment could be due to (i) the detoxification of excess ammonia, (ii) by participating in the non-enzymatic oxidative decarboxylation in the hydrogen peroxide decomposition process and (iii) by enhancing the proper metabolism of fats which could suppress oxygen radicals generation and thus prevent the lipid peroxidative damages in rats.
