A case of Bergeyella zoohelcum bacteremia after ingestion of a dish prepared with goat blood.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Muhammad M Zaman.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Upregulation of the multidrug resistance protein 1 (LeMDR1) in the protozoan parasite, Leishmania enriettii, confers resistance to hydrophobic drugs such as vinblastine, but increases the sensitivity of these parasites to the mitochondrial drug, rhodamine 123. In order to investigate the mechanism of action of LeMDR1, the subcellular localization of green fluorescent protein (GFP)-tagged versions of LeMDR1 and the fate of the traceable-fluorescent LeMDR1 substrate calcein AM were examined in both Leishmania mexicana and L. enriettii LeMDR1 -/- and overexpressing cell lines. The LeMDR1-GFP chimera was localized by fluorescence microscopy to a number of secretory and endocytic compartments, including the Golgi apparatus, endoplasmic reticulum (ER) and a multivesicular tubule (MVT)-lysosome. Pulse-chase labelling experiments with calcein AM suggested that the Golgi and ER pools, but not the MVT-lysosome pool, of LeMDR1 were active in pumping calcein AM out of the cell. Cells labelled with calcein AM under conditions that slow vesicular transport (low temperature and stationary growth) inhibited export and resulted in the accumulation of fluorescent calcein in both the Golgi and the mitochondria. We propose that LeMDR1 substrates are pumped into secretory compartments and exported from the parasite by exocytosis. Accumulation of MDR substrates in the ER can result in alternative transport to the mitochondrion, explaining the reciprocal sensitivity of drug-resistant Leishmania to vinblastine and rhodamine 123.
Evidence of West Nile encephalitis virus infection has been documented in most states of the continental United States within a short period of its first introduction in 1999. Health care providers are mostly aware of the usual presentations of this disease, eg, aseptic meningitis, encephalitis and Guillain-Barré syndrome. We present a patient whose only manifestations were cerebellar ataxia and fever.
Pneumococcal bacteremia secondary to acute epiglottitis is relatively rare, and all previously reported cases occurred in immunocompromised patients. We report a case of pneumococcal bacteremia associated with acute epiglottitis and retropharyngeal soft-tissue inflammation with upper airway narrowing that occurred in an otherwise healthy patient. In light of our unique finding, we recommend that pneumococcal bacteremia be suspected in an otherwise healthy patient who has systemic manifestations associated with acute epiglottitis.
Explore the source record for details and available documents.