Effect of Iron-Chelator Deferiprone on the In Vitro Growth of Staphylococci

The standard iron-chelator deferoxamine is known to prevent the growth of coagulase-negative staphylococci (CoNS) which are major pathogens in iron-overloaded patients. However, we found that deferoxamine rather promotes the growth of coagulase-positive Staphylococcus aureus. Accordingly, we tested whether deferiprone, a new clinically-available iron-chelator, can prevent the growth of S. aureus strains as well as CoNS. Deferiprone did not at least promote the growth of all S. aureus strains (n=26) and CoNS (n=27) at relatively low doses; moreover, it could significantly inhibit the growth of all staphylococci on non-transferrin-bound-iron and the growth of all CoNS on transferrin-bound iron at relatively high doses. At the same doses, it did not at least promote the growth of all S. aureus strains on transferrin-bound-iron. These findings indicate that deferiprone can be useful to prevent staphylococcal infections, as well as to improve iron overload, in iron-overloaded patients

Severe Pulmonary Adverse Effects in Lymphoma Patients Treated with Cyclophosphamide, Doxorubicin, Vincristine, and Prednisone (CHOP) Regimen Plus Rituximab

BACKGROUND/AIMS: The aim of our study was to determine the incidence and clinical features of severe pulmonary complications in patients receiving cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or rituximab plus CHOP (R-CHOP) as the initial treatment for lymphoma. METHODS: A retrospective analysis of pulmonary infection and drug-induced interstitial pneumonitis (DIIP) was performed using lymphoma registry data. R-CHOP was administered in 71 patients and CHOP in 29 patients. RESULTS: The severe pulmonary adverse events tended to occur more frequently with R-CHOP (18.3%) than CHOP alone (13.8%), although the difference was not significant (p = 0.771). DIIP occurred in five patients in the R-CHOP arm (7%) and in one in the CHOP arm (3%). The continuous use of steroids for conditions other than lymphoma significantly increased the risk of pulmonary infection including Pneumocystis jiroveci pneumonia (p = 0.036) in the multivariate analysis. International prognostic index, tumor stage, smoking, previous tuberculosis, chronic obstructive pulmonary disease, and lymphoma involvement of lung parenchyma were not related to pulmonary adverse events. Patients who experienced severe pulmonary events showed shorter survival when compared to those without complications (p = 0.002). CONCLUSIONS: Our experiences with serial cases with DIIP during chemotherapy and the correlation of continuous steroid use with pulmonary infection suggest that the incidence of pulmonary complications might be high during lymphoma treatment, and careful monitoring should be performed.ope

Neurofibroma of the Colon: A Diagnostic Mimicker of Gastrointestinal Stromal Tumor

Gastrointestinal neurofibroma usually develops as diffuse gastrointestinal involvement in neurofibromatosis type 1 patients. Only 4 cases of sporadic colonic neurofibroma in a patient without neurofibromatosis type 1 have been reported in the English literature. A 26-year-old female patient underwent colonoscopy, and a 4-cm-sized polypoid mass was identified in the sigmoid colon. Wedge resection of the mass showed a yellowish, hard submucosal tumor. Microscopically, the tumor was composed of wavy spindle cells, fibroblasts, and strands of collagen; the stroma showed scattered myxoid areas. The differential diagnoses included gastrointestinal stromal tumor, schwannoma, and neurofibroma. Immunohistochemistry for c-Kit, DOG (discovered on gastrointestinal stromal tumors)-1, smooth muscle actin, S-100 protein, and CD34 was performed. The tumor cells were diffusely positive for CD34 and S-100 protein, while they were completely negative for c-Kit, DOG-1, and smooth muscle actin. The final diagnosis was neurofibroma. Sporadic colonic neurofibroma is very rare. Given the diffuse positivity for CD34 and its rarity, colonic neurofibroma can be easily misdiagnosed as gastrointestinal stromal tumor. Recognition of this entity would be beneficial for pathologists to avoid misdiagnosis and unnecessary treatment

Manifestation of anaplasmosis as cerebral infarction: a case report

Abstract Background Human granulocytic anaplasmosis is a tick-borne zoonotic disease caused by Anaplasma phagocytophilum, an obligate intracellular granulocytotropic bacterium. Case presentation A 70-year-old female patient was admitted with the clinical signs of fever and an altered state of consciousness 1 week after experiencing a tick bite while planting lawn grass. Magnetic resonance imaging, performed at the time of admission, indicated cerebral infarction in the left basal ganglia, whereas increasing immunofluorescence assay antibody titers for A. phagocytophilum were also documented. A. phagocytophilum was identified using groEL and ankA targeted polymerase chain reaction and sequencing. Because of severe thrombocytopenia, only doxycycline was administered, without any antiplatelet agents. Subsequently, the symptoms improved without any focal neurologic sequela. Conclusion This is the first reported case of cerebral infarction occurrence in an anaplasmosis patient

Effects of Pyrogallol on Growth and Cytotoxicity of Wild-Type and katG Mutant Strains of Vibrio vulnificus.

Vibrio vulnificus is a causative agent of fatal septicemia and necrotic wound infection and the pathogen infection became an important public health problem in many counties. Vibrio vulnificus causes RtxA1 toxin-induced acute cell death. We tried to identify natural products that inhibit the acute cytotoxicity of V. vulnificus using a lactate hydrogenase assay. A polyphenol pyrogallol protected HeLa cells from V. vulnificus-induced cytotoxicity. Pyrogallol also decreased the growth of V. vulnificus; this inhibitory effect was more significant during log phase than stationary phase. To further elucidate the inhibitory mechanism, pyrogallol-induced toxicity was compared between a V. vulnificus catalase-peroxidase mutant (katG-) and the isogenic wild-type MO6-24/O strains. No growth was observed for the katG- mutant in the presence of pyrogallol (50 μg/mL) even after 24 h, whereas the wild-type strain demonstrated growth recovery following a prolonged lag phase. Pyrogallol-mediated growth inhibition of the katG- mutant strain was partially rescued by exogenous catalase treatment. These results indicate that the mechanism by which pyrogallol inhibits the growth and cytotoxicity of V. vulnificus likely involves polyphenol-induced prooxidant damage. Taken together, these results suggest that pyrogallol has potential for development as a new paradigm drug to treat infectious diseases