Gemella haemolysans is a rare pathogen in cases of bacterial meningitis. We present a case of meningitis due to G. haemolysans in a 17-month-old boy. This is the first reported case of Gemella meningitis in a child. The patient completely recovered following intravenous therapy with linezolid and chloramphenicol.A 17-month-old boy who was diagnosed at the age of 2 months with complex congenital heart disease (a perimembranous ventricular septal defect and a small patent ductus arteriosus) was admitted to the hospital with complaints of fever, vomiting, and loss of appetite for 2 days. A physical examination revealed an ill-appearing baby with a head circumference of 46.5 cm, a weight of 10,500 g, and a height of 77 cm. His body temperature was 39.2°C, his heart rate was 164/min, and his respiratory rate was 28/min. The anterior fontanelle was closed, and he had a grade 2/6 systolic murmur at the left sternal border. There was no hepatomegaly or splenomegaly, and he had no sick contacts or trauma. He had received three doses of hepatitis B vaccine, as well as polio, diphtheria, tetanus toxoid, pertussis, and first Bacille Calmette-Guerin (recommended in the childhood immunization schedule in Turkey) vaccines, and had not received Haemophilus influenzae type b vaccine (recommended in the childhood immunization schedule in Turkey for 3 months). His medications included digoxin and spironalactone because of heart disease. There was no family history of invasive bacterial infection. Blood, cerebrospinal fluid (CSF), and urine samples were taken and sent to the laboratory for culture and biochemical analyses. The complete blood count showed a white blood cell count of 21,830/mm 3 , of which 74% were neutrophils, 8% were bands, 16% were lymphocytes, and 2% were monocytes; a hemoglobin level of 11.9 g/dl; and a platelet count of 170,000/mm 3 . His serum basic chemistry was normal, except for a glucose level of 183 mg/dl. The level of C-reactive protein was 30.4 mg/dl, and the erythrocyte sedimentation rate was 56 mm/h. Serum immunoglobulin and subclass levels were normal, and the serum was negative for anti-HIV antibody. Urine analysis and a chest radiograph were normal. Transthoracic echocardiography was negative for endocarditis. CSF analyses showed a protein concentration of 102 mg/dl, a glucose concentration of 11 mg/dl, a red blood cell count of 250/mm 3 , and a white blood cell count of 4,500/mm 3 , of which 88% were neutrophils and 12% were lymphocytes. The CSF was negative by gram staining. The diagnosis was suspicion of bacterial meningitis, and empirical antibiotic treatment was started with ampicillin (300 mg/kg/ day) and cefotaxime (200 mg/kg/day) as part of our clinical protocol. Dexamethasone (0.6 mg/kg/day, 4 days) was given intravenously before the first administrated antibiotic dose. The CSF specimen was cultured on 5% sheep blood, eosinmethylene blue, and chocolate agars at 35°C in 5 to 10% CO 2 for 48 to 72 h. Because of a suspicion of endocarditis, three pairs of aerobic and anaerobic blood cultures,...

Chryseobacterium meningosepticum is a rare pathogen in cases of bacterial meningitis in adults and adolescents. We report on the case history of a 17-year-old boy with thalassemia major and meningitis and sepsis caused by C. meningosepticum in splenectomized. The patient received vancomycin therapy for 21 days and was discharged in a state of complete recovery. CASE REPORTA 17-year-old boy was diagnosed with thalassemia major (TM) at the age of 12 months. His ␤-thalassemia mutation was IVS-I-110 (G3A), homozygous state. He was treated with regular blood transfusions at 3-to 4-week intervals to maintain pretransfusion hemoglobin levels above 9.5 g/dl. Desferrioxamine treatment was started when the boy was 3 years of age. Because of an increasing requirement for packed red cells, he was splenectomized in 2000. Despite receiving desferrioxamine therapy, he was heavily iron loaded, so an orally active chelator, deferiprone (L 1 ,1,2-dimethyl-3-hydroxypiridin-4-one), was added 6 months before the condition described here occurred. The latest serum ferritin level was 2,750 ng/dl. The patient did not have heart failure, diabetes mellitus, or cirrhosis of liver. There was no previous history of significant infection.On 20 September 2005, the patient was admitted with fever, headache, and progressive disturbances of consciousness that had lasted for 2 days. On admission, physical examination revealed a pale and toxic appearance. He had positive signs of meningeal irritation. His body temperature was 39.2°C, his heart rate was 124 beats/min, his respiratory rate was 20/min, his blood pressure was 105/50 mm Hg, his body weight was 41 kg, and his body height was 155 cm. Hepatomegaly and a scar from the splenectomy were noted. Blood and cerebrospinal fluid (CSF) samples were taken and sent to the laboratory for culture and biochemical analyses. Results of the laboratory testing showed a white blood cell (WBC) count of 9 ϫ 10 3 /l (90% neutrophils), a hemoglobin concentration of 6.1 g/dl, a hematocrit of 18.2%, a platelet count of 258 ϫ 10 3 /l, an urea concentration of 30 mg/dl, a creatinine concentration of 1.2 mg/dl, a glucose concentration of 108 mg/dl, an aspartate aminotransferase concentration of 100 U/liter, an alanine aminotransferase concentration of 102 U/liter, a sodium level of 38 meq/liter, a potassium level of 4.0 meq/liter, an erythrocyte sedimentation rate of 150 mm/h, and a C-reactive protein concentration of 4.0 mg/dl. Study of the CSF revealed the following results: a WBC count of 5,200/mm 3 , a glucose concentration of 20 mg/dl, a protein concentration of 92 mg/dl, and a chloride level of 124 meq/liter; the CSF was negative by Gram staining. All of the remaining biochemical laboratory tests were unremarkable. A chest radiograph and computed tomography of the brain were normal. Empirical therapy with intravenous vancomycin at 60 mg/kg of body weight/day (maximum dose, 2 g/day) was initiated. The CSF specimen was cultured on 5% sheep blood, eosin-methylene blue, and chocolate agars at 35°C in 5 to 10% CO 2 ...

The aim of this study was to determine the in vitro susceptibility of 170 clinical isolates of Mycobacterium tuberculosis to fusidic acid using a proportion dilution method. Nineteen isolates were resistant to at least one first-line anti-tuberculosis drug. A total of 1.8% of the isolates were resistant to fusidic acid. Fusidic acid should be evaluated clinically as a potential supplementary drug for the treatment of infections due to multidrug-resistant strains of M. tuberculosis.

This study increases the understanding of the burden of multidrug-resistant S. typhimurium infection. Nosocomial outbreaks have a major effect on healthcare delivery, costs and outcomes.

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