Intravenous trimethoprim-sulfamethoxazole in the treatment of serious infections in children.

Intravenous TMP-SMZ was used to treat 19 infectious episodes in 18 patients ranging in age from 3 weeks to 13 years. Thirteen patients with various soft tissue or skeletal infections caused by Haemophilus influenzae, Streptococcus pneumoniae, Staphylococcus aureus. Streptococcus pyogenes, or Acinetobacter anitratus were successfully treated. Three children with four episodes of CSF shunt infections due to coagulase-negative staphylococci were treated successfully also. The only treatment failures were in two newborn infants with enteric gram-negative bacterial ventriculitis. TMP-SMZ was given at a daily dose of 10 and 50 mg/kg, respectively, every six hours. The drug was administered intravenously for a mean duration of 10 days (range 4 to 32); in 11 patients this was followed by oral administration for a mean of nine days (range 2 to 18). Half-life of TMP after intravenous administration was 5 1/4 hours; that of SMA was 8 1/2 hours. Levels determined three to four days after starting therapy were generally higher than levels obtained at corresponding times after the first dose. CSF/blood TMP and SMA ratios, determined in four patients, were 0.6 and 0.5, respectively. Side effects were observed in 14 patients, and neutropenia was the most common adverse reaction. Intravenous TMP-SMZ is an effective antimicrobic agent in the treatment of infections due to susceptible organisms. The frequent side effects, although reversible and of no major clinical consequence, suggest that future use of TMP-SMZ should be monitored closely.

Kawasaki disease in an Egyptian boy.

Since its description in Japan in 1967, Kawasaki disease has been reported from several parts of the world but has been reported only once in an Arab child and never from the African continent. We report a typical case of Kawasaki disease in an Arab child in Africa who later developed coronary and several peripheral aneurysms.

Effect of glucose-6-phosphate dehydrogenase deficiency on neutrophil function.

The bactericidal activity of neutrophils depends primarily on free oxygen radicals released by the activation of NADPH oxidase when neutrophils are stimulated by microorganisms. Severe glucose-6-phosphate dehydrogenase (G6PD) deficiency is associated with decreased NADPH production. Increased susceptibility to recurrent bacterial infections in children with severe neutrophil G6PD deficiency as a consequence of decreased NADPH production has been reported earlier. In this study, the in vitro activity of neutrophils from normal and G6PD-deficient individuals was assessed by measuring the [14C]CO2 released via the hexose monophosphate shunt from radiolabeled [1-14C]-glucose and the nitroblue tetrazolium (NBT) dye reduction test. Our results show that the G6PD activity of neutrophils from 48 individuals, identified as severely erythrocyte (RBC) G6PD deficient (< 2 U/10(12) RBC) was 23% of the enzyme activity of neutrophils from 53 individuals with normal RBC G6PD levels (98.8 U/10(12) RBC). However, the results of functional assays of neutrophils as measured by hexose monophosphate shunt and the NBT test were comparable in G6PD-deficient and normal individuals, suggesting that a reduced activity of G6PD to as low as 23% of normal does not affect neutrophil function.

Genital anomaly and cardiomyopathy: a new syndrome.

Two brothers, products of a consanguineous marriage, had severe hypoplastic genitalia and cardiomyopathy. These findings are similar to those of three other brothers of another consanguineous family who in addition had evidence of mental retardation. These five boys probably represent a previously undescribed syndrome of genetic origin but of poorly understood pathogenesis.