流感嗜血杆菌性脑膜炎致听力减退1例

患儿 ,4 12 岁 ,白族 ,因发热、咳嗽 2d入院。患儿 2d前因受凉后出现发热 ,体温 39.6℃ ,干咳 ,入院当天呕吐 4次胃内容物 ,量少 ,非喷射性 ,无头痛 ,抽搐等。入院第 2天及第 3天两次出现畏寒、寒颤、面色苍白、皮肤发花、气促、口唇发绀、肢端凉 ,测体温 39.2℃～ 4 0 .5℃。入院查体 :T 37.7℃ ,P 1 2 0次 /min ,R 2 8次 /min ,神清、精神差 ,咽充血 ,双肺呼吸音粗 ,无罗音 ,心腹正常 ,神经系统检查阴性。入院第 3天查体 :意识不清 ,反应迟钝 ,不能对答 ,双瞳孔等大等圆 ,对光反射存在 ,四肢肌力 ,肌张力正常 ,生理反射正常 ,椎体束征阴…     

Sequelae of Haemophilus influenzae meningitis

Fourteen children who had had Haemophilus influenzae meningitis more than two years earlier have been compared with their siblings. WISC, Frostig and Bender psychological tests and neurological examination were performed so that subject/sibling differences could be analysed. On neurological examination, subjects overall performed worse than the controls, although no "hard" neurological signs were found. Prolonged fever during the meningitis was associated with poorer results in psychological tests. In the subjects, there was a significant increase in left lateral dominance which may have been due to brain damage by the meningitis. However, most subjects did not differ significantly from their siblings in the tests, suggesting that prompt and adequate treatment of bacterial meningitis can prevent sequelae.     

Pathogenesis of Haemophilus influenzae meningitis

The hypoxia induced by decreased cerebrocortical blood flow contributes to the neurologic deficits found in many survivors of Hib meningitis. Because reduced blood flow is measurable within 48 hours of acquisition of bacteria, the inability of antibiotic therapy to prevent sequelae is more easily understood insofar as damage has already occurred by the time treatment is initiated. Hydrocephalus is probably due to severe choroid plexus necrosis with aqueductal occlusion. These deficiencies, along with the neuronopathy, contribute to permanent cerebrocortical deficits, including impaired learning ability.     

Moxalactam therapy of Haemophilus influenzae type b meningitis in children

Thirty-four children with Haemophilus influenzae type b meningitis were given prospectively either moxalactam (200 mg/kg/day) or ampicillin (400 mg/kg/day) plus chloramphenicol (75 mg/kg/day). One patient in each group died. The mean duration of fever, clinical response, sequential cerebrospinal fluid findings, and incidence of neurologic sequelae were similar between groups. Moxalactam cerebrospinal fluid bioactivity was significantly greater than that of ampicillin or chloramphenicol throughout therapy. Neutropenia, liver enzyme abnormalities, and diarrhea were not significantly different. In eight of 11 patients given moxalactam (versus one of 14 controls) there was complete elimination of gram-negative aerobic flora in the stools by day 10 (P = 0.002); however, none acquired Clostridium difficile. Moxalactam in effective therapy for H. influenzae type b meningitis.     

Thiamphenicol in treatment of Haemophilus influenzae meningitis.

17 infants and children with pyogenic meningitis (14 Haemophilus influenzae, 2 Diplococcus pneumoniae, 1 Neisseria meningitidis) were treated with thiamphenicol, 100 mg/kg body weight/day in 4 doses i.v., as single drug. In the H. influenzae group 10 patients were cured, 4 had relapses of meningitis, 3 with documented subdural effusions. This group is compared with 14 children matched for age, initial leucocyte and CSF cell count treated with ampicillin: all of these were cured, 1 had a subdural effusion. Thiamphenicol concentrations were determined in the serum and CSF 2 h after administration. The mean serum levels were between 10-12 mcg/ml, the mean CSF levels varied from 5.4 mcg/ml at the beginning to 1-1.9 mcg/ml at the end of meningitis. The MIC of H. influenzae was 0.6-12 mcg/ml. A significant, acute, and dose related bone marrow toxicity of thiamphenicol could be documented, but was always rapidly fully reversible. We conclude that thiamphenicol cannot replace chloramphenicol in the treatment of pyogenic meningitis as single systemic antibiotic. Special indications for thiamphenicol in this disease are discussed.     

Haemophilus influenzae meningitis in Sweden 1981-1983.

Four hundred and seventy cases of meningitis caused by Haemophilus influenza in children and 30 cases in adults were identified in Sweden between 1981 and 1983. The age specific incidence in the most susceptible age group (0-4 years) was 31/100,000/year (440 cases), which is higher than previously reported from Europe. A further 30 cases were seen in children aged 5-14. The risk of developing H influenzae meningitis before the age of 15 was 1 in 669. There were 11 deaths (2%) and five cases of serious neurological sequelae among the children. Only 18 children (4%) had predisposing diseases. All but one of the 294 strains of H influenzae from children that had been serotyped were type b. Infections in adults differed from infections in children. Five of the adults died (17%), 12 had important predisposing diseases, and at least six of the infections were caused by non-typable strains. It is concluded that research into the prevention of invasive H influenzae infections in children should have high priority.     

Haemophilus influenzae meningitis: an evolving therapeutic regimen.

Ampicillin sodium has been the drug of choice in the treatment of Haemophilus influenzae meningitis. The development of ampicillin-resistant strains forces the clinician to focus on alternative therapies. We describe two patients in whom neutropenia was noted secondary to chloramphenicol administration, and streptomycin sulfate and sulfonamides were employed. An historical perspective summarizing the evolution of available therapeutic regimens is presented.     

Brain carbohydrate metabolism during experimental Haemophilus influenzae meningitis.

Five-day-old infant rats which acquire Haemophilus influenzae b bacteremia and meningitis after intranasal inoculation have a transient depression in weight gain (2 days), but then continue to grow at the same rate as strain U--11 inoculated controls. Brain lactate, glucose, and glycogen concentrations increase during the first 5 days of disease in infected animals. The increase in brain glycogen can be accounted for by an influx of glycogen containing polymorphonuclear leukocytes. The increased concentrations of glucose and lactate were found not to be due to a change in brain weight to dry weight ratio or the volume of entrapped blood. The mean cerebrospinal fluid (CSF) glucose concentration was higher in animals with meningitis (2.7 mM) in comparison to U-11 inoculated controls (1.8 mM). This increase in brain and CSF glucose concentration appeared secondary to an increased brain uptake of hexoses as manifested by an increased [3H]mannitol uptake. Brain lactate accumulation was not explicable from the data available. There was no evidence of cerebral cortical cellular damage because in vitro oxygen uptake and lactate production were equivalent in control and meningitic animals. The ability of the infant rat brain to maintain cerebral adenosine triphosphate (ATP) content in menigitis and the failure of CSF glucose concentration to decrease might be a reflection of the importance of alternative oxidative substrate (e.g., beta-hydroxybutyrate) to the cerebral metabolism of the developing rat brain.