[Purulent meningitis. Epidemiology, etiology, diagnosis, development, prognosis, prevention, treatment].
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Biomedical subjects
Publications and source records attributed to J M Decazes.
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Periostitis ossificans and sclerosing osteomyelitis are rare subtypes of non suppurative chronic osteomyelitis in which there is, additionally, a proliferation of periosteum leading to bony deposition secondary to a mild chronic infection making their diagnosis difficult. The authors report two clinical cases and try to release criteria helping to discern them because the prognosis and therapeutic management of these affections are different.
Access to the cerebrospinal fluid, which is the only objective reflection of the essential parametres, is very limited. Investigators have long tried to design an animal model. Presently, the experimental model of the newborn rat is most often used for studying pathogenic factors in haematogenous meningitis. In contrast, the rabbit model is more adapted to therapeutic investigation The main advances have been therapeutic and pathophysiologic. Good examples are the identification of optimum antibiotic levels in the cerebrospinal fluid, and the demonstration of the responsibility of mediators produced by the host in triggering the inflammation. The principle of corticosteroid treatment before induction of bacterial lysis by antibiotics in Haemophilus meningitis is a result of such work.
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We report a case of cystitis due to Toxoplasma gondii in a patient with AIDS who presented with dysuria and urinary frequency. To our knowledge, this is the first reported case of cystitis due to this organism. Microscopy of bladder specimens revealed inflammatory cystitis, with Toxoplasma cysts disseminated within the mucosa. No other pathogen could be detected by urine culture, cytoscopy, or staining of bladder specimens obtained at autopsy. Diagnosis of cystitis due to Toxoplasma gondii may be difficult because this illness is associated with misleading radiologic and endoscopic findings. Toxoplasmosis is a rare but potentially curable cause of culture-negative cystitis in patients with AIDS.
We evaluated the pharmacokinetics and therapeutic efficacies of piperacillin and tazobactam, a beta-lactamase inhibitor, given either alone or in different combinations (80:10, 200:10, and 80:25 mg/kg/h), in experimental meningitis due to a strain of Klebsiella pneumoniae producing the TEM-3 extended-spectrum beta-lactamase. Treatment was administered intravenously as a 7-h constant infusion preceded by a bolus of 20% of the total dose. The mean (+/- standard deviation) rates of penetration into the cerebrospinal fluid (CSF) of infected animals were 6.7 +/- 3.9% for piperacillin given alone and 36.3 +/- 21.9% for tazobactam given alone. Combination treatment significantly magnified the concentration of either drug in CSF. Concentrations of bacteria in CSF increased throughout therapy in animals given either drug alone, even at high dosages. In animals given the combination at dosages of 80:10 and 200/10 mg/kg/h, only a suboptimal reduction of CSF bacterial titers was obtained in vivo, i.e. -0.49 +/- 0.34 and -0.73 +/- 0.49 log CFU/ml/h, respectively. An increase in the tazobactam dosage within the combination (80:25 mg/kg/h) was required in order to obtain a significantly faster elimination of viable organisms from the CSF (-0.97 +/- 0.35 log CFU/ml/h). The study shows that tazobactam is able to provide effective protection against piperacillin hydrolysis by the TEM-3 enzyme within the CSF. Appropriate dosage regimens of various beta-lactam-tazobactam combinations may deserve comparative studies in experimental meningitis caused by organisms producing extended-spectrum beta-lactamases.
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OBJECTIVE: To identify risk factors associated with a first episode of Clostridium difficile-associated diarrhoea (CDAD) in patients with HIV infection. DESIGN: A case-control study. SETTING: University teaching hospital HIV inpatient unit. PATIENTS AND METHODS: Nineteen HIV-infected patients with CDAD, defined as diarrhoea with positive stool culture for Clostridium difficile (CD) and positive stool cytotoxin B assay, were compared with 38 randomly selected controls (HIV-infected patients hospitalized on the ward on the day the matched case was diagnosed). CD isolates were phenotyped by electrophoretic protein patterns. RESULTS: The incidence of CDAD among HIV-infected patients was 4.1/100 of patient-admissions. On univariate analysis, cases were more likely to have used clindamycin [11 out of 19 compared with four out of 38; odds ratio (OR) 19; 95% confidence interval (CI), 2-160; P = 0.0007], and pyrimethamine (14 out of 19 compared with 13 out of 38; OR, 4.8; 95% CI, 1.4-16, P = 0.02) in the month before diagnosis, and to have had cerebral toxoplasmosis (12 out of 19 compared with 13 out of 38; OR, 2.8; 95% CI, 0.9-8.6; P = 0.09). There was also a significant increase of the risk of CDAD as duration of hospitalization in the ward increased (chi 2 for trend, P = 0.007). Multivariate models associated two risk factors with CDAD: clindamycin use (OR, 42; 95% CI, 2-813; P = 0.01), and prolonged hospitalization in the ward (OR, 3.6 per week in the ward; 95% CI, 1-13, P = 0.048). Of 18 available CD isolates, 15 (83%) had identical electrophoretic protein pattern. CONCLUSIONS: Clindamycin use and prolonged hospitalization in the ward were the main risk factors associated with CDAD in this study. These observations, together with the occurrence of one major phenotype of CD, suggest nosocomial transmission of CD in the ward.
THP-1 monocytoid cells, either not infected or chronically infected with human immunodeficiency virus type 1 (HIV-1), were challenged with Toxoplasma gondii. Parasitic growth, as assessed by trophozoite counting and measurement of supernatant p30 membrane antigen, was similar in HIV-infected and noninfected THP-1 cells. Also, T. gondii did not affect HIV replication. These experiments therefore failed to demonstrate any interaction between HIV-1 and T. gondii replication in concurrently infected monocytoid cells.
This retrospective study compared the epidemiological, clinical and bacteriological characteristics of tuberculosis in HIV-infected (HIV+) and seronegative (HIV-) patients in France. It included 67 cases of tuberculosis observed in the hospital setting between 1985 and 1990. The 35 HIV+ patients (52.2%) were more frequently of European origin, while those of African origin were HIV-. Disseminated tuberculosis predominated in HIV+ patients, as opposed to pulmonary tuberculosis in HIV- patients. The tuberculin test was more often positive in HIV- patients than in HIV+ ones (65.6 versus 17.1%; p < 0.001). Direct bacteriological examination of the sputum was positive more frequently in HIV- than HIV+ patients (56.2 versus 22.8%; p < 0.01). A high percentage of the Mycobacterium tuberculosis strains isolated from HIV+ patients (20%) was resistant to anti-tuberculous drugs, primarily isoniazid, while no resistance was found in HIV- patients. The initial response to treatment and the therapy-associated side effects did not differ between the two groups. Four relapses (11.4%) occurred in HIV+ patients, raising the question of the indication of drug prophylaxis following tuberculosis in HIV-infected patients.
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A rapidly enlarging left inguinal adenitis, with positive groove sign, and fever, chills, malaise, hypotension, headache, scarlatiniform rash, choleroid diarrhea, and proteinuria developed in an homosexual man who was positive for human immunodeficiency virus. The needle aspiration of the inguinal mass showed group A beta-hemolytic streptococci and the blood cultures were negative, suggesting group A streptococcal cellulitis-adenitis with toxic strep syndrome. Treatment with penicillin and surgical drainage was successful. Bacterial infections associated with defective humoral immunity appear to be common in patients with acquired immunodeficiency syndrome (AIDS), and some of these infections have a remarkable extensive and lethal evolution. Therefore streptococcal adenitis should be considered in any patient with AIDS or AIDS-related syndrome in whom rapidly enlarging inguinal nodes develop.
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A compound potentially effective in the treatment of meningitis should reach high concentrations in CSF. In animal experimental models, ceftazidime levels of 5-25 micrograms/ml were demonstrated during administration of doses generating serum levels similar to those achieved in humans. Human studies later confirmed CSF levels of 5-10 micrograms/ml in patients with meningitis. Ceftazidime CSF kinetic properties are adequate for use of this compound in patients with meningitis due to susceptible organisms.
Subcorneal pustular dermatosis (SPD) or Sneddon-Wilkinson disease is a skin eruption in which concomitant systemic involvement has not been reported to our knowledge. We describe a patient suffering from SPD of 6 years duration with amicrobial inguinal lymph node suppuration and aseptic spleen abscesses followed by pyoderma gangrenosum.
Patients with purulent meningitis received amoxicillin-clavulanic acid (200/20 mg/kg [body weight] per day). Clavulanic acid levels in cerebrospinal fluid were less than or equal to 0.05 micrograms/ml in 5 of 18 samples and ranged from 0.1 to 0.8 micrograms/ml in the others. Of 12 cerebrospinal fluid samples tested, 10 lacked bactericidal activity in vitro against a beta-lactamase-producing strain of Haemophilus influenzae.