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PubMed1995

Headache associated with aseptic meningitis.

A retrospective analysis of all patients admitted with the diagnostic codes of aseptic or viral meningitis was performed at two institutions over 3 years. Forty-one patients with cerebrospinal fluid confirmation of aseptic meningitis (increased protein; increased white count; negative gram stain; and negative fungal, tuberculosis, and bacterial cultures) were analyzed. All the patients had headache, which was typically severe and bilateral in 39 of the 41 patients. The headache was of abrupt onset or the worst of the patient's life in 24 of the patients. The quality of the headache, when described, was usually throbbing (11 of 14). Nineteen patients had prodromal symptoms, including malaise, myalgia, gastrointestinal symptoms, and urinary tract infections. All had associated symptoms, including nausea (25), vomiting (23), photophobia (18), stiff neck (25), and back pain (11). Thirty patients were febrile. Lumbar puncture was performed for headache and fever unexplained by systemic illness in 30 patients, meningeal signs in 15, headache of abrupt onset or the worst headache ever in 24, neurologic signs or symptoms in 12, and for other reasons in 2. Computerized tomography, when performed, was negative in all cases. Focal neurologic findings were present in 5 patients, a decreased level of consciousness in 6, and papilledema in 1. A severe headache that worsens, is abrupt in onset, or is the worst of the patient's life could be due to aseptic meningitis, bacterial meningitis, or a subarachnoid hemorrhage. Although not universally present, meningeal signs, fever, and neurologic signs or symptoms should alert one to a possible central nervous system infection.

Adolescent↗
PubMed2001

Anti-interleukin-6 antibodies attenuate inflammation in a rat meningitis model.

OBJECTIVES: Interleukin-6 (IL-6) is elevated in the cerebrospinal fluid (CSF) of humans and animals with bacterial meningitis. This study's hypothesis was that anti-IL-6 antibodies will attenuate meningeal inflammation in a rat model of bacterial meningitis. METHODS: 14 male Sprague-Dawley rats were inoculated intracisternally (IC) with 0.1 mL of heat-killed pneumococci. At one hour post-inoculation, the rats received intraperitoneal doses of either 1.0 mL phosphate-buffered saline (PBS treatment group, n = 7) or 70 microg anti-IL-6 antibodies in 1.0 mL PBS (anti-IL-6 antibody treatment group, n = 7). Nine rats (normal group, n = 9) had no inoculation, and four rats (surgical sham group, n = 4) had IC inoculations of saline. At six hours post-inoculation, all the animals had CSF removed via IC tap. The CSF protein and white blood cell (WBC) count measures were compared using a t-test. RESULTS: Mean CSF WBC for the anti-IL-6 treatment group was 2,458/microL, versus the PBS controls' mean of 9,697/microL (p = 0.007). Mean CSF protein for the anti-IL-6 group was 180 mg/dL, versus 296 mg/dL for the controls (p = 0.032). The surgical sham and normal animals had normal CSF WBC and protein values. CONCLUSIONS: In this rat meningitis model, systemic treatment with anti-IL-6 antibodies after the induction of meningitis suppressed both CSF WBC count and CSF protein level, two important indices of meningeal inflammation.

Animals↗
PubMed1993

5-Hydroxytryptamine receptor characterization of human cerebral, middle meningeal and temporal arteries: regional differences.

We have studied the regional distribution of 5-hydroxytryptamine (5-HT) receptor subtypes in fresh circular segments of human cerebral, middle meningeal, and temporal arteries. Vasomotor responses induced by a series of 5-HT agonists and antagonists with some degree of selectivity were studied by using a sensitive in vitro system. Nine 5-HT agonists were examined for contractile effects on the arteries. In cerebral and meningeal arteries 5-carboxamidotryptamine (5-CT) was more potent than 5-HT. The opposite order of potency (5-HT-5-CT) was found in temporal arteries. In the cerebral arteries 5-methoxytryptamine (5-MeOHT) was more potent than sumatriptan while sumatriptan was more potent than 5-MeOHT in meningeal and temporal arteries. The 5-HT1 receptor antagonist, methiothepin, competitively antagonized 5-CT-induced contractions in cerebral arteries, with a pA2 value of 9.05. 5-HT-induced contractions were competitively antagonized by ketanserin (5-HT2) in the temporal arteries pA2 value of 9.06). Methiothepin and ketanserin had non-competitive antagonistic effects in the middle meningeal arteries. The 5-HT3 selective antagonist ondansetron did not cause any shift of the contractions induced by 2-methyl-5-HT in the temporal, cerebral and middle meningeal arteries. These results suggest that the cerebral arteries mainly contain 5-HT1D or 5-HT1-like receptors, and the temporal artery 5-HT2 receptors; the data further indicate the presence of both receptor subtypes in the middle meningeal artery.

5-Methoxytryptamine↗
PubMed1995

[Usefulness of endotoxin-specific limulus test for the measurement of endotoxin in cerebrospinal fluid in diagnosis of bacterial meningitis].

Using a new endotoxin-specific chromogneic limulus assay (Endoscopy test), endotoxin concentrations were measured in 93 specimens of cerebrospinal fluid (CSF) from 66 pediatric patients. Eighteen patients were diagnosed as having menigitios. Of these, 6 cases (group A) with gram-negative meningitis proven by culture had high CSF endotoxin concentrations of 115.3, (82-133) (median, range) pg/ml. Ten cases (group B) with gram-positive or aseptic meningitis had endotoxin concentrations of 2.15 (0.1-3.6) pg ml. Other 2 cases with bacterial meningitis (group C), in whom no pathogen was detected, had CSF endotoxin concentrations of more than 100 pg/ml. Four cases with encephalitis (group D) and 45 cases with non-meningitis or non- encephalitis (group E), had CSF endotoxin concentrations of less than 5 pg/ml. Despite a negative culture after antibiotic treatment in group A patients, endotoxin was cleared slowly from the CSF. A clearing of endotoxin from CSF was followed by alleviation of fever with a more gradual decline in CRP values. In 2 cases of group C, the negative bacterial culture appeared to be attributable to the previous treatment with antibiotics. However, these patients had high CSF endotoxin levels, indicating gram negative bacterial meningitis. In 17 CSF specimens from 5 patients of group A, in whom Haemophilus influenzae was detected on admission, an additional a latex agglutination test for the detection of H. influenzae polysaccharide antigen was performed. Only 3 specimens from 3 patients with CSF endotoxin concentrations of more than 80 pg/ml had a positive agglutination test. These results suggest that quantitation of endotoxin concentrations is useful for the diagnosis of gram-negative meningitis. And also, the clearance of endotoxin from CSF during treatment appears to be useful in determining the timing of when antibiotic should be stopped.

Adolescent↗
PubMed2000

[Serial measurement of anti-interleukin-8 IgG autoantibody in cerebrospinal fluid of infants with bacterial meningitis].

We serially measured concentrations of interleukin (IL)-8 and anti-IL-8 IgG autoantibody in cerebrospinal fluid of infants with bacterial meningitis, and also measured these concentrations in cerebrospinal fluid obtained from infants without meningitis on admission. We have reported that the IL-8 concentration in cerebrospinal fluid of infants with purulent meningitis rapidly decreases after the initiation of therapy. Thus, in the present study, the IL-8 concentration in infants with purulent meningitis only before the initiation of therapy was significantly higher compared with that in infants without meningitis. However, the concentration of anti-IL-8 IgG autoantibody was still high after the initiation of therapy. The concentration of anti-IL-8 IgG autoantibody was significantly higher compared with that in infants without meningitis until the 15th day after the initiation of therapy. The time lag between the decrease of IL-8 and anti-IL-8 IgG autoantibody demonstrated in the present study could be used to indicate the past presence of a large amount of IL-8, even if the IL-8 concentration was already low.

Autoantibodies↗
PubMed2005

[Interleukin 12 measurement in the cerebrospinal fluid of infants with purulent meningitis].

We measured IL-12 concentrations in the CSF of patients with purulent meningitis. Twenty-three infants who were admitted between 1997 and 2003 and diagnosed as having purulent meningitis were included in this study. All patients in this study were admitted by the 3rd day of illness. After admission, appropriate antibiotics were administered to all infants. Two infants died and two other infants developed cerebral palsy and mental retardation (adverse outcome group). None of the other patients showed any neurologic abnormalities at discharge (good outcome group). As a control group, 16 infants who were diagnosed with diseases other than purulent meningitis were also investigated. The CSF IL-12 p40 concentrations in meningitis infants on admission (median [range], 1,890 [< 15-7,770] pg/ml) were significantly higher compared with those in the control group (p < 0.001). Among infants with meningitis, there were no significant differences on admission between patients with adverse outcome group and those with good outcome group. Consecutive measurements were performed in 17 infants with meningitis including the 2 infants with adverse outcome group. The concentration in the infants with adverse outcome group seemed to decrease more gradually than that in those with good outcome group. IL-12 induces production of interferon-gamma, which enhances the function of polymorphonuclear leukocytes. IL-12 may contribute to local host defenses in the subarachnoid space.

Cerebral Palsy↗
PubMed2003

Neuroinflammatory role of prostaglandins during experimental meningitis: evidence suggestive of an in vivo relationship between nitric oxide and prostaglandins.

Nitric oxide (NO) and prostaglandins are inflammatory mediators produced during meningitis. The purpose of the present study was to pharmacologically inhibit cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS) to 1) explore the prostaglandin contribution to blood-cerebrospinal fluid barrier permeability alterations and 2) elucidate the in vivo concentration relationship between prostaglandin E2 (PGE2) and NO during experimental meningitis. Intracisternal injection of lipopolysaccharides (LPSs, 200 microg) induced neuroinflammation. Rats were dosed with nimesulide (COX-2 inhibitor), aminoguanidine (iNOS inhibitor), or vehicle. Evans blue was used to assess blood-cerebrospinal fluid barrier permeability. Meningeal NO and cerebrospinal fluid PGE2 were assayed using conventional methods. (Results are expressed as mean +/- S.E.M. of 5-9 rats/group.) Nimesulide failed to prevent blood-cerebrospinal fluid barrier disruption [cerebrospinal fluid Evans blue (micrograms per milliliter): control, 0.22 +/- 0.22*; LPS, 11.58 +/- 0.66; LPS + nimesulide, 10.58 +/- 0.86; *p < 0.05; ANOVA]. Although nimesulide decreased PGE2 (picograms per microliter; p < 0.01) in LPS + nimesulide rats (13.9 +/- 1.96) versus LPS + vehicle (73.8 +/- 12.4), meningeal NO production (picomoles/30 min/10(6) cells; p < 0.01) increased unexpectedly in LPS + nimesulide rats (439 +/- 47) versus LPS + vehicle rats (211 +/- 31). In contrast, aminoguanidine inhibited meningeal NO (picomoles/30 min/10(6) cells; p < 0.005) in LPS + aminoguanidine (111 +/- 20) versus LPS (337 +/- 48) but had no effects (p > 0.05) on PGE2. The in vivo relationship between PGE2 and NO was mathematically described by a biphasic, bell-shaped curve (r2 = 0.42; n = 27 rats; p < 0.0001). Based on these results, inhibition of prostaglandin synthesis not only fails to prevent blood-cerebrospinal fluid barrier disruption during neuroinflammation and but also promotes increased meningeal NO production. The in vivo concentration relationship between PGE2 and NO is biphasic, suggesting that inhibition of COX-2 alone may promote NO toxicity through enhanced NO synthesis.

Animals↗
PubMed1994

Antibiotic therapy and acute outcome of meningitis due to Streptococcus pneumoniae considered intermediately susceptible to broad-spectrum cephalosporins.

Children with meningitis due to Streptococcus pneumoniae isolates that are relatively or fully resistant to penicillin and have decreased susceptibility to broad-spectrum cephalosporins (MIC, > or = 2.0 micrograms/ml) who have failed treatment with broad-spectrum cephalosporins have been reported. The National Committee for Clinical Laboratory Standards has newly revised guidelines indicating that S. pneumoniae isolates associated with meningitis for which the MICs are > or = 0.5 micrograms/ml should be considered resistant to broad-spectrum cephalosporins. This recommendation is not clearly based on data related to clinical outcome and may be too conservative. We present data on five children who had S. pneumoniae meningitis due to isolates that were relatively or fully resistant to penicillin (MIC range, 0.125 to 4.0 micrograms/ml) and had cefotaxime or ceftriaxone MICs of 0.50 to 2.0 micrograms/ml. Their clinical courses and outcomes were comparable to those of five children with S. pneumoniae meningitis due to strains that were relatively or fully resistant to penicillin and were inhibited by cefotaxime at concentrations of < or = 0.25 micrograms/ml, as well as to those of 25 patients with S. pneumoniae meningitis due to penicillin-susceptible isolates identified during the same period. Children with meningitis due to S. pneumoniae with cefotaxime or ceftriaxone MICs of < or = 1.0 micrograms/ml may be adequately treated with these antibiotics. Further clinical data are required before solid recommendations can be made regarding cephalosporin breakpoints for S. pneumoniae.

Anti-Bacterial Agents↗
PubMed1993

Pathogenesis and pathophysiology of bacterial meningitis.

Bacterial meningitis remains a disease with associated unacceptable morbidity and mortality rates despite the availability of effective bactericidal antimicrobial therapy. Through the use of experimental animal models of infection, a great deal of information has been gleaned concerning the pathogenic and pathophysiologic mechanisms operable in bacterial meningitis. Most cases of bacterial meningitis begin with host acquisition of a new organism by nasopharyngeal colonization followed by systemic invasion and development of a high-grade bacteremia. Bacterial encapsulation contributes to this bacteremia by inhibiting neutrophil phagocytosis and resisting classic complement-mediated bactericidal activity. Central nervous system invasion then occurs, although the exact site of bacterial traversal into the central nervous system is unknown. By production and/or release of virulence factors into and stimulation of formation of inflammatory cytokines within the central nervous system, meningeal pathogens increase permeability of the blood-brain barrier, thus allowing protein and neutrophils to move into the subarachnoid space. There is then an intense subarachnoid space inflammatory response, which leads to many of the pathophysiologic consequences of bacterial meningitis, including cerebral edema and increased intracranial pressure. Attenuation of this inflammatory response with adjunctive dexamethasone therapy is associated with reduced concentrations of tumor necrosis factor in the cerebrospinal fluid, with diminished cerebrospinal fluid leukocytosis, and perhaps with improvement of morbidity, as demonstrated in recent clinical trials. Further information on the pathogenesis and pathophysiology of bacterial meningitis should lead to the development of more innovative treatment and/or preventive strategies for this disorder.

Animals↗
PubMed2000

Identification of regions of the Escherichia coli chromosome specific for neonatal meningitis-associated strains.

Specific virulence factors associated with the pathogenesis of Escherichia coli strains causing neonatal meningitis (ECNM), such as the K1 capsular polysaccharide, the S fimbriae, and the Ibe10 protein, have been previously identified. However, some other yet unidentified factors are likely to be involved in the pathogenesis of ECNM. To identify specialized unique DNA regions associated with ECNM virulence, we used the representational difference analysis technique. The genomes of two strains belonging to nonpathogenic phylogenetic group A of the ECOR reference collection were subtracted from E. coli strain C5, isolated from a case of neonatal meningitis. Strain C5 belongs to the phylogenetic group B2 as do the majority of ECNM. We have isolated and mapped 64 DNA fragments which are specific for strain C5 and not found in nonpathogenic strains. Of these clones, 44 were clustered in six distinct regions on the chromosome. The sfa and ibe10 genes were located in regions 2 and 6, respectively. A group of genes (cnf1, hra, hly, and prs) known to be present in a pathogenicity island of the uropathogenic strain E. coli J96 colocalized with region 6. The occurrence of these DNA regions was tested in a set of meningitis-associated strains and in a control group composed of non-meningitis-associated strains belonging to the same B2 group. Regions 1, 3, and 4 were present in 91, 82, and 81%, respectively, of the meningitis strains and in 40, 13, and 47% of the control strains. Together, these data suggest that regions 1, 3, and 4 code for factors associated with the ability of E. coli to invade the meninges of neonates.

Blotting, Southern↗
PubMed1989

Levels of antibody to defined antigens of Mycobacterium tuberculosis in tuberculous meningitis.

The aim of the study was to develop an antibody immunoassay for tuberculous meningitis with a sensitivity greater than that of the initial bacterial smear while maintaining a 100% specificity. Antibody titers to five purified antigens of Mycobacterium tuberculosis were measured in cerebrospinal fluid by using an enzyme-linked immunosorbent assay technique. Seventy-four patients with tuberculous meningitis (26 culture positive) were compared with 26 patients with purulent meningitis, 69 patients with suspected but excluded tuberculous meningitis, and 29 patients with other neurological diseases. Antibody responses to both the 14-kilodalton (kDa) antigen and lipoarabinomannan were immunodominant, accounting for 74% of those with any antibody titer to a soluble extract of M. tuberculosis. A sensitivity of 61% was achieved (77% for the culture-positive samples) by using immunoglobulin G titers to lipoarabinomannan and the 14-, 19-, and 38-kDa antigens. Thus, estimation of levels of antibody in cerebrospinal fluid to selected mycobacterial antigens would be valuable in the diagnosis of tuberculous meningitis. The possible reasons for the immunodominance of the 14-kDa antigen and lipoarabinomannan in the pathogenesis of tuberculous meningitis are discussed.

Antibodies, Bacterial↗
PubMed1991

Infantile meningitis in England and Wales: a two year study.

A two year prospective study identified 1922 cases of meningitis in children under 1 year of age. A further 201 cases were identified from other sources. The annual incidence of meningitis during the first year of life was 1.6/1000; during the first 28 days of life it was 0.32/1000, and among postneonatal infants it was 1.22/1000. The male:female ratio was 1.4:1. The overall case fatality rate was 19.8% for neonates and 5.4% for postneonatal infants. Two thirds of deaths identified in the study, 50% of all deaths, were not attributed to meningitis by the Office of Population Censuses and Surveys. Group B beta haemolytic streptococci (28%), Escherichia coli (18%), and Listeria monocytogenes (5%) were most frequently isolated from neonates and Neisseria meningitidis (31%), Haemophilus influenzae (30%), and Streptococcus pneumoniae (10%) from postneonatal infants. At 2-6 months of age N meningitidis meningitis was most common, and at 7-12 months H influenzae predominated. Meningitis caused by group B beta haemolytic streptococci occurred up to 6 months of age and had a consistent mortality of 25%. Neonatal meningitis due to Gram negative enteric rods had a mortality of 32%. Low birth weight was a significant predisposing factor for both neonates and postneonatal infants. In both groups mortality was significantly higher among children admitted in coma. There was no seasonal variation in incidence in either group. Neonates were treated with either group. Neonates were treated with either chloramphenicol (50%) or gentamicin (48%) usually in combination with a penicillin; 40% received a third generation cephalosporin. Of the 1472 postneonatal infants treated 84% received chloramphenicol with a penicillin and 10% received a third generation cephalosporin. Relapse occurred in 49 patients and three died. Eighteen babies coned as a result of raised intracranial pressure, including four neonates, and four died. Mortality among the 133 (7%) children who received steroids was significantly higher than in the rest of the study group.

Chloramphenicol↗
PubMed1994

Lymphomatous meningitis in AIDS-related systemic non-Hodgkin's lymphoma: a report of eight cases.

Meningeal involvement occurred in eight (22%) of 36 adult patients with AIDS-related systemic non-Hodgkin's lymphoma, seen over a 10-year period. Clinical symptoms consisted of cranial nerve palsies, radicular involvement, headache or diffuse encephalopathy. CSF examination established the diagnosis in all cases. Systemic disease had been diagnosed seven to 33 weeks before lymphomatous meningitis in six patients, whereas in the remaining two patients diagnoses of systemic and meningeal disease were made simultaneously. All patients had intermediate or high grade lymphomas and widespread disease. In contrast to non-AIDS related lymphomas, bone marrow involvement at initial staging cannot be used to select patients for prophylactic treatment, as seven of our eight patients had no initial bone marrow involvement. In this retrospective review, prognosis of lymphomatous meningitis was extremely poor, with a mean survival of only five weeks. Survival of patients with systemic lymphoma who eventually developed lymphomatous meningitis was 4.0 months compared with 7.2 months for those who did not. Lymphomatous meningitis appears to have the worst outcome of all AIDS-related neurological complications, regardless of treatment.

Adult↗
PubMed1999

Bacterial meningitis associated with lumbar drains: a retrospective cohort study.

OBJECTIVES: The infective potential of lumbar drainage is an important topic deserving particular study. The aetiology, incidence, and clinical findings associated with bacterial meningitis are described in patients having continuous lumbar CSF drainage to treat communicating hydrocephalus after subarachnoid haemorrhage or CSF leaks after traumatic dural rents. METHODS: Retrospective review of the records of patients with a positive CSF bacterial culture who underwent lumbar drain placement over a 39 month period. RESULTS: Thirteen cases of bacterial meningitis occurred subsequent to the use of 312 lumbar drain kits (4.2%). All meningitic patients had CSF pleocytosis, but not all had peripheral leukocytosis. Fever, peripheral leukocytosis, and CSF pleocytosis did not help to differentiate the presence of bacterial meningitis from other infections. Eight patients had prior CSF drainage procedures, including ventriculostomy (n=5) or lumbar drain (n=5) placements; two patients received both procedures. Six of 13 patients developed their CSF infection within 24 hours of lumbar drain insertion. Six of 13 patients developed meningitis while receiving antibiotics for other reasons. CONCLUSIONS: External lumbar drainage seems to carry a low risk of infectious meningitis and offers a safe alternative to ventriculostomy or serial lumbar punctures. Antibiotics do not seem to protect completely against developing the infection. The infection happens most often with skin organisms. The meningitis often appears within 24 hours after lumbar drain placement. Daily CSF samples should include bacterial cultures but cell counts may not offer any additional useful information in diagnosing the complication. Lumbar drain insertion and management need not be confined to the intensive care unit.

Adult↗
PubMed2000

Role of clinical, radiological, and neurophysiological changes in predicting the outcome of tuberculous meningitis: a multivariable analysis.

OBJECTIVES: The role of EEG and evoked potentials has not been evaluated in predicting the prognosis of tuberculous (TB) meningitis. The present study was aimed at evaluating the prognostic significance of clinical, radiological, and neurophysiological variables using multi-variable analysis. METHODS: Patients with TB meningitis diagnosed on the basis of clinical, radiological, and CSF criteria have been prospectively evaluated. All the patients were subjected to a detailed neurological evaluation. The outcome was defined 6 months after starting treatment on the basis of the Barthel index (BI) score into poor (BI <12) and good recovery (BI> or =12). Death was included in the poor recovery group for statistical analysis. Thirteen clinical (age, sex, seizure, focal weakness, stage of meningitis, Glasgow coma scale score, methyl prednisolone therapy), CT (infarction, hydrocephalus, tuberculoma) and neurophysiological (EEG, motor and somatosensory evoked potentials) variables were evaluated employing single variable logistic regression followed by multivariable logistic regression analysis. The best set of predictors were obtained by stepdown logistic regression analysis. RESULTS: Fifty four patients were included in the present study. Their age ranged between 5 and 62 years, 11 were children younger than 12 years and 14 were female. Nine patients were in stage I meningitis, 12 in stage II, and 33 in stage III. On single variable logistic regression analysis the significant predictors of 6 months outcome of TB meningitis included focal weakness, Glasgow coma scale (GCS), motor evoked potential (MEP) and somatosensory evoked potential (SEP). On multivariable analysis the best set of predictors comprised focal weakness, GCS, and SEP. CONCLUSIONS: In patients with TB meningitis focal weakness, GCS, and SEP are the best predictors of 6 month outcome.

Adolescent↗
PubMed2001

Clinical presentation, natural history, and cumulative death rates of 230 adults with primary cryptococcal meningitis in Zambian AIDS patients treated under local conditions.

SETTING: Inpatient medical wards, Department of Medicine, University Teaching Hospital, Lusaka, Zambia. OBJECTIVE: To define the natural history, clinical presentation, and management outcome of microbiologically confirmed cryptococcal meningitis in adult AIDS patients treated under local conditions where antifungal and antiretroviral therapies are not routinely available. DESIGN: A descriptive, longitudinal, observational study. METHODS: All adult patients admitted to the medical wards of the University Teaching Hospital, Lusaka, Zambia with cerebrospinal fluid culture proved, primary cryptococcal meningitis, during a 12 month period were enrolled into the study. The following details were acquired: clinical features, HIV status, laboratory data, treatment accorded, and survival. RESULTS: A total of 230 patients with primary cryptococcal meningitis were studied (median age 32 years; range 15-65 years; 112 males, 118 females). Cryptococcal meningitis was the first AIDS defining illness in 210 (91%) patients. One hundred and thirty of the 230 (56%) patients had received treatment with fluconazole monotherapy and 100 (43%) patients received palliative care only without any antifungal therapy. A 100% case fatality rate was observed in both groups at follow up: by seven weeks in the untreated group and at six months in the fluconazole treated group. The cumulative median survival from time of diagnosis was 19 days (range 1-164 days) for the fluconazole treated group and 10 days (range 0-42 days) for the untreated group. CONCLUSION: Cryptococcal meningitis, under current treatment accorded at the University Teaching Hospital, Lusaka, has a 100% mortality in young Zambian adults with AIDS. The current treatment accorded to Zambian adults with cryptococcal meningitis is inappropriate. An urgent need exists to improve strategies for the clinical management of AIDS patients in poor African countries. The wider ethical and operational issues of making available antifungals to African AIDS patients are discussed.

AIDS-Related Opportunistic Infections↗
PubMed2005

[Postsurgery meningitis by Staphylococcus aureus: comparison between methicillin-sensitive and resistant strains].

BACKGROUND AND OBJECTIVE: In recent years, meningitis caused by methicillin-resistant S. aureus has increased. This study was undertaken to compare the clinical characteristics and prognosis of methicillin-resistant S. aureus (MRSA) postneurosurgical meningitis and methicillin-sensible S. aureus (MSSA) postneurosurgical meningitis. PATIENTS AND METHODS: Twenty-five episodes of postneurosurgical meningitis due to S. aureus (13 methicillin-resistant strains) seen during a ten-year period were retrospectively reviewed. RESULTS: Most common underlying diseases were: intracerebral hemorrhage (50% of MRSA patients and 46% of MSSA patients) and neoplasm (53% of MRSA patients and 33% of MSSA patients). Eleven patients (6 of them with MRSA infection) had received antibiotic treatment previously. Thirteen patients were carriers of intraventricular catheters (8 with MRSA infection), 5 wore a ventriculoperitoneal shunt (4 with infections by MSSA), 5 cases had a CSF leakage (4 with infections by MRSA), and one patient with infection by MSSA wore an epidural catheter. Fifteen patients were cured (7 with MRSA infection), and 8 died due to the infection (27% with MSSA infection and 38% with MRSA infection). CONCLUSIONS: The prognosis of postneurosurgical meningitis by S. aureus does not depend on the presence of resistance to methicillin. Nowadays, the intravenous administration of vancomycin is the treatment of choice in MRSA meningitis.

Cross Infection↗
PubMed1977

A study of the levels of fosfomycin in the cerebrospinal fluid in adult meningitis.

In order to determine the liquor concentration of fosfomycin, we chose 27 patients who were suffering from meningitis with different etiology. According to route, type of administration and doses employed, we classified the patients into five groups. Blood samples were taken from the patients 1 h after concluding the administration of the antibiotic and 2 h after the CSF sample. The concentration of fosfomycin in the serum and the CSF were then determined in the laboratory. In order to evaluate the results we divided our cases into three groups according to the state of their meningeal inflammation. In the first group of patients with active meningitis, we obtained an average concentration of fosfomycin in the serum of 65.20 mug/ml and in the CSF of 10.88 mug/ml. In the second group of patients with meningitis in the remission stage, the concentration of fosfomycin in the serum was 83.58 mug/ml and in the CSF it was 9.63 mug/ml. In the third group of patients with their meningitis cured, the concentration of fosfomycin in the serum was 66.45 mug/ml and in the CSF it was 4.95 mug/ml. On the basis of the concentrations obtained and with regard to the sensitivity in vitro, we concluded that fosfomycin can be useful in the treatment of meningitis caused by Pneumococcus, Staphylococcus, E. coli and other gram-negative bacilli.

Administration, Oral↗