Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Etiologic agents of meningitis were prospectively investigated among patients admitted to Usman Danfodio University Teaching Hospital, Sokoto. Of 1097 cerebrospinal fluid (CSF) samples submitted to the microbiology laboratory from various wards of the hospital, 289 (26%) were microscopically, culturally and/or serologically proven to be bacterial meningitis. The etiologic spectrum was as follows: Neisseria meningitidis (61%), Streptococcus pneumoniae (18%), Haemophilus influenzae (10%), Staphylococcus aureus (6%), Coliform bacilli (3%), Escherichia coli (0.7%), Mycobacterium tuberculosis (0.7%), Listeria monocytogenes (0.4%), Flavobacterium meningosepticum (0.4%) and Pseudomonas putrifasciens (0.4%). Bacterial meningitis was most prevalent (195 or 68%) among children aged 1-9 y, while adults and neonates were least affected. Coliform bacilli caused five of eight neonatal cases. Males were more frequently affected than females (chi2 = 12.50; p < 0.05). Culture and microscopy were comparatively less efficient than the search for bacterial antigens, especially in the diagnosis of Haemophilus meningitis. Antimicrobial susceptibility of N. meningitidis to ampicillin and benzyl penicillin reduced progressively over the years (F = 406.98; p < 0.001). Nineteen (11%) of the isolates (5 Meningococci, 7 Staph. aureus, 1 Haem. influenza and 6 others) showed simultaneous resistance to chloramphenicol, ampicillin and benzyl penicillin.
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PMID:Etiologic spectrum and pattern of antimicrobial drug susceptibility in bacterial meningitis in Sokoto, Nigeria. 1097 35

Tuberculous meningitis is characterized by cerebral tissue destruction. Monocytes, pivotal in immune responses to Mycobacterium tuberculosis, secrete matrix metalloproteinase-9 (MMP-9), which facilitates leukocyte migration across the blood-brain barrier, but may cause cerebral injury. In vitro, human monocytic (THP-1) cells infected by live, virulent M. tuberculosis secreted MMP-9 in a dose-dependent manner. At 24 h, MMP-9 concentrations increased 10-fold to 239 +/- 75 ng/ml (p = 0.001 vs controls). MMP-9 mRNA became detectable at 24--48 h. In contrast, tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) gene expression and secretion were similar to constitutive levels from controls at 24 h and increased just 5-fold by 48 h. In vivo investigation revealed MMP-9 concentration per leukocyte in cerebrospinal fluid (CSF) from tuberculous meningitis patients (n = 23; median (range), 3.19 (0.19--31.00) ng/ml/cell) to be higher than that in bacterial (n = 12; 0.23 (0.01--18.37) ng/ml/cell) or viral meningitis (n = 20; 0.20 (0.04--31.00) ng/ml/cell; p < 0.01). TIMP-1, which was constitutively secreted into CSF, was not elevated in tuberculous compared with bacterial meningitis or controls. Thus, a phenotype in which MMP-9 activity is relatively unrestricted by TIMP-1 developed both in vitro and in vivo. This is functionally significant, since MMP-9 concentrations per CSF leukocyte (but not TIMP-1 concentrations) were elevated in fatal tuberculous meningitis and in patients with signs of cerebral tissue damage (unconsciousness, confusion, or neurological deficit; p < 0.05). However, MMP-9 activity was unrelated to the severity of systemic illness. In summary, M. tuberculosis-infected monocytic cells develop a matrix-degrading phenotype, which was observed in vivo and relates to clinical signs reflecting cerebral injury in tuberculous meningitis.
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PMID:Identification of a matrix-degrading phenotype in human tuberculosis in vitro and in vivo. 1123 75

This is Part II of a 2-part paper on fever of unknown origin (FUO) in children. It examines the aetiology and management of prolonged FUO in children and the difficulties in the management of FUO in children in developing countries. Part I of this paper discussed acute FUO in children and was published in the March 2001 issue of Paediatric Drugs. Prolonged FUO is documented fever of more than 7 to 10 days which has no apparent source and no apparent diagnosis after 1 week of clinical investigations. About 34% of cases of prolonged FUO are caused by infections, with bacterial meningitis and urinary tract infection accounting for about 6.5 and 11.4%, respectively, of cases attributable to infections. Chronic infections, particularly tuberculosis and 'old' disorders such as Kawasaki disease, cat-scratch disease and Epstein-Barr virus infection presenting with 'new' manifestations, collagen-vascular diseases and neoplastic disorders are the other issues of major concern in prolonged FUO. Overall, however, there is a trend towards an increased number of undiagnosed cases. This is due to advancements in diagnostic techniques, such that illnesses which were previously common among the causes of prolonged FUO are now diagnosed earlier, before the presentation becomes that of prolonged FUO. Clinical examination supplemented with laboratory tests to screen for serious bacterial infections should be the mainstay of initial evaluation of children with prolonged FUO. Use of scanning techniques (such as computerised tomography and ultrasound) as additional supplements to this clinical examination may allow for the earlier diagnosis of causes of prolonged FUO in children such as 'occult' abdominal tumours. A common error in management of children with prolonged FUO is the failure to perform a complete history and physical examination; repeated clinical examination and continued observation are of paramount importance in the diagnosis of difficult cases. Major difficulties in the management of FUO in children in developing countries include constraints in the availability and reliability of laboratory tests, cost, misuse of antibiotics and difficulties encountered in the diagnosis of malaria and typhoid fever. Malaria and typhoid fever are major aetiological considerations in both acute and prolonged FUO in children in developing countries. The newer quinolones may hold great promise for the treatment of serious bacterial infections, including meningitis, which are associated with prolonged FUO in developing countries.
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PMID:Management of children with prolonged fever of unknown origin and difficulties in the management of fever of unknown origin in children in developing countries. 1135 97

The diagnostic approach to the compromised host with CNS infection depends on an analysis of the patient's clinical manifestations of CNS disease, the acuteness or subacuteness of the clinical presentation, and an analysis of the type of immune defect compromising the patient's host defenses. Most patients with CNS infections may be grouped into those with meningeal signs, or those with mass lesions. Other common manifestations of CNS infection include encephalopathy, seizures, or a stroke-like presentation. Most pathogens have a predictable clinical presentation that differs from that of the normal host. CNS Aspergillus infections present either as mass lesions (e.g., brain abscess), or as cerebral infarcts, but rarely as meningitis. Cryptococcus neoformans, in contrast, usually presents as a meningitis but not as a cerebral mass lesion even when cryptococcal elements are present. Aspergillus and Cryptococcus CNS infections are manifestations of impaired host defenses, and rarely occur in immunocompetent hosts. In contrast, the clinical presentation of Nocardia infections in the CNS is the same in normal and compromised hosts, although more frequent in compromised hosts. The acuteness of the clinical presentation coupled with the CNS symptomatology further adds to limit differential diagnostic possibilities. Excluding stroke-like presentations, CNS mass lesions tend to present subacutely or chronically. Meningitis and encephalitis tend to present more acutely, which is of some assistance in limiting differential diagnostic possibilities. The analysis of the type of immune defect predicts the range of possible pathogens likely to be responsible for the patient's CNS signs and symptoms. Patients with diseases and disorders that decrease B-lymphocyte function are particularly susceptible to meningitis caused by encapsulated bacterial pathogens. The presentation of bacterial meningitis is essentially the same in normal and compromised hosts with impaired B-lymphocyte immunity. Compromised hosts with impaired T-lymphocyte or macrophage function are prone to develop CNS infections caused by intracellular pathogens. The most common intracellular pathogens are the fungi, particularly Aspergillus, other bacteria (e.g., Nocardia), viruses (i.e., HSV, JC, CMV, HHV-6), and parasites (e.g., T. gondii). The clinical syndromic approach is most accurate when combining the rapidity of clinical presentation and the expression of CNS infection with the defect in host defenses. The presence of extra-CNS sites of involvement also may be helpful in the diagnosis. A patient with impaired cellular immunity with mass lesions in the lungs and brain that have appeared subacutely or chronically should suggest Nocardia or Aspergillus rather than cryptococcosis or toxoplasmosis. Patients with T-lymphocyte defects presenting with meningitis generally have meningitis caused by Listeria or Cryptococcus rather than toxoplasmosis or CMV infection. The disorders that impair host defenses, and the therapeutic modalities used to treat these disorders, may have CNS manifestations that mimic infections of the CNS clinically. Clinicians must be ever vigilant to rule out the mimics of CNS infections caused by noninfectious etiologies. Although the syndromic approach is useful in limiting diagnostic possibilities, a specific diagnosis still is essential in compromised hosts in order to describe effective therapy. Bacterial meningitis, cryptococcal meningitis, and tuberculosis easily are diagnosed accurately from stain, culture, or serology of the CSF. In contrast, patients with CNS mass lesions usually require a tissue biopsy to arrive at a specific etiologic diagnosis. In a compromised host with impaired cellular immunity in which the differential diagnosis of a CNS mass lesion is between TB, lymphoma, and toxoplasmosis, a trial of empiric therapy is warranted. Antitoxoplasmosis therapy may be initiated empirically and usually results in clinical improvement after 2 to 3 weeks of therapy. The nonresponse to antitoxoplasmosis therapy in such a patient would warrant an empiric trial of antituberculous therapy. Lack of response to anti-Toxoplasma and antituberculous therapy should suggest a noninfectious etiology (e.g., CNS lymphoma). Fortunately, most infections in compromised hosts are similar in their clinical presentation to those in the normal host, particularly in the case of meningitis. The compromised host is different than the normal host in the distribution of pathogens, which is determined by the nature of the host defense defect. In compromised hosts, differential diagnostic possibilities are more extensive and the likelihood of noninfectious explanations for CNS symptomatology is greater. (ABSTRACT TRUNCATED)
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PMID:Central nervous system infections in the compromised host: a diagnostic approach. 1144 10

The laboratory diagnosis of CNS infection is essential for optimal therapy. Acute infection requires rapid turn-around testing with high predictive values, that is, the ability of a test to accurately identify those patients who do or do not have disease caused by a specific etiology. The Gram's stain, fungal stains of direct smears, antigen testing for C. neoformans, and culture of bacteria, fungi, mycobacteria, and some viruses are important tests for the diagnosis of acute infection. The laboratory diagnosis of chronic infection necessitates discussion between the clinician and laboratory technician to allow triaging of testing. Antigen tests for bacteria, fungi, and viruses; antibody tests for multiple microorganisms; and PCR testing for bacteria, M. tuberculosis, and many viruses are all important in limited clinical situations. All testing for acute or chronic disease depends on sufficient specimen that is transported to the laboratory in a manner that will not compromise viability or chemical integrity. Sterile containers that maintain moisture content, exclude oxygen for anaerobic requests, and are stored at proper temperatures (22 degrees C room, 4 degrees C refrigeration, or -20 degrees C freezer depending on pathogen and test) are mandatory. Many laboratory issues addressing the diagnosis of CNS infection are changing or evolving. Most important is the recognition that bacterial antigen testing for the diagnosis of acute bacterial meningitis rarely impacts patient management and is not routinely needed, CSF shunt infections differ from usual meningeal infections and require rapid diagnosis, and TB meningitis remains a difficult disease to diagnosis but may be confirmed first by PCR testing of CSF. In addition, Whipple's disease of the CNS can be confirmed using PCR with CSF; CJD has a marker protein, referred to as 14-3-3 antigen, that can be detected in CSF, and the diagnosis of fungal CNS disease requires careful interpretation of direct smears, antigen and antibody testing, and culture. Most difficult to diagnose among the CNS infections are viral meningitis and encephalitis. The appearance of new etiologies, such as West Nile virus, and the common use of PCR for the herpes viruses and enteroviruses represent important advances. Evolving methods for the laboratory diagnosis of CNS infection represent significant improvements over previous testing; however, the array of tests available demands more attention for appropriate selection, is significantly more expensive, and requires new skills for performance and interpretation. The responsibility for proper use of laboratory testing lies both with the clinician and laboratory technician.
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PMID:Laboratory diagnosis of central nervous system infections. 1178 Feb 67

OBJECTIVE: To evaluate the feasibility of using 16S rDNA universal primer PCR (followed by sequencing) and 65-kDa heat shock Mycobacterium tuberculosis protein gene PCR as a method to determine a bacterial etiology in culture---negative cerebrospinal fluid (CSF) samples. METHODS: One hundred and forty-nine CSF samples from 128 patients were processed. DNA was extracted from the CSF samples and amplified with the eubacterial 16S rDNA primers P11E and P13B, and with the 65-kDa heat shock protein gene mycobacterial primers. The amplicons were identified by sequencing and specific oligoprobe hybridization. RESULTS: Overall, a microbiological diagnosis was made in 11 of 125 ultimately culture-negative cases. The use of 65-kDa heat shock protein gene PCR was needed to improve the diagnosis of tuberculous meningitis; in four patients, prospectively studied, the outcome of antituberculous therapy could also be followed. CONCLUSIONS: In culture-negative bacterial meningitis it is possible to improve the microbiological diagnosis by use of 16S rDNA amplification and sequencing, together with amplification of a more specific gene in mycobacteria.
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PMID:Polymerase chain reaction, with sequencing, as a diagnostic tool in culture---negative bacterial meningitis. 1185 24

The role of infectious and inflammatory causes of stroke is much more significant in children than in adults. Conversely, that of atherosclerotic disease, ischaemic heart disease and hypertensive haemorrhages has a lesser prominence in children. Bacterial meningitis caused by Streptococcus pneumoniae, Haemophilus influenzae, or Neiserria meningitidis has been known to cause stroke in children. The mechanism appears to be the spread of meningeal inflammation to involve the walls of intracranial vessels, resulting in arterial thrombosis with ischaemia or rupture with haemorrhage. Other infections caused by atypical bacterial agents such as Mycoplasma tuberculosis and viral agents such as varicella-zoster virus have also been well documented as causes of stroke. Non-infectious, inflammatory causes of stroke, such as collagen vascular disease and primary angiitis of the central nervous system, have been reported in children as well as adults. In this review, we will focus on recent advances in the field of childhood stroke caused by infectious and inflammatory disorders.
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PMID:Infectious and inflammatory disorders of the circulatory system and stroke in childhood. 1192 29

A retrospective review of autopsy findings and medical records in 33 HIV-infected children living in a Kenyan orphanage is described. Their ages ranged from 1 month to 18 years and median age at death was 71 months (range 7-156). Respiratory disorders were probably the primary cause of death in 21 (64%), in 19 (90%) of whom pyogenic parenchymal lung disease was detected. A presumptive clinical diagnosis of pulmonary tuberculosis had been made in 14 (67%); these children also had a history of recurrent acute lower respiratory tract infections (more than four infections/year). At autopsy, however, only one case of tuberculosis was identified (disseminated disease). Pneumocystis carinii pneumonia was not identified. Primary bacterial meningitis was detected in 33%. The associated findings included disseminated Kaposi sarcoma in two children and cryptococcal meningitis in one child. It is concluded that pyogenic infections are common causes of morbidity and mortality in HIV-1-infected African children. Management should include prompt treatment and, if indicated, prophylaxis for recurrent bacterial infections, and early evaluation and treatment of pulmonary tuberculosis.
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PMID:The post-mortem pathology of HIV-1-infected African children. 1207 Sep 47

Throughout the history of mankind, infectious diseases have remained a major cause of death and disability. Although industrialized nations, such as the United States, have experienced significant reductions in infection-related mortality and morbidity since the beginning of the "antibiotic era," death and complications from infectious diseases remain a serious problem for older persons. Pneumonia is the major infection-related cause of death in older persons, and urinary tract infection is the most common bacterial infection seen in geriatric patients. Other serious and common infections in older people include intra-abdominal sepsis, bacterial meningitis, infective endocarditis, infected pressure ulcers, septic arthritis, tuberculosis, and herpes zoster. As a consequence, frequent prescribing of antibiotics for older patients is common practice. The large volume of antibiotics prescribed has contributed to the emergence of highly resistant pathogens among geriatric patients, including methicillin-resistant Staphylococcus aureus, penicillin-resistant Streptococcus pneumoniae, vancomycin-resistant enterococci, and multiple-drug-resistant gram-negative bacilli. Unless preventive strategies coupled with newer drug development are established soon, eventually clinicians will be encountering infections caused by highly resistant pathogens for which no effective antibiotics will be available. Clinicians could then be experiencing the same frustrations of not being able to treat infections effectively as were seen in the "pre-antibiotic era."
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PMID:Antimicrobial resistance and aging: beginning of the end of the antibiotic era? 1212 17

An obstetrician examined records of all maternal deaths that occurred in the Chatinkha Maternity Wing of Queen Elizabeth Central Hospital in Blantyre, Malawi, during 1989-1990. None of the deaths were caused by conditions unrelated to pregnancy. In 1989 there were 78 maternal deaths out of 14,272 live births (a maternal mortality ratio of 546/100,000 live births). In 1990 there were 73 maternal deaths out of 14,281 live births (a maternal mortality ratio of 511/100,000 live births). In each year, 37 women died directly from complications of pregnancy, delivery, or their management. In 1989, the leading cause of maternal death was postabortal sepsis (15 cases), followed by obstructed labor (8 cases) and puerperal sepsis (6 cases). In 1990, the leading causes were puerperal sepsis (13 cases) and postabortal sepsis (10 cases). The number of HIV-seropositive women among direct maternal deaths was 8 for both years. In 1990, the cesarean section rate was 6.5%. Women who had undergone a cesarean section faced a risk of puerperal sepsis-related death 8.5 times greater than that of women who had delivered vaginally. The 1990 mortality rate among induced abortion cases may have been as high as 8%. There were 41 and 36 indirect maternal deaths in 1989 and 1990, respectively. The leading causes of indirect maternal death were fever (8 cases) and bacterial meningitis (5 cases). The cause could not be determined in 15 cases. By 1990, the leading causes of indirect maternal death were bacterial meningitis (8 cases) and AIDS (6 cases). 5 of the 8 bacterial meningitis cases tested positive for HIV. The 4 patients with tuberculosis and 3 patients with septicemia were HIV positive. 41% and 56% of maternal deaths in 1989 and 1990, respectively, were avoidable. When one excluded uncertain avoidable factors, 21% and 45% of maternal deaths could not be avoided. The leading avoidable factors were deficient hospital care (18 cases), patient's delay (12 cases), and illegal abortion (10 cases) in 1989; they were patient's delay (10 cases) and illegal abortion (8 cases) in 1990.
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PMID:Maternal mortality at Queen Elizabeth Central Hospital, 1989 to 1990. 1231 71


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