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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many kinds of microorganisms can produce toxic septicemia in immunocompromised hosts. We are reporting alpha-hemolytic streptococcal septicemia and meningitis in two children with hematological malignancies. [Case 1] 6 year old girl who had been suffering from acute lymphocytic leukemia. She had sepsis and bacterial meningitis in maintenance-therapy for leukemia. Streptococcus sanguis was isolated from the blood and cerebrospinal fluid (CSF). [Case 2] 11 year old girl who had had malignant lymphoma (non-Hodgkin type). She also had sepsis and bacterial meningitis due to Streptococcus mitis which was isolated from blood and CSF in maintenance-therapy. Both cases had been treated with anti-cancer drugs and had severe granulocytopenia. Positive rate of blood cultures during the recent 6 years (1984.1-1989.12) at our department was 6.0% (total number of cultures were 2,019, positive cultures were 121). Strains of 131 bacteria were determined; Gram-positive cocci were 70 strains (53.4%) and Gram-negative rods were 52 strains (39.7%). Fifteen strains (11.5%) of alpha-hemolytic Streptococci were isolated during 6 years. One hundred thirteen cases of septicemia were analysed in medical charts and 12 cases of alpha-hemolytic streptococcal septicemia were observed (5 cases with infective endocarditis and 7 cases in immunocompromised states).
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PMID:[Alpha-hemolytic streptococcal septicemia and meningitis in immunocompromised children]. 191 21

In view of the significant and articulate minority view among pediatricians that breast feeding is not "worth the bother" in developed countries, this review of the literature delves into the evidence from both developed and developing countries for the advantages of breastfeeding, both in infants and for long-term health. Infants in developed settings experience twice the hospitalization rate and more severe illness from lower respiratory tract infection, primarily respiratory syncytial virus. In developing countries the mortality risk is 4-fold. for otitis media, the relative risks were 3.3-4.3 for Finnish infants. Bacterial meningitis and/or bacteremia had a 4-fold risk for hospitalization in a Connecticut study, and a 3-fold relative risk in 2 developing country studies. Human milk was the best preventative for bacteremia and necrotizing enterocolitis in prematures in British neonatal units. A 20-fold reduction in neonatal deaths occurred in Philippine study of breastfeeding, especially in low birth weight babies. Diarrhea causes the most infant mortality in developing nations, where bottle-feeding raises rates 14-fold. In the U.S. estimated relative risks is 3.7 for diarrheal mortality. Sudden infant death is about 1/5 less common in U.S. breast fed babies than in bottle fed. There is evidence for better long-term health after breast feeding in disorders such as celiac disease, Crohn disease, ulcerative colitis, insulin-dependent diabetes mellitus, thyroid disease, malignant lymphoma, chronic liver disease, atopic dermatitis, and food allergies. The design of good studies of protection conferred by breast feeding, and the possible modes of action of breast milk are discussed.
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PMID:Breast-feeding and health in the 1980s: a global epidemiologic review. 194 1

We measured the activity of adenosine deaminase (ADA) in the cerebrospinal fluid of 3 patients with tuberculous meningitis, 38 with viral meningitis, 15 with bacterial meningitis, 5 with malignant lymphoma, 11 with cerebrovascular diseases and 13 with miscellaneous neurological disorders. The highest ADA activities were observed in patients with tuberculous meningitis (median 21.3 U/l, range 20.0-23.0) and lymphoma (13.0 U/l, range 4.0-25.0). The sensitivity of the test for diagnosing tuberculous meningitis was 100% and the specificity 99% when a cut-off value of 20.0 U/l was used. We conclude that determination of ADA in cerebrospinal fluid is useful for the diagnosis of tuberculous meningitis, but that high activity also can be seen in some other CNS disorders, e.g. lymphoma with meningeal involvement.
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PMID:Diagnostic value of cerebrospinal fluid adenosine deaminase determination. 158 21

The complications associated with the use of Ommaya reservoirs in 106 patients with meningeal involvement due to malignant disease are reviewed. Twenty-seven patients had acute lymphoblastic leukemia, 12 acute myelogenous leukemia, 3 chronic lymphocytic leukemia, 34 lymphoma, 29 carcinoma, and 1 chronic myelocytic leukemia. There were 11 technical complications, including 1 death due to misplacement of the catheter, 2 mild intraventricular hemorrhages, and 5 malfunctioning reservoirs; 3 required craniotomies (1 for subdural hematoma and 2 for subdural hygroma); 13 cases of bacterial meningitis occurred in 10 patients. One patient died of Staphylococcus aureus meningitis. The organisms causing the other infections were mainly coagulase-negative staphylococci (8 cases) or Propionibacterium acnes (2 cases). The projected infection rate for all patients (by Kaplan-Meier analysis) during the first year following insertion of a reservoir was 15%. Successful use of Ommaya reservoirs requires expert surgical implantation and meticulous care during accessing to minimize complications.
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PMID:Complications associated with Ommaya reservoirs in patients with cancer. The Princess Margaret Hospital experience and a review of the literature. 240 79

Central nervous system (CNS) infections in immunocompromised hosts are often accompanied by subtle disorders because immunosuppression usually decreases the inflammatory response. CNS infections in immunocompromised patients are usually caused by organisms different from those found in the general population. The organism causing CNS infection in an immunocompromised host can often be predicted if the type of immune abnormality of the patient is known. The common causes of CNS infection in immunocompromised hosts are reviewed here. Meningitis in patients with neutropenia is usually due to enteric Gram negative bacilli that live in the patient's own digestive tract. Pseudomonas aeruginosa is most common and is followed by E. Coli, Klebsiella, Enterobacter and Proteus. A major risk in patients with abnormal immunoglobulins or splenectomy is infection with encapsulated bacteria, particularly Streptococcus pneumoniae, Haemophilus influenzae and Neisseria meningitidis. Meningitis caused by any of the encapsulated bacteria can be fulminant. Listeria monocytogenes is the most common cause of bacterial meningitis in patients with impaired cellular immunity. Nocardia asteroides is a leading cause of brain abscess in patients with hematologic malignancy. Most patients have evidence of concomitant pulmonary lesions. Fungi are among the most common organisms involving the CNS in immunocompromised hosts. Susceptible patients include those with lymphoma or leukemia and those who receive therapies aimed at suppressing delayed hypersensitivity. Cryptococcus neoformans is a common fungal cause of CNS infection in immunocompromised hosts. The primary site of infection is the lung. Spread to the CNS is via the blood stream. The clinical course is highly variable: meningitis, meningoencephalitis and focal mass lesions. Candida causes meningitis or meningoencephalitis characterized by multiple small abscesses in neutropenic hosts. Organisms reach the CNS via the blood stream usually from the digestive tract or infected intravenous catheters. Aspergillus causes brain abscess, cerebral infarction and focal meningitis in patients with neutropenia. The primary infection is in the lung. The parasites that infest the CNS of immunocompromised patients are usually those that exploit a T-lymphocyte, mononuclear phagocyte host defect. The most common are Toxoplasma gondii and Strongyloides stercoralis. There have been a few cases of amebiasis with dissemination to the brain in patients with hematologic malignancies. Toxoplasma gondii causes major CNS disease in immunocompromised hosts: meningoencephalitis or mass lesions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Infections of the central nervous system in malignant hemopathies]. 372 88

The elevation of ADA in CSF is useful as a diagnostic means for detecting tuberculous meningitis, and in other etiologies such as lymphoma, neurosarcoidosis, fulminant bacterial meningitis, cryptococcal meningitis, neurobrucellosis and AIDS. We report an increase of ADA in CSF in association with SHA. In our case the total activity of ADA was the same as that obtained in serum, which can be interpreted among the false positives of the determination.
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PMID:False positive of ADA determination in cerebrospinal fluid. 770

A 60-year-old man presented with progressive and unique neurological symptoms. Investigations identified an isolated cerebellar lesion. This lesion fulfilled the histological criteria for lymphomatoid granulomatosis, and in situ hybridization and deoxyribonucleic acid (DNA) dot blot techniques revealed significant amounts of Epstein-Barr virus DNA within the tumor cells. The patient underwent cranial radiation therapy, and 16 months after the initial presentation the lesion evolved into a malignant lymphoma. He subsequently died secondary to subdural empyema, bacterial meningitis, and bronchopneumonia. The unique clinical and etiological aspects of this case are addressed.
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PMID:Isolated cerebellar lymphomatoid granulomatosis progressing to malignant lymphoma. Case report. 828 71

The value of DNA single-cell cytometry for the detection of neoplasia in Feulgen-stained cerebrospinal fluid cytological specimens was tested on 34 cases of Non-Hodgkin's lymphoma or leukemia and on 66 cases of viral or bacterial meningitis as a disease control group. The DNA content of 200 randomly chosen nuclei was measured on one pre-existing, cytologically representative slide per case, using a TV-image analysis system TAS-plus (Leitz, Germany). Neoplasia was diagnosed, if at least three nuclei with a DNA content above 5c (5cEE > or = 3) were found. The sensitivity investigating only one slide per case was 79.4% (27/34), the specificity 78.8% (52/66). Three lymphomas and 7 inflammatory cases were classified as suspicious (0 < 5cEE < 3). In 4 lymphoma cases (11.8%) a false-negative diagnosis and in 7 cases (10.6%) of viral meningitis a false-positive diagnosis were made. No false-positive diagnosis occurred in bacterial meningitis. While the false-negative diagnoses may be due to the only slightly increased number of cells in cerebrospinal fluid, no final explanation for increased DNA values after viral infection can be given. Therefore, before using DNA single-cell cytometry to prove the malignant character of lymphocytic pleocytosis in cerebrospinal fluid, viral meningitis has to be clinically excluded.
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PMID:DNA single cell cytometry in lymphocytic pleocytosis of the cerebrospinal fluid. 831 Jul 92

We report a 64-year-old Japanese woman who died one year after the onset of progressive gait disturbance and dementia. She noted a difficulty in holding a glass and hand tremor in June of 1996 when she was 63 years old. In July of 1996, she tended to lean toward left when she walked. She also noted truncal titubation. In November of 1996, she started to have visual hallucination and delusion in which she said "I see something is flying on the wall.", "Somebody has come into my room", and things like that. She was admitted to our service on November 22, 1996. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed disturbance in recent memory. Hasegawa's dementia rating scale was 22/30. She showed vivid visual hallucination with colors in which she saw faces of dwarfs and angels, a space ship, and others. Higher cerebral functions were normal. She showed left oculomotor palsy which was a sequel of an aneurysm and subarachnoid hemorrhage nine years before. Otherwise cranial nerves were unremarkable. She showed ataxic gait, limb ataxia, truncal titubation, and postural hand tremor. She had no weakness and no muscle atrophy. Deep tendon reflexes were within normal limits. Plantar response was flexor. Sensation was intact. Laboratory examination was also unremarkable. Complete survey for occult malignancy was negative. CSF was under a normal pressure and cell count was 1/microliter, total protein 27 mg/dl, and sugar 68 mg/dl. Cranial CT scan was unremarkable. MRI was not obtained because of the presence of an aneurysm clip in the left internal carotid-posterior communication artery junction. She showed progressive deterioration in her mental function. By January 1997, she became unable to stand or walk with marked dementia. Repeated CSF exams and cranial CT scans were unremarkable. She suffered from several episodes of aspiration pneumonia. A trial of three days methylprednisolone pulse therapy was given starting on March 7, 1997, which was of no effect on her neurologic status. On March 28, 1997, she was intubated because of acute respiratory distress syndrome. In April 2, her body temperature rose to 38 degrees C. On April 9, 1997, her blood pressure dropped and resuscitation was unsuccessful. She was pronounced dead on the same day. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had primary leptomeningeal lymphoma. Other possibilities entertained among the audience included brain stem encephalitis of unknown type, carcinomatous cerebellar degeneration plus limbic encephalitis, Creutzfeldt-Jakob disease, thalamic degeneration, and progressive multifocal leukoencephalopathy. Post-mortem examination revealed thickening and clouding of the leptomeninges; Gram-positive diplococci were found in the leptomeninges. This meningitis appeared to have been an complication in the terminal stage of her illness. Microscopic examination revealed astrocytosis in the midbrain tegmentum. Cerebral cortices showed only mild astrtocytosis. No cerebellar atrophy was seen and Purkinje cells were retained which excluded paraneoplastic cerebellar degeneration. Neuropathologic diagnosis was bacterial meningitis, however, the presence of brain stem encephalitis prior to the onset of bacterial meningitis could not be excluded. It is interesting to note that the diagnosis of the primary neurologic disease of this patient was not easy even after autopsy. As autopsy permission was obtained only for the brain, it was not clear whether or not this patient had an occult malignancy somewhere in her body, however, there was no evidence to indicate paraneoplastic degeneration of the central nervous system. As the patient did not have meningeal signs until one month before her death, it is difficult to ascribe her entire neurologic problems to her meningitis. Finally, her visual hallucination was vivid and colorful; we thought this might have been
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PMID:[A 64-year-old woman with progressive gait disturbance and dementia for one year]. 978 11

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


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