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At least 19 recordsLinked to original sources
PubMed1977

Meningoencephalitis due to Acanthamoeba SP. Pathogenesis and clinico-pathological study.

Amebic Meningoencephalitis (AM) and Primary Amebic Meningoencephalitis (PAM) are infectious diseases essentially confined to the Central Nervous System (CNS) and caused by free-living amebas of the genus Acanthamoeba (A.) and Naegleria (N.) respectively. AM due to A. sp. (Acanthamoeba castellanii and Acanthamoeba culbertsoni) have been reported in chronically ill debilitated individuals, some of them under immunosuppressive therapy, or in immunologically impaired patients without a history of recent swimming in contrast to cases due to N. sp. which usually occurs in healthy, young individuals with a recent history of swimming in man-made lakes or heated swimming pools. AM due to A.sp. is characterized by a subacute or chronic granulomatous meningoencephalitis involving mainly the midbrain, basal areas of the temporal and occipital lobes and posterior fossa structures. CNS lesions in AM are perhaps secondary and the portal of entry in humans is probably from the lower respiratory tract, genitourinary system or skin reaching the CNS by hematogenous spread. The predominant host reaction is usually composed of lymphocytes, plasma cells, monocytes and multinucleated foreign body giant cells. Necrosis is moderate and hemorrhage scant or absent. Cysts as well as trophozoites may be seen within the CNS lesions. PAM is due to Naegleria fowleri and is characterized by an hemorrhagic necrotizing meningoencephalities with an acute inflammatory response. Only trophozoites are found in lesions. The portal of entry is through the olfactory neuroepithelium. CNS tissues fixed in formalin may be used for further identification and taxonomical classification of the causative protoza using immunofluorescent antibody techniques (IFAT) and electron microscopic methods.

Amebiasis↗
PubMed1978

Primary amoebic meningoencephalitis.

As a serendipitous by-product of polio virus research, a highly fatal amoebic meningoencephalitis was recognized in animals. The causative microorganisms, contaminants of the viral cultures, were identified as small soil amoebae. These organisms, previously considered non-pathogenic, are prevalent throughout the world. Based on animal studies, the original investigators suggested the possibility of a similar disease in humans. Seven years later, human cases of amoebic meningoencephalitis were reported from widely separated areas of the world. Since 1965, a total of 79 cases have been reported. The literature of primary amoebic meningoencephalitis is presented. The history of the discovery and elucidation of this disease is reviewed. The 79 cases reported in the world literature are divided into two groups, those diagnosed retrospectively after reviewing previous deaths from meningoencephalitis, and those diagnosed at the time of the illness. The classification, morphology, pathogenicity, virulence and distribution of pathogenic soil amoebae are reviewed. The presenting clinical findings, diagnostic procedures, pathology, and management of this recently recognized, highly fatal, human disease is presented along with a report of a new case. Otolaryngologists should become familiar with this serious disorder with a transnasal portal of entry.

Amebiasis↗
PubMed1976

Herpesvirus hominis type 2 meningoencephalitis following renal transplantation.

Herpesvirus hominis (HVH) type 2 meningoencephalitis, confirmed by isolation of the virus from cerebrospinal fluid and brain biopsy specimens, is described in a 44 year old man following renal transplantation. An HVH type 2 genital infection developed two weeks after renal transplantation, which was followed by meningoencephalitis 10 days later. Subsequently an intracerebral hemorrhage developed with evidence of diffuse vasculitis on arteriography. In a second transplant patient a similar clinical syndrome also developed after an HVH type 2 genital infection, but viral studies were not made to confirm the etiology of the meningoencephalitis. HVH has been recognized as a cause ot mucocutaneous diseases in recipients of renal transplants, but involvement of the central nervous system has not been reported.

Adult↗
PubMed1975

A case of hartmannellid amebic meningoencephalitis in Zambia.

A case of amebic meningoencephalitis recognized in an adult Zambian is described. This is the first authenticated case from Africa. The morphologic features of the organism, its ability to form cysts in tissue, and the granulomatous tissue response denote that the ameba is an hartmannellid rather than a Naegleria. Free-living amebas of the family Hartmannellidae have not been incriminated before as a cause of primary amebic meningoencephalitis in man. To our knowledge this is the only case where such an ameba was responsible for fulminating meningoencephalitis. The presence of the amebas in a cellulocutaneous abdominal lesion suggests hematogenous dissemination.

Amebiasis↗
PubMed1978

Viral meningoencephalitis and head injury.

Among 162 children referred with head injury (in a 3-year period) a viral meningoencephalitis was proven to be present in seven cases. Only one patient showed symptoms of infection before the accident. On admission classical signs of viral meningoencephalitis were absent or mixed with the complications of head injury. A diagnosis of viral meningitis/meningoencephalitis was documented by immunofluorescent demonstration of viral antigens in CSF cells and/or pattern of CSF cytology and/or conventional serological methods. Whether the trauma and the infection are coincidental or causally related can not be decided definitively. A hypothesis is presented suggesting diminished alertness in subclinical viral meningoencephalitis, leading to accident proneness.

Antigens, Viral↗
PubMed1979

Sensitivity of radionuclide brain scan and computed tomography in early detection of viral meningoencephalitis.

The sensitivity of radionuclide imaging and computed tomography (CT) was evaluated in 25 patients for early detection of viral meningoencephalitis. Diagnosis was based on clinical evidence, cerebrospinal fluid (CSF) studies, electroencephalography (EEG) and radionuclide imaging. Computed tomography with contrast enhancement was performed within four days after onset of neurological signs or symptoms in 23 patients; no significant findings such as low-absorption abnormalities, mass effect or abnormal enhancement were seen. Radionuclide imaging demonstrated a sensitivity of 90% in the detection of viral meningoencephalitis; the temporal lobe was most commonly involved in patients with herpes encephalitis. Radionuclide imaging should be considered as the first diagnostic procedure in suspected early viral meningoencephalitis.

Adolescent↗
PubMed1975

A comparative study of meningoencephalitis epidemics caused by echovirus type 7 and coxsackievirus type B5. Clinical and virological observations during two epidemics in northern Sweden.

Two epidemics of meningoencephalitis caused by echovirus type 7 and coxsackievirus type B 5 in the summer and autumn of 1973 in Umeå in Northern Sweden were compared. Most patients with echovirus 7 meningoencephalitis were neck stiff and 50% had a polymorphonuclear pleocytosis in the cerebrospinal fluid (CSF). The illness was usually mild. It appears to be the first time that an epidemic caused by this virus is described from Scandinavia. On the other hand most patients with coxsackievirus B 5 meningoencephalitis showed a more profound involvement of the central nervous system, with abnormal electroencephalograms in 70% and a long convalescence period. The number of cells in CSF was normal in 70% of these patients.

Adolescent↗
PubMed1979

Adenoviral meningoencephalitis in a patient with lead toxicity.

Adenovirus type 12 was recovered from the CSF of a 36-year-old woman with adenoviral meningoencephalitis and lead toxicity. The serum level of lead was 199 micrograms/dL and the CSF level was 7 micrograms/dL. After therapy with edetate disodium calcium (Calcium Disodium Versenate), she had an uneventful recovery. The possibility of exacerbation of lead poisoning with encephalopathy due to adenovirus type 12 meningoencephalitis is raised.

Acute Disease↗
PubMed1979

An unusual form of measles meningoencephalitis. A report of two cases.

Two patients are reported with a chronic progressive illness characterized by dementia, ataxia and spasticity. There were no myoclonic jerks and both had normal electroencephalograms (EEG). Pathological findings in three brain biopsies were those of viral meningoencephalitis with perivenous demyelination. Serological data in both patients indicated the presence of measles virus infection. Intracytoplasmic structures resembling measles virus nucleocapsids were found in the brain biopsy of one patient. Immunofluorescent staining showed antibody in the temporal lobe biopsy of both patients. It is suggested that these patients are examples of a chronic form of measles meningoencephalitis hitherto undescribed.

Adult↗
PubMed1979

A case of primary amebic meningoencephalitis in Zaria, Nigeria.

A case of primary amebic meningoencephalitis due to Naegleria fowleri in a Nigerian child is described. This is probably the first authentic case from West Africa. The clinical manifestations, isolation of the ameba from the cerebrospinal fluid and nasal passages, poor response to amphotericin B, and ultimate fatal outcome all are consistent with the diagnosis of primary amebic meningoencephalitis. Subsequent identification based on morphologic features, flagellation, animal pathogenicity, and nuclear division proved conclusively that the ameba was Naegleria fowleri. The route of entry of the ameba proved to be nasal. In the absence of the history of swimming and in view of the dusty harmattan period during which the child was admitted, a possibility of infection by inhalation of dust harboring amebic cysts is suggested.

Amoeba↗
PubMed1979

Micronema deletrix meningoencephalitis in an adult man.

This is apparently the second report of a case of human meningoencephalitis caused by the nematode Micronema deletrix. The patient had severe granulomatous meningoencephalitis with numerous foci of hemorrhage and encephalomalacia. Numerous adult female and larval M. deletrix were in the brain. The organisms probably inhabit decaying organic material, but occasionally parasitize the kidney, nose, or central nervous system of the horse. In its parasitic form the nematode replicates parthenogenetically.

Brain↗
PubMed1978

Persistent hypothalamic-pituitary insufficiency following acute meningoencephalitis. A report of two cases.

This report concerns two patients, a 43-year-old woman and a 53-year-old man, who developed clinical as well as laboratory signs of permanent gonodal and thyroid failure following an acute intracranial infection--in the woman a meningoencephalitis of unknown origin, and in the man an encephalitis caused by Coxsackie B5. Endocrine investigations were compatible with hypothalamic-pituitary dysfunction, with some of the results favoring a hypothalamic lesion. Perhaps hormone deficiency of hypothalamic and/or pituitary origin is a more common sequel of acute meningoencephalitis than has hitherto been reported.

Acute Disease↗
PubMed1975

Immunoglobulin synthesis in vitro by cerebrospinal fluid cells in patients with meningoencephalitis of presumed viral origin.

Cerebrospinal fluid (CSF) cells from six patients with meningoencephalitis of presumed viral origin were incubated in the presence of labeled amino acids. The cells of two of the patients synthesized IgG, IgA, and IgM (one patient) in vitro. The CSF of these two patients had an elevated level of IgG with oligoclonal distribution. The newly synthesized IgG also had an oligoclonal distribution. CSF cells of the other four patients were not shown to synthesize immunoglobulins in vitro. The CSF of these patients had a normal level of IgG with polyclonal distribution. The results demonstrate that in some patients with virus meningoencephalitis an immunoglobulin synthesis takes place locally and that at least part of the IgG shows a restricted heterogeneity. The results also suggest the presence of stimulated lymphocytes in the CSF of the same patients.

Adolescent↗
PubMed1977

Ultrastructural observations of experimental Naegleria meningoencephalitis in mice: intranuclear inclusions in amebae and host cells.

Primary amebic meningoencephalitis was experimentallly produced in mice through intranasal instillation of pathogenic Naegleria fowleri. Experimental animals had a 64% mortality with average time of onset of symtoms of death occurring on the 7-8th day following inoculation. Ultrastructural studies of the olfactory lobes from brains of dead (or sacrificed) animals revealed major concentrations of amebae in the perivascular regions; amebae were also seen to be under attack by host polymorphonuclear leukocytes, and in the lumina of blood vessels. Amebae in brain tissue contained 30 nm intranuclear particles arranged in clusters. In the brains of some mice, dead presumably as a result of amebic meningoencephalitis, particles and crystalloids were observed in the nuclei of degenerating cells of the central nervous system. Some alternatives are examined to explain a possible relationship between ameba intranuclear particles and mouse brain cell intranuclear inclusions.

Amebiasis↗
PubMed1979

Listeria monocytogenes: brain abscess or meningoencephalitis?

A brain abscess caused by Listeria monocytogenes developed in an immunosuppressed renal transplant patient. Meningitis and meningoencephalitis from this organism were encountered in three other renal transplant recipients at this medical center during the past 4 years. Focal neurologic deficits occurred in patients with either Listeria abscess or meningoencephalitis. Computerized tomography was a rapid aid to the diagnosis of abscess. Immunosuppression has increased the incidence of central nervous system Listeria infections, but ampicillin still provides effective treatment, even when immunosuppressive therapy is continued. Limited experience with Listeria brain abscess suggests that surgical intervention improves the prognosis.

Adult↗
PubMed1979

Primary amebic meningoencephalitis with cerebral and cerebellar abscesses: case report.

A case of fatal primary amebic meningoencephalitis is reported. We need to remind ourselves that, if the usual laboratory tests fail to show any microbial or fungal agents either in the CSF or in fluids or tissues obtained at operation, it is imperative that a warm wet slide preparation be made. Primary amebic meningoencephalitis is a very rare disease, and it is only by prompt recognition of the amebae that we can make an early diagnosis and institute the appropriate therapy.

Amebiasis↗
PubMed1979

Treatment of experimental Naegleria meningoencephalitis with a combination of amphotericin B and rifamycin.

The treatment of primary amoebic meningoencephalitis was examined using a mouse model. Rifamycin by itself was ineffective. However, a synergistic effect was observed when used in combination with amphotericin B. This finding may prove useful in the treatment of patients with primary amoebic meningoencephalitis, for which satisfactory treatment is currently unavailable.

Amebiasis↗
PubMed1978

Meningoencephalitis and brain abscess due to a free-living amoeba.

A 47-year-old diabetic woman developed fatal meningoencephalitis due to a free-living amoeba. The responsible organism appeared to be neither Naegleria nor Acanthamoeba-Hartmannella. Both acute and chronic (granulomatous) inflammatory reactions of the brain were present, and both cysts and trophozoite forms were readily visualized. The latest classification and methods of identification of such amoebae are reviewed and their threat to public health underscored. It should be realized that a variety of free-living amoebae exist in nature, which potentially can produce meningoencephalitis in humans, and that none of these organisms should be labeled or considered as "avirulent" or "nonpathogenic" until proved otherwise.

Amebiasis↗