Angiostrongylosis is roundworm disease caused by Angiostrongylus. Angiostrongylus including 20 species parasitize mainly in mouse, among which two species cause disease in human are Angiostrongylus cantonensis and Angiostrongylus costaricensis. Angiostrongylus cantonensis was found by Chen H.T in 1935 in China. For pediatric case records that having meningitis syndrome with symptoms of fever, headache, paralytic, cerebrospinal fluid clear or unclear but eosinophil increasing highly, it needs to think of meningitis caused by parasites and do immune test to Angiostrongylus to identify the cause. Early treatment will have good results and avoid severe consequences
Meningoencephalitis ; Angiostrongylus

No abstract available.
Choroid ; Meningoencephalitis

2 patients with tick fever had had an encephalo-meningitis complication, a rare condition with clinical symptoms similar with other type of encephalo-meningitis. In the diagnosis of encephalo-meningitis fever caused by Ricketsia, it must pay attention to the signs of conjunctive congestion, erythrema, especially the ulcerous lesions with high diagnostic value. The change in cerebro spinal fluid is not usually specific as meningitis caused by pyogenes bacteria. These are an increase of protein level, light decrease of glucose level and a minime increased of cell count. The early detection and specific treatment reduce the severity of the condition and cerebral symptoms can be reduced slower than the fever
Meningoencephalitis ; Encephalitis ; complications

No abstract available.
Adult* ; Humans ; Meningoencephalitis* ; Mumps*

No abstract available.
Meningoencephalitis* ; Psychotic Disorders*

No abstract available.
Edema ; Humans ; Meningoencephalitis

Present study aimed to elucidate the immunosuppressive effect of prednisolone on Naegleria fowleri infection in mice. N. fowleri was cultured in CGVS medium (Willert and Le Ray, 1973). White female mice, weighing about 18 g, used for experiments were divided into five groups; untreated control group, prednisolone treated groups (before, during and after infection), and only prednisolone treated group. In the prednisolone treated group, the hormone was injected intramuscularly 5 doses of 10 mg/kg every other day. According to designated time of treatment, each mouse was challenged with 1 x 10(5) N. fowleri intranasally. Changes of body weights, clinical manifestations and number of dead mouse were observed. Brain and lung tissues of dead mice were cultured in the non-nutrient agar (Kasprzak and Mazur, 1972), or stained with hematoxylin-eosin for the examination of histopathological changes. Results of the experiment are summarized as follows: Mortality among the prednisolone treated groups was higher than that in untreated control group, and among the treated groups, the pretreated group showed shorter survival time. Body weights among untreated control mice showed no significant increase, however, treated groups of mice showed the decrease during the administration and recovery of the weights were observed at 2 to 3 days after the completion of treatment. In the treated control groups, the infected mice began to show the pathologic findings 5 days after infection while the untreated mice began to show the findings 8 days after infection. Tissue damages in brain and lung occurred due to virulence of amoeba were more severe among treated mice than that in untreated control group. The above mentioned results suggest that the treatment with prednisolone weaken the resistance of mice against N. fowleri infection, and probably induce more severe primary amoebic meningoencephalitis. Especially severe pathological findings were shown in pre-treated group, compared with untreated group.
parasitology-protozoa ; Naegleria fowleri ; meningoencephalitis ; brain ; prednisolone

The role of passive cell-mediated transfer of immunity against primary amoebic meningoencephalitis(PAME) in mice was studied. Naegleria fowleri, ITMAP 359, were cultured in CGVS medium. The ICR mice used were six week-old males of average weight of 15 g. Immunization was done by three intraperitoneal injections of l x 10(6) N. fowleri trophozoites at the interval of one week. Splenocytes were obtained from normal and immune mice spleens, and 1 x 10(7) cells were administered intraperitoneally into mice 3 days before challenge infection. Mice were infected intranasally with 7 x 10(4) N. fowleri trophozoites in a 3 microliter suspension under secobarbiturate anesthesia. Transplants of normal or immune splenocytes seem to alter the pattern of the PAME development. The splenocytes transferred from immune mice reduced the mortality rate in the N. fowleri infected mice, as compared with the mice transferred with the same number of normal splenocytes or without splenocyte. The blastogenic response of the splenocytes to both lipopolysaccharide and concanavalin A was elevated on day 7 after infection the mice transinoculated with immune splenocytes. The serum antibody titers in the mice transferred with immune splenocytes were increased gradually from day 7 up to day 20 after infections by mean of ELISA. It is suggested that the transfer of splenocytes from immunized mice conferred immunity against N. fowleri infection.
parasitology-protozoa ; Naegleria fowleri ; meningoencephalitis ; brain ; immunology

Background: tuberculosis meningoencephalitis (TBME) is an acute infectious disease of the central nervous system. The disease had a high mortality rate and severe sequelae if late diagnosis and not timely treatment. However, in recent years, the patients with TBME who was transferred to National Pediatric Hospital Hospital remained to be diagnosed not exactly, affect to treatment outcomes. Objectives: study on the difficulties in diagnosing TBME in children. Subjectives and Method: a descriptive study on 34 children aged 4-14 months diagnosed with TBME at Department of infectious, National Pediatric Hospital from January 2002 to September 2005. Results: 35.29% of the patients were under 1 year old. The suggestive signs and symptoms for diagnosis included BCG\ufffd?scar (50%), tuberculosis exposure (32.4%), weight loss (31.8), fever (100%), vomiting (70.6%), stiff-neck (94.1%), meningeal sign (70.6%), Kernig\u2019s sign (61.8%), positive Tuberculin tests (35.29%) and typical lesions on chest x-rays (11.8%). In cerebrospinal fluids (CSF), mean cell count was 274/mm3 and protein concentration was 1.51g/l. These were hindrances for diagnosing TBME in children. Disease distribution was in both the urban and the rural areas. Conclusions: Clinical manifestations and disease progress are not typical for TBME diagnosis. Therefore, it is important to think about TBME in cases with acute meaningitidis lasting for more than 14 days. PCR will be a very good marker for definite diagnosis.
Meningoencephalitis/ diagnosis ; Tuberculosis ; Meningeal/ diagnosis ; Child ;

This study is to verify the protective ability against experimental Naegleria meningoencephalitis by immunization with Naegleria fowleri in mice. Naegleria fowleri, strain 0359, and Naegleria gruberi, strain EGB, were used in this study, and cultured in CGVS medium axenically. Inbred BALB/c mice, weighing about 20 g, were immunized by three intraperitoneal injection of 1 x 10(6) N. fowleri trophozoites at the interval of one week. This N. fowleri trophozoites antigen was fixed with 5 percent formaldehyde. N. fowleri trophozoites from culture were homogenized with sonicator at 4C as monitored by phase contrast microscopy, and their membrane and cell content preparations were made for the immunization of mice. Their inoculation dose in volume was equivalent to the 1 x 10(6) trophozoites in each injection for immunization. And N. gruberi trophozoites, which was fixed with 5 percent formaldehyde, were also used for immunization. Mice were inoculated intranasally with 5 x 10(4) N. fowleri trophozoites in a 5 microliter suspension under anesthesia by as intraperitoneal injection of about l mg secobarbiturate. Nervousness, rotation or sluggish behaviour were observed in the mice which were infected with N. fowleri. Necrotic lesion was demonstrated in the anterior portion of brain, especially in the olfactory lobe. The inflammatory cell infiltration with numerous N. fowleri trophozoites was noticed. This pathological changes were more extensive in the control than in the experimental groups. Mice were dead due to experimental primary amoebic meningoencephalitis that developed between 8 days and 23 days after inoculation. Mortality rate of the mice was low in the immunized experimental group. Mean survival time, which is the survival duration of mice from the infection to death, was prolonged significantly in the immunized mice except in the mice immunized with N. fowleri membrane. Even in the mice immunized with N. gruberi, survival time was delayed. In summary, the effectiveness of immunization is demonstrated in terms of protective immunity against Naegleria meningoencephalitis in mice.
parasitology-protozoa ; Naegleria fowleri ; meningoencephalitis ; immunology ; mouse ; brain