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Objective: Primary human cerebral myiasis is an exceedingly rare condition and is almost never encountered by physicians in developed countries. The case report summarizes a case of extensive cerebral myiasis in a periurban community in the United States., Clinical Presentation: After a minor motor vehicle accident, police brought a 75-year-old man to the emergency room because he was observed to have a large cranial lesion. Examination revealed a 15 x 17 cm frontal bone defect with eroded frontal dura, exposed cortex, and massive cortical maggot infestation., Intervention: The patient was empirically treated with intravenous antibiotics for meningitis. Maggots (Phaenicia sericata, or the green bottle fly) were removed by suction, attrition, and gentle contact exposure to a mild bleach solution. Biopsy of the scalp and cranium revealed angiosarcoma, for which operative treatment was refused. The patient was transferred to a skilled nursing facility for palliative care where he died 3 months later., Conclusion: This is the first published case of cerebral myiasis in the United States. Although human cerebral myiasis is rare, conditions do exist in this country that permit myiasis.

The blood brain barrier (BBB) and the blood-cerebrospinal fluid barrier (BCB) limit the influx of immune mediators and bloodstream compounds into the central nervous system (CNS). Upon injury or infection, the integrity of these barriers is compromised and leukocyte infiltration occurs. The BCB is located in the choroid plexuses (CPs) found within ventricles of the brain, and it is considered one of the main routes of cellular infiltration into the CNS into healthy individuals. Our group recently showed that in a murine model of neurocysticercosis (NCC), there is a moderate increase in infiltration of leukocytes into ventricles, but the BCB is hardly compromised. To elucidate the role played by CPs and surrounding ependyma in leukocyte infiltration at ventricular sites, we analyzed changes in the expression of junctional complex proteins in animals intracranially infected with Mesocestoides corti. The results indicate that infection does not change the expression pattern of junctional complex proteins in CPs, but structural alterations and disappearance of these proteins were evident in ependyma adjacent to the internal leptomeninges. The kinetics and magnitude of these changes directly correlated with the extent of leukocyte infiltration through ependyma and with the expression and activity of MMPs. The results of this study indicate that the anatomical elements of the BCB are minimally disrupted during the course of murine NCC. Thus, most of the leukocytes infiltrating ventricles appear to extravasate through pial vessels located in the internal leptomeninges juxtaposed to the ependyma layer and then traverse the ependyma cells. In addition, MMP activity seems to be involved in this process. These results provide evidence for a previously undescribed entry route for leukocytes into the CNS.

This article describes amebic infections in 4 horses: granulomatous amebic encephalitis caused by Balamuthia mandrillaris and Acanthamoeba culbertsoni and systemic infections caused by Acanthamoeba sp. The former infection occurred in 1 of 4 horses spontaneously without any underlying conditions; the latter amebic infection was perhaps "opportunistic" considering the visceral involvement by this protozoan in association with Aspergillus sp. and/or Escherichia coli and Pseudomonas sp. The clinicopathologic findings and demonstration of the amebic organisms using immunohistochemical techniques, culture, polymerase chain reactions, and electron microscopy are presented.

The spatial distribution and histopathological changes induced by metacercariae of the digenean trematode Diplostomum phoxini (Faust, 1918) in the brains of European minnows Phoxinus phoxinus (L.) from the River Endrick, Scotland, were studied by light and electron microscopy. Post-mortem examination of a sample of 34 minnows revealed that 50% (n = 17) of the population was infected with 13.7 +/- 2.6 (mean +/- SE; range 1 to 38) metacercariae per infected host. Serial histological sections of the infected minnow brains revealed that the metacercariae were unevenly distributed throughout the brain, with aggregations occurring in the cerebellum, the medulla oblongata and the optic lobes. In fish with highest intensities of infection, over 40% of the cerebellar area and about 30% of the medulla oblongata area were occupied by larvae. Metacercariae disrupt the integrity of brain tissue, with individuals being found in small pockets surrounded by cellular debris. Metacercariae were rarely encountered on the surface of the brain. Electron microscopic examination of infection sites revealed that the granular layer surrounding metacercariae was necrotic, exhibited nuclear degradation and was marked by vacuolation of the cytoplasm. Rodlet cells, the only inflammatory cell types recorded in this study, were found only in parasitized brains and in close proximity to the teguments of metacercariae. It is hypothesised that secretions released from the teguments of metacercariae are a counter response to protect the metacercariae from the fish brain's cellular defence mechanisms.

A 6-year-old male golden retriever, with an 8-month history of seizures and a clinical diagnosis of lymphoma in the central nervous system, was (at the owner's request) euthanized after signs of respiratory distress and shock developed. Upon postmortem examination, the diagnoses of meningoencephalitis and pneumonia were made. A histological examination of selected tissues from both the lung and central nervous system revealed a severe, acute, multifocal, amoebic, embolic pneumonia and a severe, chronic, multifocal, nonsuppurative, amoebic meningoencephalitis. Indirect immunofluorescence analysis confirmed the presence of trophozoite and cyst stages of Balamuthia mandrillaris. This is the first report of B. mandrillaris (which is a free-living amoeba) causing fatal, multifocal granulomatous amoebiasis in a dog in Australia.

The authors report the case of a 6-year-old boy with cerebral sparganosis due to infection with a plerocercoid tapeworm larva of Spirometra mansoni. Magnetic resonance imaging revealed an area of irregular long T2 signal in the right frontal lobe. When compared with images obtained 2 years earlier, the lesion appeared to have migrated into the parietal lobe. During surgery for the removal of a granuloma, the parasite was discovered and excised. Following surgery, the patient's neurological deficits markedly improved. The authors review the pathological and imaging features of cerebral sparganosis.

Several neurological complications are associated with severe falciparum malaria. Indeed, some patients experience a neurological syndrome after complete recovery from Plasmodium falciparum infection. Particularly, postmalaria neurological syndrome (PMNS) is a self-limiting post-infective encephalopathy that occurs within 2 months after an episode of P. falciparum infection. We describe the case of a 54-year-old Japanese man who was readmitted to our hospital with incoherent speech and markedly disturbed and uncooperative behavior after a high-grade fever that occurred after an earlier adequately treated severe P. falciparum infection. Peripheral blood smears were repeatedly negative for malaria parasites, no organisms were detected in the cerebrospinal fluid, and no hallmark lesions of acute disseminated encephalomyelitis were depicted by brain magnetic resonance imaging. The neuropsychiatric symptoms were thought to be due to PMNS. The etiology of PMNS remains unclear, but it could be mediated by an immunological mechanism and could possibly be caused by mefloquine treatment. PMNS must be considered when characteristic neurological signs and symptoms such as psychotic or acute confusional episodes, general convulsions, and tremor occur after recovery from severe P. falciparum infection treated with oral mefloquine. This is the first reported case of suspected PMNS in Japan.

Cerebral hytatid cysts (HC) are extremely rare, forming 2% of all intra cranial space occupying lesions even in counties where the disease is endemic. HC diagnosis is usually based on a pathognomonic computed tomography (CT) pattern. In order to assess the value of MR we reviewed the CT (n=25) and magnetic resonance (MR, n=4 including diffusion and proton magnetic resonance spectroscopy in 1) imaging of 25 patients with pathologically confirmed cerebral hydatid disease. 19 HC were seen in children under 16 years. All were supra tentorial with 22 in the middle cerebral artery territory. HC was solitary in 18 cases, unilocular in 23 and multi-vesicular in 2 with heavily calcified pericyst in 1. 2 cysts were intra ventricular and 1 intra aqueducal. The most typical features were well defined, smooth thin walled spherical or oval cystic lesions of CSF density and/or signal with considerable mass effect (20/25). Surrounding oedema with complete or incomplete rim enhancement was seen in 3 cases which were labelled as complicated and/or infected cysts. Although CT is diagnostic of hydatid disease in almost all cases (22/25), MRI including diffusion and spectroscopy precisely demonstrate location, number, cyst capsule, type of signal and enhancement and allows diagnosis of atypical or complicated HC and appears more helpful in surgical planning.

Objectives: Hydatid disease, a parasitic infestation caused by the larval stage of the cestode Echinococcus granulosus, is diagnosed commonly in the east and south-east regions of Turkey. The aim of this study is to emphasize the relatively frequent occurrences of echinococcosis in our region, and to discuss therapeutic options and treatment results according to current literature., Methods: A retrospective 10-year review of nine different clinics' records of the Research Hospital of the Medical School of Yüzüncü Yil University revealed 372 hydatid disease cases that were localized in various organs and treated surgically (271 cases) or drained percutaneously (99 cases). Hydatid disease was diagnosed by ultrasonography (US) and computed tomography scans (CT) and confirmed histopathologically., Results: The involved organ was lung in 203 cases (131 adults, 72 children), liver in 150, spleen in 9, brain in 2, kidneys in 7 cases and the retrovesical area in 1 case. The urogenital system is involved at a rate of 2.15%. Two hundred and seventy-one cases were treated surgically and 99 percutaneously. Two cases with renal hydatid cyst refused the surgical procedure (one had a solitary kidney with hydatid cyst). Albendazole was administered to 192 patients; 93 patients had open surgical procedure and 99 patients underwent percutaneous procedure. Cysts were excised totally in the open surgical procedure; however, involved kidneys were removed totally (four cases) except one. Cystectomy and omentoplasty was performed in one case. Complications were as follows: in six cases, cystic material was spilled into the bronchial cavity during the dissection and a renal hydatid cyst ruptured and spilled retroperitoneally., Conclusion: Hydatid disease is a serious health problem in Turkey. The mainly affected organs are liver and lung. It can be treated surgical or by percutaneous aspiration.

Thirteen sheep from a milk producing farm in the Canton of Grisons that presented chronic coenurosis were examined and subjected to treatment trials at the veterinary hospital in Zurich. Symptoms were first observed around two months after the import of two dogs from Italy (Abruzza) of which one was infected with Taenia multiceps and Echinococcus granulosus. The most frequently observed clinical symptoms of the sheep were reduced general condition, circling, reduced menace reflex, apathy, unsteady gait and head tilt. Analyses of cerebrospinal fluid revealed an increased leucocyte count in 3 sheep and eosinophilia in 4 sheep. In 4 animals that underwent computertomography, one or more hypodense, definable lesions were found in the brain. In 2 sheep surgical treatment and in 10 animals medical treatment with either Praziquantel (n=8) or Oxfendazol (n=2) was attempted. Only one animal treated with Praziquantel needed not to be euthanized. At necropsy, one or two coenurus cysts could be found either in a side ventricle (n=2), in the cerebellum (n=3) or in the cerebrum (n=7). The locations corresponded with the clinical findings. Despite Praziquantel or Oxfendazol treatment, living protoscoleces could be found in the parasite cysts.

The cerebral localization of the hydatid disease is rare, under 2%, and it primarily affects children. We report 4 cases of children presenting with a cerebral hydatid cyst (2 boys and 2 girls, mean age 9 years). Clinical symptoms were very progressive, the disease was frequently diagnosed several months (1-12 months) after onset of symptoms most often headaches and vomiting. One patient presented with a right tonic-clonic seizure 3 days before hospitalization. The diagnostic was confirmed in all cases by Cerebral CT scan. All the patients were screened for other localizations. One patient also presented with pulmonary and hepatic hydatid cysts. Hydatid blood tests were positive in only one case. The treatment was surgical for all the patients (using hydropulsion) without complications in 2 cases. One child presented with meningitis, and the other child with signs of secondary ICHT related to residual mass which required its puncture.

Toxocara canis, the parasitic roundworm of dogs, can infect a number of paratenic hosts, such as mice and humans, due to the widespread dissemination of its ova in the environment. In these paratenic hosts, larvae have been shown to exhibit a predilection for the central nervous system, resulting in an increasing number of parasites migrating to the brain as infection progresses. In an initial experiment, we investigated the differential brain involvement of T. canis in 7 strains of inbred mice, and chose 2 strains, susceptible (BALB/c) and resistant (NIH) to cerebral infection. In a second experiment, both strains were investigated in terms of course of migration, larval accumulation, and behavioural response to T. canis infection. Results revealed that infected BALB/c mice took significantly longer to drink from a water source (following a period of deprivation), compared with control mice, indicating some degree of memory impairment. Cerebral larval recoveries from both strains of mice demonstrated variation between the two experiments, suggesting that larval burdens may not be a reliable indicator of susceptibility or resistance to T. canis infection. The percentage of total recovered larvae in each organ may be a better representation of larval distribution. Our model system may provide insights into the impact of chronic geohelminth infection on cognitive development.

Cysts and cystic-appearing intracranial masses have a broad imaging and pathologic spectra. The authors review the pathologic findings, origin, radiologic appearance, and differential diagnosis of many different intracranial cysts. A diagnostic algorithm based on most common anatomic locations is presented that helps narrow the differential diagnosis.

We retrospectively reviewed the MR images of the brains of six children (age = 5-13 years) who had cerebral paragonimiasis in the early active stage. Diagnosis was based on a positive antibody test enzyme-linked immunosorbent assay (ELISA) for paragonimiasis in serum. The most common finding (in five patients) was irregular hemorrhage of various degrees. Moreover, in three cases some multiple irregular lesions with surrounding edema appeared to be conglomerated and aggregated. The rare appearance (in one patient) was a "tunnel sign," which showed the migrating track of the adult worm. In one patient with abscess and minimal hemorrhage, diffusion-weighted imaging (DWI) showed a heterogeneous high signal of lesions. Other findings included slight (one patient) or marked (one patient) irregular contrast enhancement, and large edematous areas surrounding small centers of hemorrhage (two patients). MR findings of conglomerated lesions with hemorrhage or tunnel sign may help to establish the diagnosis of active-stage cerebral paragonimiasis., (2006 Wiley-Liss, Inc.)

In developing countries hydatidosis is both a medical and economic problem related to environmental hygiene and healthy veterinary practice. This cestode parasitic infestation, uncommonly involving the nervous system, presents with varied clinical manifestation, at times causing diagnostic dilemmas. Multiple intracranial and spinal hydatidosis is rare. A series of 29 histologically confirmed cases of hydatidosis of neuraxis (21 intracranial and 8 spinal) from South India are presented. Among the 21 cases of intracranial hydatidosis, 12 cases were in pediatric age, while only 1 spinal lesion was noted in a 5-year-old child. The clinical presentation of intracranial lesions was predominantly that of raised intracranial pressure and visual symptoms, while spinal hydatidosis manifested with severe back pain, weakness and sphincter disturbances. The cranial cysts were usually single and uniloculated (12 cases), multiple in 7 and single but multiloculated in 2. In spinal hydatidosis, the cysts are usually multiple and extradural, rare ones being intramedullary and intradural. Based on clinical features and imaging, the differential diagnosis for intracranial lesions were cystic tumors and arachnoid cyst while metastasis and tuberculosis were considered in cases of spinal hydatidosis because of vertebral bony involvement. The majority of the cysts could be surgically resected totally and some were aspirated under control suction and resected. None of the cases had anaphylactic reaction, with no significant post-operative morbidity and no mortality. One intracranial and 2 spinal lesions caused by fertile cysts recurred to undergo repeated surgery.

Cysticercosis of the central nervous system is the main cause of late-onset epilepsy in tropical countries. The case of a 13-year-old German girl with a generalized seizure following long-term sojourns in the Tropics is reported. Cranial imaging showed two cerebral lesions with central calcifications. Serological, molecular and cultural examination of cerebrospinal fluid and blood was negative for various parasites, fungi and bacteria including mycobacteria. Histopathological examination after neurosurgical resection revealed calcareous bodies pathognomonic for platyhelminths, in particular tapeworms. Taken together, the radiological and histopathological findings indicate infection with cysticerci, the larvae of Taenia solium.

The clinical features of neurocysticercosis (NCC) largely depend on the number, type, size, localization and stage of development of cysticerci, as well as on the host immune response against the parasite. Seizures are widely reported to be the most common symptom, occurring in 70-90% of patients, while NCC is considered to be the main cause of late-onset epilepsy in endemic areas. When cysticerci lodge within the ventricular system, life-threatening acute intracranial hypertension secondary to hydrocephalus may develop. Cysts in the subarachnoid space may invade the Sylvian fissure and grow to large sizes (giant cysts) causing intracranial hypertension with hemiparesis, partial seizures or other focal neurological signs. Racemose cysts in the basal cisterns can cause an intense inflammatory reaction, fibrosis and progressive thickening of the leptomeninges at the base of the brain. In approximately 60% of the cases, there is an obstruction of the cerebrospinal fluid (CSF) circulation, resulting in hydrocephalus and intracranial hypertension. When hydrocephalus secondary to cysticercotic meningitis is present, the mortality rate is high (50%) and most patients die within 2 years after CSF shunting. Therefore, ventricular and basal cisternal locations are considered to be malignant forms of NCC. The diagnosis of NCC is based upon neuroimaging studies, laboratory analysis of the CSF and antibody detection in the serum. Nowadays, albendazole is considered the medication of choice for the therapy of NCC. Its main use is for symptomatic patients showing multiple viable brain parenchymal cysticerci.

Immunosuppression associated with HIV infection or following transplantation increases susceptibility to central nervous system (CNS) infections. Because of increasing international travel, parasites that were previously limited to tropical regions pose an increasing infectious threat to populations at risk for acquiring opportunistic infection, especially people with HIV infection or individuals who have received a solid organ or bone marrow transplant. Although long-term immunosuppression caused by medications such as prednisone likely also increases the risk for acquiring infection and for developing CNS manifestations, little published information is available to support this hypothesis. In an earlier article published in Clinical Infectious Diseases, we described the neurologic manifestations of some of the more common parasitic CNS infections. This review will discuss the presentation, diagnosis, and treatment of the following additional parasitic CNS infections: malaria, microsporidiosis, leishmaniasis, and African trypanosomiasis.

Diplostomum (Austrodiplostomum) compactum (Lutz, 1928) metacercariae (Platyhelminthes, Digenea) were found in six fish species, belonging to two orders (Characiformes and Perciformes) and three families (Erythrinidae, Sciaenidae and Cichlidae). A total of 477 individuals were collected, from August 1999 to May 2001, in the upper Paraná River floodplain, Brazil. The metacercariae were infecting the eyes of six host species and the brain of five of them. Plagioscion squamosissimus, Satanoperca pappaterra and Cichla monoculus presented the highest values of prevalence, mean intensity and mean abundance. Diplostomum (A.) compactum was over-dispersed in the population of Hoplias aff. malabaricus, S. pappaterra, P. squamosissimus, Crenicichla britskii and C. monoculus. No significant difference was observed in the metacercariae distribution in the right and left eyes. The abundance of D. (A.) compactum metacercariae was positively correlated with the host's relative condition factor in H. aff. malabaricus and S. pappaterra. No significant difference of the abundance of parasitism between the sex of the hosts was evidenced. In relation to the prevalence, significant difference was observed only in C. britskii. Positive correlations were verified between the prevalence of infection and the standard length of the specimens in C. britskii and the intensity of infection and the standard length of the hosts in P. squamosissimus and C. monoculus. In relation to parasite abundance and the standard length class of the host, significant differences were observed in P. squamosissimus, C. britskii and C. monoculus.

An unusual female case, with alveolar echinococcosis (AE) disseminated from the primary hepatic lesion to the brain by metastasis formation, was retrospectively identified during a community survey in Ningxia Hui Autonomous Region, northwest China in 2003. Among possible metastases of hepatic AE, locations to the brain are rare and usually fatal; and they have especially been assigned to concomitant immune suppression. An enhancing role of pregnancy, which may be suspected in this case, the favourable outcome after surgery and chemotherapy, and also a mental disability in a child following long-term intrauterine exposure to mebendazole, make the report particularly unique.

Cerebral signs of focalized infection or tumour with changing localisation or meningoencephalitis with a travel history should alert the clinician to consider the possibility of a worm infection. A detailed history of the stay abroad, of consumption of raw or with animal faeces contaminated food and of known preexisting helminthic disease gives further clues. The diagnostic approach compromises the check for eosinophilia in peripheral blood and CSF, serologic testing and CT scan or MRI examination. Anthelminthic treatment may induce a host reaction with inflammation and deterioration of the clinical picture and has to be performed cautiously and under protection with corticosteroids.

We are presenting magnetic resonance spectroscopy (MRS) findings of a known case of hydatid cyst operated twice in the past. A 22-years-old male patient had presented with recurrent symptoms of generalized seizures and raised intracranial tension. MRI with MRS of the lesion was performed that showed a recurrent loculated cystic lesion in right parieto-occipital lobe. MRS through the lesion was performed using repetition time (TR) of 1500 ms and time to echo (TE) of 135 ms using 2 x 2 x 2 cm voxel, from the margin of the lesion. MRS showed mildly elevated choline (Cho), depressed creatine (Cr) and N-acetyl aspartate (NAA), a large peak of lactate, pyruvate and acetate peaks.

Objectives: Although chronic calcified neurocysticercosis (NCC) has been considered a major cause of symptomatic epilepsy in developing countries, it can also be an incidental pathological finding in epileptic patients from endemic regions. The mechanisms of brain plasticity occurring in patients with NCC during and after the inflammatory process related to the parasite infection, death, degeneration, and calcification within the host brain might be an independent factor for cognitive impairment in patients with NCC and epilepsy. In order to assess this possibility cognitive performance of patients with mesial temporal lobe epilepsy related to hippocampal sclerosis (MTLE-HS) with and without NCC was investigated through structured neuropsychological testing., Methods: Cognitive performance of long term MTLE-HS patients with (HS-NCC group, n = 32) and without NCC (HS only, n = 48) was compared. Imbalances between the two groups with respect to clinical, demographic, neuroimaging, and electrophysiological variables were adjusted by linear multiple regression analysis and Bonferroni correction for multiple tests., Results and Conclusions: There were no cognitive performance differences between HS-NCC and HS only patients, leading to the conclusion that chronic calcified NCC per se does not aggravate the cognitive performance of patients with long term MTLE-HS.

Neurocysticercosis is common in Asia, Africa and South America including Mexico. A diagnosis of neurocysticercosis was made neuroradiologically in an 8-year-old Mexican girl, who had suffered from learning difficulties for a year, and subsequently developed headache, vomiting, gait disturbance, visual hallucination, apraxia and euphoric state for 4 months. Plain CT demonstrated numerous cystic lesions with or without scolex in addition to calcified lesions. The lesions were seen throughout the whole brain, although they were relatively scarce in the cerebellum and the lateral ventricular system. Although edema was prominent around the bilateral ventricles, neither ventricular dilatation, midline shift nor inflammatory reaction around the cysts was detected. The patient was treated with albendazole for a month and with steroid for two months. Headache and vomiting disappeared in the first week of treatment but other symptoms persisted, with fluctuation. CT after 2 months of treatment showed dilatations of the third and lateral ventricles. Despite massive infection in the brain, the clinical picture at onset was mild and compatible with nonencephalitic cerebral cysticercosis. The symptoms might be caused by the progressive hydrocephalus due to cerebrospinal fluid blockage, the prognosis of which is predicted to be poor.

NcMIC1 is a 460 amino acid Neospora caninum microneme protein implicated in host cell adhesion and invasion processes. In this study, we assessed the potential protectivity of NcMIC1-based vaccination against experimental N. caninum infection in mice, employing both recombinant antigen vaccines and DNA vaccines. Recombinant NcMIC1 (recNcMIC1) was expressed in Escherichia coli as gluthatione-S-transferase-fusion protein. The corresponding NcMIC1 cDNA was cloned into the pcDNA3.1 expression plasmid (pcDNA-MIC1), and expression was checked in transfected Vero cells. Mice (10 animals/group) were vaccinated either with recNcMIC1 antigen suspended in Ribi-adjuvant (3 intraperitoneal injections), pcDNA-NcMIC1 (3 intramuscular injections), or pcDNA-NcMIC1 (twice intramuscularly), followed by 1 intraperitoneal recNcMIC1 antigen boost. Control groups included corresponding treatments with adjuvant, pcDNA3.1 without insert, and PBS (= infection control). All vaccinated and control groups were then challenged intraperitoneally with 2 x 10(6) N. caninum tachyzoites. Animals were inspected daily for a period of 3 wk postinfection (PI). At day 21, all animals were killed and assessed for infection. Before day 21 PI, clinical signs such as walking disorders, rounded back, apathy, and paralysis occurred in infection controls (50% of the mice), pcDNA and adjuvant controls (20% each), and the combined pcDNA-NcMIC1/recNcMIC1-treated group (30%). No clinical symptoms were observed in the recNcMIC1 and pcDNA-NcMIC1 vaccinated groups. All mice were positive for cerebral N. caninum infection as assessed by PCR of brain tissue. However, quantitative real-time PCR revealed that the infection intensity was significantly reduced in the group vaccinated with recNcMIC1 antigen. Immunohistochemistry confirmed these findings. In contrast, the infection intensity was highest in the group vaccinated with the pcDNA-NcMIC1/recNcMIC1 combination, indicating that the sequential application of the DNA vaccine and recombinant antigen had a deleterious effect. Serological analysis showed that only recNcMIC1-immunized animals generated detectable antibody levels recognizing native NcMIC1. Thus, of all protocols applied here, only recNcMIC1 vaccination appears to be suited to reduce cerebral infection in mice challenged with N. caninum tachyzoites.

Viable cryptococci load in biopsy material from an animal model of cerebral cryptococcoma were correlated with 1H NMR spectra and metabolite profiles. A statistical classification strategy was applied to distinguish among high-resolution 1H NMR spectra acquired from cryptococcomas, glioblastomas, and normal brain tissue. The overall classification accuracy was 100% when a genetic-algorithm-based optimal region selection preceded the development of linear discriminant analysis-based classifiers. The method remained robust despite differences in the microbial load of the cryptococcoma group when harvested at different time points. These results indicate the feasibility of the method for diagnosis without isolation of the pathogenic microorganism and its potential for in vivo diagnosis based on computerized analysis of magnetic resonance spectra.

Objective: We describe a case of severe fetal hydrocephalus due to toxoplasmosis which could not be diagnosed until late gestational age due to the lack of a serologic surveillance program during pregnancy; moreover, this case points to the usefulness of molecular biology tools in the diagnostic process. Abnormal ultrasound in the 2nd trimester was noticed and Toxoplasma gondii was demonstrated in amniotic fluid at the 28th week of gestation both by PCR and by mice inoculation. Fansidar and folinic acid were administered. The newborn suffered from progressive hydrocephalus, seizures, and pathological muscular tonus; ultrasound examination showed massive cerebral calcifications. Ophthalmologic examination revealed bilateral choroidoretinitis. Congenital toxoplasmosis was confirmed by the detection of anti- T. gondii IgM and IgA in the neonatal serum., Conclusion: The presented case is an example of severe fetal toxoplasmosis diagnosed and treated in utero., (Copyright (c) 2005 S. Karger AG, Basel.)

Hydatid cysts are rarely located in the brain (1 to 3% of all cases), and these are even more rarely in calcified form. We report one case of a 20-year-old woman. She had undergone surgery for a pulmonary hydatid cyst at the age of four years. She had been subject to general epileptic seizures refractory to standard anticonvulsive drugs for the past four years. Cerebral computed tomography showed calcification in the left occipital region. A calcified hydatid cyst was discovered and removed during surgery. Subsequent course has been good and the epileptic seizures have disappeared. A calcified hydatid cyst in the brain is very rare and presents diagnostic and therapeutic problems.

Twelve sheep from 7 different flocks consisting of approximately 150-250 animals each were diagnosed with coenurosis caused by the larval stage of Taenia multiceps. Ataxia, incoordination, drowsiness, hind leg paralysis and coma were the most prominent clinical symptoms. Monocytosis and lymphocytosis were observed upon hematological examination. Creatin kinase (CKBB) levels of the animals varied between 421 and 495 U/l. Cysts were commonly localized in the parietal and frontal lobes of the brain and in the cerebellum. In two cases, cysts were found on the lumbar aspect of the medulla spinalis. Symptoms were related to cyst localization. Depression, tilting of the head either to the right or left and head pressing were seen when cysts were located in the cerebrum. Incoordination and hyperexcitability were noted if the cysts were involved with the cerebellum and when located in the spinal cord, hind leg paralysis was the typical clinical sign. On microscopic examination, atrophy was observed in the central nervous system (CNS) organs due to pression by the bladderworms. Nonpurulent meningoencephalitis with perivascular cuffings were the most common histopathological findings. In periodic acid Schiff staining (PAS), positive reaction was observed in protoscoleces. Neurons were the most affected cell type when stained by the Klüver Barrera method. This method also showed that in the CNS, Coenurus cerebralis caused a prominent glial reaction. When parasites were localized in the nervous system treatment was impossible. Animals without neurologic sings were treated with praziquantel (Tenikur tablet-Topkim A.S.) 50-100 mg/kg/day for three days.

Objective: To determine the relationship between hippocampal atrophy (HA), neurocysticercosis calcifications (NC) and seizure semiology in patients with partial epilepsy., Methods: We identified two groups of patients: mesial temporal lobe epilepsy (MTLE) and extra-temporal epilepsy (ETE) patients. Each group was subdivided according to CT findings: normal, NC in the temporal regions, and NC in extra-temporal regions. MRI was obtained in a 2-T scanner and hippocampal volumetry was performed using 3-mm coronal T1-IR images. Hippocampal volumes below 2 standard deviations from the mean of the control group determined the presence of HA., Results: We studied 89 consecutive patients: 63 with MTLE and 26 with ETE. HA was found in 43/89 (49.5 %) patients, 42 of them with MTLE. There was no difference in frequency of HA in the comparison between patients with (25/50) and without NC (18/39) (chi(2), p=0.71). Furthermore, there was no relationship between localization of NC (temporal or extra-temporal) and seizure semiology (MTLE or ETE)., Conclusions: HA was more frequent and more severe in patients with MTLE, with no differences regarding the presence and localization of NC. These findings further support the concept that NC on CT not necessarily indicate the etiology of epilepsy and may represent only a co-existent pathology.

We monitored temporal changes in the magnitude of altered host behaviour in minnows (Pimephales promelas) experimentally infected with metacercariae of a brain-encysting trematode (Ornithodiplostomum ptychocheilus). This parasite develops and then encysts in a region of the brain that mediates the optomotor response (OMR), an innate behaviour that links visual stimuli with motor performance. The OMR of infected and uninfected minnows was evaluated between 0 and 10 weeks post-infection (p.i.), an interval spanning the development period of metacercariae to infectivity in birds. Trials involved monitoring the time an individual minnow spent following a spinning drum that had been painted with alternating black and white stripes. At 2 and 4 weeks p.i., infected minnows followed the drum 40% less often than controls. Differences between controls and infected fish declined thereafter, and were undetectable by 10 weeks p.i. Both control and infected fish habituated equally rapidly to the spinning drum. However, the difference in performance between controls and infected fish was 29% for experienced fish and 48% for fish that had never experienced the drum. Because maximum parasite-induced reduction in OMR coincided with the period of maximum parasite development, the behavioural effects are most likely due to unavoidable pathology in the brain associated with developing larvae.

Single enhancing brain lesions (SELs), mostly as a result of neurocysticercosis or tuberculosis, are a common cause of seizures. Ten patients with SELs caused by neurocysticercosis (n=6) or tuberculosis (n=4) were examined by proton magnetic resonance spectroscopy. Tuberculomas had a high peak of lipids, more choline, and less N-acetylaspartate and creatine. The choline/creatine ratio was greater than 1 in all tuberculomas but in none of the cysticerci. Magnetic resonance spectroscopy differentiates SELs caused by cysticercosis or tuberculosis and may avoid brain biopsies or unnecessary antituberculosis treatments.

Eosinophilic meningitis or meningoencephalitis caused by Angiostrongylus cantonensis is endemic to the Pacific area of Asia, especially Taiwan, Thailand, and Japan. Although eosinophilia is an important clinical manifestation of A. cantonensis infection, the role of eosinophils in the progress of the infection remains to be elucidated. In this experiment, we show that A. cantonensis-induced eosinophilia and inflammation might lead to the induction of IAP/NF-kappaB, JAK/STAT1 and MEKK1/JNK signals. The phosphorylation levels of JAK and JNK, STAT1, IAP, NF-kappaB and MEKK1 protein products were significantly increased after 12 days or 15 days of A. cantonensis infection. However, no significant differences in MAPKs such as Raf, MEK-1, ERK1/2 and p38 expression were found between control and infected mice. The activation potency of JAK/STAT1, IAP/NF-kappaB and MEKK1/JNK started increasing on day 3, with significant induction on day 12 or day 15 after A. cantonensis infection. Consistent results were noted in the pathological observations, including eosinophilia, leukocyte infiltration, granulomatous reactions, and time responses in the brain tissues of infected mice. These data suggest that the development of brain injury by eosinophilia of A. cantonensis infection is associated with activation of JAK/STAT1 signals by cytokines, and/or activation of MEKK1/JNK by oxidant stress, and/or activation of NF-kappaB by increasing IAP expression.

A patient with chronic cerebral paragonimiasis began to have new motor seizures of the right face manifested by clonic contractions that occurred several hundred times a day, consistent with simple partial status epilepticus. Ictal electroencephalogram discharges started from the left frontal region and then spread to the left hemisphere with left frontal maximum. But clinical seizures were limited to the right face. The frequent partial seizures were controlled by the intravenous infusion of phenytoin. Brain magnetic resonance imaging showed multiple conglomerated round nodules with encephalomalacia in the left temporal and occipital lobes. Applying the technique of ictal-interictal single-photo emission computed tomography subtraction, the authors were able to localize the focal ictal-hyperperfusion on left precentral cortex adjacent to the lesions that correspond to the anatomical distribution of left face motor area.

Objective: Cerebral hydatid disease is very rare, representing only 2% of all cerebral space occupying lesions even in the countries where the disease is endemic. The aim of this paper is to describe the characteristic features of cerebral hydatid disease in computed tomography (CT) and magnetic resonance imaging (MRI)., Methods: We retrospectively reviewed the CT and MR imaging findings of 18 patients with pathologically confirmed cerebral hydatid disease over a period of 13 years (1990-2002)., Results: The study group consisted of 17 cases of Echinococcus granulosus and 1 case of Echinococcus multilocularis (alveolaris). They were 12 male (66.7%), and 6 female patients (33.3%), ages ranging from 7 to 50 years with an average age of 20.3 years. Headache, vomiting and seizures were the predominant symptoms. Papilloedema was present in 14 patients (77.7%). Common CT and MR imaging findings of E. granulosus lesions were welldefined, smooth thin-walled, spherical, homogeneous cystic lesions with no contrast enhancement, no calcification, and no surrounding oedema. The lesion seen with E. multilocularis was a well-defined multiseptated mass consisting of solid and cystic components with calcification in the solid portion. Cystic lesions with surrounding hyperintensity of perifocal oedema with complete or incomplete rim enhancement were seen in two patients, and were labeled as complicated and infected cysts., Conclusion: Although cystic cerebral hydatid disease is well demonstrated by CT and MR examinations, CT is superior in detecting calcification in the cyst, when present, MR is better in demonstrating cyst capsule, detecting multiplicity and defining the anatomic relationship of the lesion with the adjacent structures, and it is more helpful in surgical planning.

Raccoon roundworms (Baylisascaris procyonis) and other Baylisascaris species cause patent or latent larva migrans (LM) in a variety of mammals and birds, including humans. It is not clear whether LM by Baylisascaris transfuga, roundworms of bears, is associated with clinical neurological disorders. To clarify this issue, ICR and BALB/c mice as well as Mongolian jirds (Meriones unguiculatus) were orally inoculated with 2,000-5,000 embryonated eggs of B. transfuga. In mice, the ascarid caused symptomatic LM of limited extent and duration, whereas the infection was fatal in jirds; i.e., they exhibited general signs such as severe depression and emaciation on days 8-11 postinfection (PI) and died, or they developed progressive and fatal neurological disorders after day 14 PI. Histological examination showed B. transfuga larvae in the brain of all mice and jirds examined, and the larvae collected from them developed to a size comparable with that of B. procyonis. There existed, however, critical differences in host reactions against larvae localized in the brain of mice and jirds; B. transfuga larvae found in mice were surrounded by granulomatous reactions and immobilized, whereas larvae found in jirds were free from any host reaction and mobile, causing extensive malacia.

A Japanese woman presenting with neurologic symptoms was presumptively diagnosed with neurocysticercosis based on imaging findings. Hooklets in the scolex of the resected lesion were not confirmed through histopathological observation. However, the illness was confirmed by mitochondrial DNA analysis to be a solitary neurocysticercosis case caused by the Asian genotype of Taenia solium.

The ratio of cardiac involvement of Echinoccocus granulosus is 0.02-2% and although seen rarely, involvement of the interatrial septum has also been reported in the published literature. The present case was a 19-year-old male university student admitted to hospital with complaints of headache and dizziness. Computerized tomography of the cranium revealed a cystic mass located at the frontal region and enucleation of the cyst was performed during surgery. A cystic lesion 5 x 4 cm in size was detected within the interatrial septum on two-dimensional transthoracic echocardiography during the postoperative period and the patient was referred to our clinic. Open heart surgery was performed and a hydatid cyst that involved the interatrial septum was enucleated. The cyst wall was sutured to the interatrial septum. No complications developed during the postoperative period. The patient was discharged on the fifth day of hospitalization and medical therapy was started with albendazole.

Recent reports indicate a higher frequency of brain infections with opportunistic amebae of the genus Acanthamoeba among immune compromised individuals, including AIDS patients. We have demonstrated, using a murine model of Granulomatous Amebic Encephalitis (GAE), that the major psychoactive and immune suppressive component in marijuana delta-9-tetrahydrocannabinol (THC) exacerbates infection by these amebae. Mice administered THC and infected with Acanthamoeba exhibited dose-related higher mortalities than infected vehicle controls. The greater severity of disease for THC-treated mice was accompanied by decreased accumulation of macrophage-like cells at focal sites of infection in the brain. Furthermore, THC administration resulted in decreased levels of mRNA for the pro-inflammatory cytokines interleukin-1 alpha, interleukin-1 beta, and tumor necrosis factor alpha for neonatal rat microglia co-cultured with Acanthamoeba. These results indicate a potential for marijuana to alter the capacity of brain macrophage-like cells to mount a full complement of immune responsiveness to brain infection by opportunistic amebae.