Neuroinvasion of Toxocara canis- and T. cati-larvae mediates dynamic changes in brain cytokine and chemokine profile.

BACKGROUND: Neurotoxocarosis (NT) is induced by larvae of the dog or cat roundworm (Toxocara canis or T. cati) migrating and persisting in the central nervous system of paratenic hosts, including humans, and may be accompanied by severe neurological symptoms. Host- or parasite-induced immunoregulatory processes contribute to the pathogenesis, but detailed data on pathogenic mechanisms and involvement of signalling molecules during cerebral Toxocara species infections are scarce. METHODS: To elucidate alterations in immunomodulatory mediator pattern, comprehensive multiplex bead array assays profiling comprising 23 different cytokines and chemokines were performed during the course of T. canis- and T. cati-induced NT. To this end, cerebra and cerebella of experimentally infected C57Bl/6 J mice serving as paratenic host models were analysed at six different time points (days 7, 14, 28, 42, 70 and 98) post infectionem (pi). RESULTS: Brain-body mass ratios of T. canis and T. cati-infected mice were significantly lower than those of the uninfected control group at day 14 pi, and also at day 28 pi for T. canis-infected mice. Both infection groups showed a continuous decrease of pro-inflammatory cytokine concentrations, including TNF-α, IFN-γ, GM-CSF and IL-6, in the cerebrum over the course of infection. Additionally, T. canis but not T. cati-induced neurotoxocarosis was characterised by significantly elevated levels of anti-inflammatory IL-4 and IL-5 in the cerebrum in the acute and subacute phase of the disease. The higher neuroaffinity of T. canis led to a prominent increase of eotaxin and MIP-1α in both the cerebrum and cerebellum, while in T. cati-infected mice, these chemokines were significantly elevated only in the cerebellum. CONCLUSIONS: The direct comparison of T. canis- and T. cati-induced NT provides valuable insights into key regulatory mechanisms of Toxocara species in paratenic hosts. The cerebral cyto-/chemokine milieu is shifted to a predominantly anti-inflammatory immune response during NT, possibly enabling both survival of the parasite and the neuroinfected paratenic host. Alteration of eotaxin and MIP-1α concentrations are congruent with the higher neuroaffinity of T. canis and species-specific tropism of T. canis to the cerebrum and T. cati to the cerebellum.

Baylisascaris procyonis Central Nervous System Infection in a Four-Month-Old Gordon Setter Dog.

A 16 wk old intact female Gordon setter was examined for a 2 wk history of progressive cerebellovestibular ataxia. Eosinophilia was found on complete blood count, and the remaining blood work was normal. A trial treatment with clindamycin and anti-inflammatory prednisone did not result in improvement of clinical signs; therefore, the dog was euthanized. On histopathologic examination, cross sections of a 75 µm wide nematode larva with a 5 µm cuticle, prominent lateral cords, lateral alae, and coeloemyelian musculature were identified in a focally extensive region of cerebellar necrosis. The size and morphology of the parasites was most consistent with Baylisascaris procyonis. This case highlights a rare but important zoonotic disease that should be considered as a differential diagnosis in any dog exhibiting acute, progressive central nervous system signs, and peripheral eosinophilia. The index of suspicion should be elevated in dogs with an unknown deworming history and known or suspected exposure to raccoons. Because most anthelminthics have been shown to be effective against B. procyonis, annual deworming is recommended in the at-risk population to reduce the likelihood of aberrant migration and zoonosis.

Border zone brain lesions due to neurotrichinosis.

Trichinosis is a parasitic disease that, due to variable clinical syndromes, is often underrecognized. We present the case of a patient with eosinophilia, focal neurological signs and multiple bilateral brain lesions, distributed mainly in the border zones. The diagnostic workup revealed neurotrichinosis, which should be suspected even without a clear history of consumption of poorly cooked meat.

GRANULOMATOUS FILARIAL ENCEPHALOMYELITIS CAUSED BY CHANDLERELLA QUISCALI IN A NORTHERN CRESTED CARACARA (CARACARA CHERIWAY).

A northern crested caracara (Caracara cheriway) was presented after being found nonambulatory in a field. On physical examination, the bird had severe hind-limb paresis. The bird did not improve after 10 days of hospitalization and was euthanized. Histologic examination of the cerebrum and spinal cord revealed multiple adult filarial nematodes surrounded by granulomatous inflammation with several multinucleated giant cells. These parasites were confirmed to be Chandlerella quiscali with polymerase chain reaction. This is the first report of C. quiscali in a bird of prey.

Primary intramedullary hydatid cyst: a case report and literature review.

Intramedullary hydatid cyst is extremely rare. We present a case of pathologically confirmed primary intramedullary hydatid cyst in an otherwise healthy patient. A 17-year-old boy presented with lumbar pain, weakness, and numbness in both lower limbs, and urinate difficulty interrupted for 2 years. The patient had no other signs of systemic hydatid cyst disease. An intramedullary cystic lesion was identified with magnetic resonance imaging and was shown to be a hydatid cyst by histopathologic examination after the surgical removal. Although extremely rare, primary intramedullary hydatid cyst pathology might be the cause of lumbar pain, weakness, and numbness in both lower limbs for those living in endemic areas. Surgical removement is feasible and effective for intramedullary hydatid cyst.

Swollen eyelid reveals multiple intracranial hydatid cysts associated with a palpebral cyst.

We report a case of a hydatid cyst of the eyelid in a 12-year-old boy associated with cerebral involvement. The patient was initially treated by neurosurgeons for brain cysts. The course after an interval of two months was marked by regression of the palpebral cyst on albendazole.

Fatal human eosinophilic meningo-encephalitis caused by CNS co-infection with Halicephalobus gingivalis and West Nile virus.

The saprophytic nematode Halicephalobus is a rare cause of fatal human meningo-encephalitis, and West Nile virus is neurotropic flavivirus implicated in a variety of clinical neurologic syndromes. Here we report a case of rapidly progressive CNS encephalopathy and death. Serologic, immuno-histochemical, histopathologic and nucleic acid studies demonstrate the presence of active Halicephalobus and West Nile virus in the CNS tissue. This is the first reported case of co-infection with these neurotropic pathogens.

Neurognathostomiasis in a young child in India: A case report.

Eosinophilc meningitis is commonly associated with Angiostrongylus and Gnathostoma infection and has largely been reported from Thailand. We present the first case report of neurognathostomaisis in a pediatric patient from India. A 3.5 year old girl presented with fever, parasthesis, behavioral changes followed by flaccid quadriparesis. Neuroimaging showed haemorrhagic radiculomyelitis with cerebrospinal fluid eosinophilia. Diagnosis of Gnathostoma infection was confirmed serologically and she was treated with anthelminthic drugs and steroids. This report emphasizes the increasing importance of central nervous system helminithic infections as an alternative diagnosis to common infections like neurotuberculosis in developing countries, even in pediatric patients. Increasing intercontinental travel and migration have increased the incidence and importance in the developed world as well.

Migration: a notable feature of cerebral sparganosis on follow-up MR imaging.

BACKGROUND AND PURPOSE: Cerebral sparganosis is a rare parasitic infection caused by sparganum, which can migrate in the brain. The purpose of this study was to demonstrate the migration of cerebral sparganosis and describe its patterns on MR imaging. MATERIALS AND METHODS: MR images of 14 patients with cerebral sparganosis treated from 2005 to 2011 were retrospectively reviewed. Diagnosis was made on the basis of a constellation of clinical history, laboratory tests, imaging findings, and histopathology. At least 3 MR imaging studies were performed for each patient during the follow-up period ranging from 12 to 38 months. Time interval, sites, enhanced pattern, and presumed routes of migration were evaluated. RESULTS: Both the initial lesions and migrated ones exhibited the "tunnel" sign and multiloculated rim enhancement. Migration was detected between 4 and 18 months after the baseline MR imaging in 14 lesions (in 14 patients), while 3 of 14 lesions showed a second migration between 22 and 38 months. Nearly all migrations were limited to the same hemisphere except for 2 contralateral migrations through the thalamus. Most of the migrations were in close proximity (within the same lobe, to the adjacent lobe, from the basal ganglia to the cortex, from the cerebellum to the pons and interthalamus) except 1 from the basal ganglia to the cerebellum. A signal change along the presumed route of migration was seen in 3 patients. CONCLUSIONS: Migration is a notable feature of cerebral sparganosis. Demonstration of migration on MR imaging could be a key diagnostic clue and beneficial for the treatment policy.

[Brain hydatidosis: report of four cases]. / Hidatidosis cerebral: aspectos clínicos e imagenológicos. Reporte de 4 casos.

In only 2% of all cases of hydatidosis, the cysts are located in the brain. We report a 12-year-old male, a 5-year-old girl and a 19-year-old female consulting for intracranial hypertension and a 13-year-old male consulting for a left hemiparesis. Imaging studies found intra-cerebral cysts with characteristics of hydatidosis in all. All lesions were completely removed surgically and the pathological study of the excised piece confirmed the diagnosis of hydatidosis.

Hidatidosis cerebral: aspectos clínicos e imagenológicos. Reporte de 4 casos / Brain hydatidosis: Report of four cases

In only 2% of all cases of hydatidosis, the cysts are located in the brain. We report a 12-year-old male, a 5-year-old girl and a 19-year-old female consulting for intracranial hypertension and a 13-year-old male consulting for a left hemiparesis. Imaging studies found intra-cerebral cysts with characteristics of hydatidosis in all. All lesions were completely removed surgically and the pathological study of the excised piece confirmed the diagnosis of hydatidosis.

Toxocara canis larvae reinfecting BALB/c mice exhibit accelerated speed of migration to the host CNS.

Using a small animal imaging system, migratory activity of Toxocara canis larvae stained by carboxyfluorescein succinimidyl ester (CFSE) was observed post primary infection (PPI) and post reinfection (PR) of BALB/c mice. Each infection was performed with 1,000 larvae per mouse. Primary infections were performed with labeled larvae, while for challenge infections the reinfecting larvae were stained by CFSE. The worm burden in mouse organs was determined during a period from 6 h to 21 days and 4 months PPI and PR. In comparison with primary infections that led to the first larvae appearance in the brain after 60 h, greatly accelerated migration of the parasites administered 3 weeks PPI to the CNS and eyes of challenged mice was noted-in both organs the larvae appeared 6 h PR. In all challenged mice, reinfecting larvae prevailed in the resident parasite population. Preliminary experiments with Toxocara cati larvae also revealed early brain involvement in primarily infected mice. Staining of T. canis larvae by CFSE had no effect on the development of a humoral antibody response against T. canis excretory-secretory antigens. In ELISA, elevated levels of specific IgG and IgG1 were noted on day 14 PPI and the levels of antibodies increased till the end of experiment. Reinfection induced an increase in the levels of both antibodies. In terms of optical density, IgG1 antibodies gave higher values in all sera examined. In ELISA for IgG antibodies, an increase in the avidity index of around 50% was detected 1 month PPI; higher-avidity antibodies were also detected in sera of reinfected animals.

Clinical manifestations of eosinophilic meningitis caused by Angiostrongylus cantonensis: 18 years' experience in a medical center in southern Taiwan.

BACKGROUND: With the improvement of public health, eosinophilic meningitis associated with Angiostrongylus cantonensis infection is now seldom reported in Taiwan. Eosinophilic meningitis typically occurred sporadically in children. This study aims to analyze the clinical manifestations and change in the contemporary epidemiology of eosinophilic meningitis in Taiwan. METHODS: This is a retrospective study of patients diagnosed with eosinophilic meningitis at Kaohsiung Veterans General Hospital, from December 1991 to September 2009. The demographic characteristics, clinical presentations, laboratory data, radiographic imaging, and treatment and clinical outcome were analyzed. A PubMed search with the keywords of eosinophilic meningitis, A cantonensis, and Taiwan was performed to retrieve cases of eosinophilic meningitis caused by A cantonensis since 1960. RESULTS: Thirty-seven patients were diagnosed to have eosinophilic meningitis during a period of 18 years. The median age was 32 years (range, 2-80 years). Ninety five percent (35/37) of the patients were adults. The median incubation period was 10.5 days (range, 3-80 days). Most of the patients presented with headache (29, 78%), fever (25, 68%), and 11(30%) had hyperesthesia. Patients with hyperesthesia had longer incubation period (55 vs. 7 days, p=0.004), lower serum immunoglobulin E levels (127.5 vs. 1295 IU/mL, p<0.001), and longer duration between symptom onset and spinal taps (14 vs. 5 days, p=0.011). Three patients presented initially with lymphocytic meningitis, and eosinophilia only appeared on a second lumbar puncture. Magnetic resonance imaging of the brain disclosed leptomeningeal enhancement (17/26, 65%) and increased signal intensity (10/26, 38%) on T2-weighted and fluid-attenuated inversion recovery images. There were eight relapses and two patients died. No sequela was noted except in one 2-year-old toddler, who had weakness of both lower limbs. CONCLUSIONS: The epidemiology of eosinophilic meningitis has changed during the past two decades in Taiwan and occurs mainly in adults in the setting of outbreaks. Hyperesthesia; repeated lumbar puncture in cases with lymphocytic meningitis of uncertain cause; and a detailed history, including food consumption, are important to establish an accurate diagnosis.

Cerebral sparganosis: A case report.

Sparganosis is a rare parasitic infection in humans caused by a larval cestode of the genus Spirometra. Spargana invade muscle, subcutaneous tissue, the eye, urogenital, and abdominal viscera, but the central nervous system (CNS) is not a frequent site of invasion. Here, we describe an 18-year-old patient with cerebral sparganosis and review data from other cases reported in the medical literature.

Biochemical and immunopathological changes in experimental neurotoxocariasis.

Toxocariasis is a widespread soil-transmitted parasitic disease. Toxocara canis larvae migrate through the tissues with a special predilection for the central nervous system. Recently, neurotoxocariasis is being diagnosed in humans with increasing frequency due to improved diagnostic tools. The present study aimed at exploring the biochemical and immunopathological alterations in the brain in experimental T. canis infection. For this purpose, 75 Toxocara-infected mice were sacrificed at 2, 5, and 16 weeks post-infection. The brains were removed and assayed for total larval count, pro-inflammatory cytokines (TNF-alpha, IL-6), and central neurotransmitters (gamma-aminobutyric acid, glutamate, dopamine, norepinephrine, and serotonin). Brain sections were also stained for histopathological study, and for assessment of the expression of inducible nitric oxide synthase (iNOS), and glial fibrillary acidic protein (GFAP) by immunohistochemical methods. We found that larval recovery showed progressive increase over the course of infection. Furthermore, the infected mice displayed increased expression of pro-inflammatory cytokines and iNOS, as well as significant disturbances in neurotransmitter profile. Astrocytic activation, evidenced by enhanced expression of GFAP, was also manifest in infected animals. These changes were maximal in the chronic stage of infection or intensified over time. In conclusion, experimental neurotoxocariasis is associated with significant biochemical, immunological, and pathological changes.