Angiostrongylosis meningomyelitis without blood eosinophilia.

Angiostrongylus cantonensis and Gnathostoma spinigerum usually cause eosinophilic meningitis with associated peripheral blood eosinophilia. A 44-year-old man developed acute paraplegia with bowel and bladder dysfunction. Spinal magnetic resonance images showed a long T2W hyperintensity signal from the 1st to 8th spinal thoracic level. Cerebrospinal fluid analysis revealed eosinophilia and elevated cerebrospinal fluid protein, whereas differential leucocytes count in peripheral blood was unremarkable. Positive immunoblot tests for A. cantonensis antibody in serum and cerebrospinal fluid were reported. The patient had neither history of recent traveling to the high endemic areas of the parasite in Thailand, nor consumption the parasitic hosts. Immediate treatment with intravenous pulse methylprednisolone and oral albendazole resulted in complete recovery. Despite an unremarkable differential leucocytes count, absence a history of parasitic hosts consumption, and a less common presentation with meningomyelitis, A. cantonensis should be considered when cerebrospinal fluid eosinophilia presents.

Disseminated Neospora caninum infection in a dog with severe colitis.

A 12-y-old spayed female Schipperke dog with a previous diagnosis of inflammatory bowel disease was presented with a 2-mo history of severe colitis. The patient's condition progressed to hepatopathy, pneumonia, and dermatitis following management with prednisolone and dexamethasone sodium phosphate. Colonic biopsies identified severe necrosuppurative colitis with free and intracellular parasitic zoites. Postmortem examination confirmed extensive chronic-active ulcerative colitis, severe acute necrotizing hepatitis and splenitis, interstitial pneumonia, ulcerative dermatitis, myelitis (bone marrow), and mild meningoencephalitis with variable numbers of intracellular and extracellular protozoal zoites. PCR on samples of fresh colon was positive for Neospora caninum. Immunohistochemistry identified N. caninum tachyzoites in sections of colon, and a single tissue cyst in sections of brain. Administration of immunosuppressive drugs may have allowed systemic dissemination of Neospora from the intestinal tract.

Angiostrongylus cantonensis Meningitis and Myelitis, Texas, USA.

Infection with Angiostrongylus cantonensis roundworms is endemic in Southeast Asia and the Pacific Basin. A. cantonensis meningitis and myelitis occurred in summer 2013 in a child with no history of travel outside of Texas, USA. Angiostrongyliasis is an emerging neurotropic helminthic disease in Texas and warrants increased awareness among healthcare providers.

Parelaphostrongylus tenuis Cerebrospinal Nematodiasis in a Horse with Cervical Scoliosis and Meningomyelitis.

There are reports of horses with acute onset acquired cervical scoliosis and cutaneous analgesia. The underlying dorsal gray column myelitis that produces these neurologic signs has been only presumptively attributed to migration of Parelaphostrongylus tenuis within the spinal cord. Despite previous confirmation brain by polymerase chain reaction testing, of P. tenuis within the brain of horses by polymerase chain reaction testing, genetic testing has failed to definitively identify the presence of this parasite in cases of equine myelitis. This case report provides molecular confirmation via polymerase chain reaction of P. tenuis within the cervical spinal cord of a horse with scoliosis and cutaneous analgesia.

[A case of myelitis with eosinophilia of the cerebrospinal fluid].

A 25-year-old woman developed numbness of the right flank two weeks after a one-month stay in Thailand and Laos, which are known as areas of angiostrongylosis cantonensis infections. The signs were numbness, pain sense disorder, and vibration sense disorder on the region of the 6th to 12th dermatome. On a MRI T(2) weighted image (T(2)WI), signal hyperintensity in a longitudinal spinal lesion was seen. In the cerebrospinal fluid (CSF), eosinophils were detected. The patient was diagnosed with eosinophilic meningitis and myelitis, and then treated with intravenous methylprednisolone. This improved her signs, CSF and MRI findings. She took no drugs, did not have any allergies, any vasculitis, or neuromyelitis optica spectrum disorders. Although anti-parasite antibodies were not identified, she was probably infected by angiostrongylus cantonensis from her history and examinations.

IL-12p40 deficiency leads to uncontrolled Trypanosoma cruzi dissemination in the spinal cord resulting in neuronal death and motor dysfunction.

Chagas' disease is a protozoosis caused by Trypanosoma cruzi that frequently shows severe chronic clinical complications of the heart or digestive system. Neurological disorders due to T. cruzi infection are also described in children and immunosuppressed hosts. We have previously reported that IL-12p40 knockout (KO) mice infected with the T. cruzi strain Sylvio X10/4 develop spinal cord neurodegenerative disease. Here, we further characterized neuropathology, parasite burden and inflammatory component associated to the fatal neurological disorder occurring in this mouse model. Forelimb paralysis in infected IL-12p40KO mice was associated with 60% (p<0.05) decrease in spinal cord neuronal density, glutamate accumulation (153%, p<0.05) and strong demyelization in lesion areas, mostly in those showing heavy protein nitrosylation, all denoting a neurotoxic degenerative profile. Quantification of T. cruzi 18S rRNA showed that parasite burden was controlled in the spinal cord of WT mice, decreasing from the fifth week after infection, but progressive parasite dissemination was observed in IL-12p40KO cords concurrent with significant accumulation of the astrocytic marker GFAP (317.0%, p<0.01) and 8-fold increase in macrophages/microglia (p<0.01), 36.3% (p<0.01) of which were infected. Similarly, mRNA levels for CD3, TNF-α, IFN-γ, iNOS, IL-10 and arginase I declined in WT spinal cords about the fourth or fifth week after infection, but kept increasing in IL-12p40KO mice. Interestingly, compared to WT tissue, lower mRNA levels for IFN-γ were observed in the IL-12p40KO spinal cords up to the fourth week of infection. Together the data suggest that impairments of parasite clearance mechanisms in IL-12p40KO mice elicit prolonged spinal cord inflammation that in turn leads to irreversible neurodegenerative lesions.

Parasite meningomyelitis in cats in Uruguay.

Two outbreaks of progressive hind limb paresis in cats (Felis catus) caused by parasitic meningomyelitis in Uruguay are reported. The case studies occurred in 2008 and 2009 respectively, in the rural areas of Fray Bentos (33° 07' 40.39'' S) and were characterized by hindquarter paralysis. This paralysis was progressive and had a chronic progression of approximately 12 months until the death or euthanasia of the animals. Clinical symptoms started with ataxia of the hindquarters with lateral side-to-side swaying and culminated in total paralysis. Two animals were sent for necropsy in 2009. The main histopathological findings were severe myelitis in the lumbar spinal cord with perivascular cuffing and white matter necrosis, severe nonsuppurative meningitis with thrombi in subarachnoid blood vessels, and intravascular presence of multiple adult parasites. From the morphological characteristics of the parasites and location in the leptomeninges, the parasite was identified as the nematode Gurltia paralysans.

Parasite meningomyelitis in cats in Uruguay / Meningomielites parasitária em gatos no Uruguai

Two outbreaks of progressive hind limb paresis in cats (Felis catus) caused by parasitic meningomyelitis in Uruguay are reported. The case studies occurred in 2008 and 2009 respectively, in the rural areas of Fray Bentos (33º 07' 40.39" S) and were characterized by hindquarter paralysis. This paralysis was progressive and had a chronic progression of approximately 12 months until the death or euthanasia of the animals. Clinical symptoms started with ataxia of the hindquarters with lateral side-to-side swaying and culminated in total paralysis. Two animals were sent for necropsy in 2009. The main histopathological findings were severe myelitis in the lumbar spinal cord with perivascular cuffing and white matter necrosis, severe nonsuppurative meningitis with thrombi in subarachnoid blood vessels, and intravascular presence of multiple adult parasites. From the morphological characteristics of the parasites and location in the leptomeninges, the parasite was identified as the nematode Gurltia paralysans.

São relatados dois surtos de paralisia progressiva dos membros posteriores em gatos (Felis catus), causada por meningomielite parasitária no Uruguai. Os estudos de casos ocorreram entre os anos 2008 e 2009, respectivamente, nas zonas rurais de Fray Bentos (33º 07' 40,39" S) e foram caracterizados por paralisia dos membros posteriores. Esta paralisia era progressiva e tinha evolução crônica de aproximadamente 12 meses, até que os animais vinham a óbito ou eram eutanasiados. Os sintomas clínicos começaram com ataxia dos membros posteriores, com movimentos laterais, terminado em paralisia total. Em 2009, dois animais foram encaminhados para necropsia. Os achados histopatológicos foram caracterizados por severa mielite na medula espinhal lombar com manguitos perivasculares linfocitarios e necrose da substância branca, severa meningite não supurativa com trombos nos vasos sanguíneos subaracnóideos, e presença intravascular de múltiplos parasitos adultos. De acordo com as características morfológicas dos parasitos e localização nas leptomeninges, este foi identificado como um nematóide da espécie Gurltia paralysans.

Toxocara canis myelitis: clinical features, magnetic resonance imaging (MRI) findings, and treatment outcome in 17 patients.

Toxocara myelitis is a rare disease. Few cases have been reported in the literature. Patients present with myelopathy, occasional eosinophilia in blood and cerebrospinal fluid (CSF), with abnormal signals on magnetic resonance imaging (MRI). In the current study we report 17 cases of isolated Toxocara myelitis from a single tertiary referral center in Lebanon, with description of the clinical presentation, laboratory data, MRI findings, and response to antihelminthic treatment. Clinical and laboratory data were collected for 17 patients who presented with evidence of spinal cord disease. The clinical presentation included sensory, motor, and autonomic dysfunction, predominantly in the lower extremities. Patients exhibited a subacute or chronic course; this was either slowly progressive or remitting-relapsing with mild to moderate disability. The patients underwent extensive blood and CSF workup as well as MRI of the spinal cord and brain. Only 2 patients had a high eosinophil count in the CSF, although blood eosinophilia was seen in 6 patients. All patients tested positive for Toxocara canis antibodies in the blood and CSF. MRI of the spinal cord revealed a single characteristic lesion in the spinal cord with fusiform enlargement that was isointense on T1-weighted images and hyperintense on T2-weighted images. Nodular enhancement was seen after gadolinium injection. Treatment with albendazole, with or without steroids, resulted in marked neurologic improvement and normalization of the MRI in all patients.The finding of a single inflammatory MRI lesion in the spinal cord with positive Toxocara canis serology in the blood and CSF in cases of subacute or chronic myelitis suggests the diagnosis of Toxocara myelitis, irrespective of the presence of eosinophilia. Antihelminthic treatment is associated with a good outcome.

Diagnosis of Parelaphostrongylus spp. infection as a cause of meningomyelitis in calves.

Migration of Parelaphostrongylus spp. has been documented to cause central nervous system damage in a number of aberrant host species but appears to be uncommon in cattle. The current report describes the clinical and laboratory findings, antemortem and definitive diagnosis, and response to treatment of Parelaphostrongylus spp. infection in five 3-7- month-old Limousin calves from 2 farms. All calves had signs of acute (n = 2) and chronic (n = 3) progressive spinal cord dysfunction. Cerebrospinal fluid analysis revealed a marked eosinophilic (acute cases) or lymphocytic (chronic cases) pleocytosis and elevated protein in all calves. A necropsy and histopathologic evaluation was performed on 2 euthanized calves, and histopathology revealed lymphoplasmacytic and eosinophilic meningomyelitis with multiple intradural and intramedullary expansile hyperplastic lymphoid nodules containing germinal centers and nematode fragments. DNA sequencing was performed on nested polymerase chain reaction products amplified with parasite-specific primers obtained from formalin-fixed and frozen spinal cord; PCR products from these 2 calves were 100% identical to Parelaphostrongylus species on DNA sequencing, confirming the diagnosis. Surviving calves rapidly improved following treatment with anthelmintics and corticosteroids. This case series identified Parelaphostrongylus spp. (likely P. tenuis) as a cause of spinal cord disease in calves and highlights the need for vigilance against aberrant parasite migration in calves grazing wet, snail-infested pastures. Cerebrospinal fluid eosinophilia is useful for supporting an antemortem diagnosis of Parelaphostrongylus in calves with acute neurologic disease; however, a lymphocytosis is observed in chronic or treated cases.

Immunoblot diagnostic test for neurognathostomiasis.

Neurognathostomiasis is a rare but severe form of human gnathostomiasis. Diagnosis of neurognathostomiasis is made presumably by using clinical manifestations. Serologic tests for neurognathostomiasis are not widely available and limited. We studied 12 patients with diagnoses of neurognathostomiasis at Srinagarind Hospital, Khon Kaen University, Thailand. There were three types of neurognathostomiasis (five patients with intracerebral hemorrhage, one patient with subarachnoid hemorrhage, and six patients with myelitis). All patients were tested for antibodies against Gnathostoma spinigerum by an immunoblotting technique. The sensitivity and specificity of the 21-kD and 24-kD diagnostic bands were 83.3% and 100%, and 91.7% and 100%, respectively. The sensitivity, specificity, positive predictive value, and negative predictive value for the 21-kD and 24-kD diagnostic bands were all 100%. Both diagnostic bands are a helpful diagnostic tool for neuro gnathostomiasis and show good diagnostic properties.

Portal Doppler ultrasound evaluation in myelitis by Schistosoma mansoni.

UNLABELLED: The mechanism for development of schistosomal myelitis has not yet been completely understood. Few publications have tried to establish a link between the general clinical presentation of the illness and its neurological manifestations. OBJECTIVE: To evaluated the portal blood flow in patients with schistosomal myelitis and controls. METHOD: Forty-three individuals were evaluated using portal Doppler ultrasound. Group I consisted of 13 patients with the spinal form of schistosomiasis. Group II included 10 patients with intestinal and hepatointestinal forms of schistosomiasis, but no neurological symptoms; while group III involved 20 healthy controls. RESULTS: Portal venous speed and portal venous flow were significantly elevated in group I (p<0.001) compared with the others. CONCLUSION: Doppler ultrasound demonstrated a situation of high flow within the portal venous system of patients with schistosomal myelitis.

Portal Doppler ultrasound evaluation in myelitis by Schistosoma mansoni / Avaliação pela ultrassonografia com Doppler portal na mielite pelo Schistosoma mansoni

The mechanism for development of schistosomal myelitis has not yet been completely understood. Few publications have tried to establish a link between the general clinical presentation of the illness and its neurological manifestations. Objective: To evaluated the portal blood flow in patients with schistosomal myelitis and controls. Method: Forty-three individuals were evaluated using portal Doppler ultrasound. Group I consisted of 13 patients with the spinal form of schistosomiasis. Group II included 10 patients with intestinal and hepatointestinal forms of schistosomiasis, but no neurological symptoms; while group III involved 20 healthy controls. Results: Portal venous speed and portal venous flow were significantly elevated in group I (p<0.001) compared with the others. Conclusion: Doppler ultrasound demonstrated a situation of high flow within the portal venous system of patients with schistosomal myelitis.

A fisiopatogênese da mielopatia esquistossomótica não é completamente entendida, sendo escassas as publicações que tentam inferir a relação entre a forma clínica da esquistossomose e suas manifestações neurológicas. Objetivo: Avaliar o fluxo sanguíneo do sistema porta em pacientes com mielite esquistossomótica, contribuindo no entendimento dos mecanismos que favorecem a chegada dos parasitas e/ou seus derivados ao sistema nervoso. Método: Foram avaliados 43 indivíduos pela Dopplerfluxometria portal. O grupo I constou de 13 pacientes com esquistossomose medular, sendo o grupo II composto por 10 portadores de formas intestinal e hepatointestinal (sem doença neurológica), e o grupo III, por 20 controles sadios. Resultados: A velocidade venosa portal e o fluxo venoso portal foram significativamente elevados (p-valor<0,001) no grupo I. Conclusão: A Dopplerfluxometria demonstrou a presença de estados hiperdinâmicos do leito vascular porta em pacientes com mielite pelo Schistosoma mansoni.

Neurodegeneration and increased production of nitrotyrosine, nitric oxide synthase, IFN-gamma and S100beta protein in the spinal cord of IL-12p40-deficient mice infected with Trypanosoma cruzi.

BACKGROUND/AIM: Chagas' disease is caused by Trypanosoma cruzi and occurs in most Latin American countries. The protozoan may colonize the central nervous system (CNS) of immune-compromised human hosts, thus causing neuronal disorders. Systemic control of the intracellular forms of the parasite greatly depends on the establishment of a TH1 response and subsequent nitric oxide (NO) release. At the CNS, it is known that low concentrations of NO promote neuronal survival and growth, while high concentrations exert toxic effects and neuron death. Accounting for NO production by astrocytes is the glia-derived factor S100beta, which is overproduced in some neurodegenerative diseases. In the current work, we studied the expression of NO, interferon (IFN)-gamma and S100beta in the spinal cord tissue of IL-12p40KO mice infected with T. cruzi, a model of neurodegenerative process. METHODS: IL-12p40KO and wild-type (WT) female mice infected with T. cruzi Sylvio X10/4 (10(5) trypomastigotes, intraperitoneally) were euthanized when IL-12p40KO individuals presented limb paralysis. Spinal cord sections were submitted to immunohistochemical procedures for localization of neurofilament, laminin, nitrotyrosine, NO synthases (NOS), IFN-gamma and S100beta. The total number of neurons was estimated by stereological analysis and the area and intensity of immunoreactivities were assessed by microdensitometric/morphometric image analysis. RESULTS: No lesion was found in the spinal cord sections of WT mice, while morphological disarrangements, many inflammatory foci, enlarged vessels, amastigote nests and dying neurons were seen at various levels of IL-12p40KO spinal cord. Compared to WT mice, IL-12p40KO mice presented a decrement on total number of neurons (46.4%, p < 0.05) and showed increased values of immunoreactive area for nitrotyrosine (239%, p < 0.01) and NOS (544%, p < 0.001). Moreover, the intensity of nitrotyrosine (16%, p < 0.01), NOS (38%, p < 0.05) and S100beta (21%, p < 0.001) immunoreactivities were also augmented. No IFN-gamma-labeled cells were seen in WT spinal cord tissue, contrary to IL-12p40KO tissue that displayed inflammatory infiltrating cells and also some parenchymal cells positively labeled. CONCLUSION: We suggest that overproduction of NO may account for neuronal death at the spinal cord of T. cruzi-infected IL-12p40KO mice and that IFN-gamma and S100beta may contribute to NOS activation in the absence of IL-12.

Verminous myelitis in a pit bull puppy.

A 10-week-old, male pit bull dog presented to the referring veterinarian with hind limb paresis and epaxial muscle atrophy. No spinal lesions were identified at gross necropsy; however, histologically there was marked granulomatous myelitis in the spinal cord between T13 and L2 with occasional, intralesional nematode larvae. Based on morphologic characteristics, the nematode larvae were identified as Strongyloides spp., possibly Strongyloides stercoralis.