Cerebral Coenurosis of a Long-Tailed Goral, Naemorhedus caudatus, in Korea.

We intended to describe a case of cerebral coenurosis in a long-tailed goral, Naemorhedus caudatus, from Hwacheon-gun, Gangwon-do (Province), in the Korea. The goral, a 10-year-old male, was suffering from neurological symptoms, such as turning the circle to one side without lifting the head straight, and died at 30 days after admission to the wildlife medical rescue center in Chuncheon-si, Gangwon-do. A fluid-filled cyst was detected in the left cerebral hemisphere by computed tomography and magnetic resonance imaging. The cyst removed from the deceased goral was transparent, about 3×3 cm in size, contained a clear fluid and approximately 320 protoscolices invaginating from the internal germinal layer. The protoscolex had 4 suckers and a rostellum with 28 hooklets arranged in 2 rows. By the present study, a case of cerebral coenurosis was first confirmed in a long-tailed goral, N. caudatus, from Gangwon-do, in Korea. The residents frequently exposed in the sylvatic environment should be careful the accidental infections of zoonotic metacestode of Taenia multiceps, Coenurus cerebralis, in Korea.

Cerebral cystic echinococcosis in Mongolian children caused by Echinococcus canadensis.

Recent molecular re-evaluation of Echinococcus granulosus, which causes cystic echinococcosis (CE), has revealed that it is not a single species, but instead consists of 5 cryptic species. Among them, E. granulosus (dog-sheep strain) is predominant (75%) followed by Echinococcus canadensis (22%). The major affected organs, in humans, are the liver (88%) and lungs (11%). Primary cerebral CE comprises less than 1% of all cases. As cerebral CE cases are rare, there are few reports with molecular confirmation of the causative species. This study reports mitochondrial gene analysis from 4 Mongolian pediatric cerebral CE cases. Molecular confirmation was obtained for 3 of the 4 cases, with all 3 cases determined to be due to E. canadensis (G6/G7) infection. None of the cases had other organ involvement. This is only the third report on the molecular identification of the Echinococcus species responsible for cerebral CE, and only the second report of E. canadensis (G6/G7) being the causative agent of cerebral CE.

Meningoencephalitis caused by pathogenic Sarcocystis species in a naturally infected sheep in Turkey.

A 3-year-old sheep was examined after an acute onset of hind limb paralysis and ataxia. At necropsy, central nervous system, pulmonary and intestinal hyperaemia and ecchymoses in the aortic arch were observed. Main microscopic lesions were confined to the heart, cerebrum and cerebellum. There were a multifocal mild myocarditis and nonsuppurative meningoencephalitis together with protozoal cysts in the heart and the brain. Protozoal cystic structures were observed within many of the myocardial fibers as well as in the cerebrum and cerebellum. Using light microscopy it could not be morphologically determined whether these organisms were Toxoplasma (T.) gondii or Neospora (N.) caninum. Additional diagnostic methods like immunohistochemistry and polymerase chain reaction provided differentiation of Sarcocystis from T. gondii and N. caninum. Transmission electron microscopy demonstrated characteristic features of Sarcocystis sp. as previously described. This is the first confirmed diagnosis of Sarcocystis sp. in the central nervous system of a sheep from Turkey.

[MRI findings of cerebral schistosomiasis in acute stage：establishment of experimental model of acute cerebral schistosomiasis with rabbits].

OBJECTIVE: To establish an experimental model of acute cerebral schistosomiasis japonica and explore the MRI manifestations of acute cerebral schistosomiasis. METHODS: Rabbits were divided into 3 groups with 10 rabbits in each group. The rabbits in the experimental group were directly injected with suspension fluid of Schistosoma japonicum eggs (0.9 mg, 1 ml) by the cranial drilling method, those in the negative control group were given saline (1 ml) by the same method above-mentioned, and those in the blank control group were not given any treatment. Antibiotic was given to the first two groups after the operation. The clinical manifestations of the 3 groups were observed, and the magnetic resonance imaging (MRI) was performed in 30 days post-operation, and then the brain tissues were taken for pathological examinations. RESULTS: All the rabbits in the experimental group exhibited inappetence, various neurological symptoms including hemiplegia, and weight loss after the operation; while those in the negative control group showed inappetence in 3 days after the operation, and 1 week later, the symptom disappeared; there were no adverse reactions in the blank control group. MRI of the experimental group showed nodular or patchy enhancement on T1WI enhancement, brain edema, abnormal ventricular dilatation, and needle augmentation. SWI displayed hypointense in the abnormal enhanced nodules and flaky hypointense on the operation brain. In the negative control group, 2 rabbits showed abnormal enhancement of the needle canal, and 1 showed mild dilatation of the ventricle. The blank control group showed normal manifestations. The pathological examinations showed abnormal appearances in 10 rabbits of the experimental group, including 6 with S. japonicum egg granuloma nodules, nonspecific granuloma nodules coexisted with perivascular inflammation; no granuloma nodules were found in the negative control group, but 2 rabbits showed vascular inflammation; the blank control group showed the normal brain tissue. CONCLUSIONS: An experimental model of acute cerebral schistosomiasis is successfully established in rabbits by intracranial injection of schistosome eggs. The MRI examination combined with the clinical manifestations can improve the accuracy of early diagnosis of cerebral schistosomiasis.

[Clinical features of 14 cases of cerebral schistosomiasis in Jiangxi Province].

OBJECTIVE: To discuss the clinical features of cerebral schistosomiasis. METHODS: The clinical data of fourteen patients with cerebral schistosomiasis from March 2010 to March 2016 were collected and analyzed retrospectively. RESULTS: The schistosomiasis immunological tests of sera and cerebrospinal fluids from the fourteen patients were all positive. Eosinophils increased in ten cases, and the proportion was 5.1%-60.3%. Schistosoma eggs were found in seven cases by the fecal Kato-Katz method. Fourteen cases were all infected with Schistosome japonicum. Twelve cases were diagnosed as chronic type, and two cases as acute type. Thirteen patients received medical treatment, of which twelve were cured, and one improved. One patient received the surgical resection of the lesion. CONCLUSIONS: The clinical manifestations of cerebral schistosomiasis mainly include seizure, headache, dizziness and fever. In the enhanced head magnetic resonance imaging (MRI), the lesions are clustered and merged into lumps, which is the characteristic image of cerebral schistosomiasis japonica. The praziquantel treatment can achieve a good prognosis.

Neurotoxocarosis: marked preference of Toxocara canis for the cerebrum and T. cati for the cerebellum in the paratenic model host mouse.

BACKGROUND: Infective larvae of the worldwide occurring zoonotic roundworm T. canis exhibit a marked affinity to the nervous tissues of paratenic hosts. In humans, most cases of neurotoxocarosis are considered to be caused by larvae of T. canis as T. cati larvae have rarely been found in the CNS in previous studies. However, direct comparison of studies is difficult as larval migration depends on a variety of factors including mouse strains and inoculation doses. Therefore, the present study aims to provide a direct comparison of both roundworm species in mice as a model for paratenic hosts with specific focus on the CNS during the acute and chronic phase of disease to provide a basis for further studies dealing with neurotoxocarosis. METHODS: C57Bl/6J mice were infected with 2000 embryonated T. canis and T. cati eggs, respectively as well as Balb/c mice infected with T. cati eggs only. On 8 time points post infection, organs were removed and microscopically examined for respective larvae. Special focus was put on the CNS, including analysis of larval distribution in the cerebrum and cerebellum, right and left hemisphere as well as eyes and spinal cord. Additionally, brains of all infection groups as well as uninfected controls were examined histopathologically to characterize neurostructural damage. RESULTS: Significant differences in larval distribution were observed between and within the infection groups during the course of infection. As expected, significantly higher recovery rates of T. canis than T. cati larvae were determined in the brain. Surprisingly, significantly more T. canis larvae could be found in cerebra of infected mice whereas T. cati larvae were mainly located in the cerebellum. Structural damage in brain tissue could be observed in all infection groups, being more severe in brains of T. canis infected mice. CONCLUSIONS: The data obtained provides an extensive characterization of migrational routes of T. canis and T. cati in the paratenic host mouse in direct comparison. Even though to a lesser extent, structural damage in the brain was also caused by T. cati larvae and therefore, the potential as pathogenic agents should not be underestimated.

Toxoplasma gondii infection in llama (Llama glama): acute visceral disseminated lesions, diagnosis, and development of tissue cysts.

Clinical toxoplasmosis has been reported in many species of warm-blooded animals but is rare in camelids. Here we report acute fatal systemic toxoplasmosis involving heart, thyroid gland, stomach, intestine, diaphragm, kidneys, adrenal glands, and liver of a 13-mo-old llama (Llama glama). Many Toxoplasma gondii tachyzoites were associated with tissue necrosis in multiple organs. Death was attributed to severe myocarditis. Ulcers associated with numerous tachyzoites were present in the C3 compartment of the stomach. Tissue cyst development was followed using bradyzoite-specific T. gondii antibodies. Individual intracellular, and groups of 2 or more, bradyzoites were identified in hepatocytes, biliary epithelium, myocardiocytes, lung, diaphragm, thyroid gland, spleen, and stomach. Lesions in the brain were a few microglial nodules and very early tissue cysts containing 1-3 bradyzoites. These observations suggest that the animal had acquired toxoplasmosis recently. Diagnosis was confirmed immunohistochemically by reaction with T. gondii -specific polyclonal rabbit serum but not with antibodies to the related protozoan Neospora caninum . Genetic typing using the DNA extracted from paraffin-embedded myocardium of llama and 10 PCR-restriction fragment length polymorphism (RFLP) markers revealed a type II allele at the SAG1, SAG2, SAG3, BTUB, GRA6, c22-8, c29-2, PK1 L358, and Apico loci; therefore, this isolate belongs to the ToxoDB PCR-RFLP genotype #1, which is most common in North America and Europe.

Babesia lengau associated with cerebral and haemolytic babesiosis in two domestic cats.

BACKGROUND: Although reported sporadically from various countries, feline babesiosis appears to be a significant clinical entity only in South Africa, where Babesia felis is usually incriminated as the causative agent. Babesia lengau, recently described from asymptomatic cheetahs, has now possibly been incriminated as the causative agent in two severe clinical cases in domestic cats. FINDINGS: Both cats were euthanised in extremis. While typical feline babesiosis in South Africa is an afebrile disease with a chronic manifestation, there was acute onset of severe clinical signs in both cats and their body temperatures were above the normal range when they were presented for treatment. Haemolytic anaemia was confirmed in one case. To our knowledge, this is the first report of cerebral babesiosis in cats.On reverse line blot 18S rDNA PCR products obtained from both cats showed positive hybridization profiles with the B. lengau species-specific probe. The two partial parasite 18S rRNA gene sequences obtained, showed high sequence similarity (99.9%) to B. lengau. In a representative tree constructed by the neighbor-joining method using the two-parameter model of Kimura the two obtained partial 18S rDNA sequences and that of B. lengau formed a monophyletic group with B. conradae and sequences previously isolated from humans and wildlife in the western USA. CONCLUSION: All clinical cases of feline babesiosis in South Africa are not necessarily caused by B. felis. Other piroplasms, e.g. B. lengau, may be incriminated in clinical cases, especially those occurring outside the known endemic area.

Toxoplasma gondii infection induces dendritic retraction in basolateral amygdala accompanied by reduced corticosterone secretion.

Pathological anxiety is thought to reflect a maladaptive state characterized by exaggerated fear. Naturally occurring perturbations that reduce fear can be crucial in the search for new treatments. The protozoan parasite Toxoplasma gondii invades rat brain and removes the fear that rats have of cat odors, a change believed to be parasitic manipulation of host behavior aimed at increasing parasite transmission. It is likely that mechanisms employed by T. gondii can be used as a heuristic tool to understand possible means of fear reduction in clinical settings. Male Long-Evans rats were infected with T. gondii and compared with sham-infected animals 8 weeks after infection. The amount of circulating plasma corticosterone and dendritic arborization of basolateral amygdala principal neurons were quantified. Previous studies have shown that corticosterone, acting within the basolateral amygdala, enhances the fear response to environmental stimuli. Here we show that T. gondii infection causes a dendritic retraction in basolateral amygdala neurons. Such dendritic retraction is accompanied by lower amounts of circulating corticosterone, both at baseline and when induced by an aversive cat odor. The concerted effects of parasitism on two pivotal physiological nodes of the fear response provide an animal model relevant to interactions between stress hormones and amygdalar plasticity.

Antimalarial activity of the anticancer histone deacetylase inhibitor SB939.

Histone deacetylase (HDAC) enzymes posttranslationally modify lysines on histone and nonhistone proteins and play crucial roles in epigenetic regulation and other important cellular processes. HDAC inhibitors (e.g., suberoylanilide hydroxamic acid [SAHA; also known as vorinostat]) are used clinically to treat some cancers and are under investigation for use against many other diseases. Development of new HDAC inhibitors for noncancer indications has the potential to be accelerated by piggybacking onto cancer studies, as several HDAC inhibitors have undergone or are undergoing clinical trials. One such compound, SB939, is a new orally active hydroxamate-based HDAC inhibitor with an improved pharmacokinetic profile compared to that of SAHA. In this study, the in vitro and in vivo antiplasmodial activities of SB939 were investigated. SB939 was found to be a potent inhibitor of the growth of Plasmodium falciparum asexual-stage parasites in vitro (50% inhibitory concentration [IC(50)], 100 to 200 nM), causing hyperacetylation of parasite histone and nonhistone proteins. In combination with the aspartic protease inhibitor lopinavir, SB939 displayed additive activity. SB939 also potently inhibited the in vitro growth of exoerythrocytic-stage Plasmodium parasites in liver cells (IC(50), ~150 nM), suggesting that inhibitor targeting to multiple malaria parasite life cycle stages may be possible. In an experimental in vivo murine model of cerebral malaria, orally administered SB939 significantly inhibited P. berghei ANKA parasite growth, preventing development of cerebral malaria-like symptoms. These results identify SB939 as a potent new antimalarial HDAC inhibitor and underscore the potential of investigating next-generation anticancer HDAC inhibitors as prospective new drug leads for treatment of malaria.

Encephalitozoonosis in pet rabbits (Oryctolagus cuniculus): pathohistological findings in animals with latent infection versus clinical manifestation.

Encephalitozoon cuniculi is a common infectious agent of rabbits. The aim of this study was to determine the distribution and extent of histological lesions in the brain and in the kidney of naturally infected pet rabbits with or without clinical encephalitozoonosis. In 71 animals (33 with symptoms) which died or were euthanised, histopathological examination including staining of spores (Ziehl-Neelsen, acid-fast trichrome) was performed and changes were described quantitatively. The cerebrum was the most frequently affected brain region (97.5%), whilst the cerebellum (55%) and the vestibular cores (37.5%) were less commonly concerned. Granulomas were found in 77.5% of animals with encephalitis and in 12.5% of rabbits with interstitial nephritis. Although cerebral granulomas were found irrespective of the grade of histological changes, they were significantly correlated with changes at higher grades. There was no correlation between the severity of encephalitis and neurological symptoms. Since severe lesions were also found in clinically inconspicuous animals, histological findings of inflammatory lesions are not indicative of overt encephalitozoonosis as the causative agent for neurological signs. Other diseases causing neurological symptoms, such as suppurative encephalitis, otitis media as well as malignant lymphoma were also detected in the rabbit population that was examined in the present study.

Initial stage of development and migratory behavior of Toxocara canis larvae in BALB/c mouse experimental model

In the present study, the initial developmental stage of Toxocara canis eggs and larvae, and number of recovered larvae from BALB/c mouse-infected organs are described. In vitro culture of T. canis detects the frequencies of interphasic, mitotic and embryonated eggs only within a 7-day period. Analysis by egg counting was carried out for 32 days. The results showed that at 7 days after cultivation, the frequency of larvae was 50.4% and that this frequency reached 52.8% in 32 days. In the experimental infection of BALB/c mice with T. canis, the number of recovered larvae statistically increased in the brain and liver, with doses of approximately 200 and 1000 eggs. After 7 days of infection, a larger number of larvae were obtained in the lung and liver, although a maximum amount was found in the brain after a 15- or 30-day post-infection period.

Endemic avian toxoplasmosis on a farm in Illinois: clinical disease, diagnosis, biologic and genetic characteristics of Toxoplasma gondii isolates from chickens (Gallus domesticus), and a goose (Anser anser).

Clinical toxoplasmosis in chickens (Gallus domesticus) has been rarely reported in literature. Here we report that three chickens on a farm in Illinois developed neurological signs. One of these chickens was examined postmortem and it had non-suppurative encephalitis with numerous Toxoplasma gondii tachyzoites and tissue cysts. The identity of the protozoa was confirmed immunohistochemically by staining with T. gondii specific antibodies, and by transmission electron microscopy. The owner of the 3 chickens donated all 11 remaining chickens and a goose on his property for the present study. All 11 chickens and a goose were euthanized, and blood, heart, brain, and 1 leg were obtained for T. gondii examination. Antibodies to T. gondii were found in sera of all chickens with titers of 1:40 in one, 1:320 in three, and 1:640 or higher in seven chickens tested by the modified agglutination test (MAT). The goose had a MAT titer of 1:320. For isolation of T. gondii, whole heart and brain and 50 g of leg muscles were digested in an acid-pepsin solution and bioassayed in four mice for each tissue. Viable T. gondii was isolated from tissues of all 11 chickens and the goose. Genotyping of these 12 T. gondii isolates using polymorphism at the genetic loci SAG1, SAG2, SAG3, BTUB, GRA6, c22-8, c29-2, L358, PK1, a new SAG2 and Apico revealed that all isolates had Type II alleles at all loci, indicating these T. gondii isolates belong to the predominant clonal Type II lineages. This is the first report of isolation of viable T. gondii from a domestic goose (Anser anser).

Human neurocysticercosis: rightward hemisphere asymmetry in the cerebral distribution of a single cysticercus.

The distribution of single cysticerci between cerebral hemispheres was studied in 227 adult cases of calcified and vesicular neurocysticercosis (NC). A rightward lateralization of calcified cysticerci was significant only in women, whereas vesicular cysticerci were equally distributed in both hemispheres. Factors related with the differences in the inflammatory response and in the regional cerebral blood flow between genders could be involved.

Cerebral sparganosis presenting as grand mal epilepsy.

A rare case of cerebral sparganosis is described. This is an uncommon condition particularly in Europe. It is most frequently seen in SE Asia but may be found anywhere in the world. The life cycle of the causative organism is described and contrasted with the principal differential diagnosis of parasitic inflammatory lesions of the brain, Taenia solium, the causative organism of cysticercosis. The treatment of cerebral sparganosis is surgical and diagnosis is most commonly made at the time of pathological examination. The importance of pre-surgical diagnosis is stressed as the treatment of the cysticercosis is pharmacological.

Niveles de parasitemia y alteraciones histopatológicas en Mus musculus BALB/c infectado con Trypanosoma cruzi obtenido de Panstrongylus chinai del Valle Chamán, La Libertad - Perú / Parasitemia levels and histopathologycal changes in Mus musculus balb/c infected with Typanosoma cruzi obtained from Panstrongylus chinai of Chaman Valley, la libertad - Peru

Se determinó los niveles de parasitemia y las alteraciones histopatológicas en el corazón y el encéfalo de Mus musculus cepa BALB/c infectado experimentalmente con Trypanosoma cruzi obtenido de Panstrongyius chinai capturados en el valle de Chamán, La Libertad-Perú. El trabajo se hizo en 10 ejemplares de M. musculus machos (nueve experimentales y un control) de 20 días de edad. A cada uno de los ejemplares del grupo experimental se les inoculó intraperitonealmente 5x104 tripomastigotes (0,1 mL inoculo original) suspendidos en sangre, y al control 0,1 mL de solución salina fisiológica estéril. La parasitemia se inició a partir del quinto día de la inoculación del T. cruzi, elevándose hasta niveles comprendidos entre 2,5x106 y 7,0x106 tripomastigotes/mL, antes de la muerte de los animales (18 días como máximo). El corazón y encéfalo fueron separados y conservados en formol al 10 por ciento para realizar cortes y colorearlos con la técnica H/E. Todos los ratones parasitados presentaron: erizamiento de pelo, incontinencia urinaria, parálisis de extremidades posteriores y convulsiones. A nivel histopatológico, tanto en el corazón como en el encéfalo, se observaron áreas de edema, congestión vascular, hipercromasia y nidos de amastigota. En el encéfalo se presentó, además, focos de inflamación crónica y difusa y en el corazón infiltrado inflamatorio linfocitario.