Naegleria fowleri-associated encephalitis in a cow from Costa Rica

Species of Naegleria, Acanthamoeba, and Balamuthia are soil amoebae that can cause encephalitis in animals and humans. Of these, Naegleria fowleri is the cause of often fatal primary meningoencephalitis in humans. N. fowleri-associated encephalitis was diagnosed in a cow that was suspected to have rabies. Only formalin-fixed brain was available for diagnosis. There was severe meningoencephalitis involving all parts of the brain and numerous amoebic trophozoites were present in lesions. The amoebae reacted with N. fowleri-specific polyclonal antibodies in an indirect immunofluorescent antibody test. This is the first report of amoebic encephalitis in any host from Costa Rica.     

Amoebic meningoencephalitis caused by Balamuthia mandrillaris in an orang utan

Objective
To describe a case of meningoencephalitis caused by Balamuthia mandrillaris in an orang utan.
Design
A pathological case report.
Animal
A 20 years old male orang utan (Pongo pygmaeus).
Procedure
The disease process was investigated by clinical pathology, necropsy, histopathology and immunofluorescence labelling.
Results
The orang utan developed sudden onset of depression, lethargy, inappetence and apparent head pain. The condition was considered to be related to a 2 year history of upper and lower respiratory disease, and the animal was placed on antibiotics after extensive testing. By the seventh day the animal had become ataxic and disoriented and a brain abscess was suspected. He died on the ninth day of illness. At necropsy, and subsequent sectioning, the brain showed multiple circular, soft, white to grey brown areas of varying size, the largest being in the left temporal (3.5 cm diameter) and right occipital (2.5 cm diameter) regions of the cerebrum. Histological examination of these regions revealed many amoebic trophozoites and occasional cysts associated with areas of haemorrhage and inflammatory necrosis. The trophozoites were packed in perivascular spaces and their nuclei often contained two or more prominent nucleoli. Immunofluorescent labelling of histological sections suggested that the agent was B mandrillaris.
Clinical implications
This report provides further evidence that B mandrillaris , a free living amoeba, can act as a pathogen in animals as well as people, and cause fatal meningoencephalitis. Along with Naegleria and Acanthamoeba spp, B mandrillaris should be considered amongst the causes of acute onset meningoencephalitis in animals.     

Meningoencephalitis caused by Naegleria fowleri in cattle of northeast Brazil

Primary amoebic meningoencephalitis is an acute disease of the central nervous system of humans and animals caused by Naegleria fowleri. This report describes a case of meningoencephalitis caused by N. fowleri in a crossbred, one-year-old bovine with progressive neurological signs. At necropsy there was thickening of the meninges and multifocal areas of malacia in the thalamus, caudal and rostral colliculi, parietal and occipital cortex, and cerebellum. Histologically there was multifocal necrosupurative meningoencephalitis associated with areas of malacia containing amoebic trophozoites. Immunohistochemistry of the brain was positive for N. fowleri. The disease should be included among the differential diagnosis of diseases of the central nervous system in cattle in areas where animals are exposed to hot, stagnant water.     

Seasonal meningoencephalitis in Holstein cattle caused by Naegleria fowleri.

Primary amoebic meningoencephalitis is a fulminant infection of the human central nervous system caused by Naegleria fowleri, a free-living amoeba that thrives in artificially or naturally heated water. The infection usually is acquired while bathing or swimming in such waters. The portal of entry is the olfactory neuroepithelium. This report describes fatal meningoencephalitis caused by N. fowleri in Holstein cattle that consumed untreated surface water in an area of California where summer temperatures at times exceed 42 degrees C. In the summers of 1998 and 1999, severe multifocal necrosuppurative hemorrhagic meningoencephalitis was observed in brain samples from nine 10-20-month-old heifers with clinical histories of acute central nervous system disease. Olfactory lobes and cerebella were most severely affected. Lesions were also evident in periventricular and submeningeal neuropil as well as olfactory nerves. Naegleria fowleri was demonstrated by immunohistochemistry in brain and olfactory nerve lesions and was isolated from one brain. Even though cultures of drinking water did not yield N. fowleri, drinking water was the likely source of the amoeba. The disease in cattle closely resembles primary amoebic meningoencephalitis in humans. Naegleria meningoencephalitis should be included among differential diagnoses of central nervous system disease in cattle during the summer season in areas with high ambient temperatures.     

Amebic meningoencephalitis caused by Acanthamoeba castellani in a dog

A natural infection of Acanthamoeba castellani, a free-living ameba, was determined to be the cause of acute, hemorrhagic, necrotizing amebic meningoencephalitis in a dog. This case is unique because previous reports of infection by the Acanthamoeba spp in dogs have not indicated its presence in the brain. Naturally developing meningoencephalitis by Acanthamoeba spp in the dog may have a pathogenesis similar to that of human beings. The ameba in this case also was observed in the lungs and kidneys, which are believed to be the primary sites of lesions in human beings that develop amebic meningoencephalitis from Acanthamoeba spp.     

Multisystemic infection with an Acanthamoeba sp in a dog

CASE DESCRIPTION-A 10-month-old Boxer was evaluated for fever and signs of cervical pain. CLINICAL FINDINGS-Physical examination revealed lethargy, fever, and mucopurulent ocular and preputial discharge. On neurologic examination, the gait was characterized by a short stride. The dog kept its head flexed and resisted movement of the neck, consistent with cervical pain. Clinicopathologic findings included neutrophilic leukocytosis, a left shift, and monocytosis. Cervical radiographs were unremarkable. Cerebrospinal fluid analysis revealed neutrophilic pleocytosis and high total protein content. On the basis of signalment, history, and clinicopathologic data, a diagnosis of steroid-responsive meningitis-arteritis was made. TREATMENT AND OUTCOME: The dog was treated with prednisone (3.2 mg/kg [1.45 mg/lb], PO, q 24 h), for 3 weeks with limited response. Consequently, azathioprine (2 mg/kg [0.9 mg/lb], PO, q 24 h) was administered. Three weeks later, the dog was evaluated for tachypnea and lethargy. Complete blood count revealed leukopenia, neutropenia, and a left shift. Thoracic radiography revealed a diffuse bronchointerstitial pattern. The dog subsequently went into respiratory arrest and died. On histologic evaluation, amoebic organisms were observed in the lungs, kidneys, and meninges of the brain and spinal cord. A unique Acanthamoeba sp was identified by use of PCR assay. CLINICAL RELEVANCE: This dog developed systemic amoebic infection presumed to be secondary to immunosuppression. The development of secondary infection should be considered in animals undergoing immunosuppression for immune-mediated disease that develop clinical signs unrelated to the primary disease. Although uncommon, amoebic infection may develop in immunosuppressed animals. Use of a PCR assay for identification of Acanthamoeba spp may provide an antemortem diagnosis.     

In vitro culture, serologic and molecular analysis of Acanthamoeba isolated from the liver of a keel-billed toucan (Ramphastos sulfuratus)

Members of the genus Acanthamoeba are usually free-living amebae and are found in a variety of ecological niches including soil, fresh and brackish water, dust in air, filters of heating, ventilating, and air conditioning units, swimming pools and hot tubs, etc. Occasionally, they are also known to cause central nervous system infections in humans and other animals. We isolated into culture an amoeba from the liver tissue of a keel-billed toucan and identified it as Acanthamoeba sp. based on culture characteristics and immunofluorescent analysis. Further, we characterized the cultured amoeba and also the amoeba in the liver tissue as Acanthamoeba, genotype T4, by sequencing a diagnostic region of the nuclear small subunit ribosomal RNA gene.     

Experimental encephalitozoonosis in neonatal dogs

The in vivo infection of neonatal dogs by the microsporidian protozoan parasite, Encephalitozoon cuniculi, was studied. Microscopic examination of tissues from infected animals showed granulomatous nephritis, meningoencephalitis, hepatitis, and pneumonitis. A large component of the inflammatory infiltrate consisted of plasma cells and lymphocytes. In addition, hyperplasia of B-lymphocyte-dependent regions of lymph nodes and erythrophagocytosis were consistently seen in infected dogs. Infected dogs developed lymphocytosis, hypergammaglobulinemia, anti-encephalitozoon antibodies, and an antigen-specific blastogenic response to E. cuniculi spores. Lymphocyte blastogenic responses to the lectin phytohemagglutinin A (PHA) were depressed compared to controls. Dogs dying during the 2-month experimental trial were bacteremic. The findings of these experiments suggest that postnatal infection results in a demonstrable although seemingly ineffective immune and inflammatory response without detectable clinical disease.     

Idiopathic granulomatous and necrotising inflammatory disorders of the canine central nervous system: a review and future perspectives

Granulomatous meningoencephalomyelitis, necrotizing meningoencephalitis, and necrotizing leukoencephalitis are common inflammatory conditions of the canine central nervous system. Although each disease has unique histopathological features, these canine disorders collectively seem to be aberrant immune responses directed against the central nervous system. A review of the neurological signs and general neurodiagnostic approach to canine meningoencephalitis is followed by an overview of the specific clinical and neuropathological features of granulomatous meningoencephalomyelitis, necrotizing meningoencephalitis, and necrotizing leukoencephalitis. The aetiopathogenesis of each disorder is explored including potential genetic, immunological, and environmental factors along with the current and prospective immunomodulatory therapies for meningoencephalitis.     

Torque teno virus infection in the pig and its potential role as a model of human infection

Torque teno viruses (TTVs), of the genus Anellovirus, are single-stranded circular DNA viruses that infect many vertebrate species. Although viruses of this type have quite a stable genome, they exhibit low nucleotide homology. Torque teno virus infection has not been consistently linked to specific diseases, although there is epidemiological evidence of an association with disease in humans. The recent recognition of naturally occurring TTV infection in swine and its epidemiological resemblance to human TTV raises the possibility of using the pig as a model to study human TTV infection. Such an approach will require the development of novel investigative tools to study the epidemiology, transmission, immune responses and potential pathogenesis of TTV infection. The present review summarises research on animal TTV infection, focussing in particular on TTV infection in the pig, and considers how a porcine experimental infection model might assist in the study of human TTV infection.     

Greyhound meningoencephalitis: PCR-based detection methods highlight an absence of the most likely primary inducing agents

Greyhound meningoencephalitis is currently classified as a breed-associated idiopathic central nervous system inflammatory disorder. The non-suppurative inflammatory response can be distinguished from the other breed-associated disorders based on histopathology and lesion topography, however the nature of the response primarily suggests a viral infection. In the present study PCR and RT-PCR technologies were employed on frozen cerebral tissue from confirmed cases of meningoencephalitis to target specific viruses and protozoa likely to be implicated and to exclude the presence of bacterial 16SrRNA. Secondly, degenerate primers were used to detect viruses of the herpesvirus and flavivirus families. In addition cerebral tissues were probed for West Nile Virus. Viral nucleic acid sequences to Borna disease virus, to louping ill, tick borne encephalitis, West Nile and other flaviviruses were not detected. Canine distemper virus was detected in one animal with 97% homology to strain A75/15. Degenerate PCR for herpesviruses detected viral amplification products in one animal with 90% homology to canine herpesvirus DNA polymerase gene. Protozoal amplification products were only detected in a single dog with pathological confirmation of a combination of lesions of greyhound meningoencephalitis and a protozoal encephalomyelitis. Neospora was confirmed with sequence homology to Austrian strain 1. Bacterial 16SrRNA was not detected. The present study supports previous observations that many of the known microbial causes of canine meningoencephalitis are not involved. Findings could reflect that the causal agent was not specifically targeted for detection, or that the agent is at undetectable levels or has been eliminated from brain tissue. The potential roles of genetics and of molecular mimicry also cannot be discounted.     

Hantavirus infection in East Asia

Hantaviruses are enveloped RNA viruses that belong to the Hantavirus genus of the family Bunyaviridae. These viruses persistently infect their rodent reservoirs without causing disease. The virus is transmitted to humans via the inhalation of infectious aerosols generated from contaminated animal secretions or through the contaminated saliva of animal bites. Hantaviruses cause haemorrhagic fever with renal syndrome in Euro-Asia, and hantavirus pulmonary syndrome (HPS) in North and South America. Here, we review the epidemiology and epizootiology of hantavirus infection in Asian countries.     

Animal noroviruses

Among enteric caliciviruses, noroviruses belong to the genus Norovirus, one of the four accepted genera in the family Caliciviridae. These single-stranded, positive-sense RNA viruses are highly variable both genetically and antigenically. Several animal enteric caliciviruses that are morphologically indistinguishable and genetically closely related to human noroviruses have been identified. The first bovine enteric noroviruses were described in Great Britain and are known as Newbury Agent 2. At least three genetic clusters of porcine noroviruses join together within genogroup II noroviruses. Human noroviruses are the most important cause of acute gastroenteritis illness in people of all ages. In the USA, they are associated with approximately 30-50% of all food-borne outbreaks. Until now, noroviruses have not been associated with gastroenteritis outbreaks in immunocompetent animals. Neither bovine nor porcine noroviruses can replicate in cell culture, although human norovirus can grow in a complex 3D culture system. However, the recently discovered murine noroviruses can replicate in cell culture and are therefore used as model viruses to study human noroviruses. This review focusses on virus classification, virion structure, pathogenesis, epidemiology, immune response and diagnosis of animal noroviruses in comparison with human noroviruses. The classification of animal enteric caliciviruses within the Norovirus genus raises the question of whether transmission from an animal reservoir to humans could occur. Answering this question is important in determining the risk of cross-species infections affecting the epidemiology and evolution of these viruses and so complicating the control of human norovirus infections.     

Disseminated Acanthamoeba sp. infection in a dog

Several species of free-living amoebae can cause encephalomyelitis in animals and humans. Disseminated acanthamoebiasis was diagnosed in pyogranulomatous lesions in brain, thyroid, pancreas, heart, lymph nodes, and kidney of a one-year-old dog. Acanthamoeba sp. was identified in canine tissues by conventional histology, by immunofluorescence, by cultivation of the parasite from the brain of the dog that had been stored at -70 degrees C for two months, and by PCR. The sequence obtained from the PCR product from the amoeba from the dog was compared to other sequences in the Acanthamoeba sp. ribosomal DNA database and was determined to be genotype T1, associated with other isolates of Acanthamoeba obtained from granulomatous amebic encephalitis infections in humans.     

West Nile virus and its emergence in the United States of America

Zoonotic West Nile virus (WNV) circulates in natural transmission cycles involving certain mosquitoes and birds, horses, humans, and a range of other vertebrates are incidental hosts. Clinical infections in humans can range in severity from uncomplicated WNV fever to fatal meningoencephalitis. Since its introduction to the Western Hemisphere in 1999, WNV had spread across North America, Central and South America and the Caribbean, although the vast majority of severe human cases have occurred in the United States of America (USA) and Canada. By 2002-2003, the WNV outbreaks have involved thousands of patients causing severe neurologic disease (meningoencephalitis and poliomyelitis-like syndrome) and hundreds of associated fatalities in USA. The purpose of this review is to present recent information on the epidemiology and pathogenicity of WNV since its emergence in North America.     

Japanese encephalitis virus infection in meerkats (Suricata suricatta)

Japanese encephalitis virus (JEV) infection has been recognized as a serious disease in humans. Wildlife animal infections due to JEV have not been well described. This study identified JEV infection in two deceased meerkats in Thailand, with clinical signs of neurological disease. Histopathology of brains revealed severe lymphoplasmacytic necrotizing meningoencephalitis, while similar inflammation was observed in the lung and liver. Partial JEV sequences were identified from the formalin-fixed paraffin-embedded-derived brain sections of two meerkats and were found to be genetically similar to a JEV strain detected in China but not from a local strain. Using immunohistochemistry, the virus was identified in neurons and glial cells, and also found in bronchial glands, Kupffer's cells in liver, lymphocytes in the spleen and pancreatic acini, which suggests extraneural infection. Transmission electron microscopy confirmed the presence of spheroid viral particles in the lungs. These findings may suggest that infection of extraneural organs in meerkats is similar to that described in JEV-infected humans. In conclusion, this study identified the first JEV infection in meerkats as an interesting case study. The JEV should be considered as an important differential diagnosis in meerkats with encephalitis. Further surveillance on JEV infection in meerkats and other wildlife species in a large cohort is needed in the future study.     

亨德拉病毒研究进展

亨德拉病毒(HeV)是属于副黏病毒科、副黏病毒亚科、亨尼病毒属的一种病毒,可引起马、人类和其他哺乳动物的感染。动物和人类感染该病毒后病死率很高,且缺乏有效的疫苗和治疗方法。不同动物的易感情况、发病机理、病理变化、潜在的传播途径等情况等仍有待进一步研究。论文就亨德拉病毒自然宿主和实验动物感染等情况进行重点阐述。     

Mycoplasma felis-associated meningoencephalomyelitis in a cat

Mycoplasmas are frequently isolated from many animal species. In domestic cats, mycoplasmas may be isolated from respiratory and ocular mucosae, but other sites are also occasionally colonized by these organisms. No cases of Mycoplasma species-associated neurologic disease have been reported in cats. We describe a case of Mycoplasma felis-associated meningoencephalitis in a 10-month-old domestic shorthair cat.     

Use of cyclosporine to treat granulomatous meningoencephalitis in three dogs

Use of cyclosporine to treat granulomatous meningoencephalitis in three dogs Three dogs with a presumptive diagnosis of granulomatous meningoencephalitis were treated with orally administered cyclosporine. In 2 dogs, cyclosporine administration replaced initial corticosteroid administration, and in 1 dog, cyclosporine was the only treatment used. One dog had the focal form of the disease in the brainstem, 1 dog had the focal form in the forebrain associated with a concurrent ocular form, and 1 dog had the disseminated form of disease. At 12-month follow-up, the 2 dogs with the focal form of the disease had no clinical signs. The dog with the disseminated form improved only partially, and euthanasia was performed 3 weeks after initial evaluation. Cyclosporine was considered effective at an initial dosage of 6 mg/kg (2.7 mg/lb) every 12 hours. Adverse effects associated with cyclosporine administration included transient lymphopenia, excessive shedding, and focal symmetric hair discoloration.