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.     

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.     

Necrotizing meningoencephalitis and pneumonitis in a simian immunodeficiency virus-infected rhesus macaque due to Acanthamoeba

Free-living amoebae of the genus Acanthamoeba can cause a fatal disease of the brain in humans called granulomatous amoebic encephalitis. We present a case of meningoencephalitis and pneumonitis in a simian immunodeficiency virus (SIV)-infected rhesus macaque caused by Acanthamoeba sp. The animal became ill 176 days after intravenous inoculation with SIVmac251 after a short history of weight loss and a sudden onset of hind limb paresis and abnormal head movements. Histopathologic examination of hematoxylin and eosin-stained tissues revealed multifocal to coalescing necrotizing neutrophilic meningoencephalitis and pneumonitis. Immunofluorescence and polymerase chain reaction were used to identify the genus of amoeba as Acanthamoeba. Immunohistochemistry of immune cell markers was used to characterize the animal's immune response to the opportunistic amoebic infection with features of both innate and adaptive cell-mediated immunity. Although not previously reported, the potential transmission to humans, either through environmental contamination or contact with an infected animal, makes this disease a threat to laboratory animal care staff and pathologists.     

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 associated with Staphylococcus warneri in a dog

A case of meningoencephalitis in a dog caused by Staphylococcus warneri is reported here. The history and clinical signs were suggestive of possible central nervous system infection. Analysis of cerebrospinal fluid documented a neutrophilic pleocytosis (890 cells/mul) and the presence of occasional intracellular cocci. Staphylococcus warneri was isolated from the microbiological culture of the cerebrospinal fluid. Treatment consisted of intravenous antibiotics, supportive care and anticonvulsants for the generalised seizures that developed after admission. Histological assessment confirmed the location and extension of bacterial meningoencephalitis. Thrombotic meningoencephalitis associated with Staphylococcus warneri infection has not, to the authors' knowledge, been previously reported in dogs.     

Fatal equine meningoencephalitis in the United Kingdom caused by the panagrolaimid nematode Halicephalobus gingivalis: case report and review of the literature

A fatal case of eosinophilic and granulomatous meningoencephalitis caused by the free-living panagrolaimid nematode Halicephalobus gingivalis is reported in a 10-year-old Welsh gelding in the United Kingdom. Clinical examination first revealed behavioural abnormalities which rapidly progressed to severe ataxia, reduced mentation status and cranial nerve signs. Despite symptomatic treatment no amelioration of neurological signs was achieved and the horse was subjected to euthanasia. A complete post mortem examination revealed eosinophilic and granulomatous meningoencephalitis mainly affecting the cerebellum and brain stem with intralesional adult nematodes, larvae and eggs. There was also eosinophilic meningitis of the cervical spinal cord. The intralesional nematodes were morphologically consistent with the panagrolaimid nematode H. gingivalis. Although infection by this facultative neurotropic parasite is extremely rare, it needs to be considered in the differential diagnosis of central nervous signs in horses and, in particular, other equine helminthic infection of the central nervous system. This fatal case is unusual since lesions were locally very extensive and the nematodes did not colonise haematogenously to other organs as seen often in equine halicephalobosis. As the taxonomy of H. gingivalis has changed and some recent reports in the literature still refer to this species as Micronema deletrix or Halicephalobus deletrix, we here provide a short update of the species and some insights on the order Tylenchida, which contains free-living nematodes with parasitic tendencies.     

Nonsuppurative meningoencephalitis associated with Aleutian mink disease parvovirus infection in ranch mink.

Severe nonsuppurative meningoencephalitis associated with Aleutian mink disease parvovirus (ADV) infection was observed in adult ranch mink. Brain lesions included severe, locally extensive to coalescing lymphoplasmacytic meningoencephalitis with accompanying gliosis, satellitosis, and mild extension of inflammation into the leptomeninges. ADV was identified in mesenteric lymph node, spleen, brain, and liver of affected mink by polymerase chain reaction techniques. Sequences of the ADV isolate (TH5) revealed 2 unique residues in the region of the viral genome that determines pathogenicity. These findings suggest that certain strains of ADV may preferentially cause disease in the nervous system. ADV infection should be considered in the differential diagnosis of neurologic disorders in mink.     

Distribution of bovine virus diarrhoea viral antigens in the central nervous system of cattle with various congenital manifestations.

Distribution of bovine viral diarrhoea virus (BVDV) antigens in the central nervous system (CNS) of 26 cattle persistently BVDV infected, 11 cattle with mucosal disease (MD), and 32 calves with congenital brain malformations was studied using monoclonal antibodies against BVDV epitopes. In persistently infected cattle and in cattle with MD, a widespread infection of neurons was present. Predilection sites for BVDV antigens were the cerebral cortex and the hippocampus. In calves with congenital encephalopathies, viral antigen-containing neurons could only be detected in the CNS of four animals. From the topographical distribution of BVDV antigens in these four postnatal cases with end-stage lesions, no conclusions could be drawn concerning the pathogenesis of BVDV-induced encephalopathies.     

Susceptibility of mice to bovine herpesvirus type 5 infection in the central nervous system

Bovine herpesvirus type 5 (BoHV-5) is an important pathogen that causes meningoencephalitis in cattle. Few studies have used the mouse as a model for BoHV-5 infection. Despite the fact that BoHV-5 can infect mice with immune deficiencies, little is known about viral replication, immune response, and the course of infection in the central nervous system (CNS) of wild-type mice. Therefore, the aim of this study was to evaluate the response in the CNS of BALB/c mice acutely infected with BoHV-5 at different days post-inoculation (dpi). BoHV-5, when inoculated intracranially, was able to infect and replicate within the CNS of BALB/c mice. Until 15 dpi, the mice were able to survive without showing prominent neurological signs. The infection was accompanied by a Th1 immune response, with a significant expression of the cytokines IFN-γ and TNF-α and chemokine CCL-2. The expression of these cytokines and chemokines was most significant in the early course of infection (3 and 4 dpi), and it was followed by meningoencephalitis with perivascular cuffing and periventriculitis, composed mainly of macrophages and lymphocytes. After the expression of cytokines and chemokine, the mice were able to curb BoHV-5 acute infection in the brain, since there was a decrease in the number of BoHV-5 DNA copies after 3 dpi and viable viral particles were not detected after 6 dpi. Importantly, BoHV-5 was able to infect the trigeminal ganglia during acute infection, since a large number of BoHV-5 DNA copies were detected on 1 and 2 dpi.     

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.     

Thromboembolic meningocephalitis caused by Haemophilus somnus infection in a bull calf-a new disease in New Zealand

Thromboembolic meningoencephalitis (TEME) caused by Huemophilus somnus infection was diagnosed for the first time in New Zealand in an eight month old bull calf. Clinical signs included pyrexia, excessive salivation, recumbency, opisthotonus and rigidity of the front legs. Multiple red, malacic foci (1-10 mm in diameter) were visible grossly on the surface of the cerebrum and cerebellum, and were scattered throughout the brain parenchyma. Histologically these lesions consisted of focal haemorrhage, necrosis and neutrophilic infiltration. Fibrin thrombi and colonies of gram negative bacteria were present in many small blood vessels within necrotic foci. An organism with the morphological and biochemical characteristics of Haemophilus somnus was cultured from the brain. Although TEME is an important disease of feedlot cattle in North America and Europe it is relatively uncommon in cattle grazing pasture and is therefore unlikely to become a major problem in New Zealand.     

Nonsuppurative meningoencephalomyelitis of unknown etiology in mink

A central nervous system disease of mink occurred in three unrelated fur farms in Oregon in September, 1981. Only kits four to five months old were affected. Clinical signs consisted of posterior ataxia progressing to complete posterior paralysis with loss of motor control and sensation. Complete or partial recovery occurred in approximately 1.5 months in most mink. Microscopic lesions consisted of severe nonsuppurative meningoencephalitis and meningomyelitis with vacuolation of the white matter of the brain and spinal cord. Canine distemper virus infection and other recognized causes were ruled out on the basis of clinical signs, history, lesions, or laboratory findings. Experimental inoculations of mink with brain and spinal cord specimens from affected mink failed to reproduce the disease.     

Parasitic disease of the bovine nervous system

Parasitic disease of the nervous system of cattle is mainly caused by migrating nematodes, expanding cestode cysts, or by rickettsiae and protozoa in the central nervous system. Common parasitic causes of neurologic diseases in cattle in the United States are Hypoderma larvae, toxins produced by Dermacentor ticks, and metabolic changes associated with intestinal coccidiosis.     

Bovine viral diarrhea virus type 2-induced meningoencephalitis in a heifer

The brain from a 15-month-old, black female Angus, with a 48-hour history of central nervous system disease, was submitted to the Oklahoma Animal Disease Diagnostic Laboratory. Microscopic findings consisted of acute, multifocal meningoencephalitis, with neuronal degeneration and necrosis and gliosis. Viral isolation yielded noncytopathic bovine viral diarrhea virus (BVDV). Virus genotyping classified the virus as BVDV type 2. Immunohistochemical labeling for BVDV antigens with BVD MAb 3.12F1 clone was prominent in the cytoplasm of neurons, glial cells, ependymal epithelium, perivascular macrophages and spindle cells, smooth muscle cells, and intravascular monocytes of the cerebrum and brain stem. Laboratory results support that tissue alterations occurred as a result of BVDV type 2 infection. In the absence of other clinical signs related to BVDV infection and using the microscopic and laboratory evidence presented, we propose that the BVDV type 2 isolated from this case may represent a neurovirulent strain of the virus. To the best of our knowledge, this is the first report of brain lesions and neuronal viral antigen localization in BVDV genotype 2 viral infection, acquired either congenitally or postnatally.     

Viral antigen distribution in the central nervous system of cattle persistently infected with bovine viral diarrhea virus

Distribution of viral antigens in the central nervous system of 25 cattle with a persistent bovine viral diarrhea virus (BVDV) infection was studied. Using a polyclonal antiserum produced in pigs and the direct immunofluorescence and immunoperoxidase technique, BVDV antigen was located exclusively in neurons. Predilection sites for viral persistence were cerebral cortex and hippocampus; in other areas of brain and spinal cord, viral antigens were in single neurons or small groups of neurons. There was no morphological evidence of cellular alteration due to viral persistence. Perivascular lymphocytic infiltrations were in affected nervous tissue. It is concluded that the central nervous system is an important location for persistence of BVDV.     

Disseminated infection with Balamuthia mandrillaris in a dog

Bilateral chronic granulomatous nephritis and meningoencephalitis were diagnosed on necropsy of a 2-year-old male Great Dane dog. The causative agent was identified as Balamuthia mandrillaris, based on morphologic features, immunohistochemical staining, and deoxyribonucleic acid detection using the polymerase chain reaction with newly designed primer pairs. Trophozoite and cystic forms of the amoeba were evident within the kidneys and brain parenchyma. This is the first report on a B. mandrillaris infection in a dog.     

Combined cytosine arabinoside and prednisone therapy for meningoencephalitis of unknown aetiology in 10 dogs

OBJECTIVES: The differential diagnosis for young to middle-aged dogs with progressive neurological signs, focal or multifocal computed tomography/magnetic resonance imaging lesions, mononuclear cerebrospinal fluid pleocytosis and negative infectious titres includes granulomatous meningoencephalomyelitis, breed-specific meningoencephalitis, infectious meningoencephalitis of unknown origin and central nervous system neoplasia. The terminology meningoencephalitis of unknown aetiology may be preferable for cases that lack histopathological diagnoses. The safety and efficacy of a combination of cytosine arabinoside and prednisone protocol is evaluated, in this study, for the treatment of meningoencephalitis of unknown aetiology in 10 dogs. METHODS: Cases were selected based on neuroanatomical localisation, negative regional infectious disease titres, cerebrospinal fluid pleocytosis and brain imaging. Clinical response was gauged through follow-up examinations, owner and referring veterinarian surveys and review of medical records. RESULTS: Partial or complete remission was achieved in all dogs; the median survival time for the 10 dogs was 531 days (range 46 to 1025 days), with five of the 10 dogs alive at the time of writing. CLINICAL SIGNIFICANCE: Prednisone/cytosine arabinoside is a safe empirical therapy for dogs with meningoencephalitis of unknown aetiology; this drug combination may prolong survival time.     

Pathogenesis of experimental vesicular stomatitis virus (New Jersey serotype) infection in the deer mouse (Peromyscus maniculatus)

The pathogenesis of vesicular stomatitis virus (VSV) infection has not been investigated previously in native New World rodents that may have a role in the epidemiology of the disease. In the present study, 45 juvenile and 80 adult deer mice (Peromyscus maniculatus) were inoculated intranasally with VSV New Jersey serotype (VSV-NJ) and examined sequentially over a 7-day period. Virus was detected by means of immunohistochemistry and in situ hybridization in all tissues containing histologic lesions. Viral antigen and mRNA were observed initially in olfactory epithelium neurons, followed by olfactory bulbs and more caudal olfactory pathways in the brain. Virus also was detected throughout the ventricular system in the brain and central canal of the spinal cord. These results support both viral retrograde transneuronal transport and viral spread within the ventricular system. Other tissues containing viral antigen included airway epithelium and macrophages in the lungs, cardiac myocytes, and macrophages in cervical lymph nodes. In a second experiment, 15 adult, 20 juvenile, and 16 nestling deer mice were inoculated intradermally with VSV-NJ. Adults were refractory to infection by this route; however, nestlings and juveniles developed disseminated central nervous system infections. Viral antigen also was detected in cardiac myocytes and lymph node macrophages in these animals. Viremia was detected by virus isolation in 35/72 (49%) intranasally inoculated juvenile and adult mice and in 17/36 (47%) intradermally inoculated nestlings and juveniles from day 1 to day 3 postinoculation. The documentation of viremia in these animals suggests that they may have a role in the epidemiology of vector-borne vesicular stomatitis.     

Amebae and ciliated protozoa as causal agents of waterborne zoonotic disease

The roles free-living amebae and the parasitic protozoa Entamoeba histolytica and Balantidium coli play as agents of waterborne zoonotic diseases are examined. The free-living soil and water amebae Naegleria fowleri, Acanthamoeba spp., and Balamuthia mandrillaris are recognized etiologic agents of mostly fatal amebic encephalitides in humans and other animals, with immunocompromised and immunocompetent hosts among the victims. Acanthamoeba spp. are also agents of amebic keratitis. Infection is through the respiratory tract, breaks in the skin, or by uptake of water into the nostrils, with spread to the central nervous system. E. histolytica and B. coli are parasitic protozoa that cause amebic dysentery and balantidiasis, respectively. Both intestinal infections are spread via a fecal-oral route, with cysts as the infective stage. Although the amebic encephalitides can be acquired by contact with water, they are not, strictly speaking, waterborne diseases and are not transmitted to humans from animals. Non-human primates and swine are reservoirs for E. histolytica and B. coli, and the diseases they cause are acquired from cysts, usually in sewage-contaminated water. Amebic dysentery and balantidiasis are examples of zoonotic waterborne infections, though human-to-human transmission can occur. The epidemiology of the diseases is examined, as are diagnostic procedures, anti-microbial interventions, and the influence of globalization, climate change, and technological advances on their spread.