Severe outbreak of avian encephalomyelitis in laying hens in Northeastern Brazil

This paper describes the epidemiological, clinical and pathological aspects of an avian encephalomyelitis (AE) outbreak in commercial laying hens in Northeastern Brazil. The disease affected 23,409 layers (from day one until 100 weeks) leading to mortality of 16.5% (5,049/30,600) of the flock. Twenty laying hens were clinically examined, and blood samples were collected and tested by Enzyme-Linked Immunosorbent Assay (ELISA). Five laying hens with neurological signs were necropsied and samples of the brain, cerebellum, spinal cord, sciatic nerve, heart, ceca tonsils, proventriculus and liver were collected, fixed in formalin buffered solution and processed according to routine methods for histological examination. Clinical signs were observed in approximately 60% of the chicken flock and included depression, ataxia, head and neck tremors, head tilt, motor incoordination and corneal opacity and of lens. All laying hens presented seroconversion for AE, with a geometric mean titer (GMT) of 6,854 and CV of 9.6%. At necropsy, there were bilateral opacity of the cornea and lens and the blood vessels of the cerebral cortex were hyperemic. The main microscopic lesions in the central nervous system consisted of red and shrunken neurons in the cerebral cortex, cerebellum and spinal cord. Significant areas of gliosis were observed in the cerebral cortex and in the molecular layer of the cerebellum. Hyperplasia of the proventricular lymphoid tissue and the ceca tonsils were observed with different degrees of intensity. In Northeastern Brazil, there haven’t been previous reports of AE in commercial laying hens and this outbreak possibly occurred by inefficient immunization of laying breeders at the genetic supply company.

Severe outbreak of avian encephalomyelitis in laying hens in Northeastern Brazil

This paper describes the epidemiological, clinical and pathological aspects of an avian encephalomyelitis (AE) outbreak in commercial laying hens in Northeastern Brazil. The disease affected 23,409 layers (from day one until 100 weeks) leading to mortality of 16.5% (5,049/30,600) of the flock. Twenty laying hens were clinically examined, and blood samples were collected and tested by Enzyme-Linked Immunosorbent Assay (ELISA). Five laying hens with neurological signs were necropsied and samples of the brain, cerebellum, spinal cord, sciatic nerve, heart, ceca tonsils, proventriculus and liver were collected, fixed in formalin buffered solution and processed according to routine methods for histological examination. Clinical signs were observed in approximately 60% of the chicken flock and included depression, ataxia, head and neck tremors, head tilt, motor incoordination and corneal opacity and of lens. All laying hens presented seroconversion for AE, with a geometric mean titer (GMT) of 6,854 and CV of 9.6%. At necropsy, there were bilateral opacity of the cornea and lens and the blood vessels of the cerebral cortex were hyperemic. The main microscopic lesions in the central nervous system consisted of red and shrunken neurons in the cerebral cortex, cerebellum and spinal cord. Significant areas of gliosis were observed in the cerebral cortex and in the molecular layer of the cerebellum. Hyperplasia of the proventricular lymphoid tissue and the ceca tonsils were observed with different degrees of intensity. In Northeastern Brazil, there havent been previous reports of AE in commercial laying hens and this outbreak possibly occurred by inefficient immunization of laying breeders at the genetic supply company.(AU)

Lyme Neuroborreliosis is a Severe and Frequent Neurological Disease in Mexico.

OBJECTIVE: To describe clinical cases with neurological manifestations associated with Borrelia burgdorferi infection in a large cohort of children and adults from Mexico. MATERIAL AND METHODS: Patients with neurological manifestation (cranial neuritis, radiculoneuritis, meningitis and encephalomyelitis) were recruited in one pediatric and two general hospitals, during January 2006-December 2015. Blood and cerebrospinal fluid (CSF) samples were drawn from each patient at inclusion. IgM and IgG antibodies against B. burgdorferi were detected using a commercial ELISA test, and confirmed by Western-Blot test (WB) using three different antigens from Borrelia burgdorferi complex. Following CDC criteria were considered true cases with both positive tests. RESULTS: Of 606 patients recruited, 403 (66.5%) were adults and 203 (33.4%) children, 50.5% were male. B. burgdorferi infection was diagnosed in 168 patients (27.7%), 97 adults, mean age 42 ± 14.7 years and 71 children, mean age 9.6 ± 5 years; early disseminated disease occurred in 130 cases (77.4 %) and chronic stage in 38 (22.6 %). A previous tick bite was reported by 21% cases, and 5% recalled an erythema migrans lesion. Polyradiculoneuropathy and encephalomyelitis were the most common manifestations, whereas 14.8% presented an initial Guillain-Barré Syndrome. B. burgdorferi sensu stricto was identified in 142 (84%) cases, B. garinii in 14 (8%), B. afzelii in three, and nine cases presented coinfection with two species. CONCLUSION: Lyme neuroborreliosis is a frequent condition in patients with neurological diseases in Mexico.

Tuberculous meningoencephalomyelitis and coinfection with HTLV-I + HTLV-II: case report.

HTLV-I and HTLV-II are endemic in some areas of Brazil, where an associated disease, HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) have been diagnosed in significant number of infected individuals. Tuberculosis has been demonstrated among those individuals, with higher prevalence than in the general population, suggesting that there is an increased risk for this comorbidity. We report the case of an individual coinfected with HTLV-I and HTLV-II, suffering from an insidious meningoencephalomyelitis caused by Mycobacterium tuberculosis. The patient was a 44 years old man successfully treated with steroids and antituberculous drugs, improving clinically and turning to a negative PCR and to a normal blood-cerebrospinal fluid barrier.

Tuberculous meningoencephalomyelitis and coinfection with HTLV-I + HTLV-II: case report

Os vírus HTLV-I e HTLV-II são endêmicos em algumas regiões do Brasil, onde uma das doenças associadas, a paraparesia espástica tropical/mielopatia associada ao HTLV (PET/MAH), tem sido diagnosticada em significativo número de pacientes infectados. Nesses indivíduos, a prevalência de tuberculose é maior que na população geral, sugerindo que possa haver um maior risco para esta comorbidade. Relatamos o caso de um homem de 44 anos coinfectado HTLV-I + HTLV-II que desenvolveu meningoencefalomielite por Mycobacterium tuberculosis. O paciente apresentou recuperação clínica parcial, correção da disfunção de barreira hemato-liquórica e negativação no PCR, mediante o tratamento com corticoesteróides e tuberculostáticos.

Brucellosis and polyneuroradiculomyeloencephalitis. A case report.

Reports on simultaneous central and peripheral nervous system involvement in a patient with brucellosis are very rare. We report of one young female patient with a long history of consumption of non-pasteurized dairy products in which clinical and laboratory findings confirmed the existence of an active brucellosis with nervous system impairment. Cerebrospinal fluid (CSF) analyses were negative. Electrophysiology and positive findings on sural nerve biopsy complemented the diagnosis of polyneuroradiculomyeloencephalitis. Treatment with a combination of doxycycline and rifampin for 2 months was successfully applied. No relapse or sequelae occurred in the patient after 12 months of follow up.

[Rabies encephalomyelitis with myocarditis and pancreatitis. Report on a case recently imported into France]. / Encéphalomyélite rabique avec myocardite et pancréatite. Observation d'un cas récent importé en France.

We report the case of a 29 year-old man who died from rabies in France, following a dog-bite during a trip in Mexico. Although it was clinically suspected, the diagnosis was uncertain until he died because of digestive, cardiac and psychiatric misleading symptoms associated to the neurologic disorders. Post mortem diagnosis was based upon virological study in immunofluorescence on cerebral smears, viral isolation on cell-culture, and ELISA. It was confirmed by light microscopy examination which showed numerous Negri bodies, and ultrastructural study of the rhabdovirus in the central nervous system. Extranervous lesions, especially myocarditis and pancreatitis, were observed and their meaning is discussed. The physician is exceptionally confronted to the diagnosis of human rabies in France. Nevertheless, the lack of compulsory antirabic vaccination and the increase of touring in enzootic countries increase the risk of infection. As an intra vitam diagnosis in frequently lacking, the diagnosis of rabies infection needs a complete post mortem virological study as well as an histological and ultrastructural examination of the central nervous system.

A local outbreak of paralytic rabies in Surinam children.

A rapidly fatal encephalomyelitis, which was in most cases characterized by ascending paralysis, developed in seven children of the age of 3 to 10 years in a bushnegro village in the interior of Surinam. Rabies virus was recovered from the central nervous system of three autopsied children. Although the source of infection has not been detected, there is an indication that, at least in some cases, the disease has been transmitted by rat-bite rather than by vampire bats. During the same period a few cases of minor febrile illness occurred in the same community. Since virological and serological evidence of a wide-spread distribution of Coxsackie A virus type 4 was obtained, the latter illness may presumably be attributed to this virus.