scholarly journals An outbreak of Avian Encephalomyelitis in broilers in Greece

2018 ◽  
Vol 66 (2) ◽  
pp. 93
Author(s):  
K. C. KOUTOULIS (Κ.Χ. ΚΟΥΤΟΥΛΗΣ) ◽  
I. HORVATH-PAPP ◽  
D. TONTIS (Δ. ΤΟΝΤΗΣ) ◽  
N. PAPAIOANNOU (Ν. ΠΑΠΑΙΩΑΝΝΟΥ) ◽  
K. EVANGELOU (Κ. ΕΥΑΓΓΕΛΟΥ)

Avian Encephalomyelitis Virus (AEV) is an infectious viral disease, member in the family of Picornaviridae, with a preference for the central nervous system and various parenchymatous organs of chickens. AEV is an enteric infection and can be transmitted by oral ingestion, but also vertically from infected broiler breeders to the chick, resulting in clinical signs at hatching. A flock of 18,000 broilers, located in the Southern part of Ipirus, exhibited sudden neurological signs. Clinical examination of 16 days old chicks showed rapid head tremors, ataxia and paralysis, often falling on their sides and lie with their legs at unusual angles. No gross lesions were noted during post mortem examinations conducted at 16, 20 and 26 days of age, apart from gross lesions on the brain. Morbidity of the flock exceeded 25% and total mortality reached 20.9% at the end of flock’s cycle. In order to diagnose the suspected AEV, histological and serological examinations were performed. The results showed typical “flame-shape” proliferation of glia, neuron necrosis and neuronocytophagia in the gray matter and Purkinje cells as well. Also, foci of infiltrating lymphocytes were seen in the brain, the glandular part of pancreas, muscular layer of heart and muscle layer of proventriculus. All observed lesions were characteristic of AEV infection. Serological results in affected flock, conducted by ELISA, showed a consecutive marked increase in serum encephalomyelitis virus antibody titers through time. At 30 days of age onwards, no clinical signs appeared. This clinical case of AEV in broilers was the first case reported in Greece.

Parasitology ◽  
2020 ◽  
pp. 1-4
Author(s):  
Barbora Fecková ◽  
Priyanka Djoehana ◽  
Barbora Putnová ◽  
Michaela Valašťanová ◽  
Michaela Petríková ◽  
...  

Abstract Angiostrongylus cantonensis causes severe neurological disorders in a wide range of warm-blooded animals, including several avian species. A laboratory isolate of A. cantonensis originating from French Polynesia, genotyped as clade 2, was used to assess the effect of experimental infection in chicken and Japanese quail. Low dose groups of birds were infected orally by 100 L3 larvae, high dose groups by 1500 L3 larvae and the birds in the third group were fed three infected snails, mimicking a natural infection. Clinical signs during the first week after infection, haematology, biochemistry, gross lesions and histology findings were used to assess the pathology of the infection. Some of the infected birds showed peripheral eosinophilia, while mild neurological signs were seen in others. No larvae were observed in serial sections of the central nervous system of infected birds 1 week after infection and no major gross lesions were observed during necropsy; histopathology did not reveal lesions directly attributable to A. cantonensis infection. Our results suggest that galliform birds are not highly susceptible to A. cantonensis infection and open a question of the importance of Galliformes in endemic areas as natural pest control, lowering the number of hosts carrying the infective larvae.


2017 ◽  
Vol 37 (9) ◽  
pp. 926-930 ◽  
Author(s):  
Daniele M. Bassuino ◽  
Guilherme Konradt ◽  
Matheus V. Bianchi ◽  
Matheus O. Reis ◽  
Saulo P. Pavarini ◽  
...  

ABSTRACT: Sida carpinifolia poisoning causes a chronic neurodegenerative disorder associated with lysosomal storage by indolizidine alkaloids (swainsonine). The epidemiological, clinical, pathological and lectin histochemistry findings of an outbreak of natural poisoning by S. carpinifolia in horses in Rio Grande do Sul state, Brazil, are described. Five horses from a total of 15 that were kept on native pasture with large amounts of S. carpinifolia presented during 90 days clinical signs of progressive weight loss, incoordination, stiff gait and ramble, in addition to exacerbated reactions and locomotion difficulty after induced movement. Four horses died, and one of them was submitted for necropsy. At necropsy, no significant gross lesions were observed. Histological findings observed in the central nervous system were characterized by swollen neurons with cytoplasm containing multiple microvacuoles; these abnormalities were more severe in the thalamus, hippocampus, cerebellum and pons. Using lectin histochemistry, the pons and hippocampus sections stained positive for commercial lectin Con-A, sWGA and WGA. This study aimed to detail S. carpinifolia poisoning in horses to be included in the differential diagnoses of neurological diseases of horses.


2011 ◽  
Vol 20 (2) ◽  
pp. 97-102 ◽  
Author(s):  
Elisangela de Oliveira ◽  
Elisa Teruya Oshiro ◽  
Rebeca Vieira Pinto ◽  
Bruna Corrêa de Castro ◽  
Karla Borges Daniel ◽  
...  

Visceral leishmaniasis (VL) is a severe chronic disease caused by Leishmania (Leishmania) infantum chagasi. Better knowledge on the effects caused by this disease can help develop adequate clinical management and treatment. Parasitological and immunohistochemical studies were performed golden hamsters Mesocricetus auratus infected with bone marrow from individuals with VL in the State of Mato Grosso do Sul, central-west Brazil. The effects of parasitism in the spleen, liver, kidneys, lungs, heart and brain of the animals were examined. Eighteen hamsters were inoculated intraperitoneally, and six healthy animals were used as negative controls. The animals were kept in the animal house and checked for clinical signs. Specimens of each organ were examined for the presence of amastigotes. Immunohistochemical technique was performed in all brain specimens and organs negative on the direct examination of parasites. Direct examination of amastigotes was positive in the spleen and liver of all infected animals; 33.3% showed the parasite in the kidneys and lungs, and 16.7% in the heart. Parasitic forms were seen in 83.3% (15/18) of the brain examined. Immunohistochemistry confirmed the results of the direct examination, except in two specimens of lung tissue and in the brain specimens. Other studies are needed to further clarify the effect of the parasite in the central nervous system.


1985 ◽  
Vol 22 (6) ◽  
pp. 548-551 ◽  
Author(s):  
D. H. Embury ◽  
I. V. Jerrett

Mannosidosis was diagnosed in four stillborn Galloway calves and an autolyzed full-term fetus from experimental matings of carrier animals. Gross lesions were moderate internal hydrocephalus, and pallor and enlargement of the liver and kidneys and arthrogryposis. Histologic changes in the central nervous system of each calf were marked foamy vacuolation of the cytoplasm of neurones in the cerebral cortex, thalamus and brainstem, and vacuolation of the Purkinje cells of the cerebellum. Spheroids were common throughout the brain and there was also consistent severe foamy cytoplasmic vacuolation of renal tubular epithelial cells and hepatocytes. The activities of α-mannosidase, the lysosomal enzyme whose activity is deficient in mannosidosis, and activities of five other lysosomal enzymes were compared in brain, liver, and kidney tissues of three mannosidosis-affected calves and normal calf tissues. Tissues from the affected calves had a marked deficiency of α-mannosidase activity compared with the normal tissues; the greatest deficiency was in the liver (99%) and brain (98%). Activities of the other lysosomal enzymes were elevated in the affected tissues compared with normal. Mannosidosis is a lysosomal storage disease that results from a defect in glycoprotein metabolism and affects man,18 Angus and Angus-related breeds of cattle, such as Murray greys,12,21 and the cat.4 The congenital disease is caused by an inherited deficiency of the lysosomal enzyme α-mannosidase,14 and is inherited in an autosomal recessive manner. Mannosidosis was recently reported in a number of aborted and stillborn Australian Galloway calves3 from an experimental breeding trial. This is more detailed account of the histological and biochemical results obtained during the trial.


2013 ◽  
Vol 62 (2) ◽  
pp. 217-219 ◽  
Author(s):  
ROBERT WALTEREIT ◽  
ULRICH HERRLINGER ◽  
MAIK STARK ◽  
STEFAN BORGMANN

Infection of the central nervous system by streptococci is known to result in severe bacterial meningitis, however some strains have low pathogenic potential and affect the brain only in immunocompromised patients. Here we report the first case of an otherwise healthy non immunocompromised young adult woman who developed meningitis caused by Streptococcus dysgalactiae subspecies equisimilis. The patient was in the 17th week of her 3rd pregnancy. The course of the disease was quickly remittent under antibiotic treatment.


2021 ◽  
Vol 95 ◽  
Author(s):  
E.P.F. de Souto ◽  
A.M. Oliveira ◽  
É.M. Campos ◽  
V.L.R. Vilela ◽  
C.S.L. de Barros ◽  
...  

Abstract The present report describes two cases of infection by Molossinema wimsatti in the brain of Pallas's mastiff bats (Molossus molossus). The first bat was captured and killed by a domestic cat in a suburban area of the municipality of Patos, Paraiba, northeastern Brazil. The second bat was found crawling on the ground in the same area before dying. No gross lesions were found at necropsy. Histology of the central nervous system revealed filarioid nematodes in the brain ventricles and cerebellum. There were adults, subadults and eggs, the latter sometimes containing microfilariae. No inflammatory response was observed in bat 1, while bat 2 presented a mild lymphoplasmacytic meningoencephalitis. Three nematodes were recovered and submitted for parasitological examination. The diagnosis of M. wimsatti infection was based on the histomorphological and parasitological characteristics of the agent and its location in the brain ventricular system of insectivorous bats. The infection likely occurs in other insectivorous bats from South American and Caribbean countries but may be overlooked.


2014 ◽  
Vol 89 (5) ◽  
pp. 559-564 ◽  
Author(s):  
E.M. Mkupasi ◽  
H.A. Ngowi ◽  
C.S. Sikasunge ◽  
P.S. Leifsson ◽  
M.V. Johansen

AbstractNeurocysticercosis (NCC) caused byTaenia soliumcysts is a frequent but neglected parasitic disease of the central nervous system (CNS) worldwide. The aim of this study was to describe anatomical locations of cysts in the CNS and the corresponding inflammation. A total of 17 naturally infected pigs were used to evaluate the distribution of cysts and, of these, seven were used to evaluate the corresponding inflammation further, through histopathology. Clinical signs in the pigs included dullness, sluggishness, somnolence, apathy and loss of consciousness. Cysts were distributed in all cerebral lobes, i.e. 39.7% in the frontal lobe, 20.3% in the parietal lobe, 20.0% in the occipital lobe and 19.7% in the temporal lobe, and only 0.4% in the cerebellum. No cysts were found in the spinal cord. Cysts were localized as follows: 47.9% in the dorsal subarachnoid, 46.9% in the parenchyma, 4.4% in the subarachnoid base and 0.9% in the ventricles. The results of the histopathology revealed lesions in an early inflammatory stage, i.e. stage I, in all anatomical locations except for two, which showed more of an inflammatory reaction, stage III, in one pig. It was concluded that clinical signs in pigs were neither pathognomonic nor consistent. These signs, therefore, cannot be used as a reliable indicator of porcine NCC. Furthermore,T. soliumcysts were found to be in abundance in all cerebral lobes, and only a few were found in the cerebellum. Regarding the inflammatory response, no significant differences were found in the location and total number of cysts. Thus, further studies are needed to explain the determinants of cyst distribution in the CNS and assess in detail clinical signs associated with porcine NCC.


2016 ◽  
Vol 44 (8) ◽  
pp. 1128-1136 ◽  
Author(s):  
Jean-Rene Galarneau ◽  
Emily K. Meseck ◽  
Robert L. Hall ◽  
Wenkui Li ◽  
Margaret L. Weaver

Naphthoquine phosphate (NP) was considered as a partner drug with a promising antimalarial drug candidate. Here we report unexpected adverse clinical signs and microscopic findings in a canine pilot toxicology study with NP. Male and female dogs were dosed daily by oral gavage with NP at 2, 10, or 50 mg/kg/day for a maximum of 14 days. NP was not tolerated at ≥10 mg/kg/day; several animals were sacrificed in moribund condition and marked neurological clinical signs were noted at 50 mg/kg/day. The main microscopic observation was central nervous system vasculocentric inflammation (mainly lymphocytes and macrophages) in the white and gray matter of various regions of the brain at ≥2 mg/kg/day and at lower incidence in the spinal cord at ≥10 mg/kg/day. Vasculocentric microscopic changes predominantly centered on the centrilobular vein were also observed in the liver at ≥2 mg/kg/day. Females were more sensitive than males with comparable NP plasma exposure. In conclusion, under the conditions of this study, the administration of NP to dogs via daily oral gavage for up to 2 weeks was not tolerated causing moribundity, marked neurological clinical signs, and vasculocentric microscopic changes in the central nervous system and the liver.


1994 ◽  
Vol 6 (3) ◽  
pp. 326-334 ◽  
Author(s):  
Rachel Y. Reams ◽  
Lawrence T. Glickman ◽  
Daniel D. Harrington ◽  
H. Leon Thacker ◽  
Terry L. Bowersock

A retrospective study of 256 cases of naturally acquired Streptococcus suis infections in swine submitted to the Indiana Animal Disease Diagnostic Laboratory from 1985 to 1989 was undertaken to describe the clinical signs, lesions, and coexisting organisms associated with S. suis serotypes 1–8 and 1/2. Infected pigs generally had clinical signs and gross lesions referable to either the respiratory system or to the central nervous system (CNS), but not both. Neurologic signs were inversely related to gross lesions in the respiratory tract ( R2 = −0.19, P = 0.003), as were respiratory signs and gross lesions in the CNS ( R2 = −0.19, P = 0.003). Suppurative bronchopneumonia was the most common gross lesion observed (55.2%, overall). Fibrinous and/or suppurative pleuritis, epicarditis, pericarditis, arthritis, peritonitis, and polyserositis were also reported. In 68% of the pigs, other bacteria in addition to S. suis were isolated. Escherichia coli (35.0%) and Pasteurella multocida (30.0%) were the most commonly recovered bacterial agents. Mycoplasma and viral agents were identified less often, and their role in the development of streptococcosis was difficult to assess. In pigs infected with serotypes 2–5, 7, 8, and 1/2, suppurative meningitis with suppurative or nonsuppurative encephalitis, suppurative bronchopneumonia, fibrinopurulent epicarditis, multifocal myocarditis, and cardiac vasculitis were the most common microscopic lesions observed, whereas pigs infected with serotype 1 generally presented with suppurative meningitis and interstitial pneumonia. Microscopic lesions were morphologically similar among serotypes and were also similar to those reported with other pyogenic bacteria. The distribution of clinical signs and the gross and microscopic lesions in pigs infected with S. suis varied among serotypes. However, these differences were not statistically significant and could not be used to distinguish between the various serotypes. These findings suggest that in pigs infected with S. suis, suppurative or fibrinopurulent inflammation in brain, heart, lungs, and serosae predominates and that bacterial culture is needed to confirm a diagnosis of streptococcosis in swine and to differentiate this disease from those caused by other pyogenic bacteria.


2019 ◽  
Vol 49 (1) ◽  
Author(s):  
Letícia Batelli de Oliveira ◽  
Matheus Vilardo Lóes Moreira ◽  
Willian Henrique de Magalhães Santos ◽  
Líslie Caroline Oliveira Stuart ◽  
Maria Dolors Pi Castro ◽  
...  

ABSTRACT: A three-year-old female African pygmy hedgehog (Atelerix albiventris), born and domiciled in Brazil, presented apathy, prostration, and difficulty to stay standing. Its parents were siblings but did not present clinical signs related to this condition. As its clinical condition worsened, the animal was euthanized and referred for necropsy. No gross lesions were found in the central nervous system (CNS). Histologically, there was vacuolation with axonal degeneration in the white matter of the CNS and in peripheral nervous tissue. The Kluver-Barrera (KB) stain confirmed demyelination in vacuolated areas. Immunohistochemistry using several neural markers confirmed astrocytosis and microgliosis associated with vacuolated areas. In addition, there was a mild decrease in the immuno intensity of myelin proteolipid protein (PLP) in these areas. These results suggest a genetic origin of the present demyelination, which resulted in the wobbly syndrome described in this report.


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