Background: Encephalitozoonosis is caused by the protozoan Encephalitozoon cuniculi, in rabbits, and can affect humans. The disease can be fatal and difficult to diagnose. It can be asymptomatic or cause vestibular neurological disease, paralysis, uveitis in addition to chronic kidney disease in rabbits. The transmission of the microorganism's spores occurs by ingestion, inhalation, or by the transplacental route. The aim of this work is to report a case of encephalitozoonosis in a pet rabbit (Oryctolagus cuniculus).Case: An Oryctolagus cuniculus with a history of paraparesis of the thoracic and pelvic limbs was referred for necropsy, the evolution of the clinical picture happened in one day. After death, a necropsy was performed. Organ fragments were collected, fixed, and processed routinely for histology. Macroscopically, there was evidence of hepatic lobes, without injury to the other organs. Microscopically it was observed in the white and gray substance of the telencephalon multiple circumscribed granulomas composed of a necrotic center surrounded by macrophages, giant multinucleated cells in addition to lymphocytes and plasmocytes in the periphery, delimited by fibrous connective tissue. Around the vessels, perivascular cuffs with two to four layers of lymphocytic infiltrate were observed. Besides, special staining of Schiff's Periodic Acid (PAS) and Ziehl-Neelsen was performed, in which numerous cylindrical, eosinophilic structures of approximately 2.5 x 1.0 µm were observed, compatible with E. cuniculi spores. Besides, histiocytic lymphoblasts pericoronitis was noted in the liver. There were no relevant changes in the kidney.Discussion: The diagnosis of encephalitozoonosis in rabbits was based on clinical and anatomopathological findings. Tetraparesis was the predominant sign in the present case and was justified by telencephalic lesions. This clinical sign is included in the literature but is less common than the syndrome such as head tilt and paralysis. The diagnosis of the disease is usually made by post-mortem examination when it is possible to identify the spores in the lesions. Multifocal granulomatous encephalitis was the most significant finding in this case, which is also consistent with other studies. The pathogenesis of granulomatous lesions is still controversial. It is known that spores allow phagocytosis by macrophages, which induce the production of interleukins and other cytokines by TCD4 + lymphocytes, thereby activating the action of TCD8 + (cytotoxic) lymphocytes. Natural killer cells, granulocytes, other macrophages, and B lymphocytes are also recruited. Although there is such an inflammatory response, the antibodies produced are not efficient to eliminate the agent from the host organism, however, they contribute to the process of opsonization and consequent phagocytosis, facilitating the destruction of the microsporidium by macrophages. The neurological form was predominant in this case, with no chronic or ocular renal forms, possibly due to the rapid clinical evolution. Special stains were useful for visualizing intralesional spores. Although PAS staining is considered to be of little use, it was relevant in this case. The visualization of the agent made it possible to distinguish differential diagnoses, among them vestibular syndrome secondary to otitis due to pasteurellosis, toxoplasmosis, neoplasms, traumas, or diseases of the spine. Thus, a diagnosis of encephalitozoonosis was made in a rabbit through clinical and anatomopathological correlation using Ziehl-Neelsen and PAS stains.Keywords: granuloma, Encephalitozoon cuniculi, central nervous system.Descritores: granuloma, Encephalitozoon cuniculi, sistema nervoso central.Título: Encefalitozoonose em coelho (Oryctolagus cuniculus)
Background: Brazil has a vast territory and favorable climatic conditions that allow the cultivation of freshwater fish. The intensification of the productive system can cause an imbalance in the aquatic environment as a result of poor water quality, nutritional deficiencies and infectious or parasitic diseases. The laboratory diagnosis and the determination of the prevalence of the main lesions, which occur in a certain region, help to guide towards the etiological diagnosis. This study aimed to describe the main parasitic lesions in fish in the routine at the Veterinary Pathology Laboratory of the Universidade de Brasília. Material, Methods & Results: All records of fish with parasitic lesions were recovered. Those cases in which there was an intralesional parasite and which presented lesions compatible with the parasite were included. The screening of ectoparasites was done by scraping the superficial mucus from the gills and skin. Organ sections were routinely processed for histopathologyand stained with hematoxylin-eosin (HE). In some records, parasitological identification was carried. The information was divided into the species of the affected fish, epidemiology of the outbreak (water quality, temperature, type of breeding), lesion distribution, etiology and macroscopic and microscopic changes. The resulting data was organized in absolute frequency and percentage. In this study, 22 cases were counted, between individual deaths and outbreaks, totaling 83 necropsied teleost fish.Inflammatory changes of parasitic origin were seen in 13/22 (59%) of the cases had lesions of parasitic origin. Skin lesions and gills were the most relevant. Macroscopically, red areas or spots of hyperemia or hemorrhage on the body surface were the most prevalent findings. Under microscopy, proliferative gill inflammation was the most relevant diagnosis. Pscinoodinium pilullare (Dinoflagellida), Ichthyophthirius multifiliis (Ciliophora), and monogenetic worms (Monogenea) were the main parasites found. Trichodina sp. (Ciliophora), Ichtyobodo sp. (Kinetoplastida), Amoebas, and Chilodonella sp. (Ciliophora), were seen in fewer numbers. An unusual case suggestive of parasitism by Eustrongylides sp. (Nematoda), in a pirá-brasília (Simpsonichthys boitonei), specimen has been recorded.Discussion: The diagnoses were based on epidemiology, anatomopathological and parasitological findings. The most frequent and significantly lethal lesion in the study was proliferative and / or hyperplastic branchitis. Proliferative branchitis with lamellar epithelial hyperplasia (LEH) is a response to some type of chemical or mechanical injury to the gill epithelium in order to protect the capillaries from further damage or microbial penetration. However, it also increases the diffusion distance between capillaries and the environment and, therefore, hinders breathing, excretory and osmoregulatory functions. Protozoan infections and monogenetic worms in general generated LEH and skin lesions of mechanical origin. Secondary bacterial infection, were observed in this parasitosis determining the cause of death of the fish. Its pathogenicity comes from the lesions caused by the colonization and histophagy of the epithelial surfaces, mainly gills and skin, causing epithelial proliferation, lamellar cell fusion, epithelial cell degeneration and necrosis forming several ulcers in the epithelium after the release of mature trophies. The pathogenesis of parasitism by Eustrongylides spp. is considerable when there is a large quantity of these larvae that can cause intestinal obstruction, rupture and compression of viscera, of greater importance in small fish. The main parasites of necropsied fish were protozoa and monogenetic worms, which mainly cause branquitis and dermatitis in varying grades.
Background: Toxoplasmosis is caused by Toxoplasma gondii, an obligate intracellular protozoan that belongs to the Aplicomplexa phylum, coccidian subclass, and affects all warm-blooded animals. The role of opossums in the epidemiology of toxoplasmosis in Brazil is not fully understood, and there are very few descriptions of toxoplasmosis lesions in these animals. This report describes the anatomopathological, molecular and immunohistochemical findings of a case of encephalic toxoplasmosis in free-living white-eared possum (Didelphis albiventris).Case: A young male opossum (D. albiventris), was treated at the Veterinary Hospital of Wild Animals of the University of Brasília, Federal District. The animal was apathetic, uncoordinated, reluctant to move, and had an exposed proximal fracture in the left radius and ulna with laceration of muscles and adjacent tendinous structures. Amputation on the left thoracic limb was performed followed by analgesia and antibiotic therapy. The environment is frequented by other wild animals, and stray cats have access to the patio of the building. Twenty-five days after arriving at the hospital, the animal was found dead in its cage. After death, a necropsy was performed. Organ fragments from the abdominal cavity, thoracic and central nervous system were collected, processed routinely for histology and stained with hematoxylin and eosin. Macroscopic lesions in the central nervous system were not observed. On microscopy, the brain showed moderate random glial nodules throughout the neuropil associated with the presence of spherical to elongated parasitic cysts of about 20 µm, with a thin wall and with its interior full of bradyzoites, consistent with Toxoplasma gondii. There was also moderate fibrinoid necrosis and moderate multifocal lymphoplasmacytic infiltrate surrounding the blood vessels (perivascular cuffs) To investigate the etiology of the brain injury, brain sections were subjected to immunohistochemistry (IHC) and real-time polymerase chain reaction (qPCR) technique for detection of T. gondii and Neospora caninum. Immunostaining for T. gondii in the cyst wall and in bradyzoites and negative immunostaining for N. caninum. qPCR was positive for T. gondii and negative for N. caninum.Discussion: Diagnosis of encephalic toxoplasmosis in a Didelphis albiventris was possible based on histopathological, immunohistochemical and molecular findings. The morphological classification of the brain lesion was important for the diagnosis. Brain toxoplasmosis in opossums usually results in focal areas of malacia on macroscopy and focally extensive necrosis on microscopy, neutrophil infiltrate, calcified necrotic material, and perivascular cuffs of lymphocytes and plasma cells. In the present case, similar histopathological lesions were noted, but no significant macroscopic changes were observed. The etiology here was defined by immunohistochemistry and qPCR, techniques proven to be useful and with good specificity for diagnosing toxoplasmosis in mammals. It is believed that the positive immunohistochemical and molecular result for Toxoplasma gondii together with the negative result for Neospora caninum were conclusive for the diagnosis. Thus, we demonstrate here a post mortem diagnosis of toxoplasmosis in a free-living synanthropic opossum and the use of anatomopathology, immunohistochemistry and real-time polymerase chain reaction as a diagnostic option for this disease in opossums. Keywords: Toxoplasma gondii, marsupial, immunohistochemistry, Real time PCR, protozoal encephalitis.Título: Toxoplasmose encefálica em um gambá-de-orelha-branca (Didelphis albiventris)Descritores: Toxoplasma gondii, marsupial, imuno-histoquímica, Real time PCR, encefalite protozoal.
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