6 research outputs found

    The crypt lymphoepithelium of the palatine tonsils of pigs : a study of its structure, function and role in the pathogenesis of Streptococcus suis infection

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    The crypt epithelium of the palatine tonsils, which is the first barrier between external environment and lymphoid tissue, was investigated in 6-month-old healthy market weight pigs and in 3 week-old piglets experimentally infected with Streptococcus suis serotype 2. This pathogen enters via and persists in the palatine tonsils, and the pathogenesis of this infection is still unclear. First, the subpopulations of intra-epithelial leukocytes were characterized and quantified using immunohistochemistry and monoclonal antibodies to porcine lymphocyte markers. Different lymphocyte subpopulations, namely CD4, CD8, and γδ T lymphocytes, and B lymphocytes, were identified. Next, the alterations in the intra­epithelial leukocyte subpopulations in response to experimental infection with S. suis were described. Myeloid cells, CD4 and CD8 T lymphocytes, and B lymphocytes were increased in the first 72h post-infection. The transport of S. suis serotype 2 across the crypt epithelium was investigated by transmission electron microscopy. S. suis was observed within neutrophils, macrophages, and also in occasional epithelial cells as early as 18h post-infection, indicating that participation of the innate immune response and epithelial cellular invasion are early steps in this infection. Macrophages containing bacteria were noticed straddling the basal lamina, suggesting that they can transport S. suis from the epithelium to the subepithelial lymphoid tissue and subsequently may disseminate the bacteria systemically. Last, the ability of epithelial cells to engulf S. suis and their ultrastructural morphology were correlated to determine whether cells compatible with M (microfold/membranous) cells were involved in bacterial uptake. Although many of the features described for M cells were observed in epithelial cells of the crypt epithelium, those containing S. suis had no specific common feature to permit classification as M cells. Taken together, these data suggest that the tonsillar crypt epithelium actively participates in the early phase of S. suis infection and likely plays an important role in the initiation of immune response

    Intoxicação experimental por sementes de Crotalaria spectabilis (Leguminosae) em suínos Experimental poisoning by Crotalaria spectabilis (Leguminosae) seeds in pigs

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    Para estudar os efeitos da ingestão de sementes de Crotalaria spectabilis em suínos, 14 porcos foram divididos em 5 grupos; quatro (A-D) eram formados por 3 porcos e um (Grupo E) por dois porcos. Com exceção do grupo A, que serviu como controle, os porcos foram alimentados com ração contendo 0,3 e 0,5% (Grupos B e C) e 1% (Grupos D e E) de sementes moídas de C. spectabilis por 32 (Grupo D), 44 (Grupo E) e 120 (Grupo B e C) dias. Um suíno do Grupo D e 2 suínos do Grupo B, morreram 8, 70 e 137 dias após o início do experimento; os restantes 11 suínos foram sacrificados em períodos que variaram entre 52 e 159 dias após o início do experimento. Dez dos 11 suínos tratados apresentaram perda do apetite e subdesenvolvimento. Outros sinais clínicos observados foram depressão, perda localizada de pêlos e distúrbios respiratórios. As principais lesões ocorreram no fígado. Em um caso eram agudas e consistiam principalmente de padrão lobular acentuado resultante de necrose centrolobulara massiva. Os outros 11 suínos apresentavam lesões hepáticas crônicas; o fígado estava firme, com cápsula espessada e aderências fibrosas entre os lobos e a estruturas adjacentes. Microscopicamente havia fibrose capsular, interlobar, interlobular e intralobular; hepatomegalocitose e proliferação de ductos biliares. Bilestase foi observadada no fígado de dois suínos; num outro havia regeneração hepatocelular nodular. Os pulmões de 4 suínos estavam avermelhados e firmes. Histologicamente havia espessamento dos septos interalveolares e interlobulares por edema, fibrose e infiltração celular, e proliferação de pneumócitos tipo II. Alterações renais foram observadas apenas microscopicamente e incluíam, principalmente, hepatomegalocitose das células epiteliais tubulares. Em 6 porcos observaram-se edemas cavitários (ascite, hidrotórax e hidropericárdio) de intensidade discreta a moderada. Alterações vasculares microscópicas consistindo de espessamento e hialinização da parede arterial foram observadas no pulmão de 5 suínos e no rim de 3. Quatro suínos tinham alterações sugestivas de encefalopatia hepática. Essas alterações não foram observadas nos suínos controles.To study the effects of the ingestion of Crotalaria spectabilis seeds, fourteen pigs were alloted in 5 groups. Four groups (A-D) consisted each of three pigs and the other (Group E) of two pigs. With the exception of those from Group A, which served as control, pigs were fed a ration containing 0.3 and 0.5% (groups B and C) and 1% (Groups D and E) of ground seeds of C. spectabilis for 32 (group D), 44 (group E), and 120 (groups B and C) days. One pig from Group D and two pigs from Group B died at 8, 70, and 137 days after the beginning of the experiment; the remaining 11 pigs were euthanatized at periods varying from 52 to 159 days from the beginning of the experiment. Ten of the 11 treated pigs had loss of apetite and poor growth rate. Depression, localized loss of hair, and respiratory distress were other observed clinical signs. Main pathological changes occurred in the liver. They were acute in one case and consisted of accentuation of the lobular pattern; due to centrilobular to massive hepatic necrosis. The remaining 11 treated pigs had chronic hepatic lesions, which included firmness, thickening of the capsule and fibrous adhesions between lobes and between hepatic capsule and adjacent structures. Histologically there was capsular, interlobar, interlobular, and intralobular fibrosis, hepatomegalocytosis and proliferation of bile ducts. In two case there was bilestasis and, in one pig, nodular regeneration was observed. The lungs of 4 pigs were reddened and firm. Histologically there was thickenning of interalveolar and interlobular septa by edema, fibrosis, cell infiltration and type II pneumocytes proliferation. The kidneys were grossly unremarkable. Histologically there was megalocytosis of the tubular epithelium and of the cells of the glomerular tuft. Hialinization of the glomerular tuft was also observed. Mild to moderate cavitary edema (ascites, hydrothorax and hydropericardium) was observed in 6 pigs. Microscopic vascular lesions consisting of arterial wall thickening and hialinization were seen in the lung of 5 pigs and in the kidney of 3 pigs. Four pigs had microscopic changes suggestive of hepatic encephalopathy. Those changes were not observed in the controls

    AFLATOXICOSE EM SUÍNOS

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    RESUMO É descrito um surto de aflatoxicose em suínos Duroc de 2 a 6 meses, que consumiam ração contaminada por 519 ppb de aflatoxinas. A morbidade foi de 97%. A mortalidade foi alta, mas não determinada com exatidão. Os sinais clínicos incluíam recusa do alimento, pouco ganho ou perda de peso, diarreia e icterícia. Lesões subagudas e crônicas foram observadas em 4 porcos necropsiados. Nas lesões subagudas o fígado era escuro, com áreas centrolobulares hemorrágicas deprimidas, havia edema da parede da vesícula biliar e bile viscosa. Nos casos crônicos o fígado apresentava-se firme e amarelo-alaranjado. Havia líquido citrino nas cavidades e edema no cólon espiral. Havia avermelhamento da mucosa gástrica da região fúndica. Alterações subagudas eram necrose e hemorragias centrolobulares, hepatomegalocitose, fibrose e hiperplasia ductal. Nos casos crônicos havia fibrose, hiperplasia ductal, megalocitose e degeneração gordurosa hepatocelular. O diagnóstico de aflatoxicose foi feito baseado nos sinais clínicos, nos achados morfológicos e na presença de níveis significativos de aflatoxina na ração dos porcos (B1 = 484,3ppb, B2 = 110,8ppb, G1 = 343,7ppb e G2 = 99,2ppb). Frangos submetidos à mesma alimentação também desenvolveram lesões da toxicose
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