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Virulence genes of the streptococcus agalactiae associated with bovine mastitis in Minas Gerais livestock herds, Brazil

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Brazil has the second largest dairy herd in the world. Minas Gerais is the largest milk producer in Brazil and accounts for about 30% of all production in the country. The mastitis is a disease that causes major losses in the dairy industry under the economic point of view, because maintains a high prevalence and limited response to therapy and may be caused by more than one hundred different etiologic agents mainly bacteria. It is estimated that the loss in milk production by untreated, reach between 12 and 15%. Whatever its origin, there are chemical and physical changes in the milk, accompanied by pathological changes in the glandular tissue. Streptococcus agalactiae is highly contagious and ubiquitous in the mammary gland, is a major etiological agents of mastitis. The elucidation of the virulence factors of this agent is of great importance for the prevention and treatment of mastitis. Because of the few published studies with S. agalactiae isolates from cattle, this study aims to compare isolates from clinical and subclinical mastitis in relation to the presence of virulence genes related to polysaccharide capsule rich in sialic acid, hyaluronate lyase, fibrinogen binding protein and pili. Primers were designed to amplify the genes fbsA, cpsC, cpsD, cpsE, cpsK, neuB and the PI-1 cluster of 16 isolates of Streptococcus agalactiae from clinical mastitis and subclinical mastitis. Molecular analysis showed the presence of gene fbsA in 85.07% of the isolates, 38.80% in hylB, cpsC, cpsD and cpsE at 4.48%, cpkJ, cpsK and neuB 79.10% in the cluster and PI-1 at 1.49%. Observed diversity of strains within and between different flocks, however, no relationship was observed among virulence factors evaluated and the severity of infection.

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ARPINI, C. M. et al. Virulence genes of the streptococcus agalactiae associated with bovine mastitis in Minas Gerais livestock herds, Brazil. Applied Microbiology: Open Access, [S.l.], v. 2, n. 3, 2016.

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