Implementación del diagnóstico de mycoplasma gallisepticum y mycoplasma synoviae mediante PCR-RFLP en aves de producción

UANL

Modelling of control options for an outbreak of Mycoplasma gallisepticum in egg production: a decision support tool

Mycoplasma gallisepticum (MG) is a bacterium that causes respiratory disease in chickens, leading to reduced egg production. A dynamic simulation model was developed that can be used to assess the costs and benefits of control using antimicrobials or vaccination in caged or free range systems. The intended users are veterinarians and egg producers. A user interface is provided for input of flock specific parameters. The economic consequence of an MG outbreak is expressed as a reduction in expected egg output. The model predicts that either vaccination or microbial treatment can approximately halve potential losses from MG in some circumstances. Sensitivity analysis is used to test assumptions about infection rate and timing of an outbreak. Feedback from veterinarians points to the value of the model as a discussion tool with producers.

Interaction of Mycoplasma genitalium with host cells: evidence for nuclear localization

Mycoplasma genitalium (Mg) is a mollicute that causes a range of human urogenital infections. A hallmark of these bacteria is their ability to establish chronic infections that can persist despite completion of appropriate antibiotic therapies and intact and functional immune systems. Intimate adherence and surface colonization of mycoplasmas to host cells are important pathogenic features. However, their facultative intracellular nature is poorly understood, partly due to difficulties in developing and standardizing cellular interaction model systems. Here, we characterize growth and invasion properties of two Mg strains (G37 and 1019V). Mg G37 is a high-passage laboratory strain, while Mg 1019V is a low-passage isolate recovered from the cervix. The two strains diverge partially in gene sequences for adherence-related proteins and exhibit subtle variations in their axenic growth. However, with both strains and consistent with our previous studies, a subset of adherent Mg organisms invade host cells and exhibit perinuclear targeting. Remarkably, intranuclear localization of Mg proteins is observed, which occurred as early as 30 min after infection. Mg strains deficient in adherence were markedly reduced in their ability to invade and associate with perinuclear and nuclear sites.

Serosurvey of selected avian pathogens in brazilian commercial Rheas (Rhea americana) and Ostriches (Struthio camelus)

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Ocorrência de anticorpos contra Salmonella e Mycoplasma em aves de criatórios de fundo de quintal próximos a explorações tecnificadas do Estado de São Paulo

Pós-graduação em Medicina Veterinária - FCAV

Pesquisa de agentes etiológicos patogênicos para galinhas de produção, em aves selvagens próximas as instalações avícolas

Pós-graduação em Medicina Veterinária - FCAV

Avaliação sorológica de Parainfluenzavirus Tipo 1, Salmonella spp., Mycoplasma spp. e Toxoplasma gondii em aves silvestres

Newcastle disease, salmonellosis and mycoplamosis are the most important infectious diseases in poultry. Toxoplamosis is a common disease in urban environment. The present study investigated serologic evidence of these diseases in captive and wildlife birds, with rapid plate agglutination test, haemagglutination inhibition test, and modified agglutination test. In a total of 117 blood serum samples, 20 showed the presence of Toxoplasma gondii, Mycoplasma gallisepticum, and Salmonella spp. antibodies. Amazona aestiva was the specie with the highest number of positive individuals (13/20). We also verified the first detection of T. gondii antibodies in birds of prey from Mivalgo chimachima and Rupornis magnirostris species.

Seroprevalence of salmonella and mycoplasma in commercial broilers, backyard chickens, and spent hens in the region of Triangulo Mineiro, state of Minas Gerais, Brazil

Avian salmonellosis and mycoplasmosis are infectious diseases that, in addition of causing lack of flock uniformity, represent a hazard to human health. The objective of the present study was to evaluate the seroprevalence of mycoplasmosis and salmonellosis in commercial broilers, backyard chickens, and spent hens slaughtered at a processing plant with local health inspection in Uberlandia, MG, Brazil. A total of 210 samples were randomly collected at the time of bleeding. Samples were submitted to rapid plate serum agglutination test (RSA) for the classification of Salmonella pullorum, Salmonella gallinarum, Mycoplasma gallisepticum and Mycoplasma synoviae. In order to increase result specificity, mycoplasmosis-positive samples were submitted to hemagglutination inhibition test (HI). No samples presented detectable antibodies against Salmonella pullorum or Salmonella gallinarum in the RSA test. Only Mycoplasma synoviae was detected in 14% of the backyard chickens and 0.74% in commercial broilers, whereas no antibodies were detected in spent hens. The seroprevalence rates found in the present study emphasize the need of keeping chicken flocks free from disease using effective biosafety systems.

Density-dependent decline of host abundance resulting from a new infectious disease

Although many new diseases have emerged within the past 2 decades [Cohen, M. L. (1998) Brit. Med. Bull. 54, 523–532], attributing low numbers of animal hosts to the existence of even a new pathogen is problematic. This is because very rarely does one have data on host abundance before and after the epizootic as well as detailed descriptions of pathogen prevalence [Dobson, A. P. & Hudson, P. J. (1985) in Ecology of Infectious Diseases in Natural Populations, eds. Grenfell, B. T. & Dobson, A. P. (Cambridge Univ. Press, Cambridge, U.K.), pp. 52–89]. Month by month we tracked the spread of the epizootic of an apparently novel strain of a widespread poultry pathogen, Mycoplasma gallisepticum, through a previously unknown host, the house finch, whose abundance has been monitored over past decades. Here we are able to demonstrate a causal relationship between high disease prevalence and declining house finch abundance throughout the eastern half of North America because the epizootic reached different parts of the house finch range at different times. Three years after the epizootic arrived, house finch abundance stabilized at similar levels, although house finch abundance had been high and stable in some areas but low and rapidly increasing in others. This result, not previously documented in wild populations, is as expected from theory if transmission of the disease was density dependent.