RESUMEN
Nematodes of the Anisakidae family have the ability to infest a wide variety of aquatic hosts during the development of their larval stages, mainly marine mammals, aquatic birds, such as pelicans, and freshwater fish, such crucian carp, these being the hosts where the life cycle is completed. The participation of intermediate hosts such as cephalopods, shrimp, crustaceans and marine fish, is an important part of this cycle. Due to morphological changes and updates to the genetic information of the different members of the family, the purpose of this review was to carry out a bibliographic search of the genus and species of the Anisakidae family identified by molecular tests, as well as the geographical area in which they were collected. The Anisakidae family is made up of eight different parasitic genera and 46 different species. Those of clinical importance to human health are highlighted: Anisakis pegreffi, A. simplexsensu stricto, Contracaecumosculatum, Pseudoterranova azarazi, P. cattani, P. decipiens and P. krabbei. The geographical distribution of these genera and species is located mainly in the European continent, Asia and South America, as well as in North and Central America and Australia. Based on the information collected from the Anisakidae family, it was determined that the geographical distribution is affected by different environmental factors, the host and the ability of the parasite itself to adapt. Its ability to adapt to the human organism has led to it being considered as a zoonotic agent. The disease in humans manifests nonspecifically, however the consumption of raw or semi-raw seafood is crucial information to link the presentation of the parasite with the disease. The use of morphological and molecular tests is of utmost importance for the correct diagnosis of the genus and species of the Anisakidae family.
RESUMEN
In humans, alterations in bone metabolism have been associated with myopathies. We postulate the hypothesis that perhaps similar pathologies can also be associated in modern chickens. Hence, this study aimed to assess the fat infiltration in bone marrow and its repercussion on broiler chicken affected by Wooden Breast (WB) myopathy. Ten Cobb 500 live birds with extreme rigidity of the Pectoralis major (PM) muscle were selected as WB affected chickens by physical examination of the muscle at 49 days of age, whereas ten chickens healthy with no physical signs of hardness in the breast muscle were considered to be unaffected. Macroscopic lesions in affected chickens included areas of firm and inflamed muscle with pale appearance, hemorrhaging, and viscous exudate on the surface. Bone marrow and sections of the PM muscle were collected and analyzed for light microscopy. Additionally, transmission electron microscopy was conducted in affected or unaffected muscle. Chickens affected with WB showed significant reductions (P < 0.05) in femur diameter, calcium, and phosphorous percentage but increased breast weight, compression force and filet thickness when compared with non-affected chickens. Interestingly, bone marrow from WB chicken had subjectively, more abundant infiltration of adipose tissue, when compared with non-affected chickens. Histology of the Pectoralis major of birds with WB showed abundant infiltration of adipose tissue, muscle fibers degeneration with necrosis and infiltration of heterophils and mononuclear cells, connective tissue proliferation, and vasculitis. Ultrastructural changes of WB muscle revealed lack definition of bands in muscle tissue, or any normal ultrastructural anatomy such as myofibrils. The endomysium components were necrotic, and in some areas, the endomysium was notable only as a string of necrotic tissue between degraded myofibrils. The fascia appeared hypertrophied, with large areas of necrosis and myofiber without structural identity with degraded mitochondria adjacent to the disrupted muscle tissue. As far as we know, this is the first study that describes a subjective increase in adipose tissue in the bone marrow of chickens affected with WB when compared with non-affected chickens, and reduced bone mineralization.
RESUMEN
Con objeto de establecer un modelo animal para el estudio de la patogenia de las diátesis hemorrágicas agudas, se llevaron a cabo estudios de parámetros hemostáticos para la evaluación de los mecanismos de coagulación, así como pruebas de biometría hemática con especial énfasis en las cuentas plaquetarias, en 16 cerdos infectados experimentalmente con el virus de la fiebre porcina clásica y 4 cerdos testigos no infectados. En el estudio no se detectaron cambios signficativos en los parámetros de evaluación de la coagulación intrínseca y extrínseca, pero sí se presentó un significativa reducción en la cuenta plaquetaria a partir del tercer día posinfección. Se discute la probabilidad de que la trombocitopenia constituye la base de la diátesis hemorrágica y que es consecuencia de un daño del virus a las plaquetas o a sus precursores, e independientemente a trastornos de la coagulación
