Análisis histológico de lesiones pódales de pollos comerciales en la Planta de Sacrificio de Pollo Olympico S. A / Histological analyses of toe lesions for commercial broiler at the slaughterhouse of Pollo Olympico S. A

Realizar el análisis histológico de lesiones pódales de pollos comerciales en la planta de sacrificio de Pollo Olympico S.A., Colombia con el fin de discutir aspectos sobre su retención sanitaria en plantas de sacrificio. Materiales y métodos: Se utilizó la población avícola de 10 granjas de la empresa Pollo Olympico S.A evaluando macroscópicamente 129.551 animales y microscópicamente 330 lesiones podales. El análisis histológico evaluó el tipo y la profundidad de las lesiones inflamatorias y la presencia de estructuras micóticas. Resultados: La evaluación macroscópica evidenció lesiones podales en el 64,7% de la población total de aves. La evaluación microscópica mostró un predominio de procesos inflamatorios con presentación de heterófilos (73,1%), el 19% fueron infiltrados mixtos y el 7.9% de predominio mononuclear. Las lesiones encontradas mostraron una localización principalmente subcorneal (77.9%) y la ausencia de estructuras micóticas, células gigantes o lesiones vasculares...

To conduct histological analyses of toe lesions for commercial broiler at the slaughterhouse of Pollo Olympico S.A., Colombia, with the ultimate goal of proposing recommendations about sanitary containment. Materials and Methods: Poultry subjects were sampled in 10 farms of Pollo Olympico S.A. Macroscopic inspections were conducted on 129.551 animals while the microscopic ones were on 330 toe lesions. Histological analyses evaluated type and depth of inflammatory lesions as well as the presence of fungal infections Results: Macroscopic analyses revealed inflammatory process mediated by heterophiles (73,1%), mixed infiltrates (19%) and mononuclear (7.9%). Lesions were mainly localized at the sub-corneal level (77.9%) and showed no signs of fungal structures, giant cells or vascular presence...

Induced liver tumour further support to a genetic marker with its high correlation with chorioallantoic membrane phenotypes in selected layer lines.

The conventional chorioallantoic membrane (CAM) phenotype assay was conducted using 11-day-old embryonatic eggs of white Leghorn strains, each inoculated with 0.2 ml of subgroup A Rous sarcoma virus (RSV) and subgroup C RSV separately containing 10(3)pfu ml(-1). Eggs were further incubated for hatching. Harvesting of CAMs for counting of pocks and monitoring chicks for liver tumour (LT) mortality during 4 weeks of post-hatching period were followed. The conversely associated phenotype (CAP) incidence i.e. CAM(+) LT(-) and CAM(-) LT(+) was observed in all three lines for both subgroup A and C virus infection. The LT deaths of chicks in all strains occurred within 21 days post-hatch irrespective of virus subgroups. The regression analysis of %LT death (transformed data) distributed within pock count range (PCR) basis was performed. The regression coefficients (b(i)'s) were found to be non-significant, indicating that %LT death did not correlate with number of particles that entered the cells because the chicks that had at least 25 pock counts in CAMs died with few exceptions. This study upheld the view that the CAM phenotypes (S and R) under the control of a pair of alleles, a(s) and a(r) at the tva locus and c(s) and c(r) at the tvc locus as reported extensively. Because of a high correlation coefficients between CAM and LT phenotypes [S and LT(+)] in respect of subgroup A (r = 0.72) and subgroup C (r = 0.81) infection, it is obvious that one could postulate a pleiotropic control of the two traits by the tva and tvc genes, respectively. Indeed fitting a 4-allele model in both tva and tvc locus, suggesting that CAPs are the indicator for nullifying the conventional 2-allele model proposed for the induced tumour expression phenotypes by leukosis sarcoma viruses.

Subgroup-A Rous sarcoma virus-induced growth stimulation of chick embryos infected via the chorioallantoic membrane.

Chicks that hatch from eggs containing group specific antigen (gs antigen) of lymphoid leukosis virus (LLV) subgroups, grow poorly. In our laboratory for more precise identification of LLV-of subgroup A (LLV-A) resistant and susceptible genotypes by progeny testing, the chorioallantoic membrane (CAM) assay in complemented by liver tumour (LT) assay, wherein Rous sarcoma virus (RSV) of subgroup A (homologous to LLV-A) was used. The present study was conducted in a light breed (White Leghorn) and also in a heavy breed (Rhode Island Red) to ascertain the effect of infection on embryonic growth by RSV subgroup A. Mean relative body weight (rbw) of infected LT negative chicks of either breed exceeded the control highly significantly (P < 0.01) by 2%. However, neither the dose of virus inoculated per embryo, nor egg size influenced the relative body weight of day old chicks (P > 0.05). No difference in relative body weight of LT positive and control chicks was observed.

Response to wing-web challenge of Rous sarcoma virus subgroups in some chicken breeds.

Response to wing-web challenge (WWC) of Rous sarcoma virus (RSV) subgroups was studied in 4-8 weeks old chicks of a light breed, a heavy breed and a cross between an indigenous black plumage Bantam fowl and Australorp breed. Wing-web tumor (WWT) began to develop within one week in response to virus subgroups A (BS-RSV) and C [RSV (RAV-49)] challenge. In chicks challenged with subgroup D [RSV (RAV-50)] virus it took a minimum of 4 weeks for development of WWT. Positive response to WWC by subgroups A, C and D virus was 84%, 100% and 52%, respectively. The duration of exhibition of positive response was maximum for subgroup A virus, followed by subgroup D and minimum for subgroup C virus.

Interrelationship between tumour virus receptors, A and C, coded by host cell genes in fowl.

Bryan Standard strain of Rous Sarcoma Virus (BS-RSV) of subgroup A and pseudotype of Bryan high titre RSV(RAV-49) of subgroup C and an equal mixture of subgroup A and subgroup C virus were inoculated to 11-day old embryos of white leghorn (WL), Australorp (AL) and f1 and f2 generations of crosses between WL and AL breeds of fowl to detect and estimate the interrelationship between tumour virus receptor coding host cell genes of tva and tvc loci. Linkage values estimated on a pooled sex basis were 0.08 +/- 0.03 and 0.10 +/- 0.03 for WL and AL breeds respectively and 0.09 on pooled breed basis. This clearly indicates that the tva and tvc loci are indeed closely linked in WL and AL breeds of fowl and supports the concept of using subgroup C virus to raise stocks resistant to subgroup A virus infection.

Induced liver tumour deaths by subgroup A Rous sarcoma virus in chicks inoculated via chorioallantoic membrane, a genetic marker.

A study was made using two strains of light breed (White Leghorn strains, A and B) and four heavy beeds (Rhode Island Red, New Hampshire, Australorp, Columbian) to evaluate the breed difference in survival potential of chicks that were infected as 11-day-old embryos via chorioallantoic membranes (CAMs) with a subgroup A Rous sarcoma virus. Of the 1185 chicks hatched over multiple hatch-replicates, 845 chicks died rapidly of a fibrosarcomatous liver tumour (LT) with a peak mortality about 74% attained by the second week, post-hatch, in the heavy breeds and more than 90% by the second week in the light breed. The breeds did not differ in induced LT mortality when the chicks hatched from eggs that had at least 25 pock counts on CAMs, apparently genetically susceptible, i.e. 25 biologically active virus particles were enough to induce an unpreventable fatal LT. However, low pock-count on CAMs did not act as a pointer for predicting genetic resistance to infection because about 23% of chicks developed from eggs that had no pocks on CAMs, apparently genetically resistant, also died of LT, requiring further studies.

Nonspecific immunoprotection against Rous sarcoma tumor in chicks.

An enzyme treated preparation of saprophytic Mycobacterium phlei, referred as NSI, when administered intramuscularly has been found to protect the chicks against Rous Sarcoma Virus induced tumor. A protection level of 35.4%, 24.1% and 21.2% were observed when challenged on 10th, 20th and 30th day post NSI inoculation. The tumor growth inhibitory-activity of NSI was significant (P less than 0.01). Both, systemic and intralesional administration of NSI exhibited significant tumorostatic activity (P less than 0.05). NSI stimulated the cell mediated immune response to specific as well as to nonspecific Rous sarcoma antigen. These studies indicated the immunopreventive activity of NSI against Rous sarcoma tumor which had an immunogenic basis.

Tratamiento de tumores cerebrales experimentales / Treatment of experimental brain tumors

Los autores estudiaron los efectos de las sustancias con posibles actividades terapeuticas en el modelo murino de tumor cerebral inducido en ratas lactantes con virus del sarcoma aviar. Se emplearon timocina, extractos de plantas del Amazonas (E79SS) y extracto de Viscum Pinus, y se dejaron evolucionar los animales durante 12 meses. A las dosis y en la forma administrada ninguna de las sustancias tuvo efecto para prolongar la vida de las ratas con tumores cerebrales y la supervivencia de los grupos tratados y de los controles fue similar.