Virus mutations and their impact on vaccination against infectious bursal disease (Gumboro disease). / Les mutations virales et leur impact sur la vaccination contre la bursite infectieuse (maladie de Gumboro).

Infectious bursal disease (also known as Gumboro disease) is an immunosuppressive viral disease specific to chickens. In spite of all the information amassed on the antigenic and immunological characteristics of the virus, the disease has not yet been brought fully under control. It is still prevalent in properly vaccinated flocks carrying specific antibodies at levels normally high enough to prevent the disease. Common causes apart, failure of vaccination against infectious bursal disease is associated mainly with early vaccination in flocks of unknown immune status and with the evolution of viruses circulating in the field, leading to antigenic drift and a sharp rise in pathogenicity. Various highly sensitive molecular techniques have clarified the viral determinants of antigenicity and pathogenicity of the infectious bursal disease virus. However, these markers are not universally recognised and tend to be considered as evolutionary markers. Antigenic variants of the infectious bursal disease virus possess modified neutralising epitopes that allow them to evade the action of maternally-derived or vaccine-induced antibodies. Autogenous or multivalent vaccines are required to control antigenic variants in areas where classical and variant virus strains coexist. Pathotypic variants (very virulent viruses) remain antigenically related to classical viruses. The difficulty in controlling pathotypic variants is linked to the difficulty of eliciting an early immune response, because of the risk of the vaccine virus being neutralised by maternal antibodies. Mathematical calculation of the optimal vaccination time and the use of vaccines resistant to maternally-derived antibodies have improved the control of very virulent viruses.

La bursite infectieuse (maladie de Gumboro) est une pathologie virale immunodépressive spécifique du poulet. En dépit des informations accumulées sur les caractères antigéniques et immunologiques du virus, la maladie reste imparfaitement contrôlée. Elle sévit aujourd'hui dans des cheptels correctement vaccinés et porteurs d'anticorps spécifiques à des niveaux habituellement suffisants pour prévenir la maladie. Au-delà des causes triviales, les échecs de la vaccination contre la maladie de Gumboro sont essentiellement liés aux vaccinations précoces de cheptels au statut immunitaire inconnu et à l'évolution des virus qui circulent sur le terrain, se traduisant par une dérive antigénique et une hausse sensible de la pathogénicité. Diverses techniques moléculaires hautement sensibles ont permis d'identifier les déterminants viraux d'antigénicité et de pathogénicité du virus. Ces marqueurs ne sont cependant pas unanimement reconnus et sont pour la plupart considérés comme des marqueurs évolutionnaires. Les virus variants antigéniques possèdent des épitopes neutralisants modifiés qui leur permettent de se soustraire à l'action des anticorps résiduels ou vaccinaux. Leur contrôle passe par l'utilisation d'autovaccins ou de vaccins multivalents dans les régions où coexistent virus classiques et variants. Les variants pathotypiques (virus hypervirulents) restent antigéniquement apparentés aux virus classiques. La difficulté de contrôler ce type de variant est liée à celle d'obtenir une réponse immune précoce, en raison du risque de neutralisation du virus vaccinal par les anticorps d'origine maternelle. Le calcul mathématique de la date optimale de vaccination et l'utilisation de vaccins insensibles aux anticorps résiduels ont permis un meilleur contrôle des virus hypervirulents.

La bursitis infecciosa (enfermedad de Gumboro) es una patología viral específica del pollo, en el que provoca inmunodeficiencia. Pese al acervo de datos existentes sobre los caracteres antigénicos e inmunológicos del virus, la enfermedad no está aún del todo controlada. Hoy en día afecta a bandadas que están correctamente vacunadas y presentan niveles de anticuerpos específicos que en general son suficientes para prevenir la enfermedad. Más allá de las causas corrientes, el fracaso de las vacunaciones contra la enfermedad de Gumboro tiene que ver esencialmente con la vacunación precoz de bandadas cuyo estado inmunológico se desconoce y con la evolución de los virus circulantes sobre el terreno, que se traduce en una deriva antigénica y un sensible aumento de la patogenicidad. Gracias a diversas técnicas moleculares de gran sensibilidad se han podido discernir los determinantes de antigenicidad y patogenicidad del virus, aunque se trata de marcadores no reconocidos unánimemente y considerados en su mayor parte marcadores evolutivos. Los virus que representan variantes antigénicas poseen epitopos neutralizantes modificados que les permiten escapar a la acción de los anticuerpos residuales o inducidos por vacunación. Para combatirlos es preciso utilizar autovacunas o vacunas polivalentes allí donde coexisten los virus clásicos y las variantes. Las variantes patotípicas (virus hipervirulentos) no dejan de estar emparentadas antigénicamente con los virus clásicos. La dificultad de luchar contra este tipo de variante está ligada a la de obtener una respuesta inmunitaria precoz, en razón del riesgo de neutralización del virus vacunal por acción de los anticuerpos de origen materno. El cálculo matemático de la fecha idónea de vacunación y el uso de vacunas insensibles a los anticuerpos residuales han permitido luchar más eficazmente contra los virus hipervirulentos.

Epidemiology and Genetic Characterization of H3N8 Equine Influenza Virus Responsible for Clinical Disease in Algeria in 2011.

An outbreak of equine influenza (EI) was reported in Algeria between May and July, 2011. The outbreak started in Tiaret, in west province of Algeria, and spread to the other parts of the country affecting almost 900 horses in many provinces. The population studied was composed of 325 horses from different groups of age. Clinical sign expression was age dependent. Indeed, a morbidity rate of 14.9% was observed in horses under 15 months old and a rate of 4.95% in horses over 8 years old. Interestingly, the morbidity rate raised sharply to reach 100% in horses aged between 18 months and 7 years. The virus (H3N8) was detected in nasopharyngeal swabs (n = 11) from non-vaccinated horses using a qRT-PCR targeting a portion of the gene encoding the matrix protein (M). The virus isolates were identified as H3N8 by sequencing the haemagglutinin (HA) and neuraminidase (NA) genes and were named from A/equine/Tiaret/1/2011 to A/equine/Tiaret/10/2011. Alignment of HA1 amino acid sequence confirmed that viruses belong to Clade 2 of the Florida sublineage in the American lineage. Moreover, they are closely related to A/equine/Yokohama/aq13/2010, A/equine/Eyragues/1/2010, A/equine/Bokel/2011 and A/equine/Lichtenfeld/2012. Our data indicate that this strain was also circulating in the European horse population in 2010, 2011 and 2012.

Variations of motility and survival with storage time at 4°C of epididymal spermatozoa Ouled-Djellal breed rams in Eastern Algeria.

AIM: The aim of this study was to evaluate some reproduction performances in Ouled-Djellal rams. MATERIALS AND METHODS: This study involved genital organs removed after slaughter from 54 rams at the municipal slaughterhouse of Batna (East Algeria). RESULTS: The measurements of survival and mobility of epididymal sperm followed at 0, 24, 48 and 72 h after collection, revealed significant (p<0.05) to highly significant differences (p>0.001) according to time. Thus, concerning the sperm motility the values were 91.00±2.40%, 89.20±2.40%, 77.00±6.20% and 62.60±1.20% at 0, 24, 48 and 72 h, respectively. Indeed, in live sperm, the viability rates were 82.15±1.48%, 77.67±1.74%, 66.56±1.95% and 52.30±1.46% at 0, 24, 48 and 72 h, respectively. CONCLUSION: This study revealed that epididymal spermatozoa stored at 04°C for 72 h kept their mobility and vitality at nearly a half of their the original parameters.

Effects of age, environmental temperature and relative humidity on the colonization of the nose and trachea of calves by Mycoplasma spp.

Nasal and tracheal swabs sequentially collected from three groups of eight calves between the ages of 1 and 98 days indicated that the nose and trachea were colonized by Mycoplasma spp. during the first weeks of life. Over 92% of all calves harboured Mycoplasma spp. in their noses when they were 2 weeks old, the rate of recovery falling gradually thereafter. The peak period of recovering mycoplasmas from the noses and tracheas of calves was at 6 weeks old. M. bovirhinis, M. arginini and Acholeplasma laidlawii predominated in the nose while M. dispar and M. bovirhinis predominated in the trachea. There was no association between rates of isolation and clinical signs of respiratory disease. There were no significant differences between the frequencies of isolation of Mycoplasma spp. from groups of calves kept under different environmental temperatures and relative humidities.

The effects of age, environmental temperature and relative humidity on the bacterial flora of the upper respiratory tract in calves.

The effects of age, environmental temperature and relative humidity on the bacterial flora of the nose and trachea of calves were investigated by sequential sampling of three groups each of eight Friesian-Holstein male calves kept in three different environmental conditions. All calves were vaccinated with a live attenuated vaccine against infectious bovine rhinotracheitis (IBR) when they were 12 weeks old. Nasal and tracheal swabs were collected at 14-day intervals for bacteriological examinations. The upper respiratory tract of calves started to be colonized by various species of bacteria within the first day of life. Although they were born at different periods of the year, the calves in all three groups had similar bacterial loads in their noses and tracheas when they were 1 day old (P greater than 0.05). The total bacterial colony forming units (BCFU) were highly variable from calf to calf and from one time of sampling to another. Despite these variations, there were age-related increases in the total BCFU in nasal and tracheal swabs in all experiments. These increases were influenced by environmental temperature. Vaccination of the calves with a live IBR vaccine appeared to enhance the bacterial colonization of the upper respiratory tract.