No abstract

African swine fever (ASF) is an acute, highly contagious and deadly viral hemorrhagic fever of domestic pigs caused by African swine fever virus (ASFV), a double-stranded DNA virus of the family Asfarviridae. In this study, molecular diagnosis and characterization of outbreak ASFV in northern Tanzania, was performed on spleen, lymph node, kidney, and heart samples collected in June and July 2013 from domestic pigs that died during a hemorrhagic disease outbreak. Confirmatory diagnosis of ASF was performed using polymerase chain reaction (PCR) by partial amplification of B646L gene of ASFV encoding the major capsid protein p72 using PPA1/PPA2 primers. PCR using PPA1/PPA2 primers produced an expected PCR product size, confirming ASF outbreak in northern Tanzania. In addition, nucleotide amplification and sequencing, and phylogenetic reconstruction of the variable 3′-end of the B646L gene and complete E183L gene encoding the inner envelope transmembrane protein p54 showed that the 2013 outbreak ASFV from northern Tanzania were 100 % identical and clustered into ASFV B646L (p72) and E183L (p54) genotype X. Furthermore, the tetrameric amino acid repeats within the central variable region (CVR) of the B602L gene coding for the J9L protein had the signature BNBA(BN)5NA with a single novel tetramer NVDI (repeat code N). The results of the present study confirm an ASF outbreak in northern Tanzania in the year 2013 and show that the present outbreak ASFV is closely related to other ASFV from ticks, warthogs, and domestic pigs previously reported from Tanzania.

Newcastle Disease (ND) is a continuing global threat to domestic poultry, especially in developing countries, where severe outbreaks of velogenic ND virus (NDV) often cause major economic losses to households. Local chickens are of great importance to rural family livelihoods through provision of high-quality protein. To investigate the genetic basis of host response to NDV, three popular Tanzanian chicken ecotypes (regional populations) were challenged with a lentogenic (vaccine) strain of NDV at 28 days of age. Various host response phenotypes, including anti-NDV antibody levels (pre-infection and 10 days post-infection, dpi), and viral load (2 and 6 dpi) were measured, in addition to growth rate. We estimated genetic parameters and conducted genome-wide association study analyses by genotyping 1399 chickens using the Affymetrix 600K chicken SNP chip. Estimates of heritability of the evaluated traits were moderate (0.18–0.35). Five quantitative trait loci (QTL) associated with growth and/or response to NDV were identified by single-SNP analyses, with some regions explaining ≥1% of genetic variance based on the Bayes-B method. Immune related genes, such as ETS1, TIRAP, and KIRREL3, were located in regions associated with viral load at 6 dpi. The moderate estimates of heritability and identified QTL indicate that NDV response traits may be improved through selective breeding of chickens to enhance increased NDV resistance and vaccine efficacy in Tanzanian local ecotypes.

Twenty flocks of web-footed birds (Pekin and Muscovy ducks and geese) and eight flocks of chickens raised under intensive management were examined for the presence of carriers of Pasteurella multocida. Five hundred and seventy-eight web-footed birds and 240 chickens from healthy flocks, as well as from flocks affected by fowl cholera, were investigated. A total of 135 isolates (80 from healthy flocks and 55 from flocks affected by fowl cholera) were obtained from the pharyngeal and cloacal mucosae after mouse passage (134 isolates) and culture in selective medium (one isolate). Thirty-five percent (7/20) of the flocks of web-footed birds and 38% (3/8) of chicken flocks had birds carrying P. multocida in the pharynx and/or cloaca. Birds from flocks affected by fowl cholera carried P. multocida at a significantly higher prevalence in the mucosa of the cloaca (P < 0.001) compared with the pharynx, while the opposite was observed in birds from healthy flocks. Extended phenotypic characterization confirmed the presence of P. multocida ssp. multocida, P. multocida ssp. septica and P. multocida ssp. gallicida in the flocks examined. P. multocida ssp. gallicida was exclusively isolated from Pekin ducks, while P. multocida ssp. multocida and P. multocida ssp. septica were obtained from chickens as well as web-footed birds. Each flock was shown to be infected by a single phenotypic clone, but some clones were found in more than one flock. A different clone was found in each of four outbreaks of fowl cholera on one of the farms in the preceding 2 years. Two genotypic and phenotypic clones each of P. multocida ssp. multocida and P. multocida ssp. septica were found. This observation indicated that outbreaks are usually clonal and that elimination of P. multocida from infected farms is possible. The results suggest that healthy poultry, in addition to convalescent carriers, may also be carriers of P. multocida. However, the virulence of P. multocida isolates and resistance of carriers to clinical infection needs to be examined. This is the first report of isolation of P. multocida from the cloacal mucosa of apparently healthy domestic poultry. Sampling of the cloaca appeared to be more sensitive for detecting carriers of P. multocida. Although selective medium was used only to a limited extent, the results suggested that mouse inoculation was a more efficient method of isolating P. multocida from poultry than the use of selective media.

Pasteurella multocida and Ascaridia galli are observed with high prevalences in free range chickens in Denmark, but the impact is unknown. A study was carried out to examine the interaction between A. galli and P. multocida in chickens and the impact on production.Five groups, each with 20 18-week-old Lohmann Brown chickens were infected. Group 1 was orally infected with 1000 AE 50 embryonated A. galli eggs. Group 2 received 10 4 cfu P. multocida intratracheally. Group 3 was infected with A. galli and subsequently with P. multocida. Group 4 was infected with P. multocida followed by A. galli. Group 5 was the control. The study ran for 11 weeks where clinical manifestations, weight gain and egg production were recorded. Excretion of P. multocida was determined on individual basis and blood smears were made for differential counts. At the end of the study pathological lesions and the number of adult worms, larvae and eggs in the faeces were recorded.The birds were more severely affected when infected with both pathogens compared to single infections with A. galli or P. multocida, respectively. A lower weight gain and egg production was observed with dual infections. A. galli infection followed by a secondary P. multocida infection resulted in more birds with pathological lesions and continued P. multocida excretion.In conclusion a negative interaction between A. galli and P. multocida was observed and it is postulated that free range chickens are at higher risk of being subjected to outbreaks of fowl cholera when they are infected with A. galli. #