Effects of feed additives on the development on the ileal bacterial community of the broiler chicken

Lillehoj

Asian Australas. J. Anim. Sci

et al. 2012

: This study evaluated the effects of dietary anticoccidial drugs plus antibiotic growth promoters (AGPs) on parameters of immunity in commercial broiler chickens. Day-old chicks were raised on used litter from a farm with endemic gangrenous dermatitis to simulate natural pathogen exposure and provided with diets containing decoquinate (DECX) or monensin (COBN) as anticoccidials plus bacitracin methylene disalicylate and roxarsone as AGPs. As a negative control, the chickens were fed with a non-supplemented diet. Immune parameters examined were concanavalin A (ConA)-stimulated spleen cell proliferation, intestine intraepithelial lymphocyte (IEL) and spleen cell subpopulations, and cytokine/chemokine mRNA levels in IELs and spleen cells. ConA-induced proliferation was decreased at 14 d post-hatch in DECX-treated chickens, and increased at 25 and 43 d in COBN-treated animals, compared with untreated controls. In DECX-treated birds, increased percentages of MHC2

Section: Introductionmentioning

confidence: 99%

Effect of Dietary Antimicrobials on Immune Status in Broiler Chickens

Lillehoj

Asian Australas. J. Anim. Sci

et al. 2012

Korean Journal of Poultry Science

“…In their following study (Lu et al, 2008), gut microbiota of broiler chickens fed diet containing antibiotic growth promoters (bacitracin methylene disalicylate and virginiamycin; AGPs) was completely different from those seen in birds fed a non-medicated control diet, indicating that low levels of in-feed antimicrobials can substantially influence gut microbiota in broiler chickens.…”

Section: Introductionmentioning

confidence: 90%

Antimicrobials, Gut Microbiota and Immunity in Chickens

Lee¹,

Lillehoj²

2011

The use of antimicrobials will be soon removed due to an increase of occurrence of antibiotic-resistant bacteria or ionophore-resistant Eimeria species in poultry farms and consumers' preference on drug-free chicken meats or eggs. Although dietary antimicrobials contributed to the growth and health of the chickens, we do not fully understand their interrelationship among antimicrobials, gut microbiota, and host immunity in poultry. In this review, we explored the current understanding on the effects of antimicrobials on gut microbiota and immune systems of chickens. Based on the published literatures, it is clear that antibiotics and antibiotic ionophores, when used singly or in combination could influence gut microbiota. However, antimicrobial effect on gut microbiota varied depending on the samples (e.g., gut locations, digesta vs. mucosa) used and among the experiments. It was noted that the digesta vs. the mucosa is the preferred sample with the results of no change, increase, or decrease in gut microbiota community. In future, the mucosa-associated bacteria should be targeted as they are known to closely interact with the host immune system and pathogen control. Although limited, dietary antimicrobials are known to modulate humoral and cell-mediated immunities. Ironically, the evidence is increasing that dietary antimicrobials may play an important role in triggering enteric disease such as gangrenous dermatitis, a devastating disease in poultry industry. Future work should be done to unravel our understanding on the complex interaction of host-pathogen-microbiotaantimicrobials in poultry.

“…Ο μηχανισμός της δράσης των ΑΑΠ δεν έχει ακόμη πλήρως διαλευκανθεί, παρά τη μακρά ιστορία της χρή σης τους (Niewold 2007, Lu et al 2008. Για την ερμηνεία της δράσης τους έχουν προταθεί τέσσερις κύριοι μηχα νισμοί (Gaskins et al 2002, Dibner andRichards 2005): 1) Η αναστολή των νποκλινικών μολύνσεων, με αποτέλεσμα την εξοικονόμηση ενέργειας, λόγω της καλύτερης αξιοποίησης της τροφής και της μη διέ γερσης του ανοσοποιητικού συστήματος.…”

Section: αντιμικροβιακοί αυξητικοί παράγοντεςunclassified

“…Οι ΑΑΠ, παρ' όλο που μειώνουν τον πληθυσμό των λακτοβακίλλων (Knarreborg et al 2002, Lu et al 2008, οι οποίοι αποτελούν επωφελή βακτήρια για τον ξενιστή, προκαλούν αύξηση των αποδόσεων των ζώων. Αυτό πιθανώς να οφείλεται στο γεγονός ότι ταυτόχρονα μειώνουν και τον πληθυσμό του C perfringens, το οποίο προκαλεί διάσπαση των χολικών αλάτων και κακή απορρόφηση των λιπών, με αποτέλεσμα την καθυ στέρηση στην ανάπτυξη (Knarreborg et al 2002).…”

Section: αντιμικροβιακοί αυξητικοί παράγοντεςunclassified

Update on the emergence and pathogenesis of necrotic enteritis in broiler chickens

Tsiouris

Georgopoulou

Petridou

2018

J Hellenic Vet Med Soc

Necrotic enteritis (NE) is a disease of broiler chickens, which is caused by Clostridiumperfringens type A or C and is characterized by high mortality and severe intestinal lesions. NE is described as a disease of high economical importance which affects health and welfare of broilers and also may pose a threat to public health. Although NE was known as a disease since 1930, it did not cause serious problems to the poultry industry. The emergence of the disease occurred after 1986 in Scandinavia and 2000 in the European Union and was related with the ban of in-feed antimicrobial growth promoter. Furthermore, the ban of meat meal and bone meal from the feed of broiler chickens and their replacement by fishmeal increased further the occurrence of NE. NE breaks the Koch's postulate, which supports that "a disease-causing organism should not be present in healthy individuals", because C perfringens may be detected in high populations in the gut of birds with no visible signs of NE. Moreover, challenge of birds with C perfringens does not \eadperse to the development of the disease. It is very well accepted that NE is a multi-factorialdisease in which a number of co-factors are usually required for the proliferation and toxinogenesis of C. perfringens and manifestation of the disease. Toxin -a, since 2006, has been proposed to be the main virulence factor for NE in poultry. The origin of this assumption seems to lie to observation that crude supernatant from C perfringens type A cultures induced necrotic lesions in broilers. Moreover, the development of NE lesions prevented partially by antibodies against C. perfringens toxin -a. The interpretation of these early studies is not clear, because they used crude supernatant and the assumption was made that the effects were caused by the dominant protein present (i.e. toxin -a). However, many other proteins are also present in the supernatant ofC perfringens cultures. The most convincing evidence, that toxin -a is not essential virulence factor for the pathogenesis of NE, comes from studies using a toxin -a negative mutant (epa mutant) of a C perfringens strain from NE outbreak, which was able to produce characteristic NE lesions. Recently, netB, a novel toxin that is associated with broiler NE, has been described. A netB mutant of C perfringens was unable to cause necrotic lesions in the gut of experimentally infected broilers, but a complemented netB mutant was virulent, like the wild-type strain. However, netB per se, might not be an essential component of virulence factor for the pathogenesis of NE, because not all strains isolated from diseased birds carry the netB gene. The presence of the toxin -β2, although it has been linked with increased incidence of bovine enterotoxaemia, intestinal disorders in human, horses and diarrhea in piglets, does not seem to be involved in the pathogenesis of NE in broiler. Most C. perfringens strains isolated from cases of NE do not carry the gene (cpb2) which is responsible for the production of toxin -β2. The efficacy of antitoxin -a toxoid vaccines, the high concentration of toxin-a at the supernatant of C. perfringens culture and feces of diseased birds, as well as the high titer of antibodies against toxin-a in birds with NE, indicate that toxin -a definitely play a role, major or minor, on the pathogenesis of NE in broilers.