monensin and Enteritis

1. This study investigated the effect of Eimeria spp./Clostridium perfringens induced necrotic enteritis and traditional antibiotic preventatives on intestinal micro-architecture and mucin profile. 2. A total of 600 Cobb 500 broiler chickens were randomly assigned to the following three groups: (i) unchallenged, (ii) challenged, and (iii) zinc bacitracin/monensin (ZnB/monensin) (n = 25 chickens/pen, 8 pens/group). The challenged and ZnB/monensin chickens were individually inoculated with Eimeria acervulina, E. maxima and E. tenella and C. perfringens type A (EHE-NE18) at 9 and 15 d post-hatch respectively, to induce necrotic enteritis. 3. The challenge procedure significantly decreased villus height, increased villus width and increased crypt depth in the challenged compared to the unchallenged chickens. Zinc bacitracin and monensin maintained villus-crypt structure similar to that of the unchallenged chickens. 4. Mucin profile was not affected by Eimeria spp./C. perfringens challenge as demonstrated by periodic acid-Schiff and high iron diamine-alcian blue pH 2 x 5 staining. Zinc bacitracin and monensin decreased the number of intestinal mucin-containing goblet cells. 5. Lectin histochemistry showed a trend towards greater Arachis hypogea (PNA) reactivity in unchallenged chickens. 6. In summary, Eimeria spp./C. perfringens challenge disrupted intestinal micro-architecture; however, challenge did not appear to affect intestinal mucin profile. Traditional antibiotics, zinc bacitracin and monensin maintained micro-architecture.

Topics: Animals; Anti-Bacterial Agents; Bacitracin; Chickens; Clostridium Infections; Clostridium perfringens; Coccidiosis; Coccidiostats; Eimeria; Enteritis; Goblet Cells; Intestinal Diseases; Intestines; Lectins; Monensin; Mucins; Necrosis; Poultry Diseases; Random Allocation; South Australia; Species Specificity

Clinical signs of proliferative haemorrhagic enteropathy (PHE) including anaemia, dysentery and sudden death were observed in finisher pigs and young breeding stock on 2 farms. On farm A, PHE occurred 12 months after repopulation of the farm. Other outbreaks of PHE occurred after the withdrawal of therapeutic concentrations of in-feed antibacterial agents (farm A), or after monensin sodium (100 g/t) replaced olaquindox (100 g/t) in feed (farm B). The outbreaks, the possible sources of contamination and the role of antibacterial feed additives in the treatment and control of PHE are described.

Topics: Anemia; Animal Feed; Animals; Anti-Bacterial Agents; Antiprotozoal Agents; Bacterial Infections; Disease Outbreaks; Drug Therapy, Combination; Dysentery; Enteritis; Epithelium; Female; Gastrointestinal Hemorrhage; Intestine, Large; Intestine, Small; Male; Monensin; Pregnancy; Quinoxalines; Swine; Swine Diseases; Victoria