The incidence of Clostridium perfringens-associated necrotic enteritis in poultry has increased in countries that stopped using antibiotic growth promoters. Necrotic enteritis and the subclinical form of C. perfringens infection in poultry are caused by C. perfringens type A, producing the alpha toxin, and to a lesser extent type C, producing both alpha toxin and beta toxin. Some strains of C. perfringens type A produce an enterotoxin at the moment of sporulation and are responsible for foodborne disease in humans. The mechanisms of colonization of the avian small intestinal tract and the factors involved in toxin production are largely unknown. It is generally accepted, however, that predisposing factors are required for these bacteria to colonize and cause disease in poultry. The best known predisposing factor is mucosal damage, caused by coccidiosis. Diets with high levels of indigestible, water-soluble non-starch polysaccharides, known to increase the viscosity of the intestinal contents, also predispose to necrotic enteritis. Standardized models are being developed for the reproduction of colonization of poultry by C. perfringens and the C. perfringens-associated necrotic enteritis. One such model is a combined infection with Eimeria species and C. perfringens. Few tools and strategies are available for prevention and control of C. perfringens in poultry. Vaccination against the pathogen and the use of probiotic and prebiotic products has been suggested, but are not available for practical use in the field at the present time. The most cost-effective control will probably be achieved by balancing the composition of the feed.

The most common source of Salmonella infections in humans is food of poultry origin. Salmonella enterica serovar Enteritidis has a particular affinity for the contamination of the egg supply. In this study, the medium-chain fatty acids (MCFA), caproic, caprylic, and capric acid, were evaluated for the control of Salmonella serovar Enteritidis in chickens. All MCFA were growth inhibiting at low concentrations in vitro, with caproic acid being the most potent. Contact of Salmonella serovar Enteritidis with low concentrations of MCFA decreased invasion in the intestinal epithelial cell line T84. By using transcriptional fusions between the promoter of the regulatory gene of the Salmonella pathogenicity island I, hilA , and luxCDABE genes, it was shown that all MCFA decreased the expression of hilA , a key regulator related to the invasive capacity of Salmonella . The addition of caproic acid (3 g/kg of feed) to the feed of chicks led to a significant decrease in the level of colonization of ceca and internal organs by Salmonella serovar Enteritidis at 3 days after infection of 5-day-old chicks. These results suggest that MCFA have a synergistic ability to suppress the expression of the genes required for invasion and to reduce the numbers of bacteria in vivo. Thus, MCFA are potentially useful products for reducing the level of colonization of chicks and could ultimately aid in the reduction of the number of contaminated eggs in the food supply.

Despite considerable efforts to control bovine mastitis and explain its causes, it remains the most costly and common disease of dairy cattle worldwide. The role and impact of non-aureusstaphylococci (NAS) in udder health are not entirely understood. These Gram-positive bacteria have become the most frequently isolated group of bacteria in milk samples of dairy cows and are associated with (mild) clinical and subclinical mastitis. Different species and strains of NAS differ in their epidemiology, pathogenicity, virulence, ecology and host adaptation, and antimicrobial resistance profiles. They have distinct relationships with the microbiome composition of the udder and may also have protective effects against other mastitis pathogens. Some appear to persist on the skin and in the teat canal and udder, while others seem to be transient residents of the udder from the environment. Analyzing genotypic and phenotypic differences in individual species may also hold clues to why some appear more successful than others in colonizing the udder. Understanding species-level interactions within the microbiome and its interactions with host genetics will clarify the role of NAS in bovine mastitis and udder health.

Short-chain fatty acids (SCFA) are widely used as feed additives in poultry for the control of pathogenic bacteria, such as Salmonella enteritidis. Recently, a new range of products was developed in which SCFA are encapsulated in mineral carriers, resulting in a slow release during the transport of these carriers through the intestinal tract. To test the efficacy of this type of products against early colonization after Salmonella infection in poultry, a challenge experiment with S. enteritidis was performed. Five groups of 20 chickens were given feed with no supplement or feed supplemented with acetic acid (0.24%), formic acid (0.22%), or propionic acid (0.27%) as film-coated microbeads or butyric acid (0.15%) as spray-cooled microcapsules. The 5 groups were challenged with 5 x 10(3) cfu S. enteritidis at d 5 and 6 posthatch, and samples of ceca, liver, and spleen were taken at d 8 and analyzed for the number of colony-forming units of Salmonella per gram of tissue. Feed supplementation with acetic acid, and to a lesser extent formic acid, resulted in an increase of colonization of ceca and internal organs. Birds receiving propionic acid-coated microbeads as feed supplement were colonized with Salmonella to the same extent as controls. Butyric acid-impregnated microbeads in the feed, however, resulted in a significant decrease of colonization by S. enteritidis in the ceca but not in liver and spleen.