C. perfringens in “no antibiotics ever” broiler farms
The prevalence and virulence of Clostridium perfringens in NAE commercial broiler farms is deemed higher than in farms using antibiotics. Research underpins that and advises year-round monitoring.
BY FANCHER, THAMES, COLVIN, ZHANG, NUTHALAPATI, KIESS, DINH AND SUKUMARAN, POULTRY SCIENCE
A
sporeforming, Gram-positive anaerobe found in the gastrointestinal tract of animals and humans (Clostridium perfringens) is the etiological agent of necrotic enteritis and gangrenous dermatitis.
These diseases cause, in broilers, significant economic and welfare concerns; the economic loss is estimated between USD$ 2 and $ 6 billion per year globally and the diseases cause a significant decrease in average daily feed intake of 40% and average daily gain of 16%.
Main barrier The use of antimicrobial growth promoters (AGPs) was the main barrier against Clostridium infections in commercial broilers. AGPs protect by direct antibacterial effects, modifying the gut microbiota, reducing GIT inflammation, and improving the overall physical health of the GIT. However, due to concerns about antimicrobial resistance, broiler operations have limited their antibiotic usage. Recently, it was estimated that more than 50% of the industry raises broilers without any antibiotics and only provided antibiotics when birds were sick. This type of broiler production is referred to as “no antibiotics ever” (NAE). Broilers reared within NAE facilities are not allowed to receive any antimicrobials in feed, water, supplementation, or injec- tion, at any point in the bird’s lifetime. However, compared to conventional production the removal of AGPs has in- creased mortality in NAE broiler production by 25 to 50% (NAE mortality 4.2%, conventional broiler production 2.9%). Also, the recent shift to NAE production has increased the incidence of Clostridium-related diseases. With greater dis- ease-incidence and mortality rates, it is crucial to under- stand the prevalence and virulence characteristics of C. perfrin- gens within commercial NAE farms. C. perfringens is classified into 5 toxinotypes (A, B, C, D, and E) based on their ability to produce major toxins. Toxinotype A is most associated with ne- crotic enteritis and gangrenous dermatitis in poultry.
70 ▶ ANTIBIOTIC REDUCTION | DECEMBER 2021
Compared to conventional production the removal of AGPs has increased mortality in NAE broiler production by 25 to 50% (NAE mortality 4.2%, conventional broiler production 2.9%).
Characteristics In this study the prevalence and virulence characteristics of C. perfringens in NAE commercial broiler farms was determined. The four farms used in this study had converted to a NAE system six months before sampling and had no clinical history of necrotic enteritis or gangrenous dermatitis. Samples of litter, faeces, and cloacal swabs were collected in the summer of 2019, on d 28 and d 56 of one flock cycle. A total of 734 presumptive isolates were obtained from 192 samples collected in the study. Irrespective of the age of flock and sample type, all 192 samples contained at least one colony presumptively identified as C. perfringens, after further screening using PCR for confirmation, toxinotyping, and identification of virulence-associated genes, only 9 isolates were confirmed as C. perfringens. All confirmed isolates were toxinotype A, however more extensive studies are required to assess the prevalence and virulence of the strains. Although the prevalence of C. perfringens was very low, the isolates contained major virulence genes that may induce Clostridium- related disease. Clostridium disease should be closely monitored in NAE facilities year-round, especially in facilities that have chronic Clostridium-related outbreaks. By monitoring the prevalence of disease-causing C. perfringens in the NAE environment, NAE facilities could limit future outbreaks.
PHOTO: HENK RISWICK
Page 1 |
Page 2 |
Page 3 |
Page 4 |
Page 5 |
Page 6 |
Page 7 |
Page 8 |
Page 9 |
Page 10 |
Page 11 |
Page 12 |
Page 13 |
Page 14 |
Page 15 |
Page 16 |
Page 17 |
Page 18 |
Page 19 |
Page 20 |
Page 21 |
Page 22 |
Page 23 |
Page 24 |
Page 25 |
Page 26 |
Page 27 |
Page 28 |
Page 29 |
Page 30 |
Page 31 |
Page 32 |
Page 33 |
Page 34 |
Page 35 |
Page 36 |
Page 37 |
Page 38 |
Page 39 |
Page 40 |
Page 41 |
Page 42 |
Page 43 |
Page 44 |
Page 45 |
Page 46 |
Page 47 |
Page 48 |
Page 49 |
Page 50 |
Page 51 |
Page 52 |
Page 53 |
Page 54 |
Page 55 |
Page 56 |
Page 57 |
Page 58 |
Page 59 |
Page 60 |
Page 61 |
Page 62 |
Page 63 |
Page 64 |
Page 65 |
Page 66 |
Page 67 |
Page 68 |
Page 69 |
Page 70 |
Page 71 |
Page 72 |
Page 73 |
Page 74 |
Page 75 |
Page 76 |
Page 77 |
Page 78 |
Page 79 |
Page 80 |
Page 81 |
Page 82 |
Page 83 |
Page 84 |
Page 85 |
Page 86 |
Page 87 |
Page 88 |
Page 89 |
Page 90 |
Page 91 |
Page 92 |
Page 93 |
Page 94 |
Page 95 |
Page 96