Page 794 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Botulinum Neurotoxins Chapter | 55 753

VetBooks.ir definitive because C. botulinum may proliferate and (Shimizu and Kondo, 1978). Protection in broilers
between 3 and 8 weeks of age was variable after vaccina-
spread from the intestinal tract to surrounding tissues of
tion at 1 and 14 days of age. Chickens are most suscepti-
the carcass. The mouse bioassay can be performed on
intestinal, cecal, and crop flushes, or samples can be ble to botulism between 2 and 8 weeks of age, and
assayed for toxin or bacterium after culture enrichment. vaccinations to protect this group may be less efficacious
In order to identify the source of contamination, feed, due to interference from maternal antibody and immatu-
water, litter, carcasses, and insects should be assayed for rity of the immune system. Routine vaccination further
toxin or cultured to isolate the bacterium. Both ELISA increases production costs, and the toxoid may not pro-
and the passive hemagglutination test can be performed to vide adequate protection against the high doses of toxin
identify serum antibodies to the toxins. However, the obtained from maggot ingestion. Toxoid immunizations
levels of toxin that produce illness are usually insufficient are also impractical for waterfowl. Therefore, preventative
to stimulate an immune response in chickens and ducks. measures to minimize outbreaks of avian botulism should
Differential diagnoses for avian botulism in poultry be aimed at flock and environmental management in both
include transient brain paralysis, coccidiostat toxicity, production birds and waterfowl.
pesticide, or other chemical toxicity, New Castle disease, In broiler outbreaks, the goals are to limit further
Marek’s disease, avian encephalomyelitis, avian reovirus, exposure and eliminate C. botulinum or toxins from the
fowl tick fever (spirochaetosis), and musculoskeletal pro- environment. Unaffected birds should be moved to uncon-
blems. Fowl cholera and chemical toxicity, particularly taminated houses. Carcasses should either be incinerated
lead poisoning, are the common differentials for botulism or buried in a deep hole. Rodents should be eliminated
in waterfowl. Fowl tick fever is common in poultry in the from broiler houses because rodent carcasses may harbor
southern and southwestern United States. However, eyelid C. botulinum. Chicken houses associated with outbreaks
paresis and the lack of postmortem lesions are supportive should be emptied and cleaned. All litter should be
of botulism as the diagnosis. removed. Houses should be washed with high-pressure
When possible, clinically ill birds should be isolated steam and cleaned with a detergent agent. A surface-
and provided fresh water; once these measures are taken, active solution should be sprayed on the interior walls.
birds often recover fully within a few days. Waterfowl The walls should then be disinfected with an organic
should be herded to uncontaminated shores, and carcasses iodine solution or an organic iodine and calcium hypo-
should be removed daily in poultry operations. Antitoxin chlorite solution. Twenty-four hours later, the interior
therapy may be administered for valuable birds or zoo walls should be sprayed with 10% formalin. Soil in con-
animals, but it is impractical for most production opera- taminated areas may also be treated with calcium hypo-
tions or wildlife. Furthermore, antitoxin protection is tran- chlorite. Houses should also be sprayed with pesticides to
sient, and birds may again become susceptible to the limit flies. Iron levels in feed and water sources should be
toxins. In broiler outbreaks, antimicrobial therapy may be monitored.
instituted through watering systems or feed. Prevention of waterfowl outbreaks is best achieved by
Administration of bacterin (100 g/ton of feed) or strepto- reducing the potential for environmental contamination
mycin (500 1000 g/ton of feed or 1 g/L of water for 3 associated with the proliferation of C. botulinum in the
days) was shown to decrease mortality rates in chickens carcasses of dead vertebrate and invertebrate animals.
(Schettler, 1979; Sato, 1987). Penicillin may also be Carcasses should be collected, and flocks should be
administered, but a mixed efficacy has been reported with herded away from shores associated with outbreaks. Pond
this treatment. Periodic use of chlortetracycline was management should maintain deep waters, steep banks,
reported to reduce botulism outbreaks on one poultry and smooth bottoms to prevent deaths of invertebrates
farm. Additives such as sodium selenite (6 g/1000 L of and vertebrates. Routine flooding, which may lead to the
water for 5 days) and vitamins A, D 3 , and E may also death of terrestrial invertebrates, should be avoided in
reduce mortality (Schettler, 1979). Conversely, elevated areas utilized by waterfowl. Water in wetland areas
iron levels in water or feed may promote the intestinal should be maintained as fresh as possible because oxygen
proliferation of C. botulinum; therefore, citric acid, an depletion in shallow, stagnant waters leads to aquatic ani-
iron chelator, may be added to water as a preventative mal die-offs. Any factors that may increase deaths in sus-
(Pecelunas et al., 1999). Furthermore, citric acid may ceptible wetlands, such as overhead power lines, should
lower the pH of the GI tract, inhibiting the growth of C. be removed or avoided.
botulinum and promoting the growth of normal flora. The possibility for transmission of botulism from birds
to their predators may exist. Coincidence of avian out-
breaks with botulism in omnivorous animals has been
Prevention documented. For instance, Weiss et al. (1982) reported
Immunization with the toxoid vaccine has been explored botulism in a fox and a weasel in association with a
in broilers, pheasants, and ducks with mixed results waterfowl outbreak. In addition, there have been several