Page 758 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Avian Toxicology Chapter | 53 719

VetBooks.ir Ochratoxin and Citrinin botulinum. There are eight antigenically distinct toxin
types designated as A, B, C (alpha and beta), D, E, F, and
These nephro- and hepatotoxic mycotoxins are produced
G; with Type C alpha cultures producing three toxins des-
by multiple species of Aspergillus and Penicillium, and
ignated C1 C3. A number of factors play a role in the
occur in feedstuffs worldwide. Ochratoxin A (OTA) is
occurrence of an outbreak of botulism, including optimal
comparatively ten times more toxic than citrinin and has
environmental conditions for spore germination and bac-
been studied extensively, although both may co-occur.
terial growth, availability of suitable material to support
bacterial replication such as decomposing carcasses, and a
Avian species vary in their sensitivity to OTA; the LD 50
in chickens is reported to be 2 4 mg/kg, whereas ducks
means for toxin transfer to birds. Type C toxin produ-
and Japanese quail are susceptible to 0.5 16.5 mg/kg
cing bacterial spores are ubiquitous in wetland environ-
body weight (BW) (Peckham et al., 1971).
ments inhabited by bird populations.
OTA inhibits protein biosynthesis, causes oxidative
Botulinum toxin is one of the most toxic biotoxins
stress, accelerates lipid peroxidation, and reacts with
known, although for any given species, toxicity varies by
enzymes-utilizing phenylalanine as a substrate, thereby
toxin type and age. For example, chickens, turkeys, phea-
exerting its toxic effects. The nephrotoxic effect of OTA is
sants, and peafowl are susceptible to types A, B, C, and E
due to its action on the organic anion transport system,
but not to types D or F (Gross and Smith, 1971). As
located in basolateral and brush border membranes of the
broiler chickens age, they become less susceptible to type
proximal tubule cells of the nephron and also involved in the
C toxin. Most outbreaks of botulism in birds are due to
absorption/reabsorption and excretion of OTA in the kidney.
exposure to type C1 toxin. Avian botulism is one of the
Field outbreaks of ochratoxicosis typically result in
most important diseases of migratory birds. Exposure
decreased feed consumption, efficiency, growth rate, and
occurs when waterfowl feed on contaminated zooplank-
increased mortality. Hepatotoxicity is characterized by a
ton, and carcass-feeding maggots or raptors feed on car-
significant increase in γ-glutamyl transferase activity,
casses. Poultry and production birds are also exposed
decrease in serum total protein, albumin, globulin, choles-
through wound contamination by spores. Vultures and
terol, triglyceride, and increase in the weight of liver. An
other carrion eaters are resistant to botulinum toxin, per-
elevation in serum uric acid, creatinine, postmortem
haps, in part, due to the production of antibodies to botuli-
degenerative changes, and an increase in the weight of
num toxin, which does not occur in sensitive species such
kidney were considered to be indicative of nephrotoxicity
as chickens and ducks (Ohishi et al., 1979).
(Huff et al., 1988). For details on mechanism and toxicity
Clinical signs are consistent with neuromuscular paral-
of OTA and citrinin refer to Chapter 74, Tremorgenic
ysis. Affected waterfowl are unable to sustain flight, hold
Mycotoxins.
their head erect (limberneck) and present with paralysis
To detoxify and reduce the concentration of OTAs,
of nictitating membrane. Waterfowl often drown; affected
various probiotic bacteria, yeast or gamma-irradiation
terrestrial birds die from respiratory and cardiac failure.
have been used (Biernasiak et al., 2006).
In chickens, an ascending flaccid paralysis is noted with
symptoms similar to waterfowl. Postmortem lesions are
Zootoxins generally not observed; in affected waterfowl, lesions
may be consistent with drowning.
There are few reports of bird intoxication resulting from
A presumptive diagnosis is based on characteristic
exposure to zootoxins. Snakebite was believed to have
clinical signs, environmental conditions conducive to bac-
been responsible for the deaths of two red-tailed hawks
terial growth and toxin production, and detection of toxin
(Buteo jamaicensis) and a Cooper’s hawk (Accipiter
in serum and tissues. Treatment of affected birds with
cooperii) based on the carcasses being found in the vicin-
antitoxin is helpful in waterfowl but not in other species
ity of venomous snakes and gross findings of hemor-
such as coots, shorebirds, gulls, and grebes (Friend and
rhages, muscle degeneration, and gangrenous necrosis of
Franson, 1999). Prevention and control of outbreaks are
a limb (Heckel et al., 1994). Chickens, turkeys, and ducks
critical to minimize losses. Removing organic and decay-
have also reportedly been killed by snakes based on bite
ing material in wetlands, and proper disposal of animal
sites that were identified on postmortem examination and
carcasses can interrupt bacterial growth and toxin
compatible gross organ lesions (Lawal et al., 1992). For
production.
further details on zootoxins, see Chapter 59, Chemical-
Induced Estrogenicity.
Feed Additives
Bacterial Toxins
Botulinum Toxin Sodium
Avian botulism results from the ingestion of botulinum Sodium ion intoxication is a significant problem in poul-
toxin produced by the anaerobic bacterium Clostridium try production. Intoxication can result from excessive