Page 748 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Avian Toxicology Chapter | 53 713

VetBooks.ir detection of the toxin in the gastrointestinal contents and information pertaining to avian mycotoxicoses is pre-
A diagnosis of cyanobacterial intoxications is often by
sented in this section.
confirmation of its presence in the algal blooms.
In addition to anatoxins and microcystins produced by
cyanobacteria, the death of lesser flamingos in East
Aflatoxins
African Rift Valley revealed another class of potent cya-
nobacterial toxins the β-N-methylamino-L-alanine and Aflatoxins are secondary fungal metabolites produced by
2,4-diaminobutyric acid. These are neurotoxic amino Aspergillus flavus, Aspergillus parasiticus, and
acids produced by the cyanobacteria belonging to the Aspergillus nomius. There are different toxin types desig-
family Arthrospira (Metcalf et al., 2013). nated by letters: B1, B2, G1, and G2. Of these aflatoxin
B1 is the most frequently occurring and toxic member of
the group. Although peanuts and corn are commonly
Avian Vacuolar Myelinopathy
known substrates for the growth of aflatoxin-producing
Avian vacuolar myelinopathy (AVM) is a disease of birds fungi, other grains and nuts have been implicated as well.
that has sporadically caused mortality of bald eagles
Economic losses attributed to aflatoxin exposure in poul-
(Haliaeetus leucocephalus), American coots (Fulica ameri-
try often stem from reductions in growth rate, hatchabil-
cana), and other waterbirds in several reservoirs in the south-
ity, feed efficiency, and immunocompetence.
eastern Unites States. Studies have demonstrated an
Poultry, especially turkeys, are extremely sensitive to
association between bird mortality and the presence of the
the toxic effects of AFB 1 , with quail being intermediate
invasive plant hydrilla (Hydrilla verticillata)(Wilde et al.,
and chickens being comparatively resistant (Lozano and
2005). Earlier, the cyanobacteria belonging to
Diaz, 2006). Mortality events have been reported in
Stigonematales was suspected to be the causative agent.
migrating wild birds such as cranes, ducks, Canada geese,
However, recent studies have shown that cyanobacterial spe-
teals and other free ranging birds following consumption
cies belonging to Aetokthonus hydrillicola gen. et sp. nov.,
of grains in damaged, fungus infested standing crops
described recently, has been found to be associated with the
(Friend and Franson, 1999).
hydrilla plant (Dodd, 2016). AVM was reproduced using Clinical signs in birds include lethargy, depression,
mallard ducks and chickens exposed to Stigonematales blindness, inability to fly, tremors, and wing flapping,
blooms previously. It is believed that a currently uncharacter- although birds can also simply be found dead. Lethal afla-
ized algal neurotoxin is the etiology. AVM is characterized toxicoses in ducklings occurred as inappetence, reduced
by widespread, bilaterally symmetrical vacuolation of the growth, abnormal vocalization, feather picking, purple
white matter of the brain and spinal cord. discoloration of leg and feet, and lameness. Ataxia, con-
vulsions, and opisthotonus preceded death (Carnaghan,
Plants 1961). Turkeys develop inappetence, reduced spontaneous
activity, unsteady gait, recumbency, anemia, and death.
A number of plants are recognized for their toxicity in birds Aflatoxicosis in chickens closely resembles the clinical
(Table 53.1). Plants contain a large variety of biologically signs in ducks and turkeys. Chronic effects, which include
active constituents, including volatile oils, resins, alkaloids, appetite loss, weight loss/reduced weight gain, and gen-
polysaccharides, phenols, glycosides, and fixed oils. eral ill health due to immunosuppression, can be more
The susceptibility of different bird species to specific insidious and difficult to definitively relate to aflatoxin
toxic plants is variable. In addition, birds may be unaf- exposure.
fected by plants that are toxic to other animals such as Acute exposures over a relatively short period lead to
mammals. For example, cedar waxwings and house finches pale, swollen, and enlarged livers (and kidneys), occa-
can consume fruit from the pepper tree (Capsicum sional gallbladder distension, thickening of crop and pro-
annuum) that is toxic to mammals (Navarro, 1992). ventricular mucosa, and hemorrhages in internal organs
Feeding behaviors also influence the susceptibility to intox- especially GI tract (blackish red). Chronic exposure pro-
ication. For example, it has been suggested that parrots can duces a shrunken, fibrous liver with regenerative nodules
consume otherwise toxic plants because they remove the or tumors. Microscopically, the hepatocytes show fatty
outer covering of fruits and seeds, which can contain high changes, proliferation of bile ductules, and extensive
concentrations of toxins, before consumption. fibrosis, accompanied by vascular and degenerative
lesions in pancreas and kidney.
Measurement of aflatoxin concentrations in suspected
Mycotoxins
feed, ingesta, or the liver is crucial for confirming diagno-
Independent chapters pertaining to mycotoxins are pre- sis. Representative sampling and adequate precautions
sented elsewhere in this book; therefore, select (e.g., freezing samples) to avoid fungal growth and toxin