Page 757 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

718 SECTION | X Avian and Aquatic Toxicology

VetBooks.ir production secondary to improper postcollection storage common clinical signs (Wyatt et al., 1973). T-2 toxin can
induce necrosis and depletion of lymphoid cells in
and shipping are necessary.
the thymus, spleen, and lymph nodes of chickens and
Steps to minimize crop damage and mold growth are
crucial. Suspected feed sources should be removed from pullets. A major postmortem finding is necrotic damage
the diet. Since aflatoxin contamination of feedstuff is characterized by white-yellowish bulges containing
nearly universal, various chemopreventive and enterosorp- caseous necrotic material in various areas of the mouth,
tive approaches such as addition of synthetic zeolites and gizzard, intestinal mucosa, and liver (Wyatt et al., 1973).
sodium calcium aluminosilicate in the feed, and adminis- Diagnosis is based on history, postmortem findings
tration of the hepatoprotective agent silymarin have been including necrotic lesions in the digestive system, and
shown to be protective (Kubena et al., 1998; Tedesco detection of T-2 at significant concentrations in the sus-
et al., 2004). pected feed. Total amount of all trichothecenes including
The Food and Drug Administration (FDA) has set a T-2 toxin in poultry feed should preferably not exceed
current guidance level for AFB 1 concentrations in corn 0.5 mg/kg, based on a compilation of data including
and peanut products intended for immature and mature occurrence, toxicity, and clinical signs in poultry (Eriksen
poultry at 20 and 100 parts per billion (ppb), respectively. and Pettersson, 2004).
Deoxynivalenol (vomitoxin): DON is the least acutely
toxic tricothecene mycotoxin to poultry but a more com-
Fusariotoxins
monly occurring grain contaminant (Rotter et al., 1996).
Fungi belonging to Fusarium spp. and several other gen- Diversion of DON-infected cereals to poultry feed is com-
era produce chemically distinct mycotoxins in feed grains monly believed to be a significant route of exposure.
and nuts. Type A and type B trichothecenes, zearalenone The effects of DON on performance are highly vari-
(ZEN), and fumonisins are fusariotoxins of relatively able but reduced weight gain and feed refusal are estab-
greater importance from a poultry-production and health lished findings. DON can cause significant lipid
perspective (Girgis and Smith, 2010). Type A trichothe- peroxidation, oxidative stress and DNA damage indicating
cenes include T-2 toxin, HT-2 toxin and diacetoxyscirpe- the genotoxic potential and possibly explaining its effects
nol; type B trichothecenes include deoxynivalenol (DON, on various body systems. The immune and intestinal epi-
vomitoxin), 3- and 15-acetyl-DON, nivalenol, and thelial cells are particularly sensitive to the toxic effects
fusarenon-X. Of these, DON is the most commonly of DON. Erosions in the mucosa of the gizzard, corruga-
encountered fusariotoxin. tions in the gastric mucosa, duodenitis, jejunitis, intestinal
Fusariotoxins differ from other mycotoxins in that bleeding, and necrosis are significant postmortem findings
they tend to be produced during the colder seasons of the associated with DON exposure. Reduced immune
year. Common substrates involved in fusariotoxin produc- responses to Newcastle disease vaccine infectious bron-
tion include corn, wheat, barley, oats, and peanuts. ZEN chitis virus have been observed in laying hens and broi-
often occurs with DON in naturally contaminated cereals, lers due to feeding DON-contaminated grains (Harvey
and it is responsible for reproductive disorders due to its et al., 1991).
estrogenic effect at suitable concentrations in susceptible The FDA has established a 10 mg/kg advisory concen-
livestock and avian populations. However, in general, tration for DON in grain or grain byproducts destined for
ZEN has limited toxicity to birds. chickens, with the added recommendation that such feed
T-2 toxin: T-2 toxin is a type A trichothecene myco- may not exceed 50% of the total diet.
toxin produced by Fusarium sporotrichioides, Fusarium Fumonisins: Fumonisins are produced by Fusarium
poae, and Fusarium acuinatum and detected less fre- verticillioides and occur as a contaminant of corn and
quently in grain and other agricultural products (Li et al., other agricultural products. Fumonisins exert their toxic
2011; Murphy et al., 2006). However, T-2 is one of the effects by disruption of sphingolipid metabolism. Ducks
most acutely toxic mycotoxins of the trichothecene are very sensitive to toxicity, whereas turkeys are more
family. In 7-day-old broilers, the LD 50 of T-2 toxin is resistant.
4.97 mg/kg, and it is more toxic than aflatoxin Fumonisins in excess of 100 mg/kg in the diet have
(LD 50 5 6.8 mg/kg), HT-2 toxin (LD 50 5 7.22 mg/kg), been shown to reduce weight gain, cause diarrhea and
and DON (LD 50 5 140 mg/kg) (Summers, 1995). hepatotoxicity. In day-old broiler chicks fed 0 400 mg/kg
In poultry, toxicological effects of T-2 are observed FB 1 for 21 days and 30 mg/kg for 14 days hepatic necrosis,
on the liver and digestive system, nervous system, and biliary hyperplasia, and thymic cortical atrophy were noted
skin due to its cytotoxic and genotoxic potential, leading postmortem (Brown et al., 1992).
to impairment of performance. Incoordination, seizures, The FDA guidance concentration for fumonisins in
eggshell thinning, reduced egg production, decreased feed poultry feed is set at 50 ppm in the total ration. Feed con-
intake and weight gain, comb cyanosis, depigmentation of taining elevated fumonisin concentrations may be dis-
the skin on legs, and necrohemorrhagic dermatitis are posed or diluted with suitable feed sources.