Possible Outbreaks of Fusariotoxicosis in Avians

Wyatt, R. D.; Harris, J. R.; Hamilton, P. B.; Burmeister, H. R.

doi:10.2307/1588839

Cited by 33 publications

(10 citation statements)

References 6 publications

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“…The toxin has been associated with several naturally-occurring myoctoxicoses in man and animals (10,11,35,38). T-2 toxin is highly cytotoxic to actively dividing cells in lymphoid and hematopoietic tissues, intestinal crypt epithelium, testis, and ovary (31, 34, 37).…”

Section: Introductionmentioning

confidence: 99%

Experimental T-2 Toxicosis in Swine Following Inhalation Exposure: Effects on Pulmonary and Systemic Immunity, and Morphologic Changes

et al. 1987

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Thirty-four, 9-to 1 1-week-old, male castrated, crossbred, specific pathogen-free derived pigs were exposed to a T-2 toxin aerosol at a nebulized dose of 0 or 9 mdkg in pairs, each pair consisting of 1 control and 1 T-2 treated pig which were exposed on the same day. Twenty to 30% of the toxin (1.8 to 2.7 mdkg) was retained by the pigs. Five pairs were killed on each of 1, 3 and 7 days after dosing. Two pairs of pigs were designated as a 0.33-day group when one T-2 treated pig died and the other was killed in a moribund state at 8 to 10 hours after dosing. The pulmonary and systemic immunity and morphologic changes of the lungs and other organs were examined. Bronchoalveolar lavage was performed to obtain alveolar macrophages (AM) and pulmonary lymphocytes (PL). The phagocytic ability of AM and mitogen-induced blastogenic responses of enriched PL and peripheral blood lymphocytes were evaluated. Clinically, all of the T-2 treated pigs vomited and were cyanotic, anorexic, lethargic and laterally recumbent. In the 0.33-, 1-, and 3-day T-2 treated pigs, there was a marked reduction in AM phagocytosis and mitogen-induced blastogenic responses of PL but not of peripheral blood lymphocytes. Mild to moderate, multifocal interstitial pneumonia was seen in the majority of the T-2 treated pigs. In pigs dying following inhalation of T-2 toxin, there was a more severe pneumonia, as well as marked necrosis of lymphoid tissues, severe necrohemorrhagic gastroenteritis and edema of the gall bladder wall, and multifocal necrosis of the heart and pancreas. Thus, inhalation exposure to T-2 toxin can result in clinical signs and morphologic changes resembling those reported previously in pigs given T-2 toxin intravascularly (iv) at a dose of 1.2 mdkg (approximate LD,,) or greater, as well as death. Mild pulmonary injury as well as transient impairment of pulmonary immunity was present in pigs surviving inhalation exposure.

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Section: Introductionmentioning

confidence: 99%

Experimental T-2 Toxicosis in Swine Following Inhalation Exposure: Effects on Pulmonary and Systemic Immunity, and Morphologic Changes

et al. 1987

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“…T-2 toxin is a cause of fusariotoxicosis of chickens (Renault et al, 1979), pigeons (Wyatt et al, 1972), and geese and ducks (Greenway and Puls, 1976). Diacetoxyscirpenol is similar to T-2 toxin except at the carbon 8 moiety.…”

Section: Introductionmentioning

confidence: 99%

Mycotoxicosis produced in broiler chickens by multiple doses of either t‐2 toxin or diacetoxyscirpenol

et al. 1982

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SUMMARYT-2 toxin, a 12, 13-epoxytrichothecene mycotoxin, was given by crop gavage to 7-day-old male broiler chickens as 14 daily doses of 1.5, 2.0, 2.5, and 3.0 mg/kg body weight/day. Diacetoxyscirpenol, also an epoxytrichothecene, was given at doses of 2.5, 3.0,and 3.5 mg/kg/day. Some chickens became dehydrated and emaciated and died. In survivors, body weight and haematocrit were reduced, the feathers were malformed, and the beak and legs were pale yellow. At necropsy, the lymphoid organs were atrophic, bone marrow was pale red or yellow, the liver was discoloured yellow, and the crop mucosa was ulcerated.Microscopic lesions included necrosis and cell depletion in lymphocytic and haematopoietic tissues, and necrosis of hepatocytes, bile ductule epithelium, enteric mucosa, and germinal regions of feather barbs. Other hepatic lesions were fatty change of hepatocytes and hyperplasia of bile ductules. Thyroid follicles were small, contained pale colloid and had tall epithelial cells. T-2 toxin was more detrimental than diacetoxyscirpenol to lymphocytic and haematopoietic tissues.

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“…Avian fusariotoxicosis is considered to be caused by trichothecenes because field and experimental forms of the disease involve ulceration of the oral mucosa. T-2 toxin was a cause of avian fusariotoxicosis in the United States (Wyatt et al, 1972), Canada (Greenway and Puls, 1976) and France (Renault et al, 1979). Avian fusariotoxicosis occurred in Russia in association with human alimentary toxic aleukia (Kurmanov and Novacky, 1978).…”

Section: Introductionmentioning

confidence: 99%

Experimental trichothecene mycotoxicosis produced in broiler chickens byFusarium sporotrichiellavar.sporotrichioides

et al. 1982

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SUMMARYFusarium sporotrichiella var. sporotrichioides (Bilay), cultured on . sterilised popcorn at 23°C and then at 8°C, 16°C and 23°C and fed as 50% of the diet, was lethal to 7-day-old male broiler chickens. The 8°C culture, containing T-2 toxin at 50 parts per million (ppm) and neosolaniol at 5 ppm, was given as whole culture at dietary concentrations of 10%, 5%, 1% and 0% for 17 days and 1% for 42 days. Half the chickens that were fed the 10% diet died during the 17 days (5 ppm T-2 toxin and 0.5 ppm neosolaniol). The corresponding daily dose was 0.24 mg T-2 toxin and 0.02 mg neosolaniol/kg body weight/day. The chickens that died were dehydrated, had necrosis and depletion of lymphoid and haematopoietic tissues and necrosis of the hepatobiliary system, gastroenteric mucosa, feather epidermis and renal tubular epithelium. The survivors had anaemia, reduction of weight gain and transiently altered righting reflex. The comb and beak were pale yellow and the feather barbs were dishevelled. Survivors also had atrophied lymphoid tissues, reduced haematopoietic cellularity in the bone marrow, necrosis of oral and crop mucosa, vacuolated hepatocytes, hyperplastic bile ductules, and reduction of the thyroid follicular diameter.

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Possible Outbreaks of Fusariotoxicosis in Avians

Cited by 33 publications

References 6 publications

Experimental T-2 Toxicosis in Swine Following Inhalation Exposure: Effects on Pulmonary and Systemic Immunity, and Morphologic Changes

Experimental T-2 Toxicosis in Swine Following Inhalation Exposure: Effects on Pulmonary and Systemic Immunity, and Morphologic Changes

Mycotoxicosis produced in broiler chickens by multiple doses of either t‐2 toxin or diacetoxyscirpenol

Experimental trichothecene mycotoxicosis produced in broiler chickens byFusarium sporotrichiellavar.sporotrichioides

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