Aflatoxicosis in Iowa swine: eight cases (1983-1985)

During 1983, 1984, and 1985, aflatoxicosis was diagnosed in 8 Iowa swine herds after the herds were fed corn from the 1983 corn crop. As a result of the diagnosis, the associated environmental conditions, clinical signs of aflatoxicosis, macroscopic and microscopic lesions, aflatoxin concentrations detected in feeds, and management of affected swine were reviewed. Concentrations of aflatoxin in shelled corn and complete feed were as high as 2,020 ng and 1,200 ng of aflatoxin (B1 and B2)/g of feed, respectively. Clinical signs of aflatoxicosis included decreased feed consumption and weight loss. Some pigs died acutely, but death often was preceded by a period of clinical disease. Greater morbidity and mortality were observed in swine herds that consumed greater concentrations of aflatoxin.     

An overview of aflatoxicosis of poultry: Its characteristics,prevention and reduction

Aflatoxicosis represents one of the serous diseases of poultry, livestock and other animals. The cause of this disease in poultry and other food-producting animals has been attributed to the ingestion of various feeds contaminated with A. flavus. This toxigenic fungus is known to produce a group of extremely toxic metabolites, of which aflatoxin B₁ (AFB₁) is most potent. Avian species especially chickes, goslings, ducklings and turkey poults are most susceptible to AFB₁ toxicity. The toxic effects of AFB₁ are mainly localized in liver as manifested by hepatic necrosis, bile duct proliferation, icterus and hemorrhage. Chronic toxicity in those birds is characterized by loss of weight, decline in feed efficiency, drop in egg production and increased susceptibility to infections. The incidence of hepatocellular tumors, particularly in ducklings, is considered to be one of the serious consequences of aflatoxicosis. Even though prevention and avoidanve are the best way to control aflatoxicosis, natural contamination of crops with A. flavus is sometimes unavoidable. Such aflatoxin-contaminated feeds can be decontaminated using various methods which mainly focus on physical removal or chemical inactivation of the toxins in the feeds. Moreover, dietary additives such as activated charcoal, phenobarbital, cysteine, glutathione, betacarotene, fisetin and selenium have also been reported to be effective in the reduction of aflatoxicosis in poultry.     

Broiler aflatoxicosis with recovery after replacement of the contaminated diet

Broiler chickens were fed a diet containing 2057 and 1323 micrograms/kg feed of aflatoxins B1 and B2, respectively, for 35 d. Effects of aflatoxins on growth, food consumption, efficiency of food utilisation and manifestations of aflatoxicosis were compared with control birds at the end of the feeding trial and at 1, 2, 4, 8 and 16 d after replacing the contaminated feed. No difference in food consumption was observed between the controls and the aflatoxin-fed chickens, but efficiency of food utilisation was decreased from 2.2 for the controls to 2.4 g food/g gain for the group fed aflatoxins. Aflatoxins caused depressed growth and enlargement of the kidney, liver, heart and gall bladder. Haemorrhagic spots were present on the surface of the muscles and some of the livers. Most livers from aflatoxin-fed birds were pale and infiltrated with lipid. After withdrawal of the food containing aflatoxins, all apparent gross lesions of aflatoxicosis disappeared, with no evidence of any lesions 8 d after removal of the contaminated diet.     

An overview of aflatoxicosis of poultry: its characteristics, prevention and reduction

Aflatoxicosis represents one of the serious diseases of poultry, livestock and other animals. The cause of this disease in poultry and other food-producing animals has been attributed to the ingestion of various feeds contaminated with A. flavus. This toxigenic fungus is known to produce a group of extremely toxic metabolites, of which aflatoxin B1 (AFB1) is most potent. Avian species especially chicks, goslings, ducklings and turkey poults are most susceptible to AFB1 toxicity. The toxic effects of AFB1 are mainly localized in liver as manifested by hepatic necrosis, bile duct proliferation, icterus and hemorrhage. Chronic toxicity in those birds is characterized by loss of weight, decline in feed efficiency, drop in egg production and increased susceptibility to infections. The incidence of hepatocellular tumors, particularly in ducklings, is considered to be one of the serious consequences of aflatoxicosis. Even though prevention and avoidance are the best way to control aflatoxicosis, natural contamination of crops with A. flavus is sometimes unavoidable. Such aflatoxin-contaminated feeds can be decontaminated using various methods which mainly focus on physical removal or chemical inactivation of the toxins in the feeds. Moreover, dietary additives such as activated charcoal, phenobarbital, cysteine, glutathione, betacarotene, fisetin and selenium have also been reported to be effective in the reduction of aflatoxicosis in poultry.     

The effect of high doses of aflatoxin on the pig]

In two experiments, 18 pigs were given feed contaminated with aflatoxin which had been prepared by the extraction of the cultures of toxinogenic strains of the fungus Aspergillus flavus. After the ingestion of aflatoxin (AFB1) at a dose of 5.4 to 10.5 mg per kg of live weight, the pigs showed symptoms of peracute aflatoxicosis and died within 12--20 hours. After ingestion of AFB1 at a dose of 1.4 or 3.1 mg per kg live weight, the pigs suffered from acute aflatoxicosis and died within 3 to 26 days from the administration of the contaminated feed. In the cases of these experimental aflatoxicoses, clinical symptoms, haematological and biochemical changes in the blood and the patho-anatomical and histological findings in the swine organism were described.     

Effects of aflatoxin ingestion on the development of Moraxella bovis infectious bovine keratoconjunctivitis

A study was conducted to determine whether measured doses of aflatoxin given under different schedules would influence the pathogenesis of Moraxella bovis induced infectious bovine keratoconjunctivitis (IBK). Calves were allotted to 4 groups (groups I-IV) of 9, 9, 9, and 8 calves, respectively. Group I calves were given aflatoxin for 11 consecutive days starting 5 days before their eyes were exposed to M. bovis. Group II calves were given aflatoxin for 5 consecutive days starting 7 days after their eyes were exposed to M. bovis. Group III calves were given aflatoxin for 5 consecutive days starting 21 days after their eyes were exposed to M. bovis. Group IV calves were not given aflatoxin; but their eyes were exposed to M. bovis on the same day as were the eyes of calves in groups I-III; these calves served as controls. Aflatoxin had little if any influence on the pathogenesis of IBK under the conditions of this study. The results did not rule out an exacerbating effect of M bovis infection on aflatoxicosis in calves. Calves with the highest concentration of aflatoxin in their blood had the more severe signs of aflatoxicosis. Possible reasons for the equivocal results are discussed.     

Molds, mycotoxins, and mycotoxicosis

Interest in mycotoxins and mycotoxicosis in humans and animals has greatly increased in recent years. Horses have long been considered very susceptible to molds. The signs, treatment, and prevention of several conditions, such as leukoencephalomalacia, aflatoxicosis, ergotism, fescue toxicity, slobbering disease, ryegrass staggers, and moldy sweet clover disease, are discussed.     

Aflatoxicosis in feeder cattle

Aflatoxicosis was diagnosed as the cause of deaths in a group of crossbred feeder steers. Corn used in the ration being fed the steers was found to be contaminated with 1,500 ng of aflatoxin/g. Residues of the mycotoxin were detected in kidney tissue, and microscopic examination of liver sections revealed lesions typical of aflatoxicosis.     

Protective effect of L-carnitine against oxidative damage caused by experimental chronic aflatoxicosis in quail (Coturnix coturnix)

This study was designed to evaluate the effect of L-carnitine supplementation on the plasma malondialdehyde (MDA) and whole blood reduced glutathione (GSH) concentrations in experimentally-induced chronic aflatoxicosis in quails. For this purpose, a total of 80 quails up to 8 weeks old were divided into four equal groups. Group I served as control, Group II was given L-carnitine at the dose of 200 mg/litre in the drinking water for 60 days, Group III was given 60 microg total aflatoxin/kg diet for 60 days, and Group IV was given both 60 microg total aflatoxin/kg diet and 200 mg L-carnitine/litre in the drinking water for 60 days. Aflatoxin treatment caused a significant increase in plasma MDA and a significant decrease in blood GSH concentrations. On the other hand, there was a significant decrease in plasma MDA and a significant increase in whole blood GSH in the L-carnitine-supplemented group. The present study demonstrated that L-carnitine brought about the inhibition of lipid peroxidation by enhancing antioxidant capacity in quails with chronic aflatoxicosis.     

Retinol Values in the Plasma of the Arabian Camel (Camelus dromedarius) and the Influence of Aflatoxicosis

The normal values are reported of the concentration of vitamin A (retinol) in the plasma of 44 male and female adult camels (Camelus dromedarius) in the United Arab Emirates. The concentrations of the vitamin in the plasma of eight camels of both sexes afflicted with aflatoxicosis were also determined. The mean concentration (±SD) of the vitamin in healthy camels was 460.1±49.3 ng/L. Sex had no significant effect on the concentration of the vitamin. Camels with aflatoxicosis had a mean concentration of retinol in the plasma of 243.4±32.3 ng/L. The concentrations of aflatoxins in the liver and ruminal contents of these animals were 18.2±1.3 and 243.4 g/kg, respectively.     

黄曲霉毒素及其致病机理简述

针对蒙牛牛奶产品中检出黄曲霉毒素的问题,本文从黄曲霉毒素的分子结构、理化性质、污染途径和程度、致病机理和限量标准及快速检测等方面做了简述。同时对牛的黄曲霉毒素中毒提出了防治的具体措施。     

Interaction between Eimeria uzura infection and aflatoxicosis in Japanese quail (Coturnix coturnix japonica)

The clinical signs and gross lesions caused by Eimeria uzura (10(5) oocysts) in Japanese quail (Coturnix coturnix japonica) exhibited little or no influence in the face of intercurrent dietary aflatoxicosis (1 p.p.m. of aflatoxin B1 from Day 0 to 55). Similarly, no significant differences in the mucosal morphology of the intestine were evident histologically between the two groups of Japanese quail. The nervous signs of ataxia, leg weakness, incoordination of movement, torticollis and terminal opisthotonos were toxin-induced manifestations. In the aflatoxic quail, hypoplastic changes and selective depletion of lymphocytes were more prominent in the bursa of fabricius. Increased relative mean weights of liver, kidney, spleen, crop, proventriculus and gizzard were observed in birds due to aflatoxin sensitivity. The combination of E. uzura infection and aflatoxicosis in Japanese quail may cause significant weight loss, and increased oocyst production and reproductive potential.     

Method for the simultaneous determination of aflatoxins B1 and M1 in the liver of slaughter animals

The method used by Egmond et al. (1979) was chosen from a number of methods recommended for the determination of aflatoxins in raw materials of animal origin. This method is described in detail to facilitate its use in practice in cases of forced slaughters of animals suspected of aflatoxicosis. The sensitivity of the method for aflatoxin B1 and M1 is about 0.05 micrograms . kg-1. On the whole, 88 liver samples were examined for the presence of the aflatoxins B1 and M1. The samples had been obtained from the slaughtered pigs (52), bulls (23), cows (6), calves (5), and from deceased pigs (2). Positive findings were obtained in five of sixteen pork liver samples and in two of the tested five samples of calf liver. All of these animals were suspected of aflatoxicosis. At current slaughter, only one case of 36 examined pigs was found to be positive. Aflatoxin M1 was found more frequently than aflatoxin B1. However, the findings never exceeded the concentration of 100 ng . kg-1; this is less by 1.5 orders than the proposed tolerated concentration for adult animals (5 micrograms . kg-1).     

A Study of Free Amino Acids in Rice Moth Larvae During Mycotoxicosis

Free amino acid pattern has been studied in rice moth larvae during aflatoxicosis and compared with normal in ground nut meal and wheat bran. It was observed that there is an increase in free amino acids in intoxicated larvae and this was directly proportional to the degree of toxicity as indicated by decrease in growth of these larvae. The study of excretary pattern of amino acids shows that intoxicated larvae excrete less amino acids than the normal larvae. The results have been discussed.     

Effects of various treatments on induced chronic aflatoxicosis in rabbits

Male New Zealand White rabbits were orally given 0.05 mg of aflatoxin B1 (AFB1)/kg of body weight daily for 10 days and were treated with glutathione-precursors and depletor, antibacterial agents, or sodium thiosulfate. The drug administered, the mortality, and the mean survival time were as follows: corn-oil controls (0), euthanatized at 25 days; AFB1-controls (2), 21 days; AFB1 and saline controls (2), 22 days; cysteine and AFB1 (5), 13 days; methionine and AFB1 (5), 12 days; sodium thiosulfate and AFB1 (2), 21 days; sulfadimethoxine and AFB1 (1), 24 days; oxytetracycline and AFB1 (0), euthanatized at 25 days; and ethyl maleate and AFB1 (3), 21 days. Clinical signs of toxicosis included decreased feed consumption during AFB1 administration, loss of body weight or failure to gain, and death. Clinicopathologic changes included increases in serum bilirubin concentration and alanine aminotransferase and aspartate aminotransferase activities. Prothrombin and activated partial thromboplastin times were lengthened. Plasma fibrinogen concentration was decreased. Changes in PCV, hemoglobin concentration, and serum alkaline phosphatase were unremarkable. Oxytetracycline had protective effects against chronic aflatoxicosis in rabbits. Cysteine and methionine enhanced chronic aflatoxicosis.     

Interaction of aflatoxin with Eimeria tenella infection and monensin in young broiler chickens.

Young broiler chicks inoculated with Eimeria tenella and given a diet containing 2.5 mug aflatoxin/g had significantly higher mortality than birds with aflatoxicosis or coccidiosis alone or uninoculated controls. This effect was seen even when a light coccidial infection alone did not increase mortality or cause weight depression. In addition this higher mortality with the combination began earleir and occurred at a higher rate than did mortality from aflatoxin or cecal coccidiosis alone. Dietary monensin sodium (99 umg/g) did not completely prevent mortality and weight depression when aflatoxin and E. tenella were in combination. Aflatoxin and E. tenella singly significantly depressed three-week body weights; however, the depression was most severe when the two were in combination. Both dietary aflatoxin and E. tenella significantly reduced hemoglobin, packed cell volume, and plasma pigmentation, and in combination resulted in more severely reduced hemoglobin, packed cell volume, and plasma pigmentation. Coccidial lesion scores were significantly less for the combination of E. tenella and aflatoxicosis than for coccidiosis alone. This atypical response of the ceca to E. tenella in the presence of dietary aflatoxin was characterized by less distended ceca, very little coagulated blood in the ceca, and apparently more profuse cecal hemorrhage.     

Major biological consequences of aflatoxicosis in animal production.

Aflatoxins, a family of closely related, biologically active mycotoxins, have been known as a prominent cause of animal disease for 30 yr. The toxins occur naturally on several key animal feeds, including corn, cottonseed, and peanuts. Occurrence of aflatoxin on some field crops tends to spike in years when drought and insect damage facilitate invasion by the causative organisms, Aspergillus flavus and A. parasiticus, which abound in the crop's environment. Acute aflatoxicosis causes a distinct overt clinical disease marked by hepatitis, icterus, hemorrhage, and death. More chronic aflatoxin poisoning produces very protean signs that may not be clinically obvious; reduced rate of gain in young animals is a sensitive clinical register of chronic aflatoxicosis. The immune system is also sensitive to aflatoxin, and suppression of cell-mediated immune responsiveness, reduced phagocytosis, and depressed complement and interferon production are produced. Acquired immunity from vaccination programs may be substantially suppressed in some disease models. In such cases the signs of disease observed are those of the infectious process rather than those of the aflatoxin that predisposed the animal to infection. Mixtures of aflatoxin with other mycotoxins can result in greatly augmented biological responses in terms of rate of gain, lethality, and immune reactivity. Because of its great biological activity, its wide-spread potential presence in areas where critical feed crops are grown, and its propensity to spike in problem years, aflatoxin promises to be a continuing problem in animal production.     

Spontaneous and experimental aflatoxicosis in goats.

Naturally occurring aflatoxicosis is described in goats fed a concentrate mixture containing polkudu meal (defatted residue from grated coconut after juice extraction). Toxigenic strains of Aspergillus flavus were present in the concentrate and aflatoxins were recovered from the liver and urine of affected animals. Hepatic lesions in poisoned goats consisted of bile duct hyperplasia and periportal fibrosis; renal lesions included necrosis of tubular epithelial cells and proteinaceous exudation in the glomerular space. Similar lesions were produced experimentally in goats with aflatoxin and the coconut cultures of A flavus. High doses of aflatoxin B1 produced, in addition, hepatic centrilobular congestion, haemorrhage and periportal fatty change.     

ACUTE AFLATOXICOSIS IN CALVES FED PEANUT HAY

SUMMARY Acute aflatoxicosis was believed to be the cause of death of 12 of 90 drought-stricken Hereford calves fed peanut hay on the southern Darling Downs in Queensland. Jaundice, photosensitisation, diarrhoea, anorexia and depression were seen before death. Serum levels of enzymes of hepatic origin and bilirubin were elevated. After death haemorrhage, hepatocyte damage, bile ductule proliferation were found. Total aflatoxin levels up to 2230 μg/kg were detected in the peanut hay with most toxin concentrated in nut-in-shell.     

Clinical and clinicopathologic features of dogs that consumed foodborne hepatotoxic aflatoxins: 72 cases (2005-2006)

OBJECTIVE: To characterize clinical signs, clinicopathologic features, treatments, and survival in dogs with naturally acquired foodborne aflatoxicosis. DESIGN: Retrospective case series. ANIMALS: 72 dogs that consumed aflatoxin-contaminated commercial dog food. PROCEDURES: Medical records of affected dogs were reviewed. Between December 2005 and March 2006, dogs were identified as having foodborne aflatoxin hepatotoxicosis on the basis of the history of consumption of contaminated food or characteristic histopathologic lesions (subject dog or a recently deceased dog in the same household or kennel). Recorded information included signalment, clinical features, clinicopathologic test results, treatments, and survival. Data were analyzed by survival status. RESULTS: Most dogs were of large breeds from breeding kennels. No significant differences were found in age or weight between 26 (36%) survivor dogs and 46 (64%) nonsurvivor dogs. Severity of clinical signs varied widely; 7 dogs died abruptly. In order of onset, clinical features included anorexia, lethargy, vomiting, jaundice, diarrhea (melena, hematochezia), abdominal effusion, peripheral edema, and terminal encephalopathy and hemorrhagic diathesis. Common clinicopathologic features included coagulopathic and electrolyte disturbances, hypoproteinemia, increased serum liver enzyme activities, hyperbilirubinemia, and hypocholesterolemia. Cytologic hepatocellular lipid vacuolation was confirmed in 11 dogs examined. In comparisons of clinicopathologic test results between survivor and nonsurvivor dogs, only granular cylindruria (7/21 dogs) consistently predicted death. Best early markers of aflatoxicosis were low plasma activities of anticoagulant proteins (protein C, antithrombin) and hypocholesterolemia. Despite aggressive treatment, many but not all severely affected dogs died. CONCLUSIONS AND CLINICAL RELEVANCE: Serum liver enzyme activities and bilirubin concentration were unreliable early markers of aflatoxin hepatotoxicosis in dogs. Hypocholesterolemia and decreased plasma protein C and antithrombin activities may function as exposure biomarkers.