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Effect of tryptophan supplementation on aflatoxicosis in laying hens.

Two experiments were conducted to determine the relationship of supplemental Trp on liver fat accumulation and egg production during aflatoxicosis in laying hens. In Experiment 1, two levels of Trp (0 and 2,000 ppm; basal = .16% Trp) and two levels of aflatoxin (AFLA) (0 and 10 ppm) were supplemented to a complete layer ration. In Experiment 2, a third level of AFLA (5 ppm) was added to the design. Single Comb White Leghorn hens (58 and 68 wk old) were fed the diets for 3 wk for Experiments 1 and 2, respectively. Henday production and egg weights were measured daily. Feed intake was measured weekly. Liver weights, liver moisture, and liver total lipids were determined at the end of each trial. In Experiment 1, supplemental Trp by itself caused a significant (P less than .01) reduction in total liver lipids compared to the controls (no Trp or AFLA). Adding trp and AFLA increased total liver lipids and caused a significant (P less than .05) decrease in egg production compared with adding AFLA alone. Total liver lipids were 41.1, 32.8, 54.8, and 62.4% (dry weight basis) for 0 Trp:0 AFLA, 2,000 Trp:0 AFLA, 0 Trp:10 AFLA, and 2,000 Trp:10 AFLA, respectively. Similar results were observed in Experiment 2. It was concluded that supplemental Trp by itself caused a reduction in total liver lipids, but when supplemented to a diet containing AFLA, Trp caused an increased severity of lesions associated with aflatoxicosis in layers.

Acute Disease↗

Effects of a hydrated sodium calcium aluminosilicate on growing turkey poults during aflatoxicosis.

Effects of adding .5% of a hydrated sodium calcium aluminosilicate (HSCAS) to diets containing 1 or .5 mg aflatoxin (AF)/kg were determined in male turkey poults from 1 day to 3 wk of age. Body weight gains were significantly reduced by 51 and 19% in turkey poults fed 1 and .5 mg AF/kg, respectively; efficiency of feed utilization was not affected. There were no deaths in poults fed .5 mg AF/kg; however, the mortality rate was 88% in poults fed 1 mg AF/kg. The addition of .5% dietary HSCAS resulted in a 68% decrease in mortality to 28% for the 3-wk experimental period. Treatment-related changes in relative organ weights, hematological values, serum biochemical values, and enzyme activities were observed. The HSCAS in the absence of AF did not alter any of the parameters measured. The HSCAS diminished the adverse effects of AF on body weight gains, most relative organ weights, hematological values, serum biochemical values, and enzyme activities associated with .5 mg AF/kg, but not 1 mg AF/kg. These findings indicate that HSCAS may diminish many of the adverse effects of AF in an AF-sensitive species, the turkey.

Aluminum Silicates↗

Acute aflatoxicosis: case report.

The objective of this presentation is to document the salient clinical findings in a case of aflatoxicosis and to review the literature on the same so as to increase the index of suspicion, enhance early diagnosis and improve management. The case was a 17-year-old schoolboy presenting with vomiting, features of infection and gastrointestinal tract symptoms. Examination revealed a very ill looking pale patient with abdominal distension, tenderness and rectal bleeding and easy bruisability. Investigations showed abnormal liver function tests, pancytopenia and elevated serum levels of aflatoxins. Management consisted of supportive care including antibiotics and antifungal therapy, transfusion of red blood cells and fresh frozen plasma. His recovery was uneventful. The literature on human aflatoxicosis shows that the presentation may be acute, subacute and chronic. The degree of emanating clinical events also conforms to status of the aflatoxicosis. Overall, the features are protean and may masquerade many other forms of toxaemias. In conclusion, the diagnosis of aflatoxicosis takes cognisance of geographical location, past events, staple diet and clinical features to exclude other infections. Also required are high index of suspicion and importantly serum levels of aflatoxin. Treatment strategies involved use of antimicrobials and supporting the damaged multi-organs.

Acute Disease↗

Waterfowl mortality caused by aflatoxicosis in Texas.

Waterfowl mortality caused by aflatoxicosis occurred in two separate areas in Texas during the 1977-78 wintering season. The first outbreak occurred in snow geese (Anser caerulescens) on the Gulf Coast prairies, followed by an outbreak in mallards (Anas platyrhynchos) in the north-central portion of the state. Aflatoxin B1 levels in geese were 500 ng/g (dry weight). Aflatoxin B1 levels in the second mortality were 10-250 ng/g (dry weight). The exact source of the toxin was not demonstrated in the first outbreak, but in the second outbreak was traced to waste peanuts, which constituted a major portion of the diet of wintering waterfowl in north-central Texas. Aflatoxin B1 levels in the field peanuts collected in the general areas were 110 ng/g.

Aflatoxin B1↗

Effect of climate and type of storage container on aflatoxin production in corn and its associated risks to wildlife species.

The effects of grain storage containers on aflatoxin production, and the relationship between the level of aflatoxin and the number and weight of fluorescing kernels were determined in corn (Zea maize) stored in controlled climate regimes. Two hundred and forty 100-g samples were held up to 3 mos using four types of storage containers placed in four climates. Storage containers included corn placed in metal cans, paper bags, plastic bags, and paper bags placed in plastic bags. Climates were constant during the duration of the project and included a combination of temperatures and humidities. Temperatures were 29-32 C and 14-18 C; relative humidities were 85-88% and 35-40%. In addition, corn was exposed to environmental conditions conductive for aflatoxin production and 100 g samples were randomly collected, examined under ultraviolet light for fluorescence, and then quantified for aflatoxin levels. Corn samples tested negative for aflatoxin at the beginning of the project. Main (i.e., container, climate, and month) and interactive effects were not observed. Mean levels of aflatoxin ranged from 0 to 151 microg/kg. Aflatoxin was produced regardless of type of storage container, time of storage, and climatic conditions; however, only 8% of the samples produced aflatoxin levels that exceeded 50 microg/kg. Fluorescing corn ranged from 0 to 19 kernels per sample, while aflatoxin levels ranged from 0 to 1,375 microg/kg for the same samples. No relationships were found between the number and weight of fluorescing kernels of corn and aflatoxin levels. The black light test yielded a false negative rate of 23% when in fact the aflatoxin concentrations exceeded 50 microg/kg. Therefore, quantifying fluorescing grain under UV light should not be considered a feasible alternative for aflatoxin testing of grain intended for wildlife.

Aflatoxins↗

Aflatoxin production in supplemental feeders provided for northern bobwhite in Texas and Oklahoma.

Mycotoxins are toxic metabolites produced by varous species of fungi. Aflatoxin (AF), a particular type of mycotoxin, can negatively impact many wildlife species in the laboratory; however, the magnitude of the problem in the field environment is unclear. Wild birds generally consume a combination of native foods and agricultural grains. A common practice in which birds, such as northern bobwhite (Colinus virginianus), contact stored agricultural grain is through supplemental feeding. This feeding practice may promote the production of AF. The objectives of this study were to (1) examine AF production in supplemental feeders and (2) examine the relationship between weather and AF production in supplemental feeders. Samples were collected from supplemental feeders from November through February of 1996-97 and 1997-98. Mean monthly AF concentration of samples from feeders ranged from 0.57+/-2.86 to 15.47+/-14.69 ppb. Aflatoxin concentration in supplemental feeders increased from pre-sample to one month after filling the feeders each year. AF production in supplemental feeders was highly variable among months with no real temporal pattern between years. Instead, AF production was related to the highly variable relative humidity of the study area which influences moisture content of grain. Average relative humidity can be used to predict AF production.

Aflatoxins↗

Aflatoxin levels in corn available as wild turkey feed in Georgia.

Samples of corn available as wildlife feed from retailers throughout Georgia (USA) were collected during April 1997 and analyzed for aflatoxin to determine if levels harmful to wild turkeys (Meleagris gallopavo) were present. Three of 31 (10%) samples collected from a 40-country area were positive. An enzyme-linked immunosorbent assay qualitatively determined that two samples contained from 0 to 20 ppb aflatoxin. A chromatography analysis of a third sample measured 380 ppb total aflatoxin. A small percentage of our sample of wildlife feed collected during one season contained levels of aflatoxin that may cause harm to turkeys, especially poults. However, because aflatoxin levels ranging from 100 to 400 ppb may cause liver dysfunction and immunosuppression in turkey poults and other wildlife, grains known to be contaminated with aflatoxin at levels unacceptable for domestic animal feeds (> or =100 ppb) should not be sold as wildlife feed. Further analyses of grains sold as wildlife feed should be conducted to address this potential problem.

Aflatoxins↗

Sequential histological and histochemical study of the rat liver after single-dose aflatoxin B1 intoxication.

Rats were given a single dose of aflatoxin B1 lethal to 50% of the animals (7.20 mg/kg). Their livers were examined histochemically in correlation with sequential histological lesions. Early periportal liver cell necrosis and marked biliary cell proliferation were observed. Periportal cytoplasmic glycogen and RNA depletion occurred during this early period and subsequently extended to the whole lobule. The enzymes investigated decreased or disappeared in the periportal area; but alkaline phosphatase increased strikingly in the centrolobular area, whereas canalicular adenosinetriphosphatase completely disappeared throughout the liver lobule. The histochemical changes reverted to normal after cessation of the necrosis. Histochemical techniques were more sensitive in detecting the vulnerability of the periportal parenchyma to aflatoxin. After the necrosis, regenerative foci appeared. They showed a variable content in glycogen and RNA and were characteristically enzyme deficient. This reflects the immaturity of regenerating hepatocytes. These early foci subsequently disappeared and are thus considered irrelevant to hepatomagenesis.

Adenosine Triphosphatases↗

Risk assessment to humans of mycotoxins in animal-derived food products.

This paper addresses approaches for assessing potential human health hazards from the presence of natural toxicants, such as mycotoxins, in animal food products. At high levels in feed these mycotoxins may cause loss or illness of farm animals, through development of animal toxicoses, such as aflatoxicosis. At lower levels in feed these mycotoxins may have no apparent effect on livestock production, but their residues and related substances may move up the food chain. This indirect intake of mycotoxins and related substances from the consumption of animal food products may pose a health hazard to humans. These health hazards are compared to the possible health hazards from the direct intake by humans of cereal and other food crops that may contain mycotoxins.

Animal Feed↗

Detection and detoxification of aflatoxins: prevention of aflatoxicosis and aflatoxin residues with hydrated sodium calcium aluminosilicate.

Our recent findings demonstrate that HSCAS can prevent aflatoxicosis in chickens and swine and significantly decreases the level of aflatoxin M1 residues in the milk of lactating dairy cattle. The basic mechanism for this action appears to involve sequestration of aflatoxin in the gastrointestinal tract and chemisorption (i.e., tight binding) to HSCAS which results in a reduction in aflatoxin bioavailability. Research is in progress to elucidate the specificity of HSCAS action and to construct a series of selective chemisorbents for mycotoxin control in livestock and poultry.

Aflatoxins↗

An outbreak of aflatoxicosis in Angora rabbits.

An outbreak of aflatoxicosis in Angora rabbits involving a large number of rabbitries was investigated. Mortality was more in weaners than in adults. Affected animals showed anorexia, dullness and weight loss followed by jaundice in terminal stages. Death occurred within 3-4 d of the appearance of clinical signs. Livers were moderately to severely congested, icteric and were hard to cut. Gall bladders were distended and had inspissated bile. Liver sections showed degenerative changes of hepatic cells along with dilatation and engorgement of sinusoids. Bile ducts had mild to severe periportal fibrosis. Focal areas of pseudolobulation and regenerative foci were also predominant. The level of aflatoxin B1 in feed samples from various farms submitted at the time of the investigation varied from 90 to 540 ug aflatoxin B1/kg of feed. Withdrawal of feed and supplementary therapy resulted in gradual disappearance of signs and mortality.

Aflatoxins↗