Development of a genetic evaluation for hair shedding in American Angus cattle to improve thermotolerance.

BACKGROUND: Heat stress and fescue toxicosis caused by ingesting tall fescue infected with the endophytic fungus Epichloë coenophiala represent two of the most prevalent stressors to beef cattle in the United States and cost the beef industry millions of dollars each year. The rate at which a beef cow sheds her winter coat early in the summer is an indicator of adaptation to heat and an economically relevant trait in temperate or subtropical parts of the world. Furthermore, research suggests that early-summer hair shedding may reflect tolerance to fescue toxicosis, since vasoconstriction induced by fescue toxicosis limits the ability of an animal to shed its winter coat. Both heat stress and fescue toxicosis reduce profitability partly via indirect maternal effects on calf weaning weight. Here, we developed parameters for routine genetic evaluation of hair shedding score in American Angus cattle, and identified genomic loci associated with variation in hair shedding score via genome-wide association analysis (GWAA). RESULTS: Hair shedding score was moderately heritable (h2 = 0.34 to 0.40), with different repeatability estimates between cattle grazing versus not grazing endophyte-infected tall fescue. Our results suggest modestly negative genetic and phenotypic correlations between a dam's hair shedding score (lower score is earlier shedding) and the weaning weight of her calf, which is one metric of performance. Together, these results indicate that economic gains can be made by using hair shedding score breeding values to select for heat-tolerant cattle. GWAA identified 176 variants significant at FDR < 0.05. Functional enrichment analyses using genes that were located within 50 kb of these variants identified pathways involved in keratin formation, prolactin signalling, host-virus interaction, and other biological processes. CONCLUSIONS: This work contributes to a continuing trend in the development of genetic evaluations for environmental adaptation. Our results will aid beef cattle producers in selecting more sustainable and climate-adapted cattle, as well as enable the development of similar routine genetic evaluations in other breeds.

Deoxynivalenol induces cytotoxicity and genotoxicity in animal primary cell culture.

Deoxynivalenol (DON), a mycotoxin produced by Fusarium graminearum, is widely found as a contaminant of food. DON is responsible for a wide range of toxic activities, including gastro-intestinal, lymphoid, bone-marrow and cardiotoxicity. But, the complete explorations of toxicity in terms of hepatotoxicity, nephrotoxicity, cytotoxicity and genotoxicity as well have not been documented well. Again, the mechanisms through which DON damages the DNA and promotes cellular toxicity are not well established. Considering the above fact, this research article is focused on the effects of DON-induced toxicities on experimental animal model as well as its effects on cellular level via various toxicological investigations. DON treatment showed cytotoxicity and DNA damage. Further, flow cytometric analysis of hepatocytes showed cellular apoptosis, suggesting that DON-induced hepatotoxicity is, may be partly, mediated by apoptosis. Moreover, significant differences were found in each haematology and clinical chemistry value, either (p > 0.05). No abnormality of any organ was found during histopathological examination. Hence, it can be concluded that DON induces oxidative DNA damage and increases the formation of centromere positive micronuclei due to aneugenic activity.

Nanosilver effects on growth parameters in experimental aflatoxicosis in broiler chickens.

Aflatoxicosis is a cause of economic losses in broiler production. In this study, the effect of one commercial nanocompound, Nanocid (Nano Nasb Pars Co., Iran) was evaluated in reduction of aflatoxin effects on the growth and performance indices in broiler chickens suffering from experimental aflatoxicosis. For this, a total of 300 one-day-old broiler chicks (Ross strain) were randomly divided into 4 groups with 3 replicates of 15 chicks in each separated pen during the 28-day experiment. Treatment groups including group A: chickens fed basal diet, group B: chickens fed 3 ppm productive aflatoxin in basal diet, group C: chickens fed basal diet plus 2500 ppm Nanocid, and group D: chickens fed 3 ppm productive aflatoxin and 2500 ppm Nanocid, in basal diet. Data on body weight, body weight gain (BWG), feed intake, and feed conversion ratio (FCR) were recorded at weekly intervals. Also cumulative data were assessed. Results showed, although supplement of Nanocid to conventional diet had no effect on performance but addition of Nanocid to diet containing 3 ppm aflatoxin increased significantly the cumulative BWG, cumulative feed consumption and decreased FCR in the last 2 weeks of experimental period. The improvement in these performance indices by supplement of Nanocid to diet containing aflatoxin showed the ability of Nanocid to diminish the inhibitory effects of aflatoxin.

Immunopathological effects of experimental T-2 mycotoxicosis in Wistar rats.

It is well known that T-2 toxin has cytotoxic radiomimetic like effects on the immune system. Because of scant research data demonstrating the chronic effects of low doses of the T-2 toxin on humoral and cellular responses in rats, the present experiment was undertaken. The animals were divided into four groups, namely, group I (0.5 ppm), group II (0.75 ppm) and group III (1.0 ppm) and group IV (control) were given toxin-free diet for 12 weeks and eight animals each were sacrificed at 2, 4, 6, 8, 10, and 12-week of the experimental period. The humoral immune response was evaluated based on hemagglutination test (HA), and levels of serum immunoglobulins (IgA, IgG, IgM) while the cell-mediated immune response was evaluated by delayed-type hypersensitivity (DTH) response to ovalbumin, lymphocyte stimulation index, analyses of CD4+ and CD8+ T lymphocytes and mRNA expression levels of selected cytokines like IL-2, IFN-γ, IL-4 and IL-10 by quantitative Real-time PCR in experimental groups. T-2 treatment caused suppression in both humoral and cell-mediated immune responses as evidenced by a decrease in all these parameters in toxin fed animals compared to the control in the dose and duration-dependent manner. This dose-dependent effect on the immune system has been further reflected largely by the depletion of lymphocytes from lymphoid organs as observed histopathologically in the spleen, thymus, and Peyer's patches in the present study.

Physiological response, function of sweat glands, and hair follicle cycling in cattle in response to fescue toxicosis and hair genotype.

Fescue toxicosis is a syndrome that results when cattle consume toxic endophyte-infected tall fescue. The objective of this study was to compare the response in physiological variables, sweat gland function, hair follicle cycling, and gene expression to feeding a total mixed ration that included tall fescue haylage and tall fescue seed containing a toxic endophyte (EI) or tall fescue haylage containing a nontoxic novel endophyte (EN) in beef heifers (Angus × Senepol heifers, n = 31) with 2 different hair genotypes. Numbers in each subgroup were as follows: novel endophyte, heterozygous slick (EN-S; n = 8), novel endophyte, homozygous hairy (wild type, EN-W; n = 7), endophyte-infected, heterozygous slick (EI-S; n = 10), and endophyte-infected, homozygous hairy (wild type, EI-W; n = 6). Physiological measurements were taken weekly for 7 wk. Data were analyzed using the MIXED procedure of SAS including dietary fescue treatment (EN vs. EI) and hair genotype (S vs. W) as main effects, day as a repeated measure, and temperature-humidity index (THI) as a covariate. Skin biopsies were taken before treatment initiation and on day 37 of treatment. Average surface temperature (ST) increased as the THI increased (P < 0.0001). Average ST was greater (P < 0.01) for animals fed EI than for animals fed the EN fescue diet, and greater (P < 0.01) for animals with the W genotype compared with animals with the S genotype. The difference between heifers with the S and W genotype was greater at greater THI (genotype × day interaction, P < 0.01). Transepidermal water loss (TEWL) was greater (P < 0.05) for animals with the S genotype compared with the W genotype and greater (P < 0.05) for heifers with the S genotype than for heifers with the W genotype when fed EI (36.7, 38.5, 30.0, and 38.7 g/m2 per hour for EN-W, EN-S, EI-W, and EI-S, respectively). The fraction of follicles in telogen in plucked hair samples for heifers fed EI was greater for animals with the S genotype than the W genotype (fraction in telogen: 0.456, 0.565, 0.297, 0.702 for EN-W, EN-S, EI-W, and EI-S, respectively; diet × genotype interaction, P < 0.05). Fraction of follicles in anagen was the opposite. EI fescue resulted in increased ST, changes in hair follicle cycling that support greater hair growth, and decreased TEWL for heifers with the W genotype compared with S genotype, suggesting greater heat stress in response to EI.

Do terbutaline- and mold-associated impairments of the brain and lung relate to autism?

Increased prevalence of the autism spectrum disorders (ASD) and the failure to find genetic explanations has pushed the hunt for environmental causes. These disorders are defined clinically but lack objective characterization. To meet this need, we measured neurobehavioral and pulmonary functions in eight ASD boys aged 8 to 19 years diagnosed clinically and compared them to 145 unaffected children from a community with no known chemical exposures. As 6 of 35 consecutive mold/mycotoxin (mold)-exposed children aged 5 to 13 years had ASD, we compared them to the 29 non-ASD mold-exposed children, and to the eight ASD boys. Comparisons were adjusted for age, height, weight, and grade attained in school. The eight ASD boys averaged 6.8 abnormalities compared to 1.0 in community control boys. The six mold-exposed ASD children averaged 12.2 abnormalities. The most frequent abnormality in both groups was balance, followed by visual field quadrants, and then prolonged blink reflex latency. Neuropsychological abnormalities were more frequent in mold-exposed than in terbutaline-exposed children and included digit symbol substitution, peg placement, fingertip number writing errors, and picture completion. Profile of mood status scores averaged 26.8 in terbutaline-exposed, 52 in mold exposed, and 26 in unexposed. The mean frequencies of 35 symptoms were 4.7 in terbutaline, 5.4 in mold/mycotoxins exposed and 1.7 in community controls.

Effects of Fusarium mycotoxin butenolide on myocardial mitochondria in vitro.

Fusarium mycotoxin toxicosis has been implicated in the etiology of Keshan disease, an endemic mitochondrial cardiomyopathy prevailing in certain areas of China. Butenolide (4-acetamido-4-hydroxy-2-butenoic acid gamma-lactone) is one of the Fusarium mycotoxins which are frequently detected from cereal grains in endemic areas. A recent study indicates that this mycotoxin induces rat cardiotoxicity, but its effect on the myocardial mitochondria remains unclear. The present study is therefore undertaken to explore the toxic effect potential of butenolide on the myocardial mitochondria. Exposure of cultured cardiac myocytes to 50 microg/ml of butenolide provoked dissipation of mitochondrial membrane potential. Incubation of isolated rat myocardial mitochondria with butenolide of 100 microg/ml for 60 min resulted in mitochondrial swelling, indicating the occurrence of mitochondrial permeability transition. Furthermore, marked oxidative damage in myocardial mitochondria was observed after incubation of isolated myocardial mitochondria with butenolide ranging from 0 to 50 microg/ml for 60 min, as manifested by concentration-dependent increases in the production of thiobarbituric acid reactive substances, the indicator of lipid peroxidation. Contrarily, a representative antioxidant glutathione significantly alleviated this oxidative mitochondrial damage induced by butenolide. In conclusion, these observations clearly show that butenolide can induce dysfunction of myocardial mitochondria, and oxidative damage appears to play a crucial role in these deleterious effects. The present study supports the hypothesis that mycotoxin toxicosis is a probable etiological factor of Keshan disease, the mitochondrial cardiomyopathy.

Effects of feeding blends of grains naturally contaminated with Fusarium mycotoxins on performance, metabolism, hematology, and immunocompetence of ducklings.

Experiments were conducted to determine the effects of feeding grains naturally contaminated with Fusarium mycotoxins on performance, metabolism, hematology, and immune competence of ducklings. Four hundred sixty-four 1-d-old White Pekin male ducklings were fed starter (0 to 2 wk), grower (3 to 4 wk), and finisher (5 to 6 wk) diets formulated with uncontaminated grains, a low level of contaminated grains, a high level of contaminated grains, or the higher level of contaminated grains + 0.2% polymeric glucomannan mycotoxin adsorbent. Body weight gains, feed consumption, and feed efficiency were not affected by diet. However, consumption of contaminated grains decreased plasma calcium concentrations after 2 wk and plasma uric acid concentrations at the 4-wk assessment point. Mean corpuscular hemoglobin concentrations and hematocrit decreased when ducks were fed contaminated grains for 4 or 6 wk, respectively. In contrast, total numbers of white blood cells and lymphocytes increased transiently in birds fed contaminated grains for 4 wk. The antibody response to sheep red blood cells (CD4+ T cell dependent) and the cell-mediated response to phytohemagglutinin-P (also CD4+ T cell dependent) were not affected by diet, but consumption of contaminated grains for 6 wk decreased the duration of peak cell-mediated response to dinitrochlorobenzene (CD8+ T cell dependent) assessed in a skin test. Feeding grains naturally contaminated with Fusarium mycotoxins, even at levels widely regarded as high, exerted only minor adverse effects on plasma chemistry and hematology of ducklings, and production parameters were unaffected in this avian species. Mycotoxin-contaminated feeds may, however, render these animals susceptible to infectious agents such as viruses against which the CD8+ T cell provides necessary defence. Glucomannan mycotoxin adsorbent was not effective in preventing alterations caused by Fusarium mycotoxins.

Human aflatoxicosis in developing countries: a review of toxicology, exposure, potential health consequences, and interventions.

Aflatoxins are well recognized as a cause of liver cancer, but they have additional important toxic effects. In farm and laboratory animals, chronic exposure to aflatoxins compromises immunity and interferes with protein metabolism and multiple micronutrients that are critical to health. These effects have not been widely studied in humans, but the available information indicates that at least some of the effects observed in animals also occur in humans. The prevalence and level of human exposure to aflatoxins on a global scale have been reviewed, and the resulting conclusion was that approximately 4.5 billion persons living in developing countries are chronically exposed to largely uncontrolled amounts of the toxin. A limited amount of information shows that, at least in those locations where it has been studied, the existing aflatoxin exposure results in changes in nutrition and immunity. The aflatoxin exposure and the toxic affects of aflatoxins on immunity and nutrition combine to negatively affect health factors (including HIV infection) that account for >40% of the burden of disease in developing countries where a short lifespan is prevalent. Food systems and economics render developed-country approaches to the management of aflatoxins impractical in developing-country settings, but the strategy of using food additives to protect farm animals from the toxin may also provide effective and economical new approaches to protecting human populations.

3-Nitropropionic acid-exogenous animal neurotoxin and possible human striatal toxin.

3-Nitropropionic acid (3-NPA)--a suicide inhibitor of succinate dehydrogenase--is a widely distributed plant and fungal neurotoxin known to induce a damage to basal ganglia, hippocampus, spinal tracts and peripheral nerves in animals. Recent reports from Northern China indicate that 3-NPA is also likely to be responsible for the development of putaminal necrosis with delayed dystonia in children after ingestion of mildewed sugar cane. This article discusses the role of 3-NPA in the causation of the disease in China, its neurotoxic effects in animals and the potential role for this compound as a probe of selective neuronal vulnerability.

Influence of the antibiotics lincomycin and tylosin on aflatoxicosis when added to aflatoxin-contaminated diets of growing swine.

Effects of dietary aflatoxin (AF) and the antibiotics lincomycin (L) and tylosin (T) were evaluated in growing crossbred pigs. Six barrows (3 replicates of 2 each, mean body weight 14.0 kg) per group were assigned to 1 of 6 treatment groups (for a total of 36): 0 mg L, 0 mg T, and 0 mg AF/kg of feed (control); 220 mg L/kg of feed (200 g/ton); 110 mg T/kg of feed (100 g/ton); 2.5 mg AF/kg of feed; 2.5 mg AF plus 220 mg L/kg of feed; 2.5 mg AF plus 110 mg T/kg of feed. Barrows were administered their respective diets for 28 days. Body weight, body weight gain, and feed consumption were reduced by the AF alone, the AF plus L, and the AF plus T treatments, compared with control, L, and T treatments. Altered serum biochemical or hematologic measurements induced by AF treatments included increased serum activities of alkaline phosphatase and gamma-glutamyltransferase, increased hematocrit, hemoglobin, RBC count, WBC count, and mean cell hemoglobin, decreased serum concentrations of albumin, cholesterol, inorganic phosphorus, unsaturated iron binding capacity, total protein, and urea nitrogen, and decreased lymphoblastogenic response. Liver weight was increased, and microscopic lesions were consistent with those observed in cases of aflatoxicosis. With some other minor exceptions for hematologic and immunologic variables, these data indicate that the feed antibiotics lincomycin and tylosin, when added to aflatoxin-contaminated diets, do not have beneficial or detrimental effects on aflatoxicosis in growing swine.

Influence of dietary aflatoxin on Eimeria uzura infection in Japanese quail (Coturnix coturnix japonica).

A study was conducted to assess the influence of dietary aflatoxin on Eimeria uzura in Japanese quail (Coturnix coturnix japonica). Quail receiving 1 part per million (ppm) of dietary aflatoxin B1 and inoculated with 10(5) sporulated oocysts of E. uzura gained significantly less weight than chicks receiving either aflatoxin or coccidia alone. Increased morbidity, mortality and decreased efficiency of feed utilization were also evident. The combination of E. uzura infection and aflatoxicosis resulted in reduction in packed cell volume (PCV) and haemoglobin (Hb). The combination of E. uzura infection and aflatoxicosis in Japanese quail may influence the course of coccidial infection due to the additive effects of aflatoxin.

Association of Fusarium mycotoxicosis with failure in applying an induction of parturition program with PGF2alpha and oxytocin in sows.

This trial was conducted in a farrow-to-finish pig unit from November 1999 to February 2000. Since November 1998 an induction-of-parturition program was applied in gilts and sows with PGF2alpha (2 mL Dinolytic, i.m.) 113 d post service, followed by oxytocin (1 mL Intertocine-S, i.m.) 24 h later. This program resulted in a high proportion of animals farrowing within the working hours of the day. At mid December 1999 splay-legs and edematous swelling and reddening of the vulva started to be observed in newborn piglets. A concurrent decline of parameters related to parturition also was noticed. Mycotoxicological analyses of the feeds revealed a co-occurring contamination with deoxynivalenol and zearalenone. For a 4-week period, sows were divided into two groups: (a) an induction-of-parturition and (b) a non-induction-of-parturition group. Significant differences were found between the two groups relating to prevalence of dystocia (<.05) and pregnancy duration (<.05). Moreover, it was found that prevalence of splay-legs and swelling of the vulva were highly correlated (<.05) with reduction of percentage of sows farrowing within the working day and increase of pre-weaning mortality. It was concluded that such an induction-of-parturition program should be avoided during a Fusarium mycotoxicosis.

Effect of aflatoxicosis on the kinetic behaviour of ceftiofur in chickens.

The kinetic behaviour of ceftiofur sodium was studied in aflatoxin treated chickens for 30 days and in non-treated chickens, following oral, intramuscular and intravenous administrations of 10 mg kg(-1) bodyweight of ceftiofur. Aflatoxicosis resulted in a more significant decrease in ceftiofur serum concentration in the treated than in non-treated chickens following oral and intravenous administrations. The kinetic behaviour showed that following intravenous injection the elimination half life time t0.5 (el) was significantly shorter in the treated chickens (1.75+/-0.03 hours) than in non-treated chickens (4.23+/-0.05 hours). Following oral administration, the kinetic behaviour revealed a longer absorption half-life [t0.5 (ab), 62.74+/-1.59 minutes] in the treated chickens than in non-treated (50.46+/-5.07 minutes), with lower Cmax 23.25+/-0.42 microg ml(-1) at long tmax (3.05+/-0.07 hour) in treated chickens than in non-treated (Cmax 27.83+/-1.28 at tmax 2.39+/-0.07 hours).

Effect of aflatoxin in growing lambs fed ruminally degradable or escape protein sources.

Thirty-two crossbred (Suffolk x Rambouillet) wether lambs were used to examine the effectiveness of protein source (soybean meal [SBM] or fish meal [FM]) in alleviating decreased performance associated with dietary aflatoxin (AF) in growing lambs. After a 21-d adaptation period to concentrate diets, lambs were assigned to the following dietary treatments: 1) SBM, 0 mg of AF; 2) FM, 0 mg of AF; 3) SBM + 2.5 mg of AF/kg diet; or 4) FM+2.5 mg of AF/kg diet (two lambs/pen; four pens/treatment). Diets were fed 35 d, at which time AF was removed from the diet (except one pen/protein source) and lambs continued on study for an additional 32 d. On d 67, all lambs were killed and necropsied. Average daily gain, feed intake, and gain/feed were similar (P > .10) among lambs fed SBM or FM; however, lambs fed AF had lower (P < .01) feed intakes, daily gain, and gain/feed. Feed intake remained lower (P < .01) after AF was removed from the diet. Aflatoxin elevated (P < .01) aspartate amino transferase and gamma-glutamyl transferase activities and total protein and cholesterol concentrations while decreasing (P < .05) alkaline phosphatase, glucose, cholinesterase, albumin, inorganic phosphorus, iron, and total-iron-binding capacity. Hematocrit, white blood cell count, and prothrombin time increased (P < .01) in lambs fed AF. No AF or protein effects were seen on ruminal VFA, pH, or lymphocyte blastogenesis (P > .10).(ABSTRACT TRUNCATED AT 250 WORDS)

The involvement of slaframine and swainsonine in slobbers syndrome: a review.

The history of "slobbers syndrome," a mycotoxicosis associated with Rhizoctonia leguminicola infestation of pastures and stored forages, is discussed. The chemistry and physiological effects of the two known biologically active alkaloids of R. leguminicola, slaframine and swainsonine, are described. Slaframine administration is generally associated with increased exocrine function, especially salivation. Ingestion of swainsonine may be linked to serious and potentially lethal central nervous system defects similar to that described for locoism. However, the singular effects of these alkaloids do not completely account for the total clinical picture noted in the field during the occurrence of slobbers syndrome. It is possible that this phenomenon is the result of an interaction between both known and unidentified biologically active metabolites of R. leguminicola.

Effects of feeding diets containing endophyte-infected fescue seed on luteinizing hormone secretion in postpartum beef cows and in cyclic heifers and cows.

Two experiments were conducted to investigate the effect of feeding endophyte (Acremonium coenophialum)-infected fescue (Festuca arundinacea Shreb.) seed on LH secretion in postpartum beef cows and in cycling heifers and cows. In Exp. 1, spring-calving primiparous Angus cows (n = 16) were pair-fed for 75 d diets that contained endophyte-free or endophyte-infected (95%) fescue seed that contained 1.3 micrograms/g of ergovaline and 5.2 mg/g of saturated pyrrolizidines. Serial blood samples for basal and GnRH-stimulated serum LH analysis were obtained on d 7, 28, 42, and 56 of the study. The endophyte had no effect on LH secretion (basal, pulse frequency, and amplitude) or milk production. Average daily gain was decreased (P < .05) in cows that consumed infected fescue seed compared with controls (-.20 vs -.01 kg, respectively). Basal serum prolactin concentrations were reduced (P < .01) in treated compared with control cows (8.9 vs 25.4 ng/mL, respectively) on d 70. In Exp. 2, cycling Angus heifers (n = 8; age = 2 yr) and cows (n = 8; age = 4 yr) stratified by age were pair-fed for 40 d diets that contained the noninfected or the highly infected fescue seed. Estrus was synchronized by prostaglandin F2 alpha (d 18 and 28). Serial blood samples for serum LH analysis were obtained on d 28 (luteal phase) and d 30 (follicular phase). The endophyte did not affect LH (P > .28) or prolactin (P > .16) secretion, whereas ADG was decreased (P < .05) in treated compared with control animals (.32 vs .70 kg/d, respectively).

Mycotoxins and reproduction in domestic livestock.

Molds are parasitic plants that are ubiquitous in livestock feedstuffs. Even though molds themselves reduce the quality of grains, their synthesis of chemical substances termed mycotoxins causes the greatest monetary loss to the animal industry. Five major mycotoxins that impair growth and reproductive efficiency in North America are aflatoxins, zearalenone, deoxynivalenol, ochratoxin, and ergot. Aflatoxins are produced by Aspergillus flavus and Aspergillus parasiticus. Consumption of grains containing aflatoxins by swine affects reproduction indirectly by reducing feed intake and growth. In swine, aflatoxins impair liver and kidney function, delay blood clotting, increase susceptibility to bruising, and interfere with cellular humoral immune systems. Ruminants are comparatively resistant to aflatoxicosis, but presence of aflatoxins in milk of dairy cows is closely monitored for human safety. Depending on environmental conditions, Fusarium roseum can produce either zearalenone or deoxynivalenol. Days 7 to 10 postmating seem to be a critical period of gestation for zearalenone to exert its detrimental actions on early embryonic development. Presence of deoxynivalenol in swine feedstuffs decreases feed intake, causes feed refusal, and induces occasional vomiting. Several species of Penicillium and Aspergillus produce ochratoxin, a mycotoxin that causes necrosis of kidney tissue. Ergot alkaloids produced by Claviceps purpurea on wheat can cause reproductive problems and are associated with lactational failure in swine. Various methods have been developed to remove mycotoxins from infected feedstuffs. Chemical analyses in laboratories as well as diagnostic kits suitable for use at the elevator or farm can be used successfully to identify which mycotoxins are present in suspect feedstuffs.

The neurological significance of abnormal natural killer cell activity in chronic toxigenic mold exposures.

Toxigenic mold activities produce metabolites that are either broad-spectrum antibiotics or mycotoxins that are cytotoxic. Indoor environmental exposure to these toxigenic molds leads to adverse health conditions with the main outcome measure of frequent neuroimmunologic and behavioral consequences. One of the immune system disorders found in patients presenting with toxigenic mold exposure is an abnormal natural killer cell activity. This paper presents an overview of the neurological significance of abnormal natural killer cell (NKC) activity in chronic toxigenic mold exposure. A comprehensive review of the literature was carried out to evaluate and assess the conditions under which the immune system could be dysfunctionally interfered with leading to abnormal NKC activity and the involvement of mycotoxins in these processes. The functions, mechanism, the factors that influence NKC activities, and the roles of mycotoxins in NKCs were cited wherever necessary. The major presentations are headache, general debilitating pains, nose bleeding, fevers with body temperatures up to 40 degrees C (104 degrees F), cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, vertigo/dizziness, and in some cases, seizures. Although sleep is commonly considered a restorative process that is important for the proper functioning of the immune system, it could be disturbed by mycotoxins. Most likely, mycotoxins exert some rigorous effects on the circadian rhythmic processes resulting in sleep deprivation to which an acute and transient increase in NKC activity is observed. Depression, psychological stress, tissue injuries, malignancies, carcinogenesis, chronic fatigue syndrome, and experimental allergic encephalomyelitis could be induced at very low physiological concentrations by mycotoxin-induced NKC activity. In the light of this review, it is concluded that chronic exposures to toxigenic mold could lead to abnormal NKC activity with a wide range of neurological consequences, some of which were headache, general debilitating pains, fever, cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, and seizures.

Altered renal function in broilers during aflatoxicosis.

Experiments were conducted to determine the effects of aflatoxicosis on acid-base balance, urine flow rate (V), glomerular filtration rate (GFR), clearance of para-aminohippuric acid (CPAH), plasma osmolality, and the renal handling of Na, K, Ca, and P. Three-week-old broilers were gavaged with aflatoxin at a dose of 2 mg/kg of BW per day for 10 consecutive days. Control birds received an equal volume of corn oil, the aflatoxin carrier vehicle. On the eleventh day, the birds were anesthetized and prepared for renal function analysis. A solution containing inulin, para-aminohippuric acid, and mannitol was infused at a low infusion rate (.1 mL/kg of BW per min) and a high infusion rate (.4 mL/kg of BW per min) to determine if aflatoxin affects the renal response to an acute volume load. Aflatoxicosis decreased the fractional excretion of phosphorous (FEP) and plasma Ca concentration but did not significantly alter any other renal function or acid-base variables. The decrease in FEP and plasma Ca may be a direct result of renal tubular damage, decreased Ca absorption from the gut, or a result of altered circulating levels of parathyroid hormone (PTH), and possibly decreased renal sensitivity to PTH.