Nicotinic acid treatment for Paralepistopsis acromelalga intoxication: assessment using magnetic resonance imaging.

CONTEXT: Paralepistopsis acromelalga, formerly known as Clitocybe acromelalga, is a rare poisonous mushroom. The mycotoxins in this mushroom cause symptoms resembling those of erythromelalgia; however, its pathogenesis remains unclear. In this report, a patient who received nicotinic acid treatment for P. acromelalga poisoning and radiological evaluation for erythromelalgia has been presented. Case detail: A 59-year-old woman was hospitalized for redness, swelling, and burning pain in her extremities that rendered difficulty in walking, and a diagnosis of P. acromelalga poisoning was made by detailed interview and mushroom identification. She was treated with intravenous nicotinic acid for 17 days followed by oral nicotinic acid amide for 2 months. She exhibited rapid symptomatic improvement and walked independently after 11 days of initial treatment. Initial MRI of her feet revealed toe-dominated subcutaneous thickening. After nicotinic acid treatment, those radiological findings improved dramatically. DISCUSSION: The subcutaneous thickening evident on MRI indicated P. acromelalga poisoning-induced erythromelalgia involved subcutaneous inflammatory edema. The typical duration of edema without treatment is more than a month. The improvement on MRI after nicotinic acid treatment indicated that the adequate vasodilation induced by nicotinic acid contributed to resolution of the symptoms. Nicotinic acid was associated with the improvement of the edematous changes caused by the P. acromelalga intoxication.

A review of the mechanism of injury and treatment approaches for illness resulting from exposure to water-damaged buildings, mold, and mycotoxins.

Physicians are increasingly being asked to diagnose and treat people made ill by exposure to water-damaged environments, mold, and mycotoxins. In addition to avoidance of further exposure to these environments and to items contaminated by these environments, a number of approaches have been used to help persons affected by exposure to restore their health. Illness results from a combination of factors present in water-damaged indoor environments including, mold spores and hyphal fragments, mycotoxins, bacteria, bacterial endotoxins, and cell wall components as well as other factors. Mechanisms of illness include inflammation, oxidative stress, toxicity, infection, allergy, and irritant effects of exposure. This paper reviews the scientific literature as it relates to commonly used treatments such as glutathione, antioxidants, antifungals, and sequestering agents such as cholestyramine, charcoal, clay and chlorella, antioxidants, probiotics, and induced sweating.

Comparison of human health risks resulting from exposure to fungicides and mycotoxins via food.

The interest in holistic considerations in the area of food safety is increasing. Risk managers may face the problem that reducing the risk of one compound may increase the risk of another compound. An example is the potential increase in mycotoxin levels due to a reduced use of fungicides in crop production. The Integrated Probabilistic Risk Assessment (IPRA) model was used to compare the estimated health impacts on humans caused by crops contaminated with the fungicides spiroxamine (SPI) and tebuconazole (TEB) or with the mycotoxins deoxynivalenol (DON) and zearalenone (ZEA). The IPRA model integrates a distribution characterising the exposure of individuals with a distribution characterising the susceptibility of individuals towards toxic effects. Its outcome, a distribution of Individual Margins of Exposure (IMoE), served as basis to perform comparisons of compounds, effects, countries, and population groups. Based on the available data and the assumptions made, none of the four compounds was found to have impact on human health in the addressed scenarios. The IMoE distributions were located as follows: DON

Antioxidant nutrients and mycotoxins.

Mycotoxins are fungal secondary metabolites that are toxic to vertebrates produced by organisms that occur as plant pathogens, soilborne fungi, airborne fungi and aeroallergens. They are distributed worldwide and may be recovered from a wide range of substrates. Their presence in food and feeds, as the result of fungal diseases in crops, can present a danger to animal and human health. Many mycotoxins have also been shown to be phytotoxic and in some cases, such as with trichothecenes produced by the wheat head blight fungus Fusarium graminearum, mycotoxins may act as virulence factors. Several natural (vitamin, provitamins, carotenoids, chlorophyll and its derivatives, phenolics, and selenium) and synthetic (butylated hydroxyanisole and butylated hydroxytoluene) compounds with antioxidant properties seem to be potentially very efficacious in protecting against the toxic effects of mycotoxins. The protective properties of antioxidants are probably due to their ability to act as superoxide anion scavengers, thereby protecting cell membranes from mycotoxin-induced damage and in some cases, antioxidant vitamins may play a role in preventing mycotoxicosis. However, much less information is available from studies carried out on antioxidants and mycotoxins, such as OTA, FB(1), T-2 toxin, ZEN, and citrinin. No such studies have been performed on recently discovered toxins such as beauvericin, fusaproliferin, moniliformin, and fusaric acid. However, supplementation with antioxidant nutrients to prevent mycotoxicosis has been controversial. The case for the use of supplemental antioxidant vitamins at the present time needs further research.

Feed and forage toxicants affecting embryo survival and fetal development.

Early embryonic and fetal development in mammals is sensitive to deficiencies and excesses of specific nutrients and toxicants. Operating directly and/or indirectly, these deficiencies and excesses can result in embryonic death or, in less severe circumstances, disruption of normal embryo and fetal growth. This paper explores the threats posed by feed and forage toxicants to the developing embryo and their impact on early programming of fetal development. Using significant examples, we consider the relevance of temporal sensitivities during early development in utero, and their implications for the morphology and functional competence of specific organs and tissues.

Witchcraft or mycotoxin? The Salem witch trials.

BACKGROUND: The Salem witchcraft trials of 1692 have been studied by many historians looking for the complex social, political, and psychological determinants behind the community-wide hysteria that led to a travesty of justice and the deaths of 20 innocent Puritans. Recently, ergot poisoning has been put forth by some as a previously unsuspected cause of the bizarre behaviors of the young adolescent girls who accused the townsfolk of witchcraft. In this essay the circumstances behind the ergot poisoning theory for this historical event are described. When the evidence is weighed carefully both pro and con, it seems unlikely that ergotism explains much of what went on in colonial Salem.

A survey of moniliformin contamination in rice and corn from Keshan disease endemic and non-KSD areas in China.

Keshan Disease (KSD) is an endemic heart disease and moniliformin (MF) has been suggested as one of the etiological factors. In this paper, thin layer chromatographic (TLC) and high pressure liquid chromatographic (HPLC) methods were used for the determination of MF in the rice and corn samples collected from KSD areas and non-KSD areas. One hundred and twenty-three rice samples were analyzed and showed MF contamination in only 8 samples (KSD areas: 8.4% positive; non-KSD areas: 2.5% positive) ranging from 73.6 to 265.3 ng/g (mean concentration: KSD areas 156.3 ng/g; non-KSD areas 179.5 ng/g). One hundred and four corn samples in KSD areas and non-KSD areas were determinated by HPLC method, 45.2% samples were contaminated with MF (KSD areas: 81.4%; non-KSD areas: 19.7%) ranging from 52.3 to 1116.0 ng/g (mean concentration: KSD areas 488.9 ng/g; non-KSD areas 457.4 ng/g). The results showed that the contamination of MF in grains were significantly different between rice and corn, but not between the grains from the KSD areas and non-KSD areas, then casting doubt on the role of MF as an etiological factor of KS.

The clinical biochemistry of experimentally produced lupinosis in the sheep.

Lupinosis was produced in sheep in four experiments by administering a toxic extract of Phomopsis leptostromiformis by various routes and at various dose rates. The course of the intoxication was followed by plasma biochemical analyses for a number of electrolytes, metabolites and enzymes. Results from these analyses suggested that in addition to being an hepatotoxicity, lupinosis also resulted in injury to muscle, kidney and adrenal cortex. This was confirmed by microscopic examination of these tissues.

A lupinosis-associated myopathy in sheep and the effectiveness of treatments to prevent it.

A lupinosis-associated myopathy occurred in 26 of 48 sheep given a crude toxic extract of Phomopsis leptostromiformis, and in 18 of 34 sheep that grazed a toxic lupin stubble. Treatment with selenium or alpha-tocopherol alone neither prevented nor cured the myopathy, but selenium and alpha-tocopherol together may have been partially effective. Among the group of 48 intoxicated sheep, those with myopathy had a significantly lower mean terminal concentration of alpha-tocopherol in their livers than those with no myopathy. There was no relationship between the severity of liver injury and the occurrence of the myopathy. It was considered that this lupinosis-associated myopathy may have a similar pathogenesis to nutritional myopathy. Data on plasma creatine phosphokinase and erythrocyte glutathione peroxidase activities, plasma alpha-tocopherol concentrations and terminal tissue concentrations of selenium and alpha-tocopherol are presented.

Thiamin supplementation and the ingestive behavior of beef cattle grazing endophyte-infected tall fescue.

Livestock grazing endophyte (Acremonium coenophialum Morgan-Jones and Gams)-infected tall fescue (Festuca arundinacea Schreb.) perform poorly due to tall fescue toxicosis, especially when animals are under heat stress. In order to determine whether thiamin promotes recovery from tall fescue toxicosis, 1 or 0 g of thiamin per day, as mononitrate, was fed orally to adult Angus (Bos taurus) cows (380 +/- 8 kg) grazing either tall fescue pasture with and without endophyte or alfalfa (Medicago sativa L.). A tethered grazing system employing a split-plot design was used to estimate intake and components of ingestive behavior. No significant differences attributable to thiamin supplements were seen in rates of intake and biting, grazing time and intake per bite when cows grazed endophyte-infected tall fescue during the first 4 d of exposure. When cows grazed endophyte-infected (greater than 95%) tall fescue with 2,091 micrograms/g loline alkaloids after 4 d of exposure, the untreated animals ingested herbage dry matter (DM) at 1.19 kg/h, whereas the cows receiving thiamin ate 1.57 kg/h (P less than .05). Cattle achieved these rates of DM intake by forming bites of 1.0 and 1.2 g DM at 24 and 26 bites/min when treated with 0 and 1 g of thiamin per day, respectively. Thiamin supplements had no effect on ingestive behavior of cows grazing endophyte-free tall fescue or alfalfa after exposure to these forages for 4 d. Responses to thiamin generally were greater when cattle grazing endophyte-infected tall fescue were exposed to heat stress. Oral thiamin supplementation may alleviate tall fescue toxicosis of beef cattle during warm weather.

Physiological responses of cattle consuming tall fescue to environmental temperature and supplemental phenothiazine.

The influence of supplemental phenothiazine (P) on growth and physiological criteria was studied in parasite-controlled calves consuming endophyte (Acremonium coenophialum)-infected tall fescue (TF). In Exp. 1, nine Angus heifer calves (312 kg) were supplemented with 227 g corn-mineral (CM) mix twice daily and allowed ad libitum access to either high-endophyte (HE) G1-307 (greater than 90% infected) or low-endophyte (LE) Kenhy (less than 1% infected) tall fescue hay, or HE G1-307 plus 2 g/d P in the daily supplement. Calves were kept in temperature-controlled rooms for 12 d at 21 degrees C followed by 7 d at 34 degrees C. In Exp. 2, 48 Angus steer calves (312 kg) were assigned to treatment groups consisting of calves grazing HE Kentucky-31 (57% infected) or LE Johnstone (less than 1% infected) TF, and supplemented daily with either .91 kg of a control CM mix or .91 kg of the CM mix containing 2 g P. The 112-d experiment was initiated on May 4 with BW and rectal temperature (RT) measurements and blood collected at 28-d intervals. In both experiments, calves receiving HE TF had lower (P less than .01) serum prolactin concentrations (PRL) at elevated ambient temperature and lower (P less than .01) serum alkaline phosphatase activities (AP) but higher (P less than .01) RT than calves consuming LE TF regardless of ambient temperature.(ABSTRACT TRUNCATED AT 250 WORDS)

Photosensitivity in South Africa. II. The experimental production of the ovine hepatogenous photosensitivity disease geeldikkop (Tribulosis ovis) by the simultaneous ingestion of Tribulus terrestris plants and cultures of Pithomyces chartarum containing the mycotoxin sporidesmin.

The mycoflora of toxic pastures were surveyed during a number of outbreaks of ovine hepatogenous photosensitivity in South Africa. Pure cultures of several isolates were dosed to sheep, but only those of Pithomyces chartarum and Myrothecium verrucaria proved to be toxic. Photosensitization was induced in sheep by dosing them with cultures of a P. chartarum isolate (GA10) obtained from Tribulus terrestris plants collected during an outbreak of geeldikkop in the Karoo. Thus for the first time a mechanism whereby T. terrestris plants can contribute to the causation of ovine hepatogenous photosensitivity was demonstrated. When cultures of GA10 equivalent to approximately 0,75--4,0 mg/kg sporidesmin were dosed at Onderstepoort Veterinary Research Institute to Highveld and Karoo sheep on a diet of lucerne, facial eczema was produced. Dosing the same cultures at levels equivalent to c. 1,0 mg/kg of sporidesmin in the Karoo resulted in lesions characteristic of both facial eczema and geeldikkop. Typical hepatic lesions of geeldikkop could be elicited by dosing GA10 at levels equivalent to c. 0,25--0,7 mg/kg of sporidesmin to Karoo sheep grazing on predominantly T. terrestris pastures in the Karoo. In the latter experiment geeldikkop was induced in the sheep on T. terrestris pastures, while those receiving identical doses on veld with little T. terrestris developed facial eczema. Geeldikkop, therefore, can be brought about by the ingestion of T. terrestris plants together with toxic cultures of P. chartarum. The plant appears not only to act as a vehicle for ingestion of spores, but also to interact with sporidesmin to induce lesions typical of geeldikkop, whereas sporidesmin alone results in facial eczema. Indications are that it can enhance the ability of sporidesmin to cause photosensitivity or, possibly, vice versa. The histopathological findings of these experiments are described in detail.

The effect of lupinosis on liver copper, selenium and zinc concentrations in merino sheep.

Merino wether weaners were exposed to toxic lupin stubbles for periods of one, two and six to nine weeks, and the effect on their liver copper, selenium and zinc concentrations studied. After the one week period there was a slight decrease in liver copper and selenium concentrations in sheep severely affected with lupinosis. This was attributed to loss of these elements from necrotic cells, and greatly increased quantities of fat in the liver. In the same period liver zinc concentrations declined and were negatively correlated with the degree of liver injury. After two weeks or more of exposure to toxic lupins a positive correlation existed between both the liver copper and selenium concentrations, and the degree of liver injury. Furthermore, total liver copper and selenium levels were also positively correlated with the degree of liver injury. Liver zinc concentrations were negatively correlated with the degree of liver injury. It is suggested that when the liver is under the influence of the toxins causing lupinosis for more than two weeks, it stores copper and selenium, and loses zinc.

Veterinary toxicology: the epidemiology of poisonings in domestic animals.

Animals are constantly exposed to a wide variety of foreign chemicals, many of which are potentially toxic and some of which result in the clinical poisonings. Pesticides are applied on or around animals for the control of insects and rodents. These chemicals may be placed in areas without regard for accessibility to household pets and domestic livestock. Insecticides, herbicides, and fungicides are routinely and haphazardly applied to animal and environmental surfaces alike with apparent disregard for differences in absorptive capability. Fortunately, newer herbicides and fungicides are relatively nonhazardous. Drugs are considered to have therapeutic effects, but the lay and professional person's disregard for species differences and variations in recommended dosages can result in poisonings. Adverse reactions may be misnomers for errors in judgment. Failure to provide satisfactory storage facilities for animal feeds and the improper preservation and handling of feedstuffs allow the growth and development of a variety of mycotoxins. Ignorance on the part of animal owners and livestockmen can result in a number of unusual and sometimes fatal clinical syndromes. The dependence of domestic animals and livestock upon their owners for the total environment makes these animals extremely susceptible to environmental pollutants. Exposure to noxious gases, irritating and hazardous industrial materials and wastes, water contaminants, and casually discarded compounds of our own use can and frequently do result in animal illnesses and death. Persons responsible for animals may be unaware of the potential hazard or lack good judgment in the use of these chemicals. Forceful and continuing education for the safe and sensible use of all foreign compounds on and around domestic animals and livestock is needed. Persons handling and applying these materials must recognize their responsibility, not only to themselves but also to their neighbors and the animals in their care.