fumonisin-b1 and Pulmonary-Edema

Fumonisin B(1) (FB(1)) is a mycotoxin produced by Fusarium spp. moulds that contaminate crop, predominantly maize, all around the world. More than 15 types of fumonisins have been indentified so far, but FB(1) is the most abundant and toxicologically the most significant one. FB(1) has a wide range of toxic effects, depending on animal species. In horses FB(1) causes equine leukoencephalomalacia (ELEM), in pigs pulmonary oedema and in experimental rodents nephrotoxicity and hepatotoxicity. In humans exposure to FB(1) is linked with higher incidence of primary liver cancer and oesophageal cancer, which are frequent in certain regions of the world (such as Transkei region in South Africa) where maize is staple food. The occurrence of neural tube defect in children in some countries of Central America (such as Mexico and Honduras) is connected with the consumption of FB(1)-contaminated maize-based food. However, possible involvement of FB(1) in the development of human diseases is not clear. Nevertheless, the International Agency for Research on Cancer (IARC) has classified FB(1) as a possible carcinogen to humans (group 2B). FB(1) is a causative agent of ELEM, a brain disorder in equines, indicating that brain is a target organ of FB(1) toxicity. Several studies on experimental animals or on cell cultures of neural origin have established that FB(1) has a neurodegenerative potential, although the mechanism of its neurotoxicity is still vague. The aim of this article is to give an overview of available literature on FB(1) neurotoxicity and involved mechanisms, and to offer a new perspective for future studies.

Topics: Animals; Carcinogens; Cell Culture Techniques; Disease Models, Animal; Esophageal Neoplasms; Food Contamination; Food Microbiology; Fumonisins; Fusarium; Humans; Leukoencephalopathies; Liver Neoplasms; Neural Tube Defects; Neurotoxins; Neurotransmitter Agents; Pulmonary Edema; Zea mays

Fumonisin toxicosis in swine was named porcine pulmonary edema (PPE) after outbreaks of a fatal disease in pigs fed Fusarium verticillioides (F. moniliforme)-contaminated corn screenings from the 1989 corn crop in Iowa, Illinois, and Georgia. Pigs that died had severe pulmonary edema, which has not been identified in other species after exposure to fumonisins. The disease has been reproduced experimentally by feeding of naturally contaminated corn, F. verticillioides culture material, and by intravenous administration of fumonisin B1 (FB1). Hepatic lesions consisting of apoptosis, necrosis, and hepatocyte proliferation also are observed. As in other species, alterations in clinical pathology reflect hepatic injury as well as elevated serum cholesterol concentration. In chronic studies, esophageal plaques, hyperplastic hepatic nodules, and right ventricular hypertrophy were found. In pigs, as in other species, fumonisin alters sphingolipid biosynthesis, with the greatest alterations in sphingosine and sphinganine concentrations in kidney, liver, lung, and heart. Our recent studies on fumonisin toxicosis in pigs have focused on immune effects and the pathogenesis of pulmonary edema. The specific immune system was not affected; however, FB1 inhibited phagocytosis and sphingolipid biosynthesis in pulmonary macrophages. Fumonisin induced an accumulation of membranous material in pulmonary capillary endothelial cells; this change appears specific to this cell type and to swine. In short-term cardiovascular studies, fumonisin decreased left ventricular dP/dt(max) (an index of cardiac contractility), mean systemic arterial pressure, heart rate, and cardiac output, and increased mean pulmonary artery pressure and pulmonary artery wedge pressure. These changes are compatible with the inhibition of L-type calcium channels by increased sphingosine and/or sphinganine concentration. Therefore, fumonisin-induced pulmonary edema in swine appears to result from acute left-sided heart failure mediated by altered sphingolipid biosynthesis.

Topics: Animals; Carboxylic Acids; Fumonisins; Immunity; Liver; Mycotoxins; Myocardium; Pulmonary Edema; Sphingolipids; Swine Diseases

Topics: Animal Feed; Animals; Diagnosis, Differential; Fumonisins; Fusarium; Hydrothorax; Mycotoxicosis; Mycotoxins; Pulmonary Edema; Swine; Swine Diseases; Zea mays

Fumonisins are the most recently discovered group of mycotoxins with important implications in animal health. Equine leucoencephalomalacia and porcine pulmonary edema are diseases observed for many years, but their etiology was unknown. These 2 syndromes were recently reproduced experimentally after administration of purified fumonisin B1 (FB1). The main target organs for the toxic actions of FB1 are the brain in horses and the lungs in the case of swine. However, severe liver damage in both species and pancreatic lesions in swine are also observed, especially when Fusarium moniliforme culture material (FCM) or naturally contaminated corn are used as the source of the fumonisins. Experimentally induced fumonisin toxicosis has been studied in poultry and cattle using FCM or naturally contaminated corn or corn screenings as the mycotoxin source. Results have shown a much lower sensitivity of these species to the toxic action of fumonisins when compared to horses and pigs. However, adverse effects on performance parameters of broiler chickens and turkey poults and on selected immune parameters of chickens and cattle were reported. In order to confirm these observations, toxicological studies using purified fumonisins are required. Studies to determine the interaction of fumonisin with other Fusarium toxins and other mycotoxins are also needed. No studies on the toxicokinetics of fumonisins have been reported. The toxicodynamics (mechanism of action) of fumonisins appears to be a blockage in the synthesis of sphingolipids and thus constitute a unique toxicological action among the known mycotoxins.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Animals, Domestic; Carcinogens, Environmental; Cattle; Encephalomalacia; Fumonisins; Horse Diseases; Horses; Mycotoxins; Poisoning; Poultry; Poultry Diseases; Pulmonary Edema; Structure-Activity Relationship; Swine; Swine Diseases

During the 1989 corn harvest season, numerous reports of equine leukoencephalomalacia (ELEM) outbreaks and a pulmonary edema (PPE) syndrome in swine from several regions of the United States were received by the National Veterinary Services Laboratories (NVSL), Ames, Iowa. Previous and concurrent research linked Fusarium moniliforme and fumonisin-contaminated feeds to both diseases. Chemical and mycological investigations revealed fumonisin B1 (FB1) concentrations of 20 to 360 ppm in suspect swine feeds and 8 to 117 ppm in suspect equine feeds. Nonproblem feeds contained concentrations below 8 ppm. Fusarium moniliforme and Fusarium proliferatum were isolated from both problem and nonproblem equine and swine feeds. When cultured on autoclaved corn, the F. moniliforme and F. proliferatum isolated produced respective FB1 and fumonisin B2 (FB2) that range from less than 5 to more than 2450 ppm and less than 5 to more than 1000 ppm, respectively. Isolates from both problem and nonproblem feeds produces high levels (greater than 500 ppm) in culture. Reported here is a review of chemical and mycological data resulting from the study of several cases of PPE and ELEM.

Topics: Animal Feed; Animals; Encephalomalacia; Food Microbiology; Fumonisins; Fusarium; Horse Diseases; Horses; Mycotoxins; Pulmonary Edema; Swine; Swine Diseases; Zea mays

Mycoplasma hyopneumoniae has a primary role in the porcine respiratory disease complex (PRDC). The objective of this study was to determine whether fumonisin mycotoxins influence the character and/or the severity of pathological processes induced in the lungs of pigs by Mycoplasma hyopneumoniae. Four groups of pigs (n = 7/group) were used, one fed 20 ppm fumonisin B1 (FB1) from 16 days of age (group F), one only infected with M. hyopneumoniae on study day 30 (group M), and a group fed FB1 and infected with M. hyopneumoniae (group MF), along with an untreated control group (group C). Computed tomography (CT) scans of infected pigs (M and MF) on study day 44 demonstrated lesions extending to the cranial and middle or in the cranial third of the caudal lobe of the lungs. The CT images obtained on study day 58 showed similar but milder lesions in 5 animals from group M, whereas lungs from 2 pigs in group MF appeared progressively worse. The evolution of average pulmonary density calculated from combined pixel frequency values, as measured by quantitative CT, was significantly influenced by the treatment and the age of the animals. The most characteristic histopathologic lesion in FB1-treated pigs was pulmonary edema, whereas the pathomorphological changes in Mycoplasma-infected pigs were consistent with catarrhal bronchointerstitial pneumonia. FB1 aggravated the progression of infection, as demonstrated by severe illness requiring euthanasia observed in 1 pig and evidence of progressive pathology in 2 pigs (group MF) between study days 44 and 58.

Topics: Animals; Disease Models, Animal; Fumonisins; Lung; Mycoplasma hyopneumoniae; Mycotoxins; Pneumonia of Swine, Mycoplasmal; Pulmonary Edema; Random Allocation; Swine; Swine Diseases; Tomography, X-Ray Computed

Fumonisin B1 is a mycotoxin that causes lethal pulmonary edema in swine. Sphinganine, sphingosine, and the sphinganine to sphingosine ratio are important biomarkers for fumonisin B1 exposure. Currently, tissues selected for sphinganine and sphingosine analyses are frozen at -80 degrees C until analyses take place. However, for diagnostics and some research projects, formalin is used more routinely as a preservative for long-term storage of tissues. To determine whether formalin-fixed tissues could be used for sphinganine and sphingosine analyses, sphinganine and sphingosine concentrations were quantified in both frozen and formalin-fixed lung, liver, kidney, and heart from fumonisin B1-treated and control pigs. Tissues were evaluated 3 months after freezing and 3, 6, and 12 months after formalin fixation. Sphinganine, sphingosine, and the sphinganine to sphingosine ratio of both frozen and formalin-fixed lung and liver from fumonisin B1-treated pigs were elevated. Formalin-fixed tissues had lower sphinganine and sphingosine concentrations but higher sphinganine to sphingosine ratios than the corresponding frozen tissues. Storage in formalin for up to 12 months did not affect the results. Sphingosine analysis could not be performed in formalin-fixed heart and kidney because of noninterpretable chromatograms. Therefore, formalin-fixed lung and liver can be used to determine fumonisin B1-induced sphinganine and sphingosine alterations in swine, with the sphinganine to sphingosine ratio being the most useful.

Topics: Animals; Formaldehyde; Fumonisins; Heart; Kidney; Liver; Lung; Pulmonary Edema; Sphingolipids; Sphingosine; Swine; Swine Diseases; Tissue Fixation

Acute and subacute intraperitoneal doses of fumonisin B(1) (FB(1)) were administered to test the efficacy of the FB(1)-glucose reaction products in detoxifying FB(1) in swine. In the acute study at 11 mumol of FB(1)/kg of body weight, five of six pigs administered FB(1) and four of six pigs administered FB(1)-glucose died from acute pulmonary edema. Analysis of weight gain, serum aspartate aminotransferase and gamma-glutamyltransferase, total cholesterol, and pathological evaluation did not provide evidence of protection against FB(1) toxicity by the FB(1)-glucose reaction products. In the subacute study at 5.5 mumol of FB(1)/kg of body weight, one pig administered FB(1) died from liver damage. Analysis of serum aspartate aminotransferase, gamma-glutamyltransferase, and total bilirubin showed protection against FB(1) toxicity by the FB(1)-glucose reaction products. The levels of sphinganine and sphinganine/sphingosine ratios in serum and liver as well as pathologic findings provided definitive evidence of protection against the FB(1) toxic effects by this detoxification procedure (p < 0.05).

Topics: Animals; Chemical and Drug Induced Liver Injury; Fumonisins; Glucose; Liver Diseases; Pulmonary Edema; Swine; Swine Diseases

From the point of view of human exposure, fumonisins (FB1, FB2, FB1, FB4), a relatively recently (1988) discovered and identified group of mycotoxins, represent one of the five most important mycotoxin groups causing human disease. In an earlier experiment studying the effects of relatively low doses (10, 20 and 40 p.p.m.) of FB1 in weaned piglets, it was established that the 4-week feeding of 10 p.p.m. (mg/kg feed) FB1 produced mild pulmonary oedema. This suggested the importance of studies with even lower doses of the toxin to determine the tolerable limits. The objective of this experiment was therefore to study the effects of prolonged (8-week) exposure to still lower concentrations (0, 1, 5 and 10 mg/kg feed) of FB1. The 8-week feeding of FB1 in low concentrations (1-10 p.p.m.) did not cause clinical signs and significant performance impairment in pigs, but rendered irreversible the chronic changes that had already developed in the animals in a dose-dependent manner. Dissection revealed pathological alterations of the lungs in one of the animals given 1 p.p.m. (n = 4), in two animals exposed to 5 p.p.m. (n = 5), and in three animals given 10 p.p.m. (n = 4). In all three treatment groups, proliferation of the connective tissue fibres, primarily of those around the lymphatic vessels, in the subpleural and interlobular connective tissue of the lungs, extending to the peribronchial and peribronchiolar areas, was seen. The results of this experiment call attention to the risk of prolonged low-dose toxin exposure, which has very important public health implications.

Topics: Animal Feed; Animals; Carboxylic Acids; Carcinogens, Environmental; Dose-Response Relationship, Drug; Environmental Exposure; Fumonisins; Lung; Male; Mycoses; Mycotoxins; Pulmonary Edema; Swine; Swine Diseases; Time Factors

Fumonisins, mycotoxins that commonly contaminate corn, induce cardiovascular toxicity and pulmonary edema in pigs, leukoencephalomalacia in horses, and nephropathy in rats, rabbits, and lambs. The mechanisms of these species-specific target organ toxicoses are poorly understood. We have previously reported perinuclear accumulation of membranous material in pulmonary capillary endothelial cells of pigs fed fumonisin-containing culture material. We hypothesized that these endothelial accumulations may be important in the pathogenesis of fumonisin-induced pulmonary edema and target organ toxicity in other species. Both target and non-target tissues from fumonisin-exposed pigs, sheep, rabbits, and rats were examined ultrastructurally. Specifically, lung, liver, heart and kidney were examined. In agreement with our previous work (Gumprecht, L.A., Beasley, V.R., Weigel, R.M., Parker, H.M., Tumbleson, M.E., Bacon, C.W., Meredith, F.I., Haschek, W.M., 1998. Development of fumonisin-induced hepatotoxicity and pulmonary edema in orally dosed swine: morphological and biochemical parameters. Tox. Pathol. 26, 777-788), endothelial alterations were present in the pulmonary capillary endothelial cells of pigs fed fumonisin-containing culture material, but at doses that did not induce pulmonary edema, as well as in pigs injected intravenously with purified fumonisin B(1). These alterations were present only in the pulmonary capillary endothelium of pigs and not in other species. In addition, these endothelial alterations were not present in any other organ of pigs or other species examined. Thus, these endothelial alterations are induced by fumonisin B(1), but only in pulmonary capillary endothelium and only in pigs. Although evidence that these alterations play a role in fumonisin-induced pulmonary edema is limited, other endothelial functions may be affected by fumonisin treatment.

Topics: Animals; Capillaries; Carboxylic Acids; Coronary Vessels; Endothelium, Vascular; Fumonisins; Kidney; Liver; Male; Microscopy, Electron; Mycotoxins; Myocardium; Organ Specificity; Pulmonary Alveoli; Pulmonary Edema; Rabbits; Rats; Rats, Sprague-Dawley; Species Specificity; Swine

This article describes the events leading to the discovery of the fumonisins in South Africa in 1988 and highlights the first 10 years (1988-1998) of fumonisin research. The predominant fungus isolated from moldy corn implicated in a field outbreak of equine leukoencephalomalacia (ELEM) in South Africa in 1970 was Fusarium verticillioides (F. moniliforme). This fungus was also prevalent in moldy home-grown corn consumed by people in high-incidence areas of esophageal cancer (EC) in the Transkei region of South Africa. Culture material on corn of F. verticillioides strain MRC 826, which was isolated from moldy corn in Transkei, was shown to cause ELEM in horses, porcine pulmonary edema (PPE) syndrome in pigs, and liver cancer in rats. A short-term cancer initiation/promotion assay in rat liver was used to purify the carcinogen(s) in the culture material. These efforts finally met with success when fumonisins B1 and B2 novel mycotoxins with cancer-promoting activity in rat liver, were isolated from culture material of F. verticillioides MRC 826 at the Programme on Mycotoxins and Experimental Carcinogenesis of the Medical Research Council in Tygerberg, South Africa. Following the elucidation of the chemical structure of the fumonisins, these carcinogenic mycotoxins were shown to occur naturally in moldy corn in Transkei. Shortly thereafter, high levels of fumonisins in the 1989 U.S. corn crop resulted in large-scale field outbreaks of ELEM and PPE in horses and pigs, respectively, in the United States. Subsequently the fumonisins were found to occur naturally in corn worldwide, including corn consumed as the staple diet by people at high risk for EC in Transkei and China. These findings, together with the fact that the fumonisins cause field outbreaks of mycotoxicoses in animals, are carcinogenic in rats, and disrupt sphingolipid metabolism, have resulted in much worldwide interest in these compounds during the first 10 years after the discovery of the fumonisins in 1988.

Topics: Animals; Carboxylic Acids; Disease Outbreaks; Encephalomalacia; Esophageal Neoplasms; Female; Fumonisins; Fusarium; History, 20th Century; Humans; Male; Mycoses; Mycotoxins; Pulmonary Edema; South Africa; Zea mays

In Hungary almost 70% of mould-affected maize inspected since 1993 was found to be contaminated with fumonisin B1 (FB1) (mean 2.6-8.65 mg/kg; maximum 9.8-75.1 mg/kg), the degree of this contamination was found to increase from year to year (Fazekas et al., 1997b). In this experiment, in order to define tolerance limit values, the effect of exposing weaned piglets to FB1 in low doses over a 4-week period was examined. The experiment was performed with 20 weaned barrows of Danish Landrace breed. After a 5-day adaptation period cultures of the fungus Fusarium moniliforme were mixed into the animals' feed in concentrations that resulted in a daily intake of fumonisin B1 of 0, 10, 20 and 40 mg/kg feed. Feeding with the toxin was observed to exert no significant effect on body weight gain or feed consumption in the animals, no clinical signs were observed and no mortality traceable to toxic effects occurred. In computer tomography examinations performed in the second and fourth weeks mild and more severe pulmonary oedema was diagnosed in the experimental animals. The processes developing in the pulmonary parenchyma were corroborated by the mathematical and statistical evaluation procedures applied. The haematological parameters examined revealed no change attributable to toxic effects, while with respect to the biochemical parameters, an increase in aspartate aminotransferase (AST) activity dependent on dosage, indicating a pathological change in the liver, was ascertained in all three experimental groups. The free sphinganine to sphingosine ratio (SA/SO), which is regarded as the most sensitive bioindicator of fumonisin toxicosis, showed an increase proportionate to toxin concentration for all three dosages. Dissection revealed mild cases of pulmonary oedema in three of the animals given doses of 10 p.p.m. (n = 4), two mild and two severe cases in those exposed to 20 p.p.m. (n = 5), and severe cases in all five animals given 40 p.p.m. The oedema of non-inflammatory origin was confirmed by histopathological examinations. The findings of this experiment which indicate that in this study FB1 administered in substantially lower concentrations than those reported in the literature resulted in severe pathological changes, point to the importance of studies involving even lower doses.

Topics: Animal Feed; Animals; Animals, Newborn; Carboxylic Acids; Fumonisins; Fusarium; Magnetic Resonance Imaging; Male; Mycoses; Mycotoxins; Pulmonary Edema; Swine; Swine Diseases; Tomography, X-Ray Computed

Fumonisins are mycotoxins produced by Fusarium verticillioides, which induce acute pulmonary edema in swine. We previously reported that ingestion of fumonisin-containing culture material decreases cardiovascular function in swine (1996,a,b; Fundam. Appl. Toxicol. 31, 169-172; 33, 140-148; 1999, Am. J Vet. Res. 60, 1291-1300). The main purpose of this study was to confirm that fumonisin B(1) was responsible for the observed cardiovascular changes. Treated pigs (n = 6) were given daily intravenous injections of purified fumonisin B(1) at 1 mg/kg for 4 days, while controls (n = 6) were injected with equal volumes of saline. On day 5, pigs were anesthetized with butorphanol-chloralose and instrumented for hemodynamic studies. Terminally, bronchoalveolar lavage was performed on each pig to determine the relative permeability index of the pulmonary endothelium. Fumonisin B(1)-treated pigs had marked decreases in the maximal rate of change of left ventricular pressure (dP/dt(max)), mean aortic pressure, cardiac output, and arterial pO(2), accompanied by increases in mean pulmonary artery pressure, oxygen extraction ratio, and blood hemoglobin concentration. Plasma and left ventricular sphingosine and sphinganine concentrations were markedly increased in treated pigs at day 5; however, there was no difference in the relative permeability index between groups. Serum cholesterol concentrations and activities of hepatic-derived enzymes were increased, and hepatocyte apoptosis and mitoses were present in the livers of fumonisin-treated pigs. In the lungs of treated pigs, there was proteinaceous edema and membranous accumulations in capillary endothelial cells. These results indicate that cardiovascular function is altered by fumonisin B(1), and that fumonisin-induced pulmonary edema is caused by left-sided heart failure and not by altered endothelial permeability. Because of the potential for contamination of human foodstuffs by fumonisins, the cardiovascular toxicity of these compounds must be taken into consideration.

Topics: Animals; Apoptosis; Blood Chemical Analysis; Bronchoalveolar Lavage; Capillary Permeability; Carboxylic Acids; Cell Division; Fumonisins; Heart Ventricles; Hemodynamics; Injections, Intravenous; Liver; Lung; Male; Mycotoxins; Organ Size; Pulmonary Alveoli; Pulmonary Edema; Sphingosine; Swine; Ventricular Function, Left

To determine the sequence of cardiovascular and blood gas changes induced by ingestion of fumonisin-containing culture material in swine and to examine the temporal relationship of these changes to plasma sphinganine and sphingosine concentrations.. 12 healthy castrated pigs (38 to 50 kg).. Pigs were instrumented to permit cardiovascular monitoring and collection of blood samples. Baseline values were obtained, and pigs were randomly assigned to 1 of 2 groups. Control pigs (n = 6) were fed a standard grower diet, whereas culture material that contained 20 mg of fumonisin B1/kg of body weight was added to the feed of treated pigs (n = 6) each day. Hemodynamic data, results of arterial and mixed venous blood gas analyses, and plasma sphinganine and sphingosine concentrations were recorded every 12 hours until treated pigs were euthanatized because of impending death from pulmonary edema.. Sphinganine and sphingosine concentrations were increased in plasma of treated pigs within 24 hours of initial fumonisin exposure and continued to increase dramatically until euthanasia. Fumonisin-treated pigs had increased respiratory rate, mean pulmonary artery pressure, and pulmonary artery wedge pressure, along with decreased heart rate and cardiac output in the 12-hour period before euthanasia. Fumonisin-treated pigs also had systemic arterial hypotension, arterial and mixed venous hypoxemia, metabolic acidosis, decreased oxygen delivery, and increased oxygen consumption immediately before euthanasia.. Fumonisin-induced pulmonary edema in swine is probably caused by acute left-sided heart failure. Onset of hemodynamic changes was associated with plasma sphinganine concentration > or = 2.2 microM/L and plasma sphingosine concentration > or = 1 microM/L.

Topics: Animal Feed; Animals; Blood Pressure; Carbon Dioxide; Carboxylic Acids; Cardiac Output; Food Microbiology; Fumonisins; Heart Rate; Hemodynamics; Male; Orchiectomy; Oxygen; Pulmonary Artery; Pulmonary Edema; Random Allocation; Respiratory Mechanics; Sphingosine; Swine; Swine Diseases; Vascular Resistance

Sera obtained from a group of pigs (n = 5) fed a diet amended with fumonisin containing Fusarium moniliforme culture material was used to determine the levels of Tumor Necrosis Factor-Alpha (TNF) activity by a functional bioassay utilizing the TNF sensitive WEHI 140 mouse fibrosarcoma cell line. Two pigs developed signs consistent with pulmonary edema which was confirmed by pathologic examination in only one pig. Significant, time dependent increases in TNF-like activity were observed in all pigs during the five days of the trial. Another group of pigs (n = 5) was given a defined daily dose of the same culture material by gastric intubation. Two pigs developed fulminant pulmonary edema and sharp increases in TNF activity were observed during the 3 days of the trial in all pigs. In both cases the activity was not abrogated by addition of a neutralizing anti-human TNF monoclonal antibody suggesting that other factors may have been responsible for these effects, possibly the increased levels of sphingoid bases in the serum. Since the pig has become an important model in the study of TNF mediated endotoxic shock, these studies illustrate the relevance of certifying the absence of this important mycotoxin from corn based animal diets, specially if functional assays are used to monitor the activity of TNF in serum.

Topics: Animals; Antibodies, Monoclonal; Carboxylic Acids; Culture Media; Cytotoxins; Diet; Female; Fumonisins; Fusarium; Humans; Infant, Newborn; Mycotoxins; Pulmonary Edema; Respiration Disorders; Swine; Tumor Necrosis Factor-alpha

From a series of experimental studies with pigs (12-16 kg), either pulmonary edema or liver failure emerged as a distinct pathogenetic expression of fumonisin B1 (FB1) toxicosis. The primary determinant as to which pathogenetic consequence developed was the quantity (dose) of the mycotoxin fed or intubated per kilogram of body weight per day. Pigs intubated with a minimum of 16 mg FB1/kg/day developed severe interlobular edema with or without hydrothorax and variably severe pulmonary edema. Pigs intubated with < 16 mg FB1/kg/day or pigs fed diets containing 200 mg FB1/kg of feed developed marked icterus and hepatocellular necrosis. The spectrum of degrees of severity of pulmonary edema observed in the experimental pigs allowed rational speculation regarding evolution of the pathologic changes.

Topics: Animals; Fumonisins; Liver Failure; Mycotoxins; Pulmonary Edema; Swine; Swine Diseases

Pulmonary edema and hydrothorax were observed in mature swine that died approximately 5 days after consuming corn screenings. These postmortem observations were reproduced in younger pigs that died within 1 week when fed the corn screenings under experimental conditions. Additionally, pulmonary edema and hydrothorax were induced in a pig that died after receiving 4 daily intravenous injections of fumonisin B1, a toxic metabolite produced by Fusarium moniliforme.

Topics: Animal Feed; Animals; Food Microbiology; Fumonisins; Fusarium; Hydrothorax; Injections, Intravenous; Liver; Lung; Mycotoxins; Pulmonary Edema; Swine; Swine Diseases; Zea mays

In 1989, corn screenings were associated with acute interstitial pulmonary edema, hydrothorax, and death in swine. Attack rate was 5-50%, case fatality rate was 50-90%, and clinical course was 1-2 days. Screenings from farms with pigs affected with pulmonary edema contained 20-330 micrograms fumonisin B1 per gram. Screenings containing 92 micrograms fumonisin B1 per gram fed to weanling pigs caused pulmonary edema and death. Sterilized corn inoculated with Fusarium moniliforme and diluted 1:1 with clean corn contained fumonisin B1 (17 micrograms/g) and caused acute pulmonary edema when fed for 5 days. Survivors developed subacute hepatotoxicosis with individual hepatocellular necrosis, hepatomegalocytosis, and increased numbers of mitotic figures. Similar liver lesions occurred in pigs given fumonisin B1 intravenously at 0.8 mg/kg body weight for 14 days.

Topics: Animal Feed; Animals; Death, Sudden; Disease Outbreaks; Female; Food Microbiology; Fumonisins; Fusarium; Illinois; Iowa; Liver; Lung; Mycotoxins; Pulmonary Edema; Swine; Swine Diseases; Zea mays

Ninety-eight samples of feeds associated with 44 cases of equine leukoencephalomalacia (ELEM) and 83 samples of feed associated with 42 cases of a porcine pulmonary edema syndrome (PPE) were analyzed for fumonisin B1 (FB1). For comparison purposes, 51 feed samples not associated with PPE or ELEM were also analyzed. Feed associated with ELEM contained FB1 ranging from less than 1 microgram/g to 126 micrograms/g with 75% of the cases having at least 1 sample above 10 micrograms/g. Feeds associated with PPE ranged from less than 1 microgram/g to 330 micrograms/g with 71% of the cases having at least 1 sample greater than 10 micrograms/g. Quantitation was by high performance liquid chromatography (HPLC)/fluorescence using the fluorescamine derivative with confirmation by thin layer chromatography (TLC) and/or gas chromatography/mass spectroscopy (GC/MS).

Topics: Animal Feed; Animals; Carcinogens, Environmental; Chromatography, High Pressure Liquid; Chromatography, Thin Layer; Encephalomalacia; Food Microbiology; Fumonisins; Gas Chromatography-Mass Spectrometry; Horse Diseases; Horses; Mycotoxins; Pulmonary Edema; Swine; Swine Diseases; Zea mays

Pulmonary edema and hydrothorax were observed in mature swine that died approximately 5 days after consuming corn screenings. These postmortem observations were reproduced in younger swine (16-24 kg) that died within 1 week when fed the corn screenings under experimental conditions. Additionally, pulmonary edema and hydrothorax occurred in a pig (7.1 kg) that died after receiving 4 daily intravenous injections of fumonisin B1. A fungus was isolated from the corn screenings that is identical to Fusarium moniliforme MRC-826 in colony morphology and under microscopic examination.

Topics: Animal Feed; Animals; Chromatography, High Pressure Liquid; Food Microbiology; Fumonisins; Fusarium; Hydrothorax; Liver; Lung; Mycotoxins; Pancreas; Pulmonary Edema; Swine; Swine Diseases; Zea mays

Fumonisin B1 (FB1) and FB2 were isolated from corn cultures of both Fusarium moniliforme and Fusarium proliferatum. Respective concentrations in culture materials of FB1 and FB2 ranged from 960 to 2,350 and 120 to 320 micrograms/g for F. moniliforme and from 1,670 to 2,790 and 150 to 320 micrograms/g for F. proliferatum. Thin-layer chromatography, gas chromatography-mass spectroscopy, high-performance liquid chromatography, and liquid secondary ion mass spectroscopy were used for detection. Fumonisins from F. proliferatum have not previously been reported.

Topics: Animal Feed; Animals; Disease Outbreaks; Encephalomalacia; Food Contamination; Food Microbiology; Fumonisins; Fusarium; Horse Diseases; Horses; Mycotoxins; Pulmonary Edema; Swine; Swine Diseases; Zea mays