Fumonisin toxicity in broiler chicks.

The effects of dietary fumonisin B1 were evaluated in young broiler chicks. The experimental design consisted of 5 treatments each with 9 randomly allotted male broiler chicks. Day-old chicks were fed diets containing 0 (feed control), 100, 200, 300, or 400 mg fumonisin B1/kg feed for 21 days. Response variables measured were chick performance, organ weights, serum biochemistry, and histologic parameters. Body weights and average daily gain dramatically decreased with increasing dietary fumonisin B1, and liver, proventriculus, and gizzard weights increased. Diarrhea, thymic cortical atrophy, multifocal hepatic necrosis, biliary hyperplasia, and rickets were present in chicks fed diets containing fumonisin B1. Serum calcium, cholesterol, and aspartate aminotransferase levels all increased at higher fumonisin dietary levels. Results indicate that fumonisin, from Fusarium moniliforme culture material, is toxic in young chicks.     

Experiment to determine limits of tolerance for fumonisin B1 in weaned piglets

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.     

Fumonisin mycotoxicosis in broilers: performance and pathology.

Fusarium moniliforme culture material containing fumonisin B1 at 300 mg/kg was incorporated into a broiler starter ration and fed ad libitum to 1-day-old broiler chicks for 2 weeks in two experiments. Clinical features of the disease produced included diarrhea, a 19% reduction in body weight, a 30% increase in relative liver weight, and a worsening of feed conversion by 20 points at 2 weeks of age. Histologically, chicks fed fumonisin had multifocal hepatic necrosis, biliary hyperplasia, muscle necrosis, intestinal goblet-cell hyperplasia, and rickets. Simultaneous feeding of 0.5% aluminosilicate had no effect on the clinical disease or lesions. The clinical disease and lesions induced mimicked those of a viral enteritis.     

Characterization of an epizootic of pulmonary edema in swine associated with fumonisin in corn screenings.

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.     

The pathology of Cestrum laevigatum (Schlechtd.) poisoning in cattle

The clinical features and pathological findings of 6 steers drenched with dried plant material of Cestrum laevigatum are described. Doses ranging from 0.5 to 10 g/kg/day were given intraruminally for 1 to 38 days. Animals that received 5 to 10 g/kg/day showed nervous signs including ataxia, muscle tremors, hypersensitivity and intermittent chewing. Clinical signs in the steers which received 0,5 to 4 g/kg/day were mild. High doses induced moderate to severe hepatosis characterized by centrilobular to midzonal coagulative necrosis, haemorrhage and congestion. At lower rates only mild hepatic lesions, characterized by disappearance of hepatocytes and collapse of the reticulin stroma in the centrilobular areas were evident. Ultrastructural changes were primarily limited to the hepatocytes and comprised degeneration, necrosis and fatty change. Degeneration and necrosis of endothelial cells and disruption of sinusoidal walls were occasionally observed.     

Poisoning of horses by bamboo, Bambusa vulgaris

The clinical and pathological aspects of a neurological disease observed in 16 horses in Pará, Amazonia, Brazil, are presented. The symptoms were mainly motor incoordination, paresis of the tongue, somnolence, difficulties in apprehension, chewing and swallowing of food, as well as instability and standing with abducted members. The clinical course was subacute or chronic and in most cases was not fatal. Postmortem examination performed in one already very sick, euthanized animal, did not show significant macroscopic lesions; histopathological examination revealed slight edema and degenerative alterations of a few axons, mainly in the medulla oblongata. In all pastures where horses were affected, plenty of bamboo had been eaten, probably because of scarcity of pasture. By feeding large amounts of fresh bamboo leaves of this region, in different growing stages, to three horses (horse 1, 47 g/kg/d for 30 days; horse 2, 10 g/kg/d for 60 days; horse 3, 18 g/kg on the first day, and 31 g/kg/d for 6 more days)—the animals ate the leaves unassisted—it was possible to reproduce nervous symptoms essentially identical to those observed in the natural disease 24 to 72 hours after the first feeding of the plant. In spite of continuous administration of the plant, intensity of the clinical signs did not increase. Based on field observations and comparison of the clinical and pathological pictures seen in the natural and experimental disease, the described illness can be concluded to be caused by the ingestion of large amounts of the leaves of Bambusa vulgaris f. vulgaris.     

Effect of dietary fumonisin B1 on certain immune parameters of weaned pigs

Only few data are available on the effect of fumonisins on the immune response. The aim of the present study was to examine whether dietary fumonisin B1 (FB1) has any effect on the humoral and cellular immune response in weaned pigs, depending on the dose and the time of toxin exposure. Fusarium moniliforme fungal culture was added to the experimental animals' diet to ensure an FB1 intake of 1, 5 and 10 ppm (first experiment) or 100 mg per animal per day (second experiment). The control animals were fed a toxin-free diet. In order to determine the immune response, the animals were vaccinated against Aujeszky's disease with inactivated vaccine (Aujesping K, Phylaxia-Sanofi, Budapest, Hungary). Specific and nonspecific in vitro cellular immune response was measured by the lymphocyte stimulation test (LST) induced by PHA-P, Con A, LPS and inactivated suspension of the Aujeszky's disease virus. Humoral immune response, e.g. specific antibody titre, was measured by the virus neutralisation (VN) test. None of the immunological parameters examined showed significant differences between groups. It could be concluded that fumonisin B1 had no significant effect on the humoral and cellular specific and nonspecific immune response when fed in a high dose (100 mg/animal/day for 8 days) or in a low concentration even for a longer period (1, 5 and 10 ppm for 3-4 months).     

ORIGINAL ARTICLE: Brain and hypophyseal acetylcholinesterase activity of pubertal boars fed dietary fumonisin B1

The effects of dietary fumonisin B₁ (FB₁) on regional brain and hypophyseal activities of AChE (EC 3117), the enzyme which catalyses the hydrolysis of acetylcholine, were studied using 24 male Large White weanling pigs divided into four groups. Each group received one of the four diets containing 0.2, 5.0, 10.0 and 15.0 mg FB₁/kg in a 6‐month feeding trial. All animals were slaughtered at the end of the feeding trial; the brains and the hypophyses obtained were carefully dissected out. Significant (p < 0.05) influence of dietary FB₁ on regional brain and hypophyseal AChE activities were observed. The AChE activities in the pons, amygdala, hypothalamus and the medulla oblongata declined significantly (p < 0.05) with increased dietary FB₁ concentrations. The findings of this study suggest that diets containing 5.0 mg FB₁/kg and above significantly (p < 0.05) altered regional brain and hypophyseal AChE activities in the animals. Dietary exposure to FB₁ at a concentration of approximately 5.0 mg/kg or more for a 6‐month period is a potential health risk that may induce adverse physiological response resulting from altered brain neurochemistry in growing pigs.     

Lesions in the central nervous system associated with perinatal lamb mortality

OBJECTIVE: To identify and describe the occurrence of neurological lesions that could have an effect on lamb mortality. PROCEDURE: The central nervous system was investigated macroscopically (n = 92) and microscopically (n = 72) in lambs dying in the perinatal period during 3 years in flocks of adult Corriedale ewes. The central nervous system was removed intact and samples of cerebral cortex, basal ganglia, thalamus, hippocampus, mesencephalon, cerebellar cortex, medulla oblongata, and cervical spinal cord were scored microscopically for the severity of neuronal dead, cytotoxic and perivascular oedema, and haemorrhage. RESULTS: Neurologic findings between birth and 6 days included haemorrhages in meninges, brain congestion and oedema, neuronal ischemic necrosis, intraparenchymal haemorrhages in medulla oblongata and cervical spinal cord, parasagittal cerebral necrosis, and periventricular leukomalacia. No significant lesions were found in anteparturient deaths or in those aged between 7 and 16 days. Oedema was more severe in the brain than in other regions of the central nervous system. Ischaemic neurons first appeared 24 hours post partum, increased linearly in number between 48 hours and 5 days post partum, and had a laminar distribution in the cerebral cortex, indicating a hypoxic-ischemic encephalopathy. Haemorrhages were most severe in the gray matter of medulla oblongata and cervical spinal cord, suggesting trauma due to instability of atlantoaxialis joint. CONCLUSION: Lesions in the central nervous system can explain most deaths at birth and within 6 days of birth. The lesions were hypoxic-ischemic and appeared to be related to birth injury.     

Pulmonary edema and hydrothorax in swine produced by fumonisin B1, a toxic metabolite of Fusarium moniliforme

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.     

Infarction of the pons and medulla oblongata caused by arteriolar thrombosis in a horse

Infarction of the pons and rostral medulla secondary to arteriolar thrombosis was documented histologically in a 17-year-old mixed-Arabian female horse. Clinically, the animal experienced a sudden onset of a head tilt and subsequent non-controllable seizures. There was no historical, clinical or histological evidence to suggest the presence of infection of Equine Herpesvirus-1 or the feeding of corn contaminated by Fusarium moniliforme.     

Effects of Fusarium moniliforme culture material containing known levels of fumonisin B1 on progress of Salmonella Gallinarum infection in Japanese quail: clinical signs and hematologic studies

To study the individual and combined effects of fumonisin B1 (FB1) toxicity and Salmonella serotype Gallinarum infection, Japanese quail (Coturnix coturnix japonica) were fed Fusarium moniliforme culture material (2.5%), 150 mg FB1/kg ration, and were subsequently challenged orally with Salmonella Gallinarum organisms (2 x 10(4) colony-forming units) at 21 days of age. The chicks were fed culture material containing FB1 from day 5 till the end of the experiment. After being infected with Salmonella Gallinarum, observations were made 1, 2, 3, 5, 7, 10, 14, and 21 days postinfection. The clinical signs of diarrhea with bloody discharges were more pronounced in the Salmonella-infected birds on the FB1 diet. Mortality caused by Salmonella Gallinarum increased by 12% in the presence of FB1. Mean body weights in both the Salmonella-infected and FB1-fed groups were significantly lower than those of the controls at almost all intervals. Mean values of hemoglobin, packed cell volume, and total erythrocyte count were slightly higher in birds fed FB1 but were lower in the Salmonella Gallinarum groups fed FB1 and plain chick mash. Anemia was evident, between 5 and 10 days postinfection, in quail chicks infected with Salmonella Gallinarum alone. Total leukocyte counts were higher in Salmonella-infected and FB1-fed groups because of an increase in the number of heterophils and lymphocytes. However, the increase in lymphocyte response to infection was lower by 4.27%-30.09% between 3 and 21 days postinfection in the FB1-fed chicks compared with chicks infected with Salmonella Gallinarum. Alanine transaminase and total serum protein were slightly higher in both the infected and FB1-fed groups. This study revealed that the continuous presence of fumonisins in the diets of quail chicks might increase the susceptibility to or the severity of Salmonella Gallinarum infection.     

Sequence of cardiovascular changes leading to pulmonary edema in swine fed culture material containing fumonisin

OBJECTIVES: 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. ANIMALS: 12 healthy castrated pigs (38 to 50 kg). PROCEDURE: 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. RESULTS: 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. CONCLUSIONS AND CLINICAL RELEVANCE: 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.     

Organ traits and histopathology of rabbits fed varied levels of dietary fumonisin B1

In a 196‐day feeding trial, 48 male crossbred rabbits (New Zealand × Chinchilla) were randomly assigned and fed varied dietary fumonisin levels of 0.13, 5.0, 7.5 and 10.0 mg fumonisin B₁/kg diet constituting treatments 1 (control), 2, 3 and 4 respectively. Five animals were randomly selected, stunned and killed per treatment. Relative weight of various visceral organs examined except heart and adrenal gland were significantly (p < 0.05) influenced by the dietary treatments. Liver and spleen weights of rabbits fed 10.0 mg fumonisin per kg were significantly (p < 0.05) lower than those fed control diet and diet 2. Kidney and testes weights were significantly (p < 0.05) lower in rabbits fed control diet and increased with increase in the dietary fumonisin levels. Histological examination of the organs revealed that rabbits fed diets 2, 3 and 4 showed increased severe lesion of approximately 20%, 40% and 60%, respectively, of the total slides examined for each treatment. Forty per cent and 80% of the rabbits fed diets containing 7.5 and 10.0 mg/kg fumonisin, respectively, showed severe necrosis whereas 40%, 60% and 20% of the rabbits fed 5.0, 7.5 and 10.0 mg/kg, respectively, showed mild–moderate liver necrosis/lesions as compared with non‐significant lesion observed in the controls. Testicles of rabbits fed diets 3 and 4 showed mild–moderate lesions and sertoli cell degeneration. Tunica mucosa erosion was observed and predominant in the stomach and small intestine of rabbits fed 7.5 and 10.0 mg fumonisin per kg diet. This suggested that fumonisin B₁ above 5.0 mg/kg in rabbit diet is toxic to body organs with potential to induce their hypofunction or total damage.     

Fumonisin B1 concentrations in feeds from 45 confirmed equine leukoencephalomalacia cases

During the fall of 1989 and winter of 1990, numerous reports of equine leukoencephalomalacia (ELEM) occurred from many regions of the United States. Typically, horses were consuming feed partially or entirely composed of corn and/or corn screenings. From October 1989 through May 1990, samples from 55 confirmed or suspected ELEM cases were received at the National Veterinary Services Laboratories, Ames, Iowa, for fumonisin B1 analysis. Samples from 9 cases in 1984-1985 were also obtained. Fumonisin B1, a mycotoxin produced by Fusarium moniliforme, causes ELEM, but little is known of naturally occurring toxic or safe levels in feeds. To determine what levels of fumonisin B1 in feeds are associated with ELEM, 45 selected cases were studied. The fumonisin B1 concentrations ranged from less than 1 ppm to 126 ppm, with the majority of the samples above 10 ppm. All types of feeds were included: corn, screenings, sweet feeds, and commercially pelleted rations. The length of exposure varied from 7 to greater than 35 days. Horse feed samples not associated with ELEM were also collected and analyzed. None of the nonproblem feed samples contained fumonisin B1 levels greater than 8 ppm.     

Interaction of Bordetella bronchiseptica, Pasteurella multocida, and fumonisin B1 in the porcine respiratory tract as studied by computed tomography

The interaction of Bordetella bronchiseptica, toxigenic Pasteurella multocida serotype D, and the mycotoxin fumonisin B(1) (FB(1)) was studied. On day 0 of the experiment, 28 artificially reared 3-day-old piglets were divided into 4 groups (n = 7 each): a control group (A), a group fed FB(1) toxin (B), a group infected with the 2 pathogens (C), and a group infected with the 2 pathogens and fed FB(1) toxin (D). The B. bronchiseptica infection [with 10(6) colony-forming units (CFU)/mL] was performed on day 4 and the P. multocida infection (with 10(8) CFU/mL) on day 16. From day 16 a Fusarium verticillioides fungal culture (dietary FB(1) toxin content 10 mg/kg) was mixed into the feed of groups B and D. In groups C and D, clinical signs including mild serous nasal discharge, sneezing, panting, and hoarseness appeared from day 4, and then from day 16 some piglets had coughing and dyspnea as well. Computed tomography (CT) performed on day 16 demonstrated lung lesions attributable to colonization by B. bronchiseptica in the infected groups. By day 25 the number of piglets exhibiting lesions had increased, and the lesions appeared as well-circumscribed, focal changes characterized by a strong density increase in the affected areas of the lungs. The gross pathological findings confirmed the results obtained by CT. These results indicate that, when combined with dual infection by B. bronchiseptica and P. multocida, dietary exposure of pigs to FB(1) toxin raises the risk of pneumonia and increases the extent and severity of the pathological changes.     

Fumonisin B1 causes multiple lesions in common carp (Cyprinus carpio)

Year-1 carp were fed ratios containing 100mg/kg and 10 mg/kg of added fumonisin B1 for 42 days. The experimental and control fish were examined clinically during the experiment and at the end all fish were necropsied and histological changes recorded. Blood vessels, liver, exocrine and endocrine pancreas, excretory and haematopoietic kidney, heart and brain were sensitive both to 100 and 10mg/kg of FB1 in the diet and the rodlet cell (RC) frequency was considerably increased in and around damaged tissues. Many damaged blood vessels contained stacks of RCs above the endothelium. Other changes subsequent to fumonisin exposure that have not been previously reported include scattered lesions in the exocrine and endocrine pancreas, and interrenal tissue, probably due to ischemia and/or increased endothelial permeability. Presented findings indicate the need for more intensive studies of fumonisin-induced toxicity in cultured fish.     

Equine protozoal myeloencephalitis in a pony

A 10-year-old pony died 5 days after the onset of a nervous disorder. Necropsy revealed a yellowish area of discoloration (1.5 by 1 cm) in the medulla oblongata. Microscopically, necrosis and nonsuppurative myeloencephalitis were found in the medulla oblongata. Immature and mature meronts (25 by 10 microns) were seen in neural tissue and in capillaries of the brain stem. Organisms were similar structurally to those seen in equine protozoal myeloencephalitis of horses.     

Predictive value of hypoglycin A and methylencyclopropylacetic acid conjugates in a horse with atypical myopathy in comparison to its cograzing partners

Hypoglycin A (HGA) was detected in blood and urine of a horse suffering from atypical myopathy (AM; Day 2, serum, 8290 μg/l; urine: Day 1, 574, Day 2, 742 μg/l) and in its cograzing partners with a high variability (46–1570 μg/l serum). Over the period of disease, the level of the toxic metabolites (methylencyclopropylacetic acid [MCPA]‐conjugates) increased in body fluids of the AM horse (MCPA‐carnitine: Day 2, 0.246, Day 3, 0.581 μmol/l serum; MCPA‐carnitine: Day 2, 0.621, Day 3, 0.884 μmol/mmol creatinine in urine) and HGA decreased rapidly (Day 3, 2430 μg/l serum). In cograzing horses MCPA‐conjugates were not detected. HGA in seeds ranged from 268 to 367 μg/g. Although HGA was present in body fluids of healthy cograzing horses, MCPA‐conjugates were not detectable, in contrast to the AM horse. Therefore, increasing concentrations of MCPA‐conjugates are supposed to be linked with the onset of AM and both parameters seem to indicate the clinical stage of disease. However, detection of HGA in body fluids of cograzing horses might be a promising step in preventing the disease.     

Morphological characteristics of C1 and C2 adrenergic neurone groups in marmoset monkey brainstem by using antibody against phenylethanolamine-N-methyltransferase

This work describes a mapping study of phenylethanolamine-N-methyltransferase (PNMT) immunoreactive neurones and fibres in the medulla oblongata of the marmoset monkey, Callithrix jacchus. Two groups of PNMT-immunoreactive neurones were found in the marmoset monkey medulla oblongata: a ventrolateral (C1 group) and a dorsomedial PNMT-immunoreactive cells group (C2 group). The PNMT-immunoreactive cells in the ventrolateral group C1 were found to be located around the lateral reticular nucleus. The PNMT-immunoreactive somata within the ventrolateral medulla are round to oval, and mostly multipolar with branched processes. In the dorsomedial group C2, PNMT-immunoreactive cell bodies appeared near the obex. The majority of the dorsomedial PNMT-immunoreactive neurones were observed in the nucleus tractus solitarius; although some were present in the dorsal motor nucleus of the vagus. The PNMT-immunoreactive somata in the dorsomedial medulla were small and round or ovoid. These results provide information upon the adrenergic system in the medulla oblongata of a species that presents a useful model of a small primate brain, the marmoset monkey.