Effects of feed-borne Fusarium mycotoxins on performance, serum chemistry, and intestinal histology of New Zealand White fryer rabbits.

The objective of the present study was to determine the effects of feeding diets containing grains naturally contaminated with Fusarium mycotoxins to fryer rabbits. The efficacy of a glucomannan mycotoxin adsorbent (GMA) was also examined. Thirty 5-wk-old male New Zealand White rabbits were fed a control diet, a contaminated diet, or a contaminated diet + 0.2% GMA for 21 d. Experimental diets contained deoxynivalenol (DON; vomitoxin) at a concentration of 0.25, 4.3, and 4.9 µg/g, respectively. Feed intake was measured daily and water intake was measured every 3 d. At the end of the feeding period, blood was collected for evaluation of serum chemistry and hematology. Visceral organs were excised, weighed, and processed for histopathological examination. Body weight gain and water intake were greater in rabbits fed the contaminated diet (P = 0.075 and 0.020, respectively) and those fed the contaminated + GMA diet (P = 0.026 and 0.002, respectively) compared with controls. Rabbits fed the contaminated + GMA diet had significantly increased serum urea concentrations (P = 0.023) and decreased serum alkaline phosphatase activity (P = 0.020) compared with controls. Increase in BW gain of rabbits fed the contaminated diets was caused by increased water consumption. There was no effect (P > 0.05) of diet on relative organ weights, but decreased infiltrations with eosinophilic granulocytes were observed in different regions of the intestine in rabbits fed the contaminated or the contaminated + GMA diet. It was concluded that rabbits could be adversely affected by feed-borne Fusarium mycotoxins but appear to be less sensitive than other mammalian species. Supplementation with GMA did not reduce many of the effects of feed-borne mycotoxins.

Effects of dietary Fusarium mycotoxins on intestinal lymphocyte subset populations, cell proliferation and histological changes in avian lymphoid organs.

An experiment was conducted to investigate the effects of dietary Fusarium mycotoxins on gut immunity, cell proliferation, and histology of avian lymphoid organs. The efficacy of a polymeric glucomannan mycotoxin adsorbent (GMA) was also determined. Seventy-two one-day-old male turkey poults were fed corn, wheat, and soybean meal-based diets for 21 days. Diets included control grains, contaminated grains and contaminated grains +0.2% GMA. The major contaminant was deoxynivalenol (3.9 µg/g) with lesser amounts of zearalenone (0.67-0.75 µg/g), 15-acetyl-deoxynivalenol (0.34 µg/g) and HT-2 toxin (0.078-0.085 µg/g). T- and B-lymphocyte populations and crypt cellular proliferation in duodenum, jejunum, ileum and cecal tonsil were measured immunohistochemically on day 14 and 21. Histological changes were recorded after 14 and 21 days of feeding. Feeding contaminated grains significantly increased the percentage of B-lymphocytes in ileum on day 14, and reduced (P<0.05) the percentages of CD8(+)-lymphocytes in cecal tonsil on day 21. GMA supplementation prevented these effects. The feeding of contaminated diets also caused a reduction (P<0.05) in ileal crypt proliferating cells and a significant increase in spleen secondary follicle on day 21. It was concluded that the feeding of grains naturally contaminated with Fusarium mycotoxins results in adverse effects on gut immunity and mucosal cell proliferation.

Morphologic changes in the intestine of broiler breeder pullets fed diets naturally contaminated with Fusarium mycotoxins with or without coccidial challenge.

The effects of feeding diets containing grains naturally contaminated with Fusarium mycotoxins on intestinal histology were studied in chickens raised to 10 wk of age in the absence or presence of coccidial challenge. Experimental diets included the following: controls, diets containing grains naturally contaminated with Fusarium mycotoxins, and diets containing contaminated grains + 0.2% polymeric glucomannan mycotoxin adsorbent. Contaminated diets contained up to 3.8 microg/g deoxynivalenol (DON), 0.3 microg/g 15-acetyl DON, and 0.2 microg/g zearalenone. An optimized mixture (inducing lesions without mortality) of Eimeria acervulina, Eimeria maxima, and Eimeria tenella was used to challenge birds at 8 wk of age. Intestinal tissues were collected from duodenum, jejunum, and ileum prior to challenge; at the end of the challenge period (7 days postinfection; PI); and at the end of the recovery period (14 days PI). Mean villus height (VH) in the duodenum of birds fed the contaminated diets in the absence of coccidial challenge was significantly lower than that of the controls. Mean VH in the jejunum and ileum of the same birds was significantly higher compared to controls, indicating a compensatory mechanism. Fusarium mycotoxins retarded duodenal recovery from coccidial lesions, as indicated by lower duodenal VH and apparent villus surface area comparing challenged birds fed the contaminated diets to challenged controls of the same age. Increased VH was frequently associated with cryptal hyperplasia and increased numbers of mitotic figures in crypts. It was concluded that diets contaminated with Fusarium mycotoxins below levels that negatively affect performance could alter intestinal morphology and interfere with intestinal recovery from an enteric coccidial infection.

Intracranial hemorrhage after use of tissue plasminogen activator for coronary thrombolysis.

Tissue plasminogen activator (tPA), an approved coronary thrombolytic agent, can cause serious bleeding. We report the cases of six patients with intracranial hemorrhage after tPA treatment for acute myocardial infarction. None of the patients were hypertensive at admission, and only one was hypertensive during therapy. Intravenous tPA, 100 mg, was followed by continuous intravenous heparin infusion; intracranial hemorrhage occurred between 2 and 14 hours after tPA infusion ended and between 3 and 17 hours after heparin therapy was started. The partial thromboplastin time (PTT) was excessively prolonged (from 81 s to more than 150 s) in all patients at onset of intracranial hemorrhage. The intracerebral hematomas were predominantly of lobar location, and two patients had multiple simultaneous hemorrhages. Four patients died from massive intracranial hemorrhage; the mechanism for these hemorrhages was unclear. Factors possibly related to hemorrhage include a systemic fibrinolytic state or a platelet anti-aggregant effect produced by tPA and enhanced hemorrhagic tendency caused by the combined effects of tPA and heparin. Local vascular changes at the bleeding site remain as potential contributing factors for isolated intracranial hemorrhage.

Intracerebral hemorrhage and phenylpropanolamine use.

Two patients developed intracerebral hemorrhage within hours from first-time ingestion of phenylpropanolamine-containing medications. One patient had marked hypertension, presented with three intracerebral hematomas, and developed a fourth hemorrhage 10 days later. Angiogram in one patient revealed "beading" of intracranial arteries, an abnormality also detected in a third patient who developed severe headache, vomiting, and acute hypertension following a single dose of phenylpropanolamine. These cases and others reported in the literature strongly suggest an association between phenylpropanolamine ingestion and hemorrhagic stroke. Direct questioning of use of this medication in cases of unexplained intracranial hemorrhage in previously healthy young individuals may reveal an unsuspected high frequency of this association.