Feed exposure to FB1 can aggravate pneumonic damages in pigs provoked by P. multocid a

Abstract

The possible interaction between Pasteurella multocida and the mycotoxin fumonisin B1 (FB1), recognised as one of the most often food/feed contaminant, was studied with the aim to evaluate whether and how FB1 can influence and/or complicate the development and severity of various pathological damages provoked by Pasteurella multocida in some internal organs of pigs. Heavier lung pathology was seen in pigs experimentally infected with Pasteurella multocida, when the same were exposed to 20 ppm dietary levels of fumonisin B 1 (FB 1 ) as was assessed by gross pathology, pathomorphological examinations, clinical biochemistry and some immunological investigations. The most typical damages in FB 1 treated pigs were the strong oedema in the lung and the slight oedema in the other internal organs and mild degenerative changes in the kidneys, whereas the typical pathomorphological findings in pigs infected with Pasteurella multocida was broncho-interstitial pneumonia. FB1 was found to aggravate pneumonic changes provoked by P. multocida in the cranial lobes of the lung and to complicate pneumonic damages with interstitial oedema in the lung. No macroscopic damages were observed in the pigs infected only with Pasteurella multocida. It can be concluded that the feed intake of FB1 in pigs may complicate or exacerbate the course of P. multocida serotype A infection.

Porcine Hepatic Response to Fumonisin B1 in a Short Exposure Period: Fatty Acid Profile and Clinical Investigations

“…In the present investigation, the most striking modifications seen in the liver of piglets exposed to 20 mg FB 1 /kg diet are the vacuolar degeneration of hepatocyte cytoplasm. This finding was markedly categorized as a mild to moderate effect, in agreement with the findings of Dilkin et al [20] and Kovács et al [21]. The vacuolar degeneration of hepatic cell cytoplasm is highly associated with disturbance of cellular water or lipid metabolism, indicative of an exertion of the cell’s metabolic and/or detoxification activity.…”

“…Despite a recent study illustrating that 12.2 mg FBs/kg diet developed hepatotoxicity in piglets after 28 days of exposure [10], it is interesting to study the sub-acute effect of FB 1 on the liver. From this point of view, earlier reports which applied 20 mg FB 1 /kg diet [18,21] on piglets did not provide alteration in the membrane profile of the liver, in connection with its hepatotoxicity. Monitoring alterations in lipids may assist for better understanding of FB 1 toxicity mechanism of action.…”

“…The ALT, AST, GGT, and LDH were not statistically altered by toxin exposure. In a study on piglets [21] at the same FB 1 level, but longer exposure period (two weeks), neither ALT, nor AST differed from the control. In pigs, ALP is a strongly responsive enzyme to FB 1 toxicity [57].…”

“…In swine, specifically, FB 1 was found to exert development of pulmonary edema and hepatotoxicity [4], moreover, it has been suggested as the key player behind pulmonary fibrosis [15]. With regard to the liver, several studies reported the ability of FB 1 in inducing histomorphological alterations with dose range of 3.7–190 mg/kg diet and exposure time range of 5–83 days, using different exposure methods: contaminated diet, orally gavaged, and intravenously [10,16,17,18,19,20,21]. Also, it induced clinical signs, such as respiratory distress [11].…”

Research Progress on Fumonisin B1 Contamination and Toxicity: A Review

“…FB1 also significantly increases colonization of the small and large intestine by extra-intestinal pathogenic E. coli strains [ 95 ]. Some studies have shown that administration of different doses of FB1 (11.8 mg/kg, 0.5 mg/kg, and 20 mg/kg) can complicate the infection process of Bacillus subtilis A, causing interstitial bronchial pneumonia [ 96 , 97 , 98 ]. Recent studies have shown that non cytotoxic doses of FB1 can aggravate OTA induced cytotoxicity and apoptosis.…”