Page 1075 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Fumonisins Chapter | 71 1007

VetBooks.ir Southeastern parts of the United States was heavily extract fumonisin from different matrices could account
The 1989, corn crop in many Midwestern and
for some of the variability. In addition, some reports have
reported only the concentration of fumonisin B 1 associ-
infected with F. verticillioides, and contaminated screen-
ings fed to animals led to fatal outbreaks of PPE ated with the development of pulmonary edema, while
(Harrison et al., 1990; Osweiler et al., 1992). This syn- others have reported both fumonisin B 1 and fumonisin B 2 .
drome was also reproduced experimentally with contami- Fumonisin B 2 usually occurs at about 30% of fumonisin
nated corn screenings and purified fumonisin B 1 B 1 in naturally-contaminated corn, and is generally con-
(Harrison et al., 1990; Osweiler et al., 1992). sidered to be equitoxic to fumonisin B 1 (Ross et al.,
Lung and liver are the major target organs of fumoni- 1994). Reported doses that induced pulmonary edema in
sin toxicosis in pigs; however, other organs have been swine include 100 ppm of fumonisin B 1 and fumonisin B 2
reported to be affected. Pigs that ingest fumonisin at con- in naturally-contaminated corn (Motelin et al., 1994),
centrations high enough to cause pulmonary edema usu- 16 mg fumonisin B 1 /kg/day as fumonisin-containing cul-
ally die after about 4 days in field cases (Osweiler, 1992) ture material (Colvin et al., 1993), and 20 mg fumonisin
and after 3 6 days of fumonisin exposure experimentally B 1 /kg/day as culture material (Gumprecht et al., 1998).
(Gumprecht et al., 1998; Haschek et al., 1992; Motelin Fumonisin-induced pulmonary edema has also been
et al., 1994). Pigs that survive chronic exposure to high reported with naturally-contaminated corn (330 mg of
doses of fumonisin without developing pulmonary edema fumonisin B 1 per kg of feed) in Hungary (Fazekas et al.,
typically demonstrate hepatic disease with anorexia, 1998), Brazil (Sydenham et al., 1992), and Thailand
weight loss, and generalized icterus (Colvin et al., 1993; (Patchimasiri et al., 1998).
Osweiler et al., 1992). Hepatic toxicity occurs at doses Another study has suggested that even lower concen-
significantly lower than those necessary to cause pulmo- trations of fumonisins may be able to induce pulmonary
nary edema (Colvin et al., 1993; Motelin et al., 1994). edema in swine (Zomborszky et al., 2000). Fumonisin B 1
was fed added to the feed of weaned pigs at doses of 0,
10, 20, and 40 ppm for 4 weeks as fumonisin-containing
Fumonisins in Swine-Pulmonary Effects
culture material (five pigs per group). Computed tomogra-
Pulmonary edema (Fig. 71.4) has been reported in pigs phy (CT) of the lungs and magnetic resonance imaging of
fed naturally contaminated fumonisins-containing food, the brains were performed prior to the study and at 2 and
fumonisin-containing culture material or following IV 4 weeks of fumonisin feeding. Histopathology was also
administration of fumonisin (Harrison et al., 1990; done at the time of necropsy (4 weeks). The results of this
Haschek et al., 1992; Motelin et al., 1994; Osweiler et al., study showed that all five pigs fed fumonisin B 1 at
1992). Reported concentrations of fumonisin required to 40 ppm developed “severe” pulmonary edema as assessed
produce pulmonary edema have been variable, presum- by CT and histopathology. Two of the five pigs fed fumo-
ably due to variability in susceptibility among exposed nisin B 1 at 20 ppm had “severe” pulmonary edema while
animals (Table 71.1). However, other constituents in the two other pigs in the group had “mild” edema. In the
diet and analytical detection related to the ability to 10 ppm group, three of the five pigs were reported to
have “mild” pulmonary edema. Magnetic resonance stud-
ies of the brain were not able to identify any significant
changes during the course of the study in any group.
Clinical signs associated with the development of pul-
monary edema consistently begin 3 6 days after initia-
tion of exposure to a high concentration of fumonisins.
These include dyspnea and open mouthed breathing,
increased respiratory rate, cyanosis of skin and mucous
membranes, inactivity and sudden death (Osweiler et al.,
1992). Pigs usually die within a few hours after the onset
of definitive respiratory distress. Histologically, pulmo-
nary edema is present by day three of fumonisin exposure
(Gumprecht et al., 1998) and is characterized by intersti-
tial edema around airways and vessels, in interlobular and
subpleural connective tissues, and in alveolar interstitium
(Gumprecht et al., 1998; Harrison et al., 1990; Haschek
FIGURE 71.4 Lung from a pig fed fumonisin-containing culture mate- et al., 1992; Osweiler et al., 1992). Lymphatics are dilated
rial at a dose of 20 mg fumonisin B 1 per kg of body weight for 4 days.
Pulmonary edema is characterized by severe widening of the interlobular and alveolar edema is often present. Fluid is also present
septa. within the thoracic cavity.