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Pasteurella multocida is a Gram-negative bacterium recovered from a wide variety of wild and domestic animals and has mostly been associated with infection following animal bites. We present the first reported case of a patient who developed a postoperative sternal wound infection due to P. multocida complicated by bloodstream infection. The outcome was favorable following surgical debridement and antimicrobial therapy. We also review the literature regarding P. multocida postoperative wound infections.

Feed amended with autoclaved culture material (CM) of Fusarium proliferatum containing fumonisin B1 (FB1) (61-546 ppm), fumonisin B2 (FB2) (14-98 ppm) and moniliformin (66-367 ppm) was given to 228 male chicks in three separate feeding trials. In a fourth feeding trial, purified FB1 (125 and 274 ppm) and moniliformin (27 and 154 ppm) were given separately and in combination (137 and 77 ppm, respectively). Chicks that died during the trial periods, survivors and controls were subjected to postmortem examination. Specimens (liver, kidney, pancreas, lung, brain, intestine, testis, bursa of Fabricius, heart and skeletal muscle) were examined grossly and preserved for subsequent histopathologic and ultrastructural examination. Prominent gross lesions in affected birds fed diets amended with CM or purified FB1 and moniliformin included ascites, hydropericardium, hepatopathy, nephropathy, cardiomyopathy, pneumonitis, gizzard ulceration, and enlarged bursa of Fabricius filled with caseous material. The various concentrations of FB1 and moniliformin in the amended rations produced well-defined dose-response lesions in all groups in all four trials. Histopathologic changes included hemorrhage, leucocytic infiltration, fatty change or infiltration, individual cell necrosis and fibrosis in liver, kidneys, lungs, heart, intestines, gizzard, bursa of Fabricius and pancreas. Edema and hemorrhage were prominent in brains of treated birds. Ultrastructural changes included cytoplasmic and nuclear enlargement of cells in affected liver, lungs, kidneys, heart and pancreas. There were thickened membranes of the smooth endoplasmic reticulum, dilation of the rough endoplasmic reticulum with loss of ribosomes and vacuolated or deformed mitochondria.

We investigated the validity of dogs and cats as sentinels of environmental lead exposure to humans. This paper reports findings from a study conducted in Granite City, IL, during the summer of 1991. At this site, a former secondary lead smelter had been in activity for more than 80 years. The smelter was shut down in 1982. The surrounding area was found to be contaminated with lead, with soil lead concentrations above 5000 ppm in some places. The Illinois Department of Public Health conducted a survey in the community to determine the effects of lead on the local population. We sampled dogs and cats owned by these people. Our results suggest that living near a closed lead smelter, with heavy soil contamination, was not associated with high blood lead concentrations in pets, or their owners. There was a significant relationship between BLC (blood lead concentrations), in indoor pets and younger children, which was consistent with our hypothesis that pets could be used to monitor childhood lead exposure. We also found that, when there was one pet with a high BLC in a house, the likelihood of finding one person with a BLC above 10 micrograms/dl was significantly increased.

Two hundred twenty-eight male broiler chicks (Columbia x New Hampshire) were given feed amended with autoclaved culture material of Fusarium proliferatum containing fumonisin B1 (FB1) at 61, 193, and 546 ppm, fumonisin B2 (FB2) at 14, 38, and 98 ppm, and moniliformin at 66, 193, and 367 ppm in 3 separate feeding trials (amounts of toxin in each trial, respectively). Birds were started on amended rations at days 1, 7, and 21 and continuing for 14 days. Of serum chemistry parameters, only glucose was significantly decreased. Significant increases were noted in serum cholesterol, sodium, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and gamma-glutamyl transferase. Of the hematologic parameters, significant decreases were noted in red blood cell counts, hemoglobin, packed cell volume, and white blood cell counts. Immunologic changes included impaired anti-Newcastle disease antibody hemagglutination inhibition titers associated with relative decreases in total serum globulins and increases in albumin/globulin ratios. The changes were noted in all treatment groups when compared to controls.

This paper reports the results of a study conducted in Granite City, Illinois during the months of August through October 1991. The study involved a subpopulation of 77 households having 106 dogs and cats which was a corollary to a major study conducted in humans by the Illinois Department of Public Health to evaluate lead exposure. A secondary lead smelter had been in operation in this town for almost 80 years and was shut down in 1982. Important soil contamination with lead was reported and this paper presents data regarding levels of soil and dust lead and associated blood lead concentrations in animals and their owners in a total of 77 households. Overall, blood lead concentrations (BLC) were low (0-13 micrograms/dl in the animal owners; 0-28 micrograms/dl in pets). There was no significant relationship between soil or dust lead and BLC in humans; however, the relationship was significant in animals. Odds ratios were computed to determine whether 500 or 1000 ppm lead in environmental samples was associated with increased risk of having a high BLC. We could not find any increased risk in humans, while the risk did increase in animals. It is concluded that animals are more at risk than their owners of having a high BLC when exposed to the same contaminated environment and can be used to monitor the bioavailability of lead.

A former secondary lead smelter was in operation in Granite City, Ill, until the early 1980s. As a result, the surrounding area is heavily contaminated with lead. Soil concentrations as high as 5,000 ppm have been measured in prior studies. Because of growing concerns about health defects associated with low levels of lead exposure in human beings, a major study has been conducted on people living in the area. The study reported here was a corollary to the human exposure study. Lead concentration was determined in 84 dogs and 26 cats in the town and ranged between < 5 and 28 micrograms/dl. None of the dogs had clinical signs of lead poisoning. The CBC and serum biochemical values did not indicate many significant differences between dogs with a high (> or = 10 micrograms/dl) or low blood lead concentration (BLC). Hemoglobin concentrations were lower, and WBC counts were higher in dogs and cats with higher BLC, but they were still within reference ranges. Free erythrocyte protoporphyrin concentration was determined. Normal values appeared to be similar for dogs and cats. Only animals with BLC > or = 20 micrograms/dl were found to have somewhat increased concentration of free erythrocyte protoporphyrin. delta-Aminolevulinic acid dehydratase activity was measured and found to be negatively correlated with BLC. The relation was strong, even at low BLC (5 to 10 micrograms/dl) in both species. Age or sex difference was not observed. Therefore, biological changes associated with low BLC were limited to BLC in the 10- to 30-micrograms/dl range.

Two hundred twenty-eight male chicks (Columbia x New Hampshire) were given feed amended with autoclaved culture material (CM) of Fusarium proliferatum Containing fumonisin B1 (FB1), fumonisin B2 (FB2) and moniliformin in 3 separate feeding trials. Purified FB1 and moniliformin were given separately and in combination in a fourth feeding trial. Birds were given amended rations at day 1 (Trial 1 and 4), day 7 (Trial 2), and day 21 (Trial 3) and their respective ration was given for 28 days (Trial 1), 21 days (Trial 2), 7 days (Trial 3), and 14 days (Trial 4). FB1 concentrations were 546, 193, and 61 ppm; FB2 were 98, 38 and 14 ppm; and moniliformin were 367, 193, and 66 ppm in the first 3 feeding trial regimens. Chicks in Trial 4 were given dietary concentrations of purified FB1 at 274 and 125 ppm, and moniliformin at 154 and 27 ppm. FB1 and moniliformin, both alone and in combination, produced dose-responsive clinical signs, reduced weight gains and mortality in chicks. Age of birds given amended feeds had little difference in the clinical response; however, those given the rations from days 7 or 21 were slightly less susceptible than those given rations beginning at 1 day of age. Additive effects were noted when the toxins were given in combination. When toxins were given separately, adverse effects took longer to occur. A system to monitor pattern and rate of defecation (RD) was developed for assessing the chicks' approach to feed, water and heat source as illness progressed. Our results indicate that chicks fed corn heavily infected with F. proliferatum under field conditions could suffer acute death similar to that described for 'spiking mortality syndrome' during the first 3 weeks of age.

One hundred eight fertile eggs (Columbia x New Hampshire) were assigned to 10 groups of 10 eggs each (2 control groups had 14 eggs each). Five groups of eggs were inoculated on day 1 of incubation, while the other 5 groups were inoculated on day 10. The inoculum of the 4 treatment groups on both day 1 and 10 consisted of 1,10, or 100 microM purified fumonisin B1 (FB1) or a culture material extract (CME) of Fusarium proliferatum, having known amounts of FB1, FB2 and moniliformin (FB1 20 microM; FB2 4 microM and moniliformin 7 microM). Inoculum consisted of the respective toxin(s) dissolved in 100 microliters double distilled, autoclaved water (diluent). Control eggs were inoculated with diluent only. Mortality was both dose- and time-responsive in all treatments. Eggs inoculated on day 1 with 1 microM FB1 had 50% mortality; 10 microM FB1 had 70% mortality; 100 microM FB1 had 100% mortality; and CME had 100% mortality. Eggs inoculated on day 10 with 1,10 or 100 microM FB1 or CME had 30, 60, 90 and 80% mortality, respectively. Normal chicks were hatched from all control eggs. The median death times (MDT50) were inversely dose-responsive in all treatments, ranging from 3.0 to 7.4 days in embryos exposed on day 1 and from 3.2 to 9.0 days in those exposed on day 10. Early embryonic changes in exposed embryos included hydrocephalus, enlarged beaks and elongated necks. Pathologic changes were noted in liver, kidneys, heart, lungs, musculoskeletal system, intestines, testes and brain toxin-exposed embryos.

The effects of administration of a commercially available extract of Gingko biloba (EGB) on bromethalin-induced brain lipid peroxidation and cerebral edema in adult male Sprague-Dawley rats was determined. Gingko biloba extract was given (100 mg/kg) by gavage immediately after bromethalin (1.0 mg/kg) administration. Rats were euthanatized at 24 hours after dosing. Brain lipid peroxidation was determined by measurement of brain malonaldehyde-thiobarbituric acid chromophore (MDA-TBA) concentration, brain sodium concentration, and brain water content. Treatment of bromethalin-dosed rats (10/group) with EGB was associated with a statistically significant (P less than 0.05) decrease in clinical sign severity, compared with bromethalin-dosed saline solution-treated rats. All rats given bromethalin and saline solution developed clinical signs of toxicosis including CNS depression, hind limb weakness, ataxia, paralysis, and coma. Some rats given bromethalin and EGB developed clinical signs, however, none developed hind limb paralysis. The brain MDA-TBA concentration (2.4 +/- 0.5 delta MDA-TBA concentration/mg of protein), percentage of water in brain tissue (80.3 +/- 0.30%), and brain sodium concentration (6.68 +/- 0.21 mg/g of dry weight) were significantly increased in rats given bromethalin and saline solution, compared with control rats given saline solution (1.0 +/- 0.1 delta MDA-TBA concentration/mg of protein; 78.1 +/- 0.33% water in brain tissue; 4.83 +/- 0.30 mg of brain Na+/g of dry weight) and rats given bromethalin and EGB (1.6 +/- 0.2 delta MDA-TBA concentration/mg of protein; 79.3 +/- 0.31% water in brain tissue; 5.37 +/- 0.34 mg of brain Na+/g of dry weight).(ABSTRACT TRUNCATED AT 250 WORDS)

Corn contaminated with deoxynivalenol was added to the diets of three dairy cows for 5 d and milk, urine, and 3 d following feeding of the diets. Dietary concentrations of deoxynivalenol averaged 66 mg/kg. Following exposure to deoxynivalenol, unconjugated deepoxydeoxynivalenol, a metabolite of deoxynivalenol, was present in milk at concentrations up to 26 ng/ml. Deoxynivalenol was not detected in the milk. Approximately 20% of the deoxynivalenol fed was recovered in the urine and feces in the unconjugated forms as deepoxydeoxynivalenol (96%) and deoxynivalenol (4%). After incubating urine with beta-glucuronidase, the concentration of unconjugated deepoxydeoxynivalenol increased by 7 to 15-fold whereas unconjugated deoxynivalenol increased 1.6 to 3-fold. Detectable concentrations of unconjugated deepoxydeoxynivalenol were found in urine and feces up to 72 h after the last oral exposure. Thus, urine and feces are the diagnostic specimens of choice for the determination of deoxynivalenol exposure in cows. Feeding deoxynivalenol-contaminated diets for 5 d did not alter feed intake or milk production nor were the milk concentrations of calcium, phosphorus, sodium, potassium, magnesium, or nitrogen altered.

Rat hepatic microsomal preparations were used to study the metabolism of deoxynivalenol (DON) and its metabolite 3 alpha,7 alpha,15-trihydroxytrichothec-9,12-dien-8-one (DOM-1). The N-demethylation of ethylmorphine was monitored to assess the viability of the mixed-function oxidase. DON was incubated with microsomes and an NADPH-generating system. Samples were removed from the incubation system and analysed for DON using an HPLC equipped with a UV detector. After incubation for 30 min, there was no evidence of disappearance of DON or of the presence of new metabolites; neither was microsomal NADPH oxidation altered by the addition of DON. Rat and pig hepatic microsomal preparations were used to assess DON glucuronidation, using p-nitrophenol disappearance to check the viability of the microsomal glucuronidating system. When DON was incubated with microsomes and 14C-labelled uridine 5'-diphosphoglucuronic acid, no radioactivity was detected in the TLC zone where the glucuronide was expected. Three rats and one pig were dosed orally with 2 mg DON/kg and samples of their urine and faeces were extracted and incubated with beta-glucuronidase or with buffer only. No differences in DON or DOM-1 concentrations were detected between samples incubated with or without beta-glucuronidase. These results suggest that DON was neither bioactivated to a more toxic product nor oxidized to a less toxic compound by the rat hepatic mixed-function oxidase system. Likewise, DOM-1 was not reactivated or metabolized by this system. Neither DON nor DOM-1 glucuronides were formed either in in vitro liver systems or in vivo.

During the 1981 corn harvest season in Illinois and surrounding states, cold wet weather enhanced the growth of Fusarium graminearum, with resulting contamination by vomitoxin and, to a lesser extent, zearalenone. Of 342 feed samples analyzed, 274 contained vomitoxin at a concentration ranging from 0.1 to 41.6 ppm (mean, 3.1 ppm) and 40 samples contained zearalenone at a concentration ranging from 0.1 to 8 ppm (mean, 0.66 ppm). Animal health problems and reduced growth performance were observed mainly in swine fed vomitoxin-contaminated rations. The predominant clinical complaints, in decreasing frequency were: reproductive problems (50%), feed refusal (43%), reduced weight gain (25%), diarrhea (17%), death (14%), and emesis (11%).