Ergot alkaloids are-synthesized by fungi of the Claviceps family that infect rye as well as other cereals and grains. Since a portion of the ranch mink diet is cereal, mink are at a risk of being exposed to ergot alkaloids. This study was performed to determine the reproductive toxicity of ergot alkaloids derived from ergot-contaminated oats in mink. Four groups of 12 female mink each were fed diets containing 0, 3, 6 or 12 ppm ergot alkaloids from 2w prior to the breeding season until the kits were approximately 33-d old (133 d). Females were mated with untreated males. Ergo talkaloids caused a transient decrease in feed consumption, but body weights were unaffected. The gestation period of the mink in the 6 ppm group was longer compared to controls. The number of mink whelping varied significantly with 9 mink whelping each in the control and 3 ppm groups compared to 4 mink in the 6 ppm group and 1 in the 12 ppm group. Ergot alkaloids had a significant effect on kit survivabilitywith no kits surviving in the 12 ppm group. Serum prolactin was significantly depressed in the 3 ergot alkaloid groups compared to the control group. This study indicated that ingestion of ergot alkaloids at 3 ppm or higher resulted in reproductive toxicity in mink.

In this report we describe the lesions produced by the protozoal organism, Toxoplasma gondii, in the eyes and brain of the common yellow canary (Serinus canaria). Nine of 15 birds in a flock were affected with blindness, which developed over a 3-mo span, and two birds developed torticollis. Microscopic alterations within the eye consisted of a nonsuppurative chorioretinitis with large numbers of macrophages that contained the tachyzoite form of T. gondii in the subretinal space, and aggregates of tachyzoites were found in the nerve fiber layer of the retina with and without necrosis. Tissue cysts with bradyzoites were scattered throughout the meninges and neuropil of the cerebrum and cerebellum. Both forms were confirmed by transmission electron microscopy in the eye and brain. Frozen brain samples reacted with T. gondii-specific cat sera in indirect fluorescent antibody tests. The source of infection was hypothesized to be from a stray cat the owner kept that had access to some of the bird feed. Treatment (trimethoprim 0.08 g/ml H2O and sulfadiazine 0.04 g/ml in water for 2 wk) was instituted by the referring veterinarian on the remaining birds. A second treatment regime was given for 3 wk. The owner of the canaries did not return for further treatment.

Mature female natural dark mink (Mustela vison) were fed 0.0006 (control), 0.016, 0.053, 0.180, or 1.40 ppb 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for 131-132 d to ascertain the chronic toxic effects of TCDD in mink, including reproduction. Consumption of the 1.4 ppb TCDD diet resulted in lethargy, bloody stools, and 16.7% mortality. Final mink body weights were inversely proportional to the dietary TCDD concentrations. Due to subnormal mink breeding, definitive effects of TCDD on mink reproductive performance were not ascertained; however, there were significant dose-dependent decreases in kit (young mink) birth weight and survival from birth to 3 w of age in the groups that had reproduction. There were also significant differences in adult minkwhite blood cell counts, plasma total solids, serum iron, phosphorus, albumin, total protein, total CO2, cholesterol, osmolality, and anion gap concentrations, and alanine aminotransaminase activity between the various dietary groups. During the latter stages alopecia and thickened, deformed, and elongated toenails were observed in the adult mink fed 1.4 ppb TCDD. At termination the mink fed 1.4 ppb TCDD had ascites, gastric ulcers, intestinal hemorrhages, depletion of adipose tissue, and mottled and/or discolored livers, spleens, and kidneys. Focal lymphocytic meningitis in region of the olfactory bulb was present in 42% of the mink fed 1.4 ppb TCDD. These results confirmed the high sensitivity of mink to TCDD and revealed a toenail abnormality not previously reported for mink fed TCDD.

Previous research has shown that ingestion of 3,3',4,4',5-pentachlorobiphenyl (PCB 126) by juvenile mink (kits) caused a lesion in the mandible and maxilla that consisted of proliferation of sQuamous epithelium in the periodontal ligament, osteolysis of adjacent alveolar bone, and loose and displaced teeth. Similar, but less severe changes, developed in adult mink fed 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The present study was conducted to compare similarities and differences of the lesion within the jaws of mink fed these 2 polyhalogenated hydrocarbons. Diets containing 24 ppb PCB 126 or 2.4 ppb TCDD were fed to 6-w-old kits for 36 d. Similar diets were fed to 12-w-old kits for 35 d. Some of these mink were then fed untreated feed for an additional 50 d. All mink treated with PCB 126 or TCDD had reductions in body weight gains which were more severe in the 6-w-old kits than the 12-week-old kits. By 28 days of exposure, many of the 6- and 12-week-old mink treated with PCB 126 or TCDD had loose and displaced incisor teeth. Canine teeth were grossly more prominant. Radiographs showed maxillary and mandibular osteolysis with lysis of the lamina dura in treated mink. Withdrawal of the toxicants from the diets of the 12-w-old mink failed to alleviate the lesions, which continued to be progressively more severe.

This report characterizes squamous cell proliferation in young farm mink (Mustela vison) fed a diet supplemented with 0.024 ppm 3,3',4,4',5-pentachlorobiphenyl (polychlorinated biphenyl [PCB] congener 126). One to 2 months of dietary exposure to PCB 126 resulted in gross lesions of the upper and lower jaws consisting of mandibular and maxillary nodular proliferation of the gingiva and loose teeth. The maxilla and mandible of the PCB-treated mink were markedly porous because of loss of alveolar bone. Histologically, this osteoporosis was caused by proliferation of squamous cells that formed infiltrating cords. This report clearly documents the fact that the environmental contaminant PCB 126 can cause osteoinvasive squamous proliferation in young mink, although the dose used in the present study was 7 and 36 times higher than what is typically encountered in contaminated bird eggs and fish, respectively.

The maxilla and mandible from 2 adult female mink fed 5.0 ppb 2,3.7,8-tetrachlorodibenzo-p-dioxin (TCDD) for 6 mo were grossly unremarkable, but histologically had nests of squamous epithelium within the periodontal ligament. There was osteolysis of the adjacent alveolar bone.

Environmental contaminants with estrogenic activity have recently received attention because of their potential effects on the reproductive efficiency of humans and wildlife. This study was conducted with the endogenous estrogen, 17 β-estradiol (E2), to establish the histologic response of the fathead minnow (Pimephales promelas) as a model organism. Sexually mature fathead minnows were exposed for 14 days to waterborne concentrations of 1000, 100, 10, 2, 1, 0.5, 0.25, 0.125, 0.1 or 0.0625 nM E2. Exposure to E2 caused a reduction in size of the prominent male secondary sex characteristics, the fatpads and nuptial breeding tubercles. Histological lesions observed in the testes included proliferation of Sertoli cells and degenerative changes. Electron microscopy of seminiferous tubules and their Sertoli cells revealed large phagolysosomes filled with degenerating spermatozoa and other cellular debris. Females had ovaries in which most of the follicles were in the primary stage of development. There were also more atretic follicles and fewer secondary and Graafian follicles than in unexposed females. These findings demonstrate components of sexually mature fish which may be altered by compounds that mimic E2. To determine if lesions observed in males were permanent, 50 sexually mature males and females were exposed to a single concentration of 10 nM E2 for 10 days. Samples were collected from males on the final day of E2 exposure and over a period of 16 weeks after the exposure was stopped. No E2-induced lesions were observed beyond 16 weeks post E2 exposure. Results of these studies suggest that histological lesions could occur at ecologically-relevant exposures to ‘estrogenic’ compounds. However, certain lesions caused by exposure of adult fathead minnows are not permanent.

Three Quarter Horses, a stillborn filly (horse No. 1), a female fetus aborted at approximately 6 months of gestation (horse No. 2), and a 1-month-old colt that had been weak at birth (horse No. 3), had myopathy characterized histologically by large spherical or ovoid inclusions in skeletal and cardiac myofibers. Smaller inclusions were also found in brain and spinal cord and in some cells of all other tissues examined. These inclusions were basophilic, red-purple after staining with periodic acid-Schiff (both before and after digestion with diastase), and moderately dark blue after staining with toluidine blue. The inclusions did not react when stained with Congo red. Staining with iodine ranged from pale blue to black. Their ultrastructural appearance varied from amorphous to somewhat filamentous. On the basis of staining characteristics and diastase resistance, we concluded that these inclusions contained amylopectin. A distinctly different kind of inclusion material was also present in skeletal muscle and tongue of horse Nos. 1 and 3. These inclusions were crystalline with a sharply defined ultrastructural periodicity. The crystals were eosinophilic and very dark blue when stained with toluidine blue but did not stain with iodine. Crystals sometimes occurred freely within the myofibers but more often were encased by deposits of amylopectin. This combination of histologic and ultrastructural features characterizes a previously unreported storage disease in fetal and neonatal Quarter Horses, with findings similar to those of glycogen storage disease type IV. We speculate that a severe inherited loss of glycogen brancher enzyme activity may be responsible for these findings. The relation of amylopectinosis to the death of the foals is unknown.

Feed that is typically used on commercial mink ranches is an ideal environment for bacterial growth because of the raw animal by-products used as ingredients. Recently, formaldehyde was approved for use as an antimicrobial agent in poultry feed. Experiments in our laboratory were carried out to investigate the effects of incorporating different concentrations of formalin into the feed of mink on the growth of gram-negative and gram-positive bacteria. Feed containing 0, 550 or 1100 ppm formalin was kept refrigerated for up to 7 d and the number of colony forming units of gram-negative and gram-positive bacteria derived from the feed was determined each day. Colony forming units in the formalin-treated feed were significantly fewer than colony forming units in untreated feed. In the second trial, feed containing the same concentrations of formalin was maintained at 30 C for 24 h and cultured bacterial colonies were counted at 0, 12 or 24 h of feed incubation. Both concentrations of formalin were effective in significantly reducing the number of colony forming units. A feed consumption trial determined if mink (Mustela vison) preferred formalin-treated feed to non-treated feed kept refrigerated for up to 7 d. Consumption of feed treated with 1100 ppm formalin was significantly lower than consumption of the non-treated feed on d 1, 2, 4 and 5, but body weight was not affected. A long-term feeding trial determined the effects of formalin on mink reproduction, early growth of offspring and quality of fur. Mink were fed formalin at concentrations of 0, 550 or 1100 ppm for approximately 140 d beginning 1 mo prior to mating until kits were weaned at 6 w of age. Mating success was not affected by consumption of formalin-treated diets, but kit survival at birth was adversely affected in mink consuming 1100 ppm formalin. Hemoglobin concentration, hematocrit, mean corpuscular volume, and mean corpuscular hemoglobin were significantly decreased in 6-w-old kits, but there were no significant differences in any of these parameters between the kits exposed to 0 and 550 ppm formalin. In a second phase, some kits and their dams were continued on their respective dietary treatments from weaning through pelting (approximately 220 and 320 d, respectively). At pelting, hematocrits and hemoglobin concentrations for the kits fed 1100 ppm formalin were significantly less compared to the control and 550 ppm formalin groups. There were no significant differences in body weights among female kits or adult female mink. The body weights of male kits in the 1100 ppm formalin group became significantly less than the body weights of male kits in the control and 550 ppm formalin groups as the trial progressed. The quality of fur was highest for mink in the control group and lowest for mink in the 1100 ppm formalin group. While dietary 1100 and 550 ppm formalin were effective in suppressing bacterial growth in the feed of mink, the deleterious effects of 1100 ppm formalin on kit survival, hematologic parameters, body weight, and quality of fur preclude formalin use at this concentration.

Fathead minnows were exposed to 4-nonylphenol (NP) or nonylphenol ethoxylate (NPEO) to determine the effects of these weak estrogen agonists on secondary sex characteristics and gonads of sexually mature males and females during 42-day continuous-flow exposures. Neither NP nor NPEO caused statistically significant effects on tubercles or fatpad size at the concentrations tested. Exposure to 1. 1 or 3.4 micrograms NP/L caused changes in the number and size of Sertoli cells and germ cell syncytia. Necrotic aggregates of various stages of germ cells in the spermatogenic sequence were observed in the testes of males exposed to NP. Electron microscopy of the testes of NP-exposed males revealed the presence of phagocytic cells in the lumina of seminiferous tubules. The cytoplasm of some Sertoli cells was distended with myelin figures and necrotic spermatozoa. No significant effects on the stages of follicular development were observed in females exposed to NP. There were no differences in the gonads or secondary sex characteristics of males or females exposed to 5.5 micrograms NPEO/L, the greatest concentration studied. The histologic responses observed are sensitive indicators of waterborne exposure to NP at environmentally relevant concentrations, but not as sensitive as induction of plasma vitellogenin. The secondary sex characteristics were not affected by concentrations of NP or NPEO as great as 3.4 or 5.5 micrograms/L, respectively. Histologic responses occurred at concentrations that were less than the final chronic value based on survival and approximately the same as those required to cause effects on egg production. The histologic effects caused by NP were similar to, but not exactly the same as those caused by exposure of fathead minnows to 17 beta-estradiol.

Rhodococcus equi infection was diagnosed in two goats from the same herd. At necropsy, numerous caseating granulomas were disseminated throughout the liver, lungs, abdominal lymph nodes, medulla of right humerus, and the right fifth rib of goat No. 1, and the liver of goat No. 2. Histopathologic examination confirmed the presence of multiple caseating granulomas in these organs. Numerous gram-positive and Giemsa-positive coccobacilli were identified within the cytoplasm of macrophages. Aerobic bacterial cultures of the liver and lung from both goats yielded a pure growth of R. equi. R. equi antigens were immunohistochemically identified in caseating granulomas from both goats. However, the 15- to 17-kd virulence antigens of R. equi were not detected, suggesting possible infection by an avirulent strain of this organism.

This study was conducted to determine the multigenerational effects of consumption of PCB-contaminated carp (Cyprinus carpio) from Saginaw Bay (Lake Huron) on mink (Mustela vison) reproduction and health and to examine selected biomarkers as potential indicators of polyhalogenated hydrocarbon toxicity in mink. The mink were fed diets formulated to provide 0 (control),, 0.25, 0.5, or 1.0 ppm polychlorinated biphenyls (PCBs) through substitution of Saginaw Bay carp for ocean fish in the diets. To determine whether the effects of PCB exposure were permanent, half of the parental (P-1) animals were switched from their respective treatment diets to the control diet after whelping the first of two F-1 generations. Effects of in utero and lactational exposure to PCBs on subsequent reproductive performance of the F-1 animals were examined by switching half of the first-year F-1 offspring (kits) to the control diet at weaning, while the other half was continued on their parental diet (continuous exposure). Continuous exposure to 0.25 ppm, or more, of PCBs delayed the onset of estrus (as determined by vulvar swelling and time of mating) and lessened the whelping rate, litters whelped by females continually exposed to 0.5 ppm, or more, of PCBs had greater mortality and lesser body weights than controls. Continuous exposure to 1.0 ppm PCBs had a variable effect on serum T-4 and T-3 concentrations. Compared to the controls, there were significant differences in kidney, liver, brain, spleen, heart, and thyroid gland weights of the mink continually exposed to 1.0 ppm PCBs. There was an increase in the incidence of periportal and diffuse vacuolar hepatocellular lipidosis in the P-1 mink with continuous exposure to increasing concentrations of PCBs. Plasma and liver PCB concentrations of the adult and kit mink were, in general, directly related to the dietary concentration of PCBs and the duration and time of exposure. Short-term parental exposure to PCBs had detrimental effects on survival of subsequent generations of mink conceived months after the parents were placed on "clean" feed. The lowest observed adverse effect level (LOAEL) for dietary PCBs in this study was 0.25 ppm.