Ulcerative dermatitis in C57BL/6 mice lacking stearoyl CoA desaturase 1.

Ulcerative dermatitis (UD) is a common cause of morbidity and euthanasia in mice with a C57BL/6 (B6) background. The purposes of the current study were to determine whether UD lesions could be reliably produced in B6 mice lacking stearoyl-CoA desaturase 1 (SCD1(-/-) mice), to ascertain whether the UD lesions in SCD1(-/-) mice were similar to those found in other B6 mice, and to characterize the cell invasion phenotype of Staphlococcus xylosus cultured from the lesions. S. xylosus isolates from the environment and human skin were used as controls. SCD1(-/-) (n = 8 per group) and nontransgenic B6 control mice (n = 22 mice pooled from 3 groups that received different concentrations of conjugated linoleic acid) were fed standard rodent chow or a semipurified diet (NIH AIN76A) for 4 wk. Samples from other B6 mice with UD (field cases; n = 7) also were submitted for histology and culture. All of the SCD1(-/-) mice developed UD lesions by 4 wk on NIH AIN76A. None of SCD1(-/-) fed standard rodent chow and none of the wildtype B6 mice fed NIH AIN76A developed UD. Supplementation with conjugated linoleic acid did not affect ulcerogenesis. UD lesions in SCD1(-/-) mice and field cases were grossly and histologically similar. S. xylosus was isolated from SCD1(-/-) mice with UD (71%) and field cases of UD (43%). These isolates were the most cell-invasive, followed by the environmental isolate, and finally the human skin isolate. Our results provide a basis for further pathologic and clinical study of UD.

Ulcerative disease outbreak in crayfish Orconectes propinquus linked to Saprolegnia australis in big Muskellunge Lake, Wisconsin.

Crayfish populations in the area of the North Temperate Lakes Long Term Ecological Research (LTER) project, Wisconsin, USA, have been monitored for >25 yr. In 2005, native crayfish Orconectes propinquus from Big Muskellunge Lake were found with ulcerated lesions in the cuticle. In 2006, lesions occurred in 9.5% of sampled crayfish from the lake (n=3146). Ulcers generally occurred on the appendages of affected individuals but varied in location and severity. The prevalence of ulcers varied widely among sites, sample depths, and sampling dates, ranging from < 2% to >20%. The prevalence of ulcers in crayfish increased from a minimum in early June to a maximum in late July and August. In aquarium trials, healthy crayfish representing either O. propinquus or O. rusticus co-housed with ulcerated crayfish did not develop ulcers within 4 wk of exposure. Gross and histopathologic analyses of ulcerated crayfish revealed the presence of filamentous hyphae in the lesions while hemocytic infiltrates, melanotic reactions and silver-stained sections indicated that the ulcers had an oomycete etiology. Excised samples of ulcerated crayfish cuticle grown in culture developed an oomycete that was identified as Saprolegnia australis by PCR amplification and sequence analysis of 2 different DNA fragments. This is the first report of the occurrence of ulcers in wild crayfish associated with S. australis infection in the U.S.A. The advent of the outbreak and its underlying ecological causes are still under investigation.

Clostridial enteropathy in lactating outbred swiss-derived (ICR) mice.

Reports of severe enteric disease of unknown etiology affecting lactating mice have appeared in the literature. Clostridial disease similar to that seen in cattle and sheep on high-carbohydrate rations and caused by Clostridium perfringens has been suspected in these mouse outbreaks but has not been isolated from affected mice. The present report describes a severe, necrotizing enterocolitis associated with overgrowth of C. perfringens type A in lactating Swiss-derived (ND4) mice. Mice nursing large litters of pups in the second week of life were the most severely affected. The organism isolated from dead or moribund mice was positive by polymerase chain reaction assay for the gene for the C. perfringens a toxin, but actual toxin production was not determined. The disease in this mouse colony was ameliorated by increasing the fat and calorie content of the diet of lactating dams, which each received 1 g peanut butter every 48 h.

Inguinal hernias, endometriosis, and other adverse outcomes in rhesus monkeys following lead exposure.

The Harlow Center for Biological Psychology (HCBP) has a cohort of rhesus monkeys that were exposed to low concentrations of lead acetate in utero or as infants. The lead-exposed animals have been followed for 19 years and have developed four cases of inguinal hernia (males), three cases of endometriosis (females), and one case of immunoblastic lymphoma (male). Retrospective analysis of the data from the original lead-exposed cohort indicates that there is a significant association between lead exposure and the development of inguinal hernia (P=.04). Endometriosis was not significantly associated with lead exposure (P=.36). A case control study also was done to determine the significance of neonatal lead exposure as a risk factor for the development of inguinal hernia and endometriosis. The risk of developing inguinal hernia was significantly increased in lead-exposed animals (OR=20.0, P=.009). The association between endometriosis and lead exposure was also strong (OR=10.13, P<.001). No unmatched variables were associated with inguinal hernia, including body weight, history of diarrhea, constipation, or intussusception. No unmatched variables were highly associated with endometriosis, including body weight, age at first parity, and history of stillbirths. However, parity and the number of stillbirths were associated with lead exposure (P=.011 and P=.041, respectively). There was an association between endometriosis and a history of hysterotomy (OR=2.09) but it was not statistically significant (P=.38). No other cases of lymphoma in unexposed animals were identified using HCBP animal health records. These data indicate that early lead-exposed rhesus monkeys may develop illnesses later in life, especially inguinal hernia and endometriosis, more frequently than unexposed monkeys. Studies of human populations with early lead exposure are warranted to determine their incidence of inguinal hernia, endometriosis, and hematologic neoplasia.