NURSING DISEASE IN MINK - CLINICAL AND POSTMORTEM FINDINGS

Citation
Rr. Schneider et Db. Hunter, NURSING DISEASE IN MINK - CLINICAL AND POSTMORTEM FINDINGS, Veterinary pathology, 30(6), 1993, pp. 512-521
Citations number
33
Categorie Soggetti
Veterinary Sciences",Pathology
Journal title
ISSN journal
03009858
Volume
30
Issue
6
Year of publication
1993
Pages
512 - 521
Database
ISI
SICI code
0300-9858(1993)30:6<512:NDIM-C>2.0.ZU;2-5
Abstract
One hundred fifty lactating mink on one ranch in southern Ontario were monitored over the lactation period in 1989 for evidence of clinical disease, and serial blood samples were collected for biochemical analy sis. Antemortem blood samples were collected and necropsies performed on the 17 females that developed nursing disease and on 17 controls ma tched to the same stage of lactation and on ten nonlactating controls. Twenty-two additional nursing disease cases were selected from seven ranches in the following year and processed similarly. The clinical si gns typically observed in affected females were sudden onset lethargy and anorexia followed by dehydration, ataxia, and a reluctance to move . The major clinical-pathologic findings were a marked increase in ser um osmolality and total protein, urea nitrogen, creatinine, phosphorus , glucose, and potassium concentrations and a decrease in sodium and c hloride concentration. In addition, the animals were acidotic, there w as a reduction in the urine specific gravity, and the hemogram was con sistent with a stress response. Emaciation and dehydration were the on ly pathologic changes consistently present in cases of nursing disease and not in controls. In almost all cases, bacteria were not cultured from the liver, spleen, and mammary gland, but Campylobacter jejuni wa s cultured from the intestinal contents of 15/17 affected mink and 2/5 controls. Aleutian disease virus antibody was not present in any of t he affected mink. Lipid vacuoles in hepatocytes and renal tubular epit helium, hypertrophy of cells in the adrenal cortex, and pulmonary cong estion and atelectasis were present in both diseased females and contr ols, as were various sporadic inflammatory lesions. Nursing disease ma y result from energy depletion due to lactation. All lactating females are affected by this process; clinical disease reflects the terminal physiologic decompensation of the most susceptible individuals.