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.