Notoedric
mange was responsible for a population decline of bobcats ( Lynx rufus ) in 2 Southern California counties from 2002-2006 and is now reported to affect bobcats in Northern and Southern California. With this study we document clinical laboratory and necropsy findings for bobcats with
mange. Bobcats in this study included free-ranging bobcats with
mange (n = 34), a control group of free-ranging bobcats without
mange (n = 11), and a captive control group of bobcats without
mange (n = 19). We used 2 control groups to evaluate potential anomalies due to capture stress or diet. Free-ranging healthy and
mange-infected bobcats were trapped or salvaged. Animals were tested by serum biochemistry, complete blood count, urine
protein and
creatinine,
body weight, necropsy, and assessment for
anticoagulant rodenticide residues in liver tissue. Bobcats with severe
mange were emaciated, dehydrated, and anemic with low serum
creatinine,
hyperphosphatemia,
hypoglycemia,
hypernatremia, and hyperchloremia, and sometimes septicemic when compared to control groups. Liver
enzymes and leukocyte counts were elevated in free-ranging, recently captured bobcats whether or not they were infested with
mange, suggesting capture stress. Bobcats with
mange had lower levels of serum
cholesterol,
albumin,
globulin, and total
protein due to
protein loss likely secondary to severe dermatopathy.
Renal insufficiency was unlikely in most cases, as urine
protein:
creatinine ratios were within normal limits. A primary gastrointestinal loss of
protein or blood was possible in a few cases, as evidenced by elevated blood
urea nitrogen,
anemia, intestinal parasitism,
colitis, gastric
hemorrhage, and
melena. The prevalence of exposure to
anticoagulant rodenticides was 100% (n = 15) in bobcats with
mange. These findings paint a picture of debilitating, multisystemic disease with infectious and toxic contributing factors that can progress to death in individuals and potential decline in populations.