Janet Foley | Search USGS

USGS2013

Serum chemistry, hematologic, and post-mortem findings in free-ranging bobcats ( Lynx rufus ) with notoedric mange

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.

Journal of Parasitology↗

USGS2011

Investigating and managing the rapid emergence of white-nose syndrome, a novel, fatal, infectious disease of hibernating bats

White-nose syndrome (WNS) is a fatal disease of bats that hibernate. The etiologic agent of WNS is the fungus Geomyces destructans , which infects the skin and wing membranes. Over 1 million bats in six species in eastern North America have died from WNS since 2006, and as a result several species of bats may become endangered or extinct. Information is lacking on the pathogenesis of G. destructans and WNS, WNS transmission and maintenance, individual and site factors that contribute to the probability of an outbreak of WNS, and spatial dynamics of WNS spread in North America. We considered how descriptive and analytical epidemiology could be used to fill these information gaps, including a four-step (modified) outbreak investigation, application of a set of criteria (Hill's) for assessing causation, compartment models of disease dynamics, and spatial modeling. We cataloged and critiqued adaptive-management options that have been either previously proposed for WNS or were helpful in addressing other emerging diseases of wild animals. These include an ongoing program of prospective surveillance of bats and hibernacula for WNS, treatment of individual bats, increasing population resistance to WNS (through vaccines, immunomodulators, or other methods), improving probability of survival from starvation and dehydration associated with WNS, modifying hibernacula environments to eliminate G. destructans , culling individuals or populations, controlling anthropogenic spread of WNS, conserving genetic diversity of bats, and educating the public about bats and bat conservation issues associated with WNS.

Conservation Biology↗