Migrating bats have increased mortality near moving turbine blades at wind farms. The authors evaluated competing hypotheses of barotrauma and traumatic injury to determine the cause. They first examined the utility of lungs from salvaged bat carcasses for histopathologic diagnosis of barotrauma and studied laboratory mice as a model system. Postmortem time, environmental temperature, and freezing of carcasses all affected the development of vascular congestion, hemorrhage, and edema. These common tissue artifacts mimicked the diagnostic criteria of pulmonary barotrauma; therefore, lung tissues from salvaged bats should not be used for barotrauma diagnosis. The authors next compared wind farm (WF) bats to building collision (BC) bats collected near downtown Chicago buildings. WF bats had an increased incidence in fracture cases and specific bone fractures and had more external lacerations than BC bats. WF bats had additional features of traumatic injury, including diaphragmatic hernia, subcutaneous hemorrhage, and bone marrow emboli. In summary, 73% (190 of 262) of WF bats had lesions consistent with traumatic injury. The authors then examined for ruptured tympana, a sensitive marker of barotrauma in humans. BC bats had only 1 case (2%, 1 of 42), but this was attributed to concurrent cranial fractures, whereas WF bats had a 20% (16 of 81) incidence. When cases with concurrent traumatic injury were excluded, this yielded a small fraction (6%, 5 of 81) of WF bats with lesions possibly consistent with barotrauma etiology. Forensic pathology examination of the data strongly suggests that traumatic injury is the major cause of bat mortality at wind farms and, at best, barotrauma is a minor etiology.
Bat mortality is increased near moving, but not static, turbine blades at wind farms (WFs).2,9,14,21,23,25 The 2 leading hypotheses for the mortality include blunt force trauma from being struck by moving turbine blades and barotrauma. Barotrauma is a phenomenon in which abrupt air pressure changes cause tissue damage to air-containing structures (eg, lungs). It is suggested by some to cause a high proportion of bat deaths at WFs, with up to 90% of bats reported to have lung lesions consistent with barotrauma.4 Key diagnostic features of pulmonary barotrauma include microscopic detection of hemorrhage and edema in airspaces with vascular congestion and interstitial bullae.1,4,15,29 However, pulmonary barotrauma diagnosis has primarily been based on examination of lung tissues from salvaged bat carcasses. The time from death to carcass collection (and eventual tissue fixation) in these cases is not typically known, and in some cases only an estimated window of time (eg, died the previous night) is at best available.3,4 Prior to collection, the carcasses may be exposed to various environmental conditions (eg, temperature, sunlight) that can alter tissue decomposition kinetics and tissue morphology.35,42 Additionally, biologists frequently salvage bat carcasses from WFs for study and may freeze them for long-term storage, which could cause additional morphologic changes.
We designed a 2-part forensic investigation into the etiology of bat mortality at WFs. First, we hypothesized that postmortem decomposition and environmental conditions would influence the development of morphologic artifacts in the lung that could mimic and confound the diagnosis of pulmonary barotrauma. We examined a laboratory mouse model to longitudinally study the appearance of these morphologic parameters to determine the diagnostic utility of salvaged lung tissue for barotrauma diagnosis. Second, we designed a controlled experiment to evaluate bat carcasses for signs of traumatic injury and barotrauma. To this end, we examined salvaged bats collected from a central Illinois WF compared with a control group collected from downtown Chicago that had died following collision with a building.
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