Antibodies to Pseudogymnoascus destructans are not sufficient for protection against white‐nose syndrome. Issue 11 (11th May 2015)

• Record Type: Journal Article
• Authors: Johnson, Joseph S.; Reeder, DeeAnn M.; Lilley, Thomas M.; Czirják, Gábor Á.; Voigt, Christian C.; McMichael, James W.; Meierhofer, Melissa B.; Seery, Christopher W.; Lumadue, Shayne S.; Altmann, Alexander J.; Toro, Michael O.; Field, Kenneth A.
• Is Part Of: Ecology and evolution. Volume 5:Issue 11(2015:Jun.)
• Page Start: 2203
• Page End: 2214
• Publication Date: 2015-05-11
• Subjects: Ecology -- Periodicals; Evolution -- Periodicals; 577.05
• DOI: 10.1002/ece3.1502
• Languages: English
• ISSNs: 2045-7758

Abstract

<abstract abstract-type="main" id="ece31502-abs-0001"> <title>Abstract</title> <p>White‐nose syndrome (WNS) is a fungal disease caused by <italic>Pseudogymnoascus destructans</italic> (<italic>Pd</italic>) that affects bats during hibernation. Although millions of bats have died from WNS in North America, mass mortality has not been observed among European bats infected by the fungus, leading to the suggestion that bats in Europe are immune. We tested the hypothesis that an antibody‐mediated immune response can provide protection against WNS by quantifying antibodies reactive to <italic>Pd</italic> in blood samples from seven species of free‐ranging bats in North America and two free‐ranging species in Europe. We also quantified antibodies in blood samples from little brown myotis (<italic>Myotis lucifugus</italic>) that were part of a captive colony that we injected with live <italic>Pd</italic> spores mixed with adjuvant, as well as individuals surviving a captive <italic>Pd</italic> infection trial. Seroprevalence of antibodies against <italic>Pd</italic>, as well as antibody titers, was greater among little brown myotis than among four other species of cave‐hibernating bats in North America, including species with markedly lower WNS mortality rates. Among little brown myotis, the greatest titers occurred in populations occupying regions with longer histories of WNS, where bats lacked secondary symptoms of WNS. We detected antibodies cross‐reactive with <italic>Pd</italic> among little brown myotis naïve to the fungus. We observed high titers among captive little brown myotis injected with <italic>Pd</italic>. We did not detect antibodies against <italic>Pd</italic> in <italic>Pd</italic>‐infected European bats during winter, and titers during the active season were lower than among little brown myotis. These results show that antibody‐mediated immunity cannot explain survival of European bats infected with <italic>Pd</italic> and that little brown myotis respond differently to <italic>Pd</italic> than species with higher WNS survival rates. Although it appears that some species of bats in North America may be developing resistance to WNS, an antibody‐mediated immune response does not provide an explanation for these remnant populations.</p> </abstract>