Effects of Inactivated Mycobacterium bovis Vaccination on Molokai-Origin Wild Pigs Experimentally Infected with Virulent M. bovis

Authors

Pauline Nol, US Department of Agriculture , Animal and Plant Health Inspection Service, National Wildlife Research CenterFollow
Morgan Wehte, Dinosaur National Monument, Dinosaur, COFollow
Richard A. Bowen, Colorado State University - Fort CollinsFollow
Suelee Robbe-Austerman, USDA APHISFollow
Tyler Thacker, USDA/ARS/National Animal Disease CenterFollow
Kristina Lantz, USDA APHISFollow
Jack Rhyan, US Department of AgricultureFollow
Laurie A. Baeten, USDA APHISFollow
Ramón A. Juste, Servicio Regional de Investigación y Desarrollo Agroalimentario SERIDAFollow
Iker A. Sevilla, NEIKER-Instituto Vasco de Investigación y Desarrollo AgrarioFollow
Christian Gortazar, IREC Universidad de Castilla - La ManchaFollow
Joaquín Vicente, University Castilla la Mancha & CSICFollow

ORCID IDs

Iker A. Sevilla https://orcid.org/0000-0003-3968-3390

Date of this Version

3-2020

Citation

Pathogens 2020, 9, 199;

doi:10.3390/pathogens9030199

Comments

© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license

Abstract

The wild pig population on Molokai, Hawaii, USA is a possible reservoir for bovine tuberculosis, caused by Mycobacterium bovis, and has been implicated in decades past as the source of disease for the island’s domestic cattle. Heat-inactivated vaccines have been effective for reducing disease prevalence in wild boar in Spain and could prove useful for managing M. bovis in Molokai wild pigs. We designed an experiment to test this vaccine in wild pigs of Molokai genetics. Fifteen 3–4-month-old pigs were orally administered 10⁶–10⁷ colony forming units (cfu) of heat-inactivated M. bovis (Vaccinates; n = 8; 0.2 mL) or phosphate buffered saline (Controls; n = 7; 0.2 mL). Each dose was administered in a 0.5 mL tube embedded in a fruit candy/cracked corn mix. Boosters were given seven weeks post-prime in the same manner and dose. Nineteen weeks post-prime, pigs were orally challenged with 1 × 10⁶ cfu of virulent M. bovis. Twelve weeks post-challenge, pigs were euthanized and necropsied, at which time 23 different tissues from the head, thorax, and abdomen were collected and examined. Each tissue was assigned a lesion score. Ordinal lesion score data were analyzed using non-zarametric Wilcoxon Signed Rank test. Effect size was calculated using Cohen’s d. Four of eight Vaccinates and four of seven Controls had gross and microscopic lesions, as well as culture-positive tissues. Vaccinates had statistically lower lesion scores than Controls in the following areas: gross thoracic lesion scores (p = 0.013 Cohen’s d = 0.33) and microscopic thoracic lesion scores (p = 0.002, Cohen’s d = 0.39). There were no differences in head lesion scores alone, both gross and microscopic, nor were there differences when comparing combined gross and microscopic head and thoracic lesion scores. These results are indicative that this vaccination protocol affords a modest degree of infection containment with this vaccine in Molokai wild pigs.