Biology of Disease Connection

While “bighorns + domestic sheep = many dead bighorns” is often a valid general conclusion, the equation is not necessarily that simple. Various factors and types of disease can be involved (Malmberg, Nordeen, and Butterfield 2008). According to a 2015 joint issue statement released by The Wildlife Society and American Association of Wildlife Veterinarians:

“The most important diseases affecting wild sheep populations are respiratory infections that result in pneumonia. Bacteria of the family Pasteurellaceae (Pasteurella multocida, Mannheimia haemolytica and Bibersteinia trehalosi), and Mycoplasma ovipneumoniae are the most frequently isolated respiratory pathogens from wild sheep with pneumonia. Pneumonia caused by these organisms often results in the mortality of a large proportion of the population (Cox and Carlson 2012) across all age classes (referred to as an all age epizootic or die-off) and is typically followed by enzootic disease with multiple years of lamb mortality from pneumonia (WAFWA WHC 2014). This pattern of pneumonia in wild sheep has been documented in more than 70 peer-reviewed scientific publications (TWS and AAWV 2015).”

The Desert Bighorn Council's technical staff provides futher background on bighorn disease:

“Bighorns have died from a wide variety of diseases that they have contracted from domestic sheep. These include scabies (a major cause of mortality in the 1800s and as late as the 1970s in New Mexico), chronic frontal sinusitis, internal nematode parasites (worms), pneumophilic bacteria, footrot, parainfluenza 111, bluetongue, and soremouth (contagious echthyma)” (1990, 33).

Rocky Mountain bighorns in northern Colorado

Though pneumonia is not the only type of disease bighorns can contract from domestic sheep, it frequently appears in literature covering bighorn die-offs. Tomassini et al. state:

“From the mid-1800s until the 1980s, pneumonia was frequently diagnosed in diseased bighorn found in the field, and [pneumonia] bacteria from the Pasteurellaceae family were isolated several times from these animals. One of the challenges in summarizing the literature describing pneumonic disease in the bighorn sheep is the constantly evolving nomenclature describing the primary suspected pathogen, Pasteurella haemolytica” (2009, 931).

Tomassini et al. continue by remarking: “The T biotypes [of P. haemolytica] . . . were reclassified in 1990 as Pasteurella trehalosi and as Bibersteinia trehalosi in 2007. The A biotypes . . . were reclassified in 1999 as Mannheimia haemolytica. Both of these species still belong to the Pasteurellaceae family” (2009, 931). On this site, where applicable the updated M. haemolytica name is used instead of P. haemolytica, and microbial pathogen species causing pneumonia are often simply referred to as “pneumonia bacteria.”

In a 2014 scientific journal article, Ziegler et al. provide a more detailed summary of the bighorn pneumonia situation:

“Pneumonia epizootics have played a major role in the decline of bighorn sheep (Ovis canadensis) populations in the United States [1,2], but the specific cause of bighorn sheep pneumonia has been debated for some time. Mannheimia haemolytica, Bibersteinia trehalosi, Pasteurella multocida, and Mycoplasma ovipneumoniae are all frequently detected in affected lung tissues [1–6]. Contacts between domestic sheep and goats have frequently been observed to precede bighorn sheep pneumonia outbreaks, and experimental contact with domestic sheep results in fatal pneumonia in >95% of bighorn sheep [3–11]. Recent evidence supports the hypothesis that M. ovipneumoniae is the primary agent responsible for these outbreaks but acts indirectly by impairing pulmonary defenses, predisposing to polymicrobial pneumonia with multiple secondary bacterial agents [1,2,6]. According to this hypothesis, M. ovipneumoniae, a pathogen frequently carried by domestic sheep and goats but absent from healthy bighorn sheep populations, triggers pneumonia epizootics involving animals of all ages when introduced to naive bighorn sheep populations. Bighorn sheep that survive the all-ages epizootic become immune but some individuals continue to carry M. ovipneumoniae in their upper respiratory tract, serving as a source of infection to lambs. As a result, annual lamb pneumonia epizootics may recur for many years after the initial all-ages outbreak (Ziegler et al. 2014).”

In a 2008 article, Malmberg, Nordeen, and Butterfield explain more factors that complicate understanding the biology of pneumonia infection in bighorns:

“Although it is widely known that Pasteurella causes respiratory distress in bighorn sheep and generally results in eventual death by pneumonia, the process of bacterial colonization of the lung is not well understood. It has been hypothesized that Pasteurella increases in number in the nose until an excess of organisms in the nose results in entry into the lungs. A healthy animal should be successful in clearance of the bacteria from the lungs, but the process may be inhibited by incidents of stress, concurrent viral infections, or environmental or climatic change.

These predisposing factors may compromise immunity of bighorn sheep, allowing for a shift from benign to lethal Pasteurella spp. infection or facilitating the establishment of highly pathogenic forms that would otherwise be controlled by immune system function. Factors that may result in suppression of the immune system and predisposition to pneumonia may include parasites such as lungworms (Protostrongylus spp.) or mites (Psoroptes ovis), nutritional deficiencies, periods of low forage quality and quantity, high predation or harassment, harsh weather conditions, inbreeding, or density dependent stress resulting from overcrowding. 

The respiratory disease complex in bighorn sheep is complicated by the fact that infected individuals do not always die and sometimes no harmful effects of the bacteria are observed. Because bighorn sheep infected with apparently pathogenic strains of Pasteurella sometimes show no clinical signs of respiratory disease, it is believed that certain ecological or environmental conditions play a role in the all-age die-offs” (2008, 199).

So, bighorns can carry strains of pneumonia bacteria without getting fatally sick, and various biological and ecological factors could worsen or mitigate illness. Malmberg, Nordeen, and Butterfield’s statements come from a study investigating a 2006 bighorn pneumonia outbreak in Nebraska’s Wildcat Hills that resulted in an all-age die-off of about 50% of the population (2008). While the authors did not directly implicate domestic sheep, they state that “findings suggest that [bighorn] sheep occupying private properties may be exposed to a stressor that is not present within the Wildlife Management Area, such as livestock” (2008, 198). They go on to say that the pneumonia epizootic “was more likely to have originated from domestic sheep [than from] stress and nutrition associated with cattle” (2008, 203).

desert bighorn ewe and ram in Grand Canyon National Park

As emphasized earlier, only certain types of pneumonia bacteria from domestic sheep seem to be fatal to bighorns. Heimer remarks that: “The highly virulent [Mannheimia haemolytica of] domestic sheep . . . will almost certainly cause fatal pneumonia in any wild bighorn exposed to it. The other Pasteurellas, trehalose and multocida may or may not cause pneumonia die-offs depending on circumstances” (2002, 154). George et al. state: “Mannheimia haemolytica biogroup 1 is the most common biovariant isolated from domestic sheep, and is comparatively rare in wild sheep” (2008, 399). Heimer adds: “not every bighorn sheep herd exposed to a domestic sheep perishes . . . [and] some bighorn populations experience pneumonia die-offs in the apparent absence of domestic sheep” (2002, 158).

Though M. haemolytica has been a recent prominent fatal pneumonia bacterium affecting bighorns, a number of recent studies have examined the role of M. ovipneumoniae, which may predipose bighorns to increased disease vulnerability (Ziegler et al. 2014; Besser et al. 2008, 2010, 2012 2013, 2014; Dassanayake 2010; Justice-Allen 2011; Oaks et al. 2010; Weiser et al. 2012). Washington State University veterinarian and researcher Dr. Thomas E. Besser has been central to much of the bighorn M. ovipneumoniae research. This page features a series of five videos covering a presentation Dr. Besser gave on M. ovipneumoniae at the January 30, 2013 Wild Sheep Working Group (WSWG) meeting.

Just how close do wild and domestic sheep need to be for disease transmission? Regarding pneumonia bacteria species, Dixon et al. state: “The method of transmission in bighorn sheep generally has been assumed to be by direct (nose-to-nose) contact” (2002, 6). In a study with wind tunnels, Dixon et al. found that P. multocida was much more likely to survive wind transportation than [M. haemolytica] or P. trehalosi (2002). The authors concluded that their “findings suggest a potential exists for Pasteurella spp. to be transmitted between animals without direct contact” (2002, 6).

Although components of wild-domestic sheep disease transmission can be complicated, some important trends stand out that highlight bighorns’ special susceptibility. One trend is that domestic sheep often stay healthy after fatally infecting bighorns. This trend is well-known (DBC Technical Staff 1990). According to Subramanian et al.: “Although [M. haemolytica] causes pneumonia in . . . domestic sheep . . . and wild sheep . . ., the lung pathology and mortality are much more severe in [bighorns]. Furthermore, experimental inoculation of [bighorns] . . . has resulted in fatal pneumonia in [bighorns] but not in [domestic sheep]” (2011, 332). As George et al. point out, “some [pneumonia bacteria] carried as normal commensal flora by healthy domestic sheep are highly pathogenic in bighorn sheep” (2008, 389). Why do bighorns die from exposure to pathogens that are often harmless to domestic sheep? The DBC’s technical staff explains:

“The prevailing theory on why this has occurred can be summed up as follows: New World sheep (bighorns) are so susceptible to diseases of Old World sheep (domestics) because the bighorns did not co-evolve with the above-listed diseases, as did domestic sheep. Bighorns have not developed effective immunity against these diseases. Domestic sheep are inoculated or, through natural selection over hundreds of years, have developed a resistance against some of these diseases, but carry blood titers for most of them. When there is contact between bighorns and domestic sheep, the bighorns have little defense. This theory is analogous to the accepted explanation for the transmission of human diseases carried to the Native Americans by Europeans. The Native American populations had no immunity to Old World diseases and suffered many documented die-offs” (1990, 33).

Another important trend of wild-domestic sheep disease transmission is that an illness’s effect on individual bighorn populations can be long-lasting. For example, in the 1980s, in California’s Santa Rosa Mountains, lambs regularly died from pneumonia (DeForge et al. 1997; DeForge et al. 1982). According to DeForge et al.: “[In the] Santa Rosa Mountains . . . a disease outbreak reportedly struck bighorn in the late 1970’s. This epizootic contributed to at least 13 years of poor recruitment and an 81% population decline in the . . . adult bighorn population between 1979 and 1996” (1997, 9). Cahn et al. explain the trend of suppressed lamb recruitment:

“Whether mild or severe, most respiratory disease outbreaks in bighorn populations are followed by several years of pneumonia caused mortality of lambs resulting in low recruitment rates and juvenile survival. Continuing lamb infection apparently results from females that remain infective following an outbreak, although mortality or morbidity among the females may not be detectable. Such recurring lamb infections can substantially delay the recovery of depleted populations to pre-outbreak levels” (2011, 1754).

bighorn lambs

For example, in the winter of 2009-2010, western Montana’s Lower and Upper Rock Creek bighorn populations suffered severe pneumonia die-offs (WAFWA 2010). By 2011, the number of yearlings per 100 ewes in the Rock Creek populations had dropped by 96% (Crowser 2011).

Regarding initial all-age die-offs, the Montana Department of Fish, Wildlife, and Parks notes that: “Each dieoff event can be somewhat unique. Sometimes die-offs occur rapidly with wild sheep dying within a few days, while other times a die-off may last a couple of months with the animals’ condition deteriorating slowly before death” (2010, 57).

Besser, Thomas E., E. Frances Cassirer, Margaret A. Highland, Peregrine Wolffd, Anne Justice-Allen, Kristin Mansfield, Margaret A. Davis, and William Foreyt. Bighorn sheep pneumonia: Sorting out the cause of a polymicrobial disease. 2013. Preventative Veterinary Medicine 108, no. 2-3 (February): 85-93.

Besser, Thomas E., E. Frances Cassirer, Kathleen A. Potter, John VanderSchalie, Allison Fischer, Donald P. Knowles, David R. Herndon, Fred R. Rurangirwa, Glen C Weiser, and Subramaniam Srikumaran. 2008. Mycoplasma ovipneumoniae infection with population-limiting respiratory disease in free-ranging Rocky Mountain bighorn sheep (Ovis canadensis canadensis). Journal of Clinical Microbiology 46, no. 2 (February): 423-430.

Besser, Thomas E., E. Frances Cassirer, Kathleen A. Potter, Kevin Lahmers, J. Lindsay Oaks, Sudarvili Shanthalingam, Subramaniam Srikumaran, and William J. Foreyt. 2014. Epizootic pneumonia of bighorn sheep following experimental exposure to Mycoplasma ovipneumoniae. PLoS ONE 9, no. 10 (October): 1-9.

Besser, Thomas, Catherine Yamada, E. Frances Cassirer, Donald Knowles, J. Lindsay Oaks, Shannon Swist, Caroline Herndon, Srikumaran Subramaniam. 2010. Mycoplasma ovipneumoniae as a primary agent of epidemic respiratory disease in bighorn sheep (Ovis canadensis) commingled with domestic sheep (Ovis aries). In proceedings of Northern Wild Sheep and Goat Council’s 17th Biennial Symposium, Hood River, OR. June 7-11.

Besser, Thomas E., E. Frances Cassirer, Catherine Yamada, Kathleen A. Potter, Caroline Herndon, William J. Foreyt, Donald P. Knowles, and Subramaniam Srikumaran. 2012. Survival of bighorn sheep (Ovis canadensis) commingled with domestic sheep (Ovis aries) in the absence of mycoplasma ovipneumoniae. Journal of Wildlife Diseases 48, no. 1 (January): 168-172.

Brigham, William R., Eric M. Rominger, and Alejandro Espinosa T. 2007. Desert bighorn sheep management: Reflecting on the past and hoping for the future. In transactions of Desert Bighorn Council’s 49th Annual Meeting, Las Vegas, NV. April 3-6.

Cahn, Maya L., Mary M. Conner, Oswald J. Schmitz, Thomas R. Stephenson, John D. Wehausen, and Heather E. Johnson. 2011. Disease, population viability, and recovery of endangered Sierra Nevada bighorn sheep. Journal of Wildlife Management 75, no. 8 (November): 1753-1766.

Crowser, Vivaca. 2011. News: Bighorn Lambs Still Feeling Effects of 2009-2010 Pneumonia Outbreak. Montana Department of Fish, Wildlife, and Parks. ruralftp/Newsletter/LinksFrom-eNewsletters/2011-7_BighornLambs2010Pneumonia Outbreak.pdf (accessed May 13, 2012).

Dassanayake, Rohana P., Sudarvili Shanthalingam, Caroline N. Herndon, Renuka Subramaniam, Paulraj K. Lawrence, Jegarubee Bavananthasivam, E. Frances Cassirer, Gary J. Haldorson, William J. Foreyt, Fred R. Rurangirwa, Donald P. Knowles, Thomas E. Besser, Subramaniam Srikumaran. 2010. Mycoplasma ovipneumoniae can predispose bighorn sheep to fatal Mannheimia haemolytica pneumonia. Veterinary Microbiology 145, no. 3-4 (October): 354-359.

DeForge, James R., David A. Jessup, Charles W. Jenner, and Joan E. Scott. 1982. Disease investigations into high lamb mortality of desert bighorn in the Santa Rosa Mountains, California. In transactions of Desert Bighorn Council’s 26th Annual Meeting, Borrego Springs, CA. April 7-9.

DeForge, James R., Stacey D. Ostermann, Charles W. Willmott, Kevin Barry Brennan, and Steven G. Torres. 1997. The ecology of Peninsular bighorn sheep in the San Jacinto Mountains, California. In transactions of Desert Bighorn Council’s 41st Annual Meeting, Grand Junction, CO. April 9-11.

Desert Bighorn Council (DBC) Technical Staff. 1990. Guidelines for the management of domestic sheep in the vicinity of desert bighorn habitat. In transactions of DBC’s 34th Annual Meeting, Hermosillo, Sonora, Mexico. April 4-6.

Dixon, David M., Karen M. Rudolph, Mark L. Kinsel, Lisa M. Cowan, David L. Hunter, and Alton C.S. Ward. 2002. Viability of airborne Pasteurella spp. In proceedings of Northern Wild Sheep and Goat Council’s 13th Biennial Symposium, Rapid City, SD. April 23-27.

George, Janet L., Daniel J. Martin, Paul M. Lukacs, and Michael W. Miller. 2008. Epidemic Pasteurellosis in a bighorn sheep population coinciding with the appearance of a domestic sheep. Journal of Wildlife Diseases 44, no. 2 (April): 388-403.

Heimer, Wayne. 2002. Bighorn pneumonia die-offs: An outsider’s synoptic history, synthesis, and suggestions. In proceedings of Northern Wild Sheep and Goat Council’s 13th Biennial Symposium, Rapid City, SD. April 23-27.

Justice-Allen, Anne E., Clint J. Luedtke, Matthew Overstreet, James W. Cain III, and Thomas R. Stephenson. 2011. Prevalence of Mycoplasma ovipneumoniae in desert bighorn sheep in Arizona. In transactions of Desert bighorn Council's 51st meeting, Laughlin, NV. April 6-8.

Oaks, Lindsay J., Thomas Besser, Frances Cassirer, Timothy V. Baszler, and Catherine Yamada. 2010. Diagnosis of Mycoplasma ovipneumoniae in bighorn sheep. In proceedings of Northern Wild Sheep and Goat Council’s 17th Biennial Symposium, Hood River, OR. June 7-11.

Malmberg, Jennifer L., Todd Nordeen, and Chuck Butterfield. 2008. The effects of disease, stress, and distribution on bighorn sheep restoration in Nebraska. In proceedings of Northern Wild Sheep and Goat Council’s 16th Biennial Symposium, Midway, UT. April 27-May 1.

Montana Department of Fish, Wildlife, and Parks (MFWP). 2010. Montana Bighorn Sheep Conservation Strategy: 2010. Helena. =397 46 (accessed October 15, 2011). [govt. doc.]

Subramaniam, Renuka, Caroline N. Herndon, Sudarvili Shanthalingam, Rohana P. Dassanayake, Jegarubee Bavananthasivam, Kathleen A. Potter, Donald P. Knowles, William J. Foreyt, and Subramaniam Srikumaran. 2011. Defective bacterial clearance is responsible for the enhanced lung pathology characteristic of Mannheimia haemolytica pneumonia in bighorn sheep. Veterinary Microbiology 153, no. 3 (December): 332-338. 

The Wildlife Society and American Association of Wildlife Veterinarians (TWS and AAWV). 2015. Joint Issue Statement: Domestic Sheep and Goats Disease Transmission Risk to Wild Sheep. _TWS-AAWV_JointStatement_APPROVED.pdf (accessed April 26, 2015). 

Tomassini, Letizia, Ben Gonzales, Glen C. Weiser, and William Sischo. 2009. An ecologic study comparing distribution of Pasteurella trehalosi and Mannheimia haemolytica between Sierra Nevada bighorn sheep, White Mountain bighorn sheep, and domestic sheep. Journal of Wildlife Diseases 45, no. 4 (October): 930-940.

Weiser, Glen C., Mark L. Drew, E. Frances Cassirer, and Alton C.S. Ward. 2012. Detection of Mycoplasma ovipneumoniae and M. arginini in bighorn sheep using enrichment culture coupled with genus- and species-specific polymerase chain reaction. Journal of Wildlife Diseases 48, no. 2 (April): 449-453.

Western Association of Fish and Wildlife Agencies (WAFWA). 2010. Summary on 9 BHS Die-offs in 5 Western States: Winter 2009-10 (June 22, 2010). Cheyenne: WAFWA. 2009-10.pdf (accessed May 17, 2012).

Ziegler, Jessie C., Kevin K. Lahmers, George M. Barrington, Steven M. Parish, Katherine Kilzer, Katherine Baker, and Thomas E. Besser. 2014. Safety and immunogenicity of a Mycoplasma ovipneumoniae bacterin for domestic sheep (Ovis aries). PLoS ONE 9, no. 4 (April): 1-7.