Infectious agents and diseases in brown bears

Photo: Grizzly bear with wolves on a bull elk carcass in Yellowstone National Park (YNP. While the environmental transmission across species (wolves & bears) may be rare and limited, feeding on ungulate carcasses serves to be a potential area for grizzly bears to acquire infection from other infected taxa (wolves). The time when grizzlies may be most vulnerable is when they push wolves off of recent kills. Photo courtesy NPS/Dan Stahler.

Brown bears are enormous free-ranging, omnivore generalists, subjected to numerous pathogens & diseases. Over the decades, research has documented a wide variety of diseases ranging from viral to parasitic infections. In this summary, we will discuss relevant information on viral, bacterial, parasitic infections of free-ranging brown bears (grizzlies).

Background Information:​

It is essential to realize that not all micro-organisms cause disease, and the effects of a specific disease are not consistent amongst all infectious outbreaks (Murray et al. 1999). Ecological and epidemiological conditions dictate the impacts of a specific disease. Single-host infectious diseases are very unlikely to cause extinctions unless the host population numbers are dwindling, or disease transmission is rapid, with a somewhat delayed impact. However, cases where the reservoir hosts carry the infection and exhibit the ability to sustain reinfection of the population, effects may occur regardless of the population or transmission rate (Begon & Bowers 1995, McCallum & Dobson 1995, Murray et al. 1999).

One of the primary goals and challenges for conservation and wildlife biologists is to identify conditions that are conducive to creating “the perfect storm,” or conditions where the spread of infection and severity of the disease becomes amplified to create an epidemic. The goal here is to create and implement control measures that can mitigate or prevent such epidemics of “perfect storms” from occurring. The importance of identifying and working to prevent and mitigate disease outbreak in large carnivore populations is of particular importance, given that many populations are already seriously threatened, suffer from fragmented habitat and ranges (Murray et al. 1999). In addition to threatened populations, carnivores and ursids, in general, are incredibly susceptible to a wide variety of highly lethal or extremely debilitating microparasites (Appel 1987); many of these microparasites are native to and transmitted by domestics species (dogs, cats). As large free-ranging carnivores as bears and wolves experience restrictions caused by urban landscape development & habitat barriers, in the future, we can expect increased transmission of infectious diseases from domestic animals (Murray et al. 1999). The effects surrounding infectious diseases may additionally be amplified or provoked by other complications or factors surrounding the species condition (endangered/threatened), ranging from malnutrition to stress or even in some cases, inbreeding (O’Brien & Roelke et al. 1985; Ullrey, 1993; Lloyd, 1995).

How do we test for infectious diseases? ​

Serological tests have examined a wide variety of infectious diseases. A serology test is a blood test used to detect and measure certain levels/presence of antibodies resulting from exposures to particular viruses or bacteria. When bears and other carnivores have exposure to certain bacteria and viruses (antigens), their immune systems respond by producing specific unique antibodies against the given organism antibody levels, known more frequently as an antibody titer, help scientists determine when infection occurred (CDPHE, 2019). Most surveys performed have found antibodies to be present in many sampled populations (Murray et al. 1999). However, indeed, many serological tests have not been validated for non-domestic species (Gardner, Hietala & Boyce, 1996). In the case of non-domestic species, high antibody titers may represent previous or prior infection with an avirulent strain, or micro-organisms with cross-reacting antigens. Both possibilities are, however, indistinguishable based solely on serum antibodies (Murray et al. 1999). 

Within the wildlife community, there is a strong tendency for many biologists to equate seroprevalence with past or recent infection with a disease (Choquette & Kuyt, 1974). Seroprevalence represents the cumulative number of individuals in a population who exhibit positive test results for a specific disease based on serology (blood serum) (Tusting et al. 2014). Micro-organisms do not necessarily need to be present in order for antibodies to be detected if immunity has eliminated the infection and to confirm disease presence, clinical signs, and detection of micro-organisms are required (Evermann & Eriks, 1999). For example, there are instances where antibodies and viruses were detected in carnivore species (Alexander, MacLachlan et al. 1994; Alexander, Kat et al. 1995), even though there was minimal evidence that the infections at present, caused any disease symptoms. 

The specific viral, bacterial, and parasitic diseases of bears:
 Various viruses detected in ursids (avian influenza, bluetongue, canine parvovirus, eastern, western & Venezuelan equine encephalitis) are absent of associated clinical disease (Bourne & Vila-Garcia, 2007). 

Canine Coronavirus (CCV): The only detection of antibodies to CCV have presented in one bear, from the region of Slovakia; there are no known reports to date, or evidence of direct exposure of bears to CCV (Vitásková et al. 2019). Canine coronavirus is a highly contagious intestinal infection with origins in canids. The virus spreads through contact with oral secretions or contact with infected feces or waste. Importantly, coronaviruses are relatively resistant and can remain infectious for more prolonged periods outdoors, even at cold temperatures (McCaw et al. 2006). Some of the various clinical signs of CCV are depression, loss of appetite, vomiting, acute diarrhea, and fever. For domestic dogs, several vaccines are available: Nobivac ® Canine 1-DAPPV+CV, Nobivac ® Canine 1-DAPPVL2, and Nobivac ® Canine 1-CV. Merck Animal Health Solutions distributes all three of these vaccines.

Canine Distemper Virus (CDV): Bears are known to demonstrate a particular susceptibility to canine distemper virus (CDV); however, clinical disease is rare. Prior research has documented this fatal disease in Polar bear cubs, Spectacled bears, and Giant pandas (Schonbauer et al. 1984; Deem et al. 2000).

CDV is acute, extremely transmissible, similar in many ways to morbilliviruses, such as measles and rinderpest (Greene & Appel, 2006). Measles requires a large host population so that it is provided a continuous supply of hosts for the pathogen to persist (Bartlett, 1957, 1960; Bolker & Grenfell, 1995). Carnivores (bears) are different from humans in the respect that there is a higher turnover in the population. Because of this higher turnover rate, it may allow CDV to persist within smaller populations. Models suggest a requirement of 50,000-100,000 individuals in a carnivore population for a 50% chance of persistence for ten years (Almberg, Cross & Smith, 2010).

Since wolf reintroduction in Yellowstone National Park (YNP), there have been three outbreaks of CDV. All three outbreaks overlapped with significant wolf pup mortality events (Almberg, Wayne, Sheldon & Crabtree, 2009; Almberg et al. 2010; Stahler, Macnulty, Wayne, Vonholdt & Smith, 2013).

Figure: Capture locations for grizzly bears tested for canine distemper virus (CDV) between 1984-2014. Sera neutralization (SN) tests with titer values >= 24 are positive (green) whereas SN tests with titer values <12 are negative (red). The estimated distribution of grizzly bears in the Greater Yellowstone Ecosystem (GYE) is identified in blue, where the Grizzly Bear Recovery Zone (GBRZ) is outlined in orange.

CDV virus transmits from close contact via means of aerosols, oral, respiratory, or ocular fluids. However, morbilliviruses do not survive long outside of a host (Cross et al. 2018). While the environmental transmission across species (wolves & bears) may be rare and limited, feeding on ungulate carcasses serves to be a potential area for grizzly bears to acquire infection from other infected taxa (wolves). The time when grizzlies may be most vulnerable is when they push wolves off of recent kills (Cross et al. 2018). 

Samples analyzed between 1984-2014 included 565 grizzly bear sera samples from throughout the Greater Yellowstone Ecosystem (GYE). About 6% of grizzly bear samples exhibited serum neutralization (SN) titers between 12 to 24 for CDV. Distemper seroprevalence in grizzly bears was between 30%-40% (Cross et al. 2018).

​Table(s): Canine distemper virus (CDV) antibody titer results for grizzly bears captured between 1984-2014. During this time, 565 captures were recorded. The highest CDV antibody titer recorded over three decades was 2048 (GB #756).

Grizzlies in the GYE did not have the same outbreak years as wolves. Before 1996, the IGBST only collected 16 serological tests on grizzly bears. Because of this, the estimated hazard of CDV before 1997 only reflects the prior distribution and does not reflect a decline in hazard following wolf introduction to YNP. The average time between birth and testing for a bear was approximately 7.7 years, as opposed to wolves at 1.7 years. The information provided by grizzly bears, in general, was not as informative (when they were infected, intermittent outbreaks, etc.) compared to wolves (Cross et al. 2018).

During 2005, there was supporting evidence of a minor CDV outbreak in GYE grizzlies, which coincided with a CDV outbreak in wolves. However, during two other outbreaks in wolves in 1999 and 2008, outbreaks in ursids were not apparent (Cross et al. 2018).

Canine Adenovirus 1 (CAdV-1): On several occasions, infectious canine hepatitis or referred to as canine adenovirus 1 infection, has been detected in bears. Typically, this causes extreme salivation, nausea & vomiting, diarrhea, signs of abdominal pain and neurological signs. Unfortunately, many bears with this infection succumb to the disease. Surviving bears may be subject to a 2-3 month recovery time (Murray et al. 1999; Pursell et al. 1983; Collins et al. 1984; Kritsepi et al. 1996). 

Photo: Cub of grizzly 451 (Katmai) lying deceased. Note the hair is from ravens attempting to scavenge the carcass. Photo courtesy NPS.

Photo: Grizzly 451 (Katmai) lies next to her dying cub for over two-days. Photo courtesy of NPS.

Photo: Grizzly 451 (Katmai) passes her dying cub with her present offspring. Photo courtesy NPS.

Case Study: Katmai National Park, October 2015
​During October 2015, a female brown bear cub was discovered deceased in Katmai National Park and Preserve, near Brooks Falls. In late October, the webcam captured footage of a cub, collapsing and then subsequently dying. The National Park Service recovered the carcass and submitted it to the US Geological Survey, National Wildlife Health Center in Madison, WI. The bear’s brain tissue was tested for rabies virus and canine distemper virus (CDV); both were negative. The University of Wisconsin-Madison Biotechnology Center sequenced the PCR product; the amplified sequence shared 100% identity and matched to the canine adenovirus 1 (Knowles et al. 2018)

Photo: Gross necropsy image of affected bears' brain. Petechial hemorrhages noticeable throughout the surface. -Knowles, S., Bodenstein, B. L., Hamon, T., Saxton, M. W., & Hall, J. S. (2018). Infectious canine hepatitis in a brown bear (Ursus arctos horribilis) from Alaska, USA. Journal of wildlife diseases, 54(3), 642-645.

CAdV-1 was first observed in dogs back in the 1930s, yet, now, the infection is seen globally (Decaro et al. 2008). CAdV-1 can infect members of Canidae, Mustelidae, and Ursidae (Woods 2001). The disease is transmitted either by direct contact or any type of exposure to infected membranes/secretions. The virus replicates in vascular endothelial cells (line the interior surface of blood/lymphatic vessels), hepatocytes (cells located in the central parenchymal tissue of the liver), and renal epithelial cells (Decaro et al. 2008). The first documented CAdV-1 mortality in captive black bears was documented over three-decades ago (Pursell et al. 1983). 

Photo: Grizzly 868 (from Katmai, AK) fishing on the lip of Brooks Falls during July. This bear tested negative for canine adenovirus (CAdV-1) or commonly referred to as canine hepatitis, and canine distemper virus (CDV). At the time of his death, 10-12 gallons of fluid were discovered in his abdomen; his cause of death remains unknown. Photo courtesy of NPS.

Photo: Grizzly 868 (Katmai) lies deceased with park personnel investigating. Photo courtesy NPS.

Clinical signs observed included anorexia, salivation, vomiting, diarrhea, nystagmus, ataxia, seizures, and flaccid paralysis. Gross necropsy exhibited lymphadenopathy, ascites, vascular congestion, and disseminated petechial hemorrhages; on a microscopic level, there was hemorrhage and minor inflammation in the brain (mild hepatic necrosis) (Pursell et al. 1983; Collins et al. 1984; Knowles et al. 2018). What remains a mystery, is what role CAdV-1 infections may play in brown bear cub mortality and what impact it may have on Alaskan brown bear populations, and other population segments for that matter (Knowles et al. 2018).

Photo: Grizzly 868 (Katmai) lies deceased with park personnel investigating. Photo courtesy NPS.

Photo: Grizzly 868 (Katmai) lies deceased with park personnel investigating. Photo courtesy NPS.

Neorickettsia: This disease is better known as ‘salmon poisoning’ or ‘Elokomin fluke fever’ (Murray et al. 1999). The organisms infect a trematode, eventually developing through two-hosts (snail and fish). Generally, salmonids are the fish host; the carnivore (bear) becomes infected once it consumes and eats the infected salmon. The organisms are released into the bloodstream once the fluke penetrates the mucosal lining of the gut (Reed, 2006).

Clostridial organisms: Bears, like many other species, are susceptible to clostridial organisms and infections (Clostridium difficile and Clostridium perfringens), both of which cause myonecrosis (death to muscle tissue) (Bourne & Vila-Garcia, 2007). There are documented cases of myonecrosis following the intramuscular injection of anesthetic drugs. Another case of myonecrosis was associated and attributed to a facial wound (Barnes & Rogers, 1980; Rao et al. 1988). Of more recent times, two grizzly bears in the Greater Yellowstone Ecosystem, died due to Clostridium spp infection, slightly over a decade ago (Haroldson & Frey, 2009).

Case Study: Grizzly Clostridium Trapping Deaths - Idaho, 2008
On August 24, 2008, grizzly bears 563 and 595 were captured in the Caribou-Targhee National Forest (CTNF) by members of the Interagency Grizzly Bear Study Team (IGBST). On August 31, a week after capture, bear 595 was discovered deceased by a hunter. Officials submitted the bears’ carcass to the Wildlife Health Laboratory, Idaho Department of Fish and Game, where the cause of death was determined to be attributed to a clostridial infection at the anesthesia (jab) injection site. Wildlife health pathologists believe that 563 most likely died from a similar clostridial infection; however, no one discovered the carcass until September 4. Unfortunately, at that point, the remains had been subjected to severe decomposition, inhibiting conclusive results from the necropsy. Clostridial infections can cycle with the weather, and moisture conditions; complications from bacteria were high in the ruminates in the general area surrounding these captures (P. Mamer, IDFG, personal communication)(Haroldson & Frey, 2009). 
 
​The IGBST revised their handling protocols after the two clostridium related deaths, and amended procedures to now include the application of prophylactic antibiotics effective against clostridium (Penicillin -DuraPen; and Oxytetracycline - OxyTet).

Photo: Black bear with sarcoptic mange. Photo courtesy of the Pennsylvania Game Commission.

Mites & mange: There have been several reported instances of various bear species with mites. In North America, this is most commonly black bears. North American Black bears can experience both audycoptic and sarcoptic mange. Audycoptic mange is a result of Ursicoptes americanus mites, causing alopecia, pruritis, crusting (most often observed around the head region). Sarcoptic mange may cause pruritis, alopecia, pustular dermatitis, crusting & thickening of the skin (Fowler 1986; Bourne & Vila-Garcia, 2007; Bourne et al. 2010).

Hookworm: Nematode infections have been frequently documented in bear populations and are seemingly familiar. Hookworm (Ancylostoma & Uncinaria spp), in particular, are the most severe in young bear cubs. This nematode causes diarrhea, blood in feces, anorexia, weight loss, anemia, and debilitation. Hookworm and other nematode infections can be particularly fatal in young cubs & juveniles (Bourne et al. 2010).

Figure: Graphical depiction of the life-cycle of ascarids. Courtesy of the Center for Disease Control (CDC).

Ascarid (large roundworm): Roundworm, predominantly Baylisascaris transfuga infections are extremely common in bears. Many of these infections result, causing diarrhea, and anorexia. In some cases of severe infection, it may result in poor body condition. Other severe consequences of infection may include worms fatally blocking the small intestines (Bourne et al. 2010).

Bears are subject to various other parasitic infections which include: cestodes (adult tapeworms in the intestines and larval form), trematodes (flukes), acanthocephalans, Dirofilaria ursi, toxoplasmosis (sometimes fatal), trichinellosis, lice, fleas, and ticks (Rogers & Rogers, 1976; Kiupel et al. 1987; Bourne & Vila-Garcia, 2007).

Zoonotic agents and diseases of bears

There are various modes of transmission through which disease passes from bears to humans. These include everything from bites, scratches, consumption of meat, accidental exposure to or ingestion of waste, aerosols, and arthropods (Di Salvo & Chomel, 2019). While there are several published accounts of documented bacterial infections following bear bites and scratches, trichinosis/trichinellosis dominates most concerns outlined in published literature (Kunimoto, Rennie, Citron & Goldstein, 2004; Lehtinen et al., 2005; Liu & Hsu, 2004; Thomas & Brook, 2011). In most instances, bears exposed to various pathogens do not display any clinical signs and seem relatively unaffected by disease. These observations suggest bears may play a key role as ‘reservoirs’ or ‘sentinels’ for numerous disease pathogens (Di Salvo & Chomel, 2019). Diseases which have been confirmed or designated as potential zoonoses in brown bears (Ursus arctos) include: Anaplasma phagocytophilum, Ancylostoma spp., Bacillus anthracis, Borrelia burgdorferi, Brucella spp., Coxiella burnetti, Diphyllobothrium spp., Dirofilaria ursi, Francisella tularensis, Leptospirosis spp., Mycobacterium tuberculosis ssp., Rabies, Toxoplasma gondii, Trichinella spp., Uncinaria spp., Yersinia enterocolitica, Yersinia pestis. Of these diseases, Trichinella spp. is the only confirmed and documented zoonotic disease transmitted between bears-humans (Di Salvo & Chomel, 2019).

Bacteria

​Brucellosis (Brucella spp.) - Several studies have outlined the presence of Brucella spp. antibodies in serum samples of black, brown, and polar bears. From 1988-1991, a serological survey consisting of 644 samples from Alaskan grizzlies and black bears found antibodies at 15% & 1.3% (Chomel, Kasten, Chappuis, Soulier & Kikuchi, 1998). Another study (O’Hara et al., 2010) detected antibodies in brown bears at 14% of 92 samples. An even more recent study (Ramey et al. 2018) found that 155 brown bears, occupying five geographic locations in Alaska, yielded a seroprevalence of 15%. Interestingly enough, none of the mentioned studies documented or reported any reproductive issues in bears resulting from Brucella spp., which is known to cause problems such as abortion or placentitis (Di Salvo & Chomel, 2019).

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Anthrax (Bacillus anthracis) - Rarely have anthrax infections or exposure been documented in bears. In 1993, an outbreak documented in bison within northern Canada resulted in the death of three bears; this was likely from the consumption of infected carcasses (Gates, Elkin & Dragon, 1995). While there is not nearly enough conclusive evidence from observation or study, we should still consider bears as capable of transmitting anthrax to humans (Di Salvo & Chomel, 2019).

Tularemia (Francisella tularensis) - Tularemia has been documented and reported in bears in varying locations throughout North America, and the United States. The first recorded cases of Tularemia were in black bears residing in Alaska during the 1960s. Recently, black bears have yielded an antibody prevalence of 28%, while grizzlies sit at 19% (Chomel et al., 1998; Hansen, Vogler, Keim, Wagner & Hueffer, 2011). Most research and published articles note wild rabbits as the culprits for human transmission of tularemia. In Japan between 1924-1994 (70-years), wild rabbits were responsible for nearly 93% of human tularemia infections; there were only six cases of zoonotic tranmission recorded from bears in that time frame (O’Hara, Sato & Homma, 1996).

Leptospirosis (Leptospira spp.) - There is a high prevalence of antibodies to Leptospira spp. in brown bears, documented in several locations throughout Europe. Between 1981-1991, brown bears in Croatia reflected 40% (17 of 42 bears). Again, between 1998-2007, the prevalence was at 36.5% (19 of 52 bears) (Modric & Huber, 1993; Slavica et al., 2010). It is believed that bears may contract this bacteria from living & occupying similar spaces in the proximity to rodents. In Alaska, based on serum samples collected in five locations between 2013-2016, 7% of 104 brown bears reflected seropositive results (Ramey et al., 2018). The hotspot during the study between 2013-2016 was Lake Clark National Park & Preserve (Ramey et al., 2018). An important human-health consideration is that once a bear contracts, and recovers from this bacterial infection, they are fully capable of shedding the bacteria. In this respect, humans need to avoid bear excreta (Di Salvo & Chomel, 2019; Ramey et al., 2018).

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Lyme Disease (Borrelia burgdorferi) & Anaplasma phagocytophilum & Ehrlichia spp. – Researchers who have collected ticks from bears across the United States have found antibodies to Rickettsia spp., Anaplasma phagocytophilum, and Ehrlichia spp. (Binninger et al., 1980; Bronson et al., 2014; Chern, Bird, Frey, & Huffman, 2016; Leydet & Liang, 2013; Ruppanner et al., 1982; Skinner et al., 2017; Stephenson et al., 2015; Yabsley, Nims, Savage, & Durden, 2009). Lyme disease caused via infected ticks also has been documented in brown bears in Scandinavia (Paillard et al., 2015).


​Q fever (Coxiella burnetii) – The bacteria which causes ‘Q fever’ in humans, has been frequently documented in brown bears in Europe (Croatia), and less so in brown bears in North America. Infection in humans can be caused through the inhalation of dust particles, meaning that those participating in animal husbandry of bears, or conducting den survey, should take elevated caution (Di Salvo & Chomel, 2019).

Tuberculosis (Mycobacterium tuberculosis) –Little is known about tuberculosis in brown bears globally. In recent years, researchers documented a case in Marsican brown bears in Italy (Fico et al., 2019). What we do know is that this specific bacteria, even when present in bears, poses a very low-risk threat to humans; this mainly applies to those working with bears in captive settings (Fefar et al., 2012; Kamdi & Hedau, 2016).

Virus

​Rabies - Instances of rabies have been documented in bears, but is infrequent (Krebs, Williams, Smith, Rupprecht, & Childs, 2003). There have only been four documented cases of clinical rabies in bears between 1992-2011. All cases reported and documented took place in the eastern United States and involved a raccoon variant of the rabies virus (Bronson et al., 2014). During November 2014, a rabies virus was isolated and sequenced from a brown bear which attacked an individual in the region of Primorsky Krai, Russia (Shchelkanov et al., 2016).

Influenza (H1N1 Influenza A) - Surprisingly, bears can contract influenza from humans. The 2009 H1N1 influenza A pandemic affected the sloth bears at the Smithsonian National Zoo in Washington DC. The virus itself was isolated from one bear with clinical respiratory signs, in addition to identifying all seropositive bears in this period (Boedeker et al., 2017). Giant pandas in China were also affected by H1N1 (Li et al., 2014).

Protozoa

Toxoplasmosis (Toxoplasma gondii) - The zoonotic transmissibility between bears and humans with toxoplasmosis is of great concern to bear hunters. Consuming undercooked bear meat or tissue containing cysts is a means of contracting toxoplasmosis (Tenter, Heckeroth, & Weiss, 2000). The detection of T. gondii is on a global scale, found in black, grizzly and polar bears (Bronson et al., 2014; Burridge, Bigler, Forrester, & Hennemann, 1979; Chomel, Zarnske, Karsten, Kass, & Mendes, 1995; Oksanen et al., 2009; Rah et al., 2005; Stephenson et al., 2015; Zarnske, Dubey, Kwok, & Ver Hoef, 1997). During a subsequent study, grizzly bears continued to exhibit antibody prevalence to T. gondii, reaching 44% (67 of 152 bears) within five regions in Alaska (Ramey et al., 2018).

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