Parasite provides wolves the ability to become dominant in their packs
A study of almost 200 wolves in North America found that sick wolves were more likely to take charge of their group than their healthy counterparts. Furthermore, infected animals are more inclined to abandon their social groups and venture out on their own.
Toxoplasma gondii’s parasitic effect on its hosts’ confidence is a survival mechanism. T. gondii has to enter the cat’s body through the digestive system of its host in order to reproduce sexually. If the parasite influences the host to act recklessly, that outcome becomes more likely. Although studies have found conflicting results, infection is typically associated with less fear of cats and more exploratory behavior in rodents. People’s bodies and minds shift as a result, with increased testosterone and dopamine production and risk-taking behavior.
By consuming infected animals or swallowing T. gondii forms excreted in the feces of infected cats, warm-blooded mammals can contract the parasite. Muscle and brain cysts arise after an acute infection and remain latent for the duration of the host’s life. Up to a third of the population may be permanently afflicted.
Although T. gondii infections are common in wildlife, the effects on their behavior are poorly understood. A study found that the likelihood of lions preying on diseased hyenas in Kenya increased. Wildlife ecologists Connor Meyer and Kira Cassidy from the University of Montana in Missoula identified a unique chance to connect infection and behavior in wild wolves when they saw the extensive data on grey wolves (Canis lupus) collected in Yellowstone National Park, Wyoming, over the course of nearly 27 years. Yellowstone is home to both cougars (Puma concolor) and wolves, and the latter are known to steal prey from the former on occasion. The wolves risk infection if they consume the cats or their waste.
The researchers analyzed 256 blood samples from 229 wolves that had been tracked and studied for their whole lifetimes, with information on each animal’s social position and health documented. Meyer and Cassidy found that infected wolves were 46 times more likely to become pack leaders — frequently the only wolves in the pack that reproduce — and 11 times more likely to leave their birth family to create a new pack.
Meyer said that they got the result, and they just open-mouth stared at each other. This is far larger than they anticipated. The study appears in the current issue of Communications Biology.
This study provides solid evidence of the tremendous influence that diseases can have on the ecology and behavior of wild animal populations, according to Dan Macnulty, a wolf scientist at Utah State University in Logan. He also says it illustrates how important it is to keep track of wolves and other animals over time in Yellowstone.
The group plans to investigate in the future whether or not infection improves the chances of wolf reproduction and what the ecological effects of low or high infection rates might be. Because infected wolves have the option to move anywhere, a wolf population with a high T. gondii infection rate may grow rapidly across a landscape. If the pack leader is overly bold and reckless, the entire pack may soon follow, increasing the likelihood of a run-in with a cougar and putting more pack members at danger of contracting the disease.
Meyer concludes that this tale demonstrates how parasites can function as key components of ecosystems. He suggests that parasites may play a more important function than is currently believed.
However, Meyer argues that even brave, risk-taking wolves infected with the parasite are unlikely to end up as food for a cougar because of the wolf’s reputation for hunting cougars. He theorizes that American lions (Panthera atrox), enormous feline predators weighing approximately 200 kilos, who prowled North America until they went extinct around 11,000 years ago, could have been more prone to prey on diseased wolves in the past.
Keywords: wolves become dominant
Meyer, C. J. et al. (2022). Commun. Biol. https://doi.org/10.1038/s42003-022-04122-0
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