From the humor they provide in funny pet videos to the physical comfort of waking up next to a furry friend in the morning, your ordinary housecat is probably a source of  great joy in your life. Unfortunately, cats have had a mostly negative impact in the ecosystems we’ve introduced them to. Many cats are infected with Toxoplasma gondii, a zoonotic, protozoan parasite that only sexually reproduces in the intestines of domestic and wild felids. The widespread infection of cats with T. gondii has led to its equally broad distribution across the globe, including areas where no native felids exist. The oocysts, or eggs of this parasite are masters of survival: experiments have shown that activated T. gondii oocysts can survive up to 28 days at -20°C and could potentially survive for years in cold but moist environments (4°C in water) [1], [2]. Infection with T. gondii has been linked to abortions in livestock, deaths in endangered wildlife and most concerningly, congenital defects in human infants. My research focuses on transmission on these last two fronts, specifically in Northern California and Rio de Janeiro State, Brazil.

Animals that historically have not had exposure to T. gondii often have severe symptoms after infection, including death. The relationship between T. gondii infection and deaths in the endangered Southern sea otter (Enhydra lutris nereis) is well studied and hits close to home here in Northern California [3]–[5]. Since T. gondii is a terrestrial parasite and cats are not known for their swimming ability (otherwise we might have the “kitty paddle”), you might wonder how parasites in cat poop end up in the ocean. Parasite transport can occur due to a process called surface runoff, where rainfall washes away the top layers of soil and pulls it to lower elevations until this polluted water reaches the ocean.

---

When T. gondii oocysts reach the ocean, they can attach onto kelp beds or be sucked up by an oyster or mussel that’s filtering water. A sea otter that eats an infected oyster may then unknowingly consume these oocytes. Infected otters can experience brain inflammation, which can lead to death or make the otter more vulnerable to other illnesses or attacks from larger predators [5]. There are only around 3,000 Southern sea otters in the wild today, so each individual is vital for conservation efforts .

My current research focuses on studying cat populations of highest risk, namely feral cats, that are releasing oocysts near sea otter habitat. Previous studies have shown that these outdoor, largely unmanaged cats contribute more oocysts to the environment, and we hypothesize that they also carry more of the parasite strains that have been isolated from dead sea otters [6]. Getting a more accurate picture of the quantity and type of oocysts that are regularly being defecated by cats near the California coast can tell us where sea otters are at highest risk for infection, and where human management may be beneficial to prevent further deaths.

---

The risk of toxoplasmosis has decreased over the years in high income countries, but high infection rates still persist in many middle- and low-income nations such as Brazil. Asymptomatic Toxoplasma infection is common in humans, but infection with virulent strains can be an issue for healthy adults, immunocompromised people, and developing fetuses [7]–[9]. Acute exposure and infection for the first-time during pregnancy can lead to miscarriage or significant ocular and brain deformities in children. It can be painful to lose a pregnancy to a preventable cause, or to have increased lifelong costs to treat and manage the symptoms of congenital toxoplasmosis. Brazil has one of the
highest reported prevalence of congenital toxoplasmosis in the world, with an estimated 7,396 cases per year, or 2 per 1,000 live births [10]. Some of the hypothesized reasons for the high disease burden in Brazil are the presence of many wild felid species in addition to feral cats that shed oocysts, more virulent strains of T. gondii in the environment, and lack of clean drinking water for a significant proportion of the poorest populations, which can result in a higher risk of exposure to oocysts in water [11]. This differential access to treated water is an important but understudied socioeconomic risk factor which I, as part of a collaboration with Brazilian doctors and researchers, am studying along with climate variables such as temperature and humidity to identify and highlight risks, especially in vulnerable populations. Assessing both socioeconomic and climatic factors can help us build a unique understanding of environmental risk overall, and create more accurate, targeted policies to reduce acute infection in pregnant women [12].

.

---

Despite being one of the most common and pervasive parasites globally, T. gondii research and management still has extensive room for continued advancement. Further investigation of risk factors for humans and wildlife will help us identify the most impactful management actions we can take to prevent the greatest number of cases and deaths. In both cases covered we recognize two broader themes, namely how pollution, particularly biologic pollution, can be dangerous and how a clean environment and clean water is not just a matter of preference or cleanliness but a matter of life and death.

As we take steps to decrease T. gondii transmission, some social and cultural priorities could include increasing awareness for vulnerable populations, educating people, especially cat-owners, about the role of cats in pathogen transmission, and improving methods to filter and deactivate oocysts. Personal actions we can take with additional ecosystem benefits beyond T. gondii transmission, are preventing all forms of physical and biologic pollution, spaying and neutering cats to reduce the number of potential hosts, and keeping cats indoors to prevent oocyst contamination in the environment. Humans have played a major role in the invasion of cats (and their parasite hitchhikers) across the world and this has resulted in the detrimental effects on wildlife and human health that we see today. It’s been incredible as a scientist to see how these divergent stories are connected by this wildly successful parasite, and though it is not the fault of cats and other felids for spreading T. gondii, it is imperative that we take responsibility to reduce risks for humans and wildlife.

Sophie Zhu is an Epidemiology PhD candidate in the Department of Pathology, Microbiology, and Immunology at the UC Davis School of Veterinary Medicine. She is interested in infectious diseases, mathematical modeling, and looking at pathogen transmission through a One Health lens. Currently, her research focuses on the protozoan parasite Toxoplasma gondii and its effects on marine mammals and in human pregnancy. Contact info: sozhu@ucdavis.edu and @sophiezoo on Twitter

References

[1] J. P. Dubey, “Toxoplasma gondii Oocyst Survival under Defined Temperatures,” J. Parasitol., vol. 84, no. 4, pp. 862–865, 1998, doi: 10.2307/3284606.
[2] J. K. Frenkel and J. P. Dubey, “Effects of freezing on the viability of toxoplasma oocysts,” J. Parasitol., vol. 59, no. 3, pp. 587–588, Jun. 1973.
[3] K. Shapiro, E. VanWormer, A. Packham, E. Dodd, P. A. Conrad, and M. Miller, “Type X strains of Toxoplasma gondii are virulent for southern sea otters (Enhydra lutris nereis) and present in felids from nearby watersheds,” Proc. R. Soc. B Biol. Sci., vol. 286, no. 1909, p. 20191334, Aug. 2019, doi: 10.1098/rspb.2019.1334.
[4] M. A. Miller et al., “Coastal freshwater runoff is a risk factor for Toxoplasma gondii infection of southern sea otters (Enhydra lutris nereis),” Int. J. Parasitol., vol. 32, no. 8, pp. 997–1006, Jul. 2002, doi: 10.1016/S0020-7519(02)00069-3.
[5] C. Kreuder et al., “PATTERNS OF MORTALITY IN SOUTHERN SEA OTTERS (ENHYDRA LUTRIS NEREIS) FROM 1998–2001,” J. Wildl. Dis., vol. 39, no. 3, pp. 495–509, Jul. 2003, doi: 10.7589/0090-3558-39.3.495.
[6] E. VanWormer, P. A. Conrad, M. A. Miller, A. C. Melli, T. E. Carpenter, and J. A. K. Mazet, “Toxoplasma gondii, Source to Sea: Higher Contribution of Domestic Felids to Terrestrial Parasite Loading Despite Lower Infection Prevalence,” EcoHealth, vol. 10, no. 3, pp. 277–289, Sep. 2013, doi: 10.1007/s10393-013-0859-x.
[7] R. McLeod et al., “Outcome of Treatment for Congenital Toxoplasmosis, 1981–2004: The National Collaborative Chicago-Based, Congenital Toxoplasmosis Study,” Clin. Infect. Dis., vol. 42, no. 10, pp. 1383–1394, May 2006, doi: 10.1086/501360.
[8] J. D. Vaudaux et al., “Identification of an Atypical Strain of Toxoplasma gondii as the Cause of a Waterborne Outbreak of Toxoplasmosis in Santa Isabel do Ivai, Brazil,” J. Infect. Dis., vol. 202, no. 8, pp. 1226–1233, Oct. 2010, doi: 10.1086/656397.
[9] L. M. G. Bahia-Oliveira, J. L. Jones, J. Azevedo-Silva, C. C. F. Alves, F. Oréfice, and D. G. Addiss, “Highly Endemic, Waterborne Toxoplasmosis in North Rio de Janeiro State, Brazil,” Emerg. Infect. Dis., vol. 9, no. 1, pp. 55–62, Jan. 2003, doi: 10.3201/eid0901.020160.
[10] P. R. Torgerson and P. Mastroiacovo, “The global burden of congenital toxoplasmosis: a systematic review,” Bull. World Health Organ., vol. 91, no. 7, pp. 501–508, Jul. 2013, doi: 10.2471/BLT.12.111732.
[11] M. E. Grigg, J. P. Dubey, and R. B. Nussenblatt, “Ocular Toxoplasmosis: Lessons From Brazil,” Am. J. Ophthalmol., vol. 159, no. 6, pp. 999–1001, Jun. 2015, doi: 10.1016/j.ajo.2015.04.005.
[12] E. V. M. Carellos et al., “Adverse Socioeconomic Conditions and Oocyst-Related Factors Are Associated with Congenital Toxoplasmosis in a Population-Based Study in Minas Gerais, Brazil,” PLoS ONE, vol. 9, no. 2, Feb. 2014, doi: 10.1371/journal.pone.0088588.

[Edited By: Sabrina Mederos]