Home & Garden Columns
Last week I got a salutary reminder about the consequences—sometimes unforeseeable—of bringing exotic animals and plants to a new habitat. I was interviewing Melissa Miller, a Department of Fish and Game wildlife veterinarian, who studies the pathogen loads of sea otters. Miller happened to mention a die-off six years ago during which up to four sick or dead otters were being stranded every day along the coast between Morro Bay and Pismo Beach. The sick animals exhibited clinical signs of brain damage, and necropsies showed evidence of brain inflammation and enlarged lymph nodes. The casualties tested positive for a protozoan parasite called Sarcocystis neurona.
There are many described species of Sarcocystis, all with complex life cycles and definite host preferences. Some infect only reptiles, others waterfowl, others mammals. This degree of specialization suggests a long history of co-evolution with the terrestrial vertebrates, although I don’t know if anyone has looked at Sarcocystisgenetics and sorted out the relationships.
Some species have an intermediate host in which the parasite bides its time, hanging out in muscle tissue and lymph nodes, before that host is eaten by a carnivorous definitive host. Sexual reproduction only occurs in the body of the definitive host, which sheds the organism’s oocysts—think of them as eggs—in its feces. That’s similar to the life history of the notorious Toxoplasma gondii, in which rats are the intermediate and cats the definitive host. I refer you to Carl Zimmer’s Rex, for more on T. gondii, , which among other things alters the behavior of infected rats by reducing their fear response to cat urine.
The definitive host forS. neurona, is, of all things, the Virginia opossum. (I’ll stick with “possum” from here on, although that version technically applies to a group of not-all-that-similar Australian mammals.) It’s an asymptomatic carrier, a sort of marsupial Typhoid Annie. Domestic cats, skunks, raccoons, and armadillos have been identified as intermediate hosts. Possums, inveterate scavengers, appear to acquire the parasite by eating roadkill. Since motor vehicle encounters are not a significant cause of mortality in sea otters, that pathway is pretty much a dead end.
Once they leave the possum in their egglike stage, the parasites get washed into the ocean in winter storms (along with a host of other pathogens and toxins.) They’re picked up by filter-feeding marine organisms like mussels, which are then eaten by sea otters. Or at least some sea otters: Miller says a young otter picks up its food preferences from its mother. If mom favors mussels, so will her offspring.
S. neurona, can also be a serious problem for horses, who apparently acquire it through possum-contaminated feed or water and develop a neurological condition called equine protozoal myeloencephalitis. It’s treatable but may leave the victim permanently impaired and is prone to relapse; not something any horse owner would want to deal with. For more, see a summary from Purdue’s Animal Disease Diagnostic Lab.
This whole complex is relatively new to California. Possums aren’t native here: a founding population from Tennessee was introduced to the San Jose area in 1910 by some nostalgic Southerner. (One account mentions a 1900 introduction of Missouri possums.) Low-maintenance generalists, they’ve prospered in their new habitat, which includes our crawlspaces and outbuildings. Compared with such destructive exotics as feral pigs (which I’ll admit is setting the bar high), possums are relatively benign—except for their role as vectors for S. neurona. ,
I’m not advocating a possum purge, necessarily, although concerned horse owners might want to possum-proof their grain bins. But the possum-Sarcocystis, relationship is an sobering example of the kind of baggage exotic species bring with them. Whoever released those Tennessee (or Missouri) possums in San Jose has a lot to answer for.