Ophidiomyces ophidiicola is an emerging pathogen that causes snake fungal disease, a potentially fatal infection spreading rapidly across North America. We spoke to microbiologist Dr Jeffrey Lorch about his recent work to identify the fungus causing the disease.
For the past decade, dead snakes have been turning up in the dozens across the Eastern United States, all afflicted by the same mysterious illness. The animals have lesions and blisters along their length, and their scales are thickened and yellow, making their skin rough and crusty. The snakes’ snouts can become so swollen that the jaws misalign, and the eyes sometimes develop a strange milky coating.
The first reports of this disease came in 2006, when an already fragile population of timber rattlesnakes in New Hampshire was hit by an unknown pathogen that decimated the population, from forty down to just nineteen. Then, in 2008, scientists analysed the bodies of four dead snakes in Illinois and identified what they suspected was responsible – a fungus in their infected tissue that feeds off keratin, the protein that forms hair, nails and snake scales.
Snake fungal disease (SFD), as the infection became known, has since spread across 16 States and moved across the border into Canada. The problem is of growing concern for conservationists, especially as wild snake populations are currently thought to be in global decline. But before scientists can begin to tackle the disease, they need to determine for certain what causes it.
“Even though we had a strong correlation between the fungus and the disease, it was still just a correlation,” explains Dr Jeffrey Lorch, who runs the Diagnostic Microbiology Lab at the National Wildlife Health Center in the US. “So we wanted to know, is it just a fungus that takes advantage of necrotic [dead] skin, and something else is actually causing the lesions?”
To find out, Jeff and his team ran an experiment in the lab. They infected healthy red corn snakes with the fungus thought to be the culprit, Ophidiomyces ophidiicola. And, sure enough, after a few days the snakes began to show classic signs of SFD.
“Pretty much every snake we infected got the disease, but the control snakes didn’t,” says Jeff. “Snakes developed lesions relatively quickly, often within a few days. Over the next weeks, the lesions got progressively worse, and the snakes would end up shedding their skin to try to clear the infection.” Snakes will often shed to purge themselves of parasites, and infected snakes in the experiment shed twice as often as healthy snakes.
But it’s not always as easy for snakes in the wild to shed their skin. For one thing, it’s often cooler, so the animals’ metabolisms will be lower. As well as this, the fungus may interfere with the snakes’ eating habits – wild snakes with SFD are often emaciated through lack of food, and in the experiment some of the infected snakes displayed a loss of appetite. This combination means it’s likely that infected snakes in the wild would lack the energy to grow new skin and shed their old one, resulting in a feedback loop that makes the animal sicker and even less able to fight off infection.
Loss of appetite wasn’t the only strange behaviour that Jeff and his team observed. Some of the snakes began to rest in conspicuous areas of their enclosures, instead of remaining concealed in the sheltered parts. This is unusual behaviour for snakes, which are usually quite elusive but Jeff says it’s quite common in wild snakes with SFD. People have even documented infected snakes coming out during winter when they should be hibernating.
One theory is that the snakes are trying to bask. As snakes are cold-blooded and can’t regulate their own body temperature, basking could be a way to raise their metabolism, allowing them to better fight off the infection. “In reptiles generally, the immune system functions at a certain preferred temperature,” explains Jeff. “Lizards for example have been observed to seek out warm temperatures to induce fever. The fungus can’t grow above 37ºC, so if the snakes can survive that, they could kill the fungus.”
This kind of behaviour isn’t currently well documented in snakes. But Jeff says that his team could run future experiments to see if infected snakes seek out warmer temperatures and weather that helps them fight disease.
Now that there is an established link between O. ophidiicola and SFD, the next steps will be to understand why the disease is emerging right now, and where it might have come from. Scientists aren’t sure whether the fungus has been introduced to affected areas, or has always been present and is only now causing serious disease. Factors such as climate change and fragmentation of the snakes’ natural habitats could also mean that wild populations are increasingly finding themselves in environmental microclimates that encourage infection.
If environmental changes are driving disease, Jeff and his colleagues are concerned that this could just be the tip of the iceberg. Snake conservation is tricky at the best of times, not least because snakes are so cryptic. It’s harder to monitor and track wild snake numbers compared to other animals, which means that information on population sizes isn’t easy to come by. But people’s preconceptions about the animals don’t help either.
“When I first starting studying SFD, I thought it was going to be challenging to get people to care,” admits Jeff. “Interest isn’t always there for snakes versus more charismatic animals. Particularly in the US, they’re quite maligned as wildlife, and you still get people who think snake populations should be wiped out.
“But overall, I’ve been surprised by the favourable reaction, and I think human viewpoints on snakes are changing. I think we also need more research into the economic and ecosystem services that snakes provide – they can form an important base of the food chain, and they eat large numbers of rodents. So their impact on preventing destruction of crops and reducing the spread of disease from other animals may be underappreciated.”