Invasive Species and Disease: Rabbit, Rabbit

New isn’t always better. Invasive species, those entering an environment for the first time, are often unwelcome visitors; because they are free from their native predators and pathogens, their populations can reach extraordinarily high numbers, usually to the detriment of native species. Humans are often the cause of invasive species introductions, and at times, we try to cure the disastrous results, attempting control by any means, including unleashing disease.

Australia is famous for its native marsupials, from koalas to kangaroos. Historically, because its wilderness was chockablock full of creatures with pouches, it had little ecological space for placental mammals. That all changed in 1859, when a wealthy grazier, hoping to lay the foundation for the refined sport of rabbit shooting, released two dozen rabbits on his estate in southern Victoria. The rabbits bred like, well, rabbits, and within 10 years they had become a major agricultural pest across the subtropical regions of the country. By 1888, both the Australian and New Zealand governments were offering a substantial reward for a winning rabbit control strategy2.

What doesn’t kill you

As early as 1918, myxoma virus, the cause of a fatal South American rabbit disease called myxomatosis, was suggested as a means to cull the Australian rabbit population. The idea took a while to gain traction; testing under quarantine didn’t begin until 1937, and field trials weren’t underway until 1949. A year later, the disease spread way past the trial area, and caused high rabbit mortality. Since that was in fact the goal, the authorities quickly abandoned containment efforts and continued to release the virus through the 1950s, while monitoring the disease through laboratory testing. That’s when things went awry. Evolution, pushing its nose in where it wasn’t wanted, took action, and by 1957, it was clear that less virulent strains of myxoma were outcompeting the more virulent ones in the wild, reducing the rate of mortality. Not only that, but the 10% or so of infected rabbits that survived the epidemic continued to breed like, well, rabbits, and produced offspring that were more resistant to the disease2.

Despite this Darwinian turn of events, the campaign against rabbits wasn’t a total failure. The rapid reduction of the rabbit population gave the Australian landscape some much needed ecological breathing room, and cut rabbit populations down to 5-25% of their pre-1950 numbers. The program’s early success even inspired other countries to follow suit. In 1952 myxomatosis was released in France. Over the following decade, it spread across Europe (it’s actually still spreading), until the inevitable happened: the same evolutionary processes at work in Australia took hold in the Old World. But by the time the virus’ virulence declined and the rabbits’ resistance rose, the French rabbit population had been reduced by 90-98%. Unfortunately, there also appear to be some serious side effects. The devastation of rabbits in the Iberian peninsula, where they are a keystone species, has threatened the survival of the regions apex predators, the imperial eagle and the lynx3.

invasive species
It begins.

If you can’t beat them

In the 1980s, a different rabbit pathogen, rabbit haemorrhagic disease virus (RHDV), went from being unknown to having a global spread. RHDV is terrifyingly lethal; it can cause death within 24 hours. In 1988, after outbreaks among wild rabbits in Spain, RHDV was suggested for rabbit control in Australia. Things moved along more quickly this time, and by 1995, field trials were underway. Despite taking greater precautions (such as hosting the field trials on an island offshore, delightfully named Wardang Island), RHDV escaped the quarantine area and spread to the adjacent mainland. Within six months it had spread about 360km from the quarantine site. None of the carefully planned containment measures got the disease under control, so it was declared endemic, and the measures were abandoned. By 1996, RHDV was being deliberating released into wild Australian rabbit populations1.

Although it had been a party to the RHDV field trials, the New Zealand government decided against using the disease on their own rabbits. This decision did not sit well with farmers, who promptly ignored it, and within a month of the announcement, released RHDV on their own. After a month of failing to contain the disease (largely due to the fact that farmers continued to deliberately spread it), the government relented and legalized its use.

While it is too early to predict the long-term outcomes of releasing RHDV, it has clearly had a large ecological and economic impact: changing rabbit population cycles and reducing the population in affected areas by 85% (it has been particularly successful in hot, arid regions), increasing vegetation and the amount of grazable land (at least temporarily). But again, there are side effects. RHDV may have negatively impacted native wildlife, because it has left behind a legion of hungry domestic cats; the cats (another invasive species) had been feeding on rabbits, and have begun preying on native species in their stead1.

Novelty can come at a high price, as invasive species show. New ideas and approaches are inherently challenging, because we have no way to gauge what will happen, leaving only our best guess to guide us. Ecological systems are particularly delicate; they are extremely complex, and often precariously balanced. Adding anything to the mix can cause the whole thing to collapse, so the stakes of intervention (even when well-intentioned) are high. What else is new?


  1. Cooke, BD, and F Fenner. (2002). Rabbit haemorrhagic disease and the biological control of wild rabbits, Oryctolagus cuniculus, in Australia and New Zealand. Wildlife Research, 29:689-706.
  1. Fenner, F. (2000). Adventures with poxviruses of vertebrates. FEMS Microbiology Reviews, 24:123-133.
  1. Kerr, P. (2012). Myxomatosis in Australia and Europe: A model for emerging infectious diseases. Antiviral Research, 93:387-415.

Image source: Creative Commons,

Influenza: New You, New Flu

Alias: influenza, flu

It’s traditional to ring in the New Year by making resolutions, promising ourselves that this year we’ll change for the better. While, generally speaking, the flu isn’t a great role model (let’s hope making people sick isn’t a common resolution), it could teach us a thing or two about change. Influenza A (the type that causes seasonal flu) mutates at a breakneck pace: about 1 mutation per genome per replication, which is close to the maximum rate a viable organism (one that can survive and reproduce) can reach1.

Influenza mutates in two ways: slow and steady or all at once. Small mutations that commonly occur when the virus replicates are called antigenic drift. An antigenic shift is a very rare, sudden, and dramatic change that results in new surface proteins on the virus. These shifts and drifts have created a smorgasbord of human flus, including seasonal, avian (from birds), and swine and variant (both from pigs), with a wide range of severity and symptoms. The seasonal flu can cause everything from its typical mild illness to death. The elderly are particularly vulnerable; from 1976-2006, mortality has ranged from about 3,000 to 49,000 people per year, with 90% occurring in people over 65 years old2.

Antigenic shifts are the bigger, showier mutations, and they get most of the press, because they can produce new virus subtypes that humans are highly susceptible to, sometimes from a non-human source (i.e. bird flu). However, although it’s a bit less flashy, antigenic drift can also have big effects. This year, the form of influenza virus circulating in the US, H3N2, seems to have drifted just enough to reduce the efficiency of the flu vaccine, leaving more people than usual susceptible to the illness. This virus subtype caused greater than normal amounts of disease when it struck the US in 2012-2013, and it looks like 2014-2015 will be a repeat performance. So far, forty-three states have reported high levels of the disease, and in the last week of 2014, flu accounted for 5.9% of all clinic visits2. Change isn’t always good.

High resolution.

Cause: The flu is caused by a suite of influenza viruses. Two main types (Type A and B) spread in humans. Type A is broken into subtypes based on which forms of two surface proteins it contains: there are 18 different hemagglutinin (H) and 11 neuraminidase subtypes (N), and subtypes are named accordingly. The virus is spread through droplets coughed, sneezed or spat by infected people and inhaled or ingested by the uninfected. The ill can spread the flu to people up to 6 feet away. Most adults are infectious from 1 day before they show symptoms to up to a week after they become sick2.

Consequence: Seasonal flu results in a familiar suite of symptoms, including fever, chills, cough, sore throat, nasal congestion, muscle ache, headache, and fatigue. More rarely, it can cause vomiting and diarrhea. Most people recover within two weeks, but some develop complications that can lead to more serious illnesses, such as bronchitis or pneumonia, which can result in death. Avian flu and variant flu may result in severe respiratory illness2.

Cure: Prevention is the most effective protection against influenza; the flu vaccine reduces incidence of flu-related doctor visits by 60%, and even if it is not effective against the virus and the virus is contracted, it may still prevent illness and more serious complications. Other preventative hygiene practices, like washing hands with soap and water, and disinfecting commonly touched surfaces, are also essential in combatting influenza. A small number of anti-virals, like Tamiflu, are currently the only treatment for the flu2. Hopefully, that too will change.


  1. Drake, JW. (1993). Rates of spontaneous mutation among RNA viruses. Proceedings of the National Academy of Science, 90:4171-4175.
  2. “Influenza (Flu)”. Centers for Disease Control and Prevention. 9 January 2015. Web. 11 January 2015.

Image source: Creative Commons,