Archive for the ‘Parasites: Tales of Humanity’s Most Unwelcome Guests’ Category
Reform Judaism Magazine has published an adapted excerpt from my book Parasites: Tales of Humanity’s Most Unwelcome Guests. The excerpt is a shortened version of my retelling of the story of Rahab, Joshua, and the Battle of Jericho, with the blood fluke Schistosoma hematobium as a central character.
Reform Judaism Magazine is an interesting publication. The online version features a number of articles that would appeal to any reader: titles that caught my eye include “Were the Jews Slaves in Egypt?,” “The Divinity of Dementia,” and “A Paragraph that Changed History” (“Why Jesus’ last supper could not have been a Passover meal…”). Fascinating.
It’s my pleasure to be published in this magazine. You can read Was Joshua the Hero of Jericho? on the internet.
As any good parasitology text will tell you, liver cysts caused by Echinococcus multilocularis typically occur in rodents: animals like voles, lemmings, and mice. The disease is called alveolar echinococcosis, or alveolar hydatid disease, and it occasionally occurs in people too, if eggs of the tapeworm are accidentally swallowed.
Echinococcus multilocularis liver cysts in dogs
The liver cyst caused by E. multilocularis is a larval stage – a stage that multiplies asexually in the cyst. The adult stage of the parasite is found in canids, members of the dog family: arctic foxes, red foxes, jackals, coyotes, domestic dogs. Thus, the 2009 discovery of a liver cyst in a domestic dog in British Columbia, Canada (Jenkins et al.), is puzzling and alarming.
This scenario is not actually so bizarre. Taenia solium, or pork tapeworm, has a similar story: humans normally host the adult tapeworm in the intestine after consuming the larval cysticercus in undercooked pork. But if a human swallows the tapeworm egg instead, the eggs hatches and the larva moves into the tissues – sometimes the brain – and forms a cysticercus.
When humans have T. solium cysticerci in their tissues, the disease is called cysticercosis – or, in the brain, neurocysticercosis – and this can be much worse than having the tapeworm in the intestine. Clearly, in a dog, a liver cyst that can grow large enough to compromise liver function, and spread to other parts of the body, is worse than hosting a tapeworm in the intestine as well.
In cysticercosis in humans, and presumably alveolar echinococcosis in dogs, the tissue cysts often originate from the hosts own intestinal tapeworms. In humans, it’s poor hygiene and hand to mouth transmission. In dogs, it’s grooming – licking eggs off soiled fur. This raises the question: have dogs always frequently had the liver cysts when they had the worms or has something changed?
Echinococcus multilocularis spreading to new places
Jenkins et al. remark that “compared with native North American strains, European strains of Echinococcus multilocularis appear to have greater potential to cause alveolar hydatid disease (AHD) in humans.” The strain found in British Columbia was a European strain; perhaps they have greater potential to cause AHD in dogs as well. Do we know?
The British Columbia dog apparently did not have the adult tapeworm in its intestine and the authors speculate that the parasite may have been introduced by an imported infected dog. This, too, is alarming. It brings to mind my discussion of E. multilocularis in Parasites: Tales of Humanity’s Most Unwelcome Guests, in which I relate the identification of Echinococcus multilocularis in wild canids smuggled into the Eastern US for fox hunting.
If one imported dog can introduce the worm to British Columbia, what is the likelihood that many illegally translocated infected canids have not spread the worm as well? Is alveolar echinococcosis simmering in rodents, dogs, and people in the eastern United States?
Jenkins EJ, Peregrine AS, Hill JE, Somers C, Gesy K, Barnes B, et al. Detection of European strain of Echinococcus multilocularis in North America [letter]. Emerg Infect Dis [serial on the internet]. 2012 June.
Roberts, Larry S., and John Janovy Jr. Gerald D. Schmidt & Larry S. Roberts’ Foundations of Parasitology 8th ed. Boston: McGraw Hill, 2009. Pg 354-5.
My CBC Ideas documentary, Worthy Parasites: A Villain’s Silver Lining, will air for the first time on Jan 8, 2013, at 9 PM.
Regular listeners of CBCs Ideas, hosted by Paul Kennedy, know that the program can explore virtually any topic in science, history, the arts, culture, religion or anything else you can think of. Interesting, provocative, and contemporary, it’s been on the air for decades and it’s always worth a listen.
That’s why I’m thrilled and honored to be the contributor of an episode that explores how species almost everyone loathes – parasites – are actually beneficial in many ways, even essential in our world. If you think parasites have no worth, think again, and listen to my one-hour episode in January.
CBC Ideas, Worthy Parasites: A Villain’s Silver Lining is available on CBC Radio One across Canada: Tuesday, January 8 at 9 p.m. (9:30 p.m. NT) and Monday, January 28 at 2 p.m. (2:30 p.m. NT). It will also be live streamed and streamed on demand on the CBC website, and available as a podcast.
You’ll be surprised by all the good things parasites do for you.
Would you take a drug to make yourself poisonous to mosquitoes, or black flies, or wasps? How about taking Ivermectin for bedbugs? I’m not so sure about this – the most obvious problem is that one would have to be bitten before it could work!
A recent article on Bloomberg.com suggested that giving people oral Ivermectin for bedbugs might be an effective way of dealing with a bedbug infestation. A very small study (three people) found that most bedbugs died if they fed on someone within a day of a dose of Ivermectin, and that 54 hours after the dose, 42% of bugs died after feeding.
Treating people who aren’t sick with drugs has precedent: it’s common for people traveling in places where mosquitoes carry malaria, for example, to take an anti-malarial drug to avoid infection. But while malaria can easily kill you, bedbugs have never been shown to transmit disease to humans.
Ivermectin is an antiparasitic and obviously an insecticide. Like all drugs, it comes with a risk of side effects, some of them quite serious. Would it really make sense to expose large numbers of people – people who aren’t infected with anything – to this drug? It seems to me that treating a dwelling with insecticides is one thing – sometimes not a very good thing – but turning people into insecticide laden bug traps is another.
Would it even work? Past research has indicated that bedbugs don’t feed every day. A 2009 study indicated that they might feed every two to three days and that they might synchronize their feeding (in other words, the bugs in a colony all tend to feed at the same time). Ivermectin is typically given as a single dose; how would we determine when it’s feeding day for the bedbugs? If the first twenty-four hours is crucial, you’d want to make sure you took the drug on the right day. And what if some survived or didn’t feed that day? And you’d need 100% participation from people staying in the dwelling. Imagine trying to do this in an apartment building. How many doses of Ivermectin would it take?
Finally, I suspect resistance would arise fairly quickly. If 42% of bugs died after feeding at the 54 hour mark, that means 58% survived – and they’d all been exposed to the drug. If their survival was due to them having more natural resistance than the other bugs, and they passed that along to subsequent generations, we’d see more and more resistance.
Before very long, the days of using Ivermectin for bedbugs would be over.
Gale, J. (2012) “Bed Bugs Dying After Merck Drug Suggests Possible Weapon.” Bloomberg.com
Reinhardt, K., Isaac, D. and Naylor, R. (2010), Estimating the feeding rate of the bedbug Cimex lectularius in an infested room: an inexpensive method and a case study. Medical and Veterinary Entomology, 24: 46–54. doi: 10.1111/j.1365-2915.2009.00847.x
No human parasitic disease has ever been eradicated (although we may be close to eradicating Guinea Worm), but if ever there was a target, it would be malaria. Keeping an eye on the news and medical journals convinces me that there has never been more activity in scientific research aimed at understanding the parasites that cause malaria and finding ways to thwart them. Researchers have tried to develop malaria resistant mosquitoes. They’ve uncovered how the parasites invade red blood cells. They’ve investigated enzymes and proteins essential to the parasite’s survival. They’ve developed novel drugs. Hardly a day goes by when there is not something new. One might think we’re on the cusp of success.
But the reality is still grim. If you look at the statistics, you see that things are not really changing, at least not yet. Maps released by the Malaria Atlas Project allow us to roughly compare 2007 with 2010, and though there are clearly some changes (WHO statistics do indicate that the total number of malaria cases has dropped over the last decade), in the big picture they are minor changes that could easily reverse themselves.
This is discouraging. I wonder how long it will take for all this new research to provide us with a successful (and likely multi-pronged) approach to loosening the grip of this terrible disease.
There are a lot more maps on the Malaria Atlas Project site. Anyone interested in this should have a look.
Parasites can do you good. I didn’t discuss it at length in Parasites: Tales of Humanity’s Most Unwelcome Guests (I touched on it in chapter six), but I’m fascinated by the growing evidence that at least some of our parasites have good things to contribute to our health. The latest piece of that puzzle is research showing that hookworms can initiate an immune response in the host that actually speeds healing of tissue damage.
In their paper “An essential role for TH2-type responses in limiting acute tissue damage during experimental helminth infection,” Fei Chen et al report that in mice “IL-17 initially contributed to inflammation and lung damage, whereas subsequent IL-4 receptor (IL-4R) signaling reduced elevations in IL-17 mRNA levels, enhanced the expression of insulin-like growth factor 1 (IGF-1) and IL-10 and stimulated the development of M2 macrophages, all of which contributed” to healing (Nature Medicine, published online 15 January 2012). In other words, there was an inflammatory response to the worms at first, then inflammation was suppressed while healing was enhanced.
It’s reasonable that a healing response may have evolved to help the host’s body deal with damage done by the worms themselves, but of course the potential exists for us to use that response to help heal tissue damage from other causes. This new report also ties in with previous work that suggests the ability of some of our parasites to suppress inflammation may protect us from autoimmune diseases.
It does make sense to me that organisms that have been with us for millions of years would have a relationship of both give and take with the host. While it’s true that parasitic diseases are some of the worst we face, and hookworm is a nasty parasite, I think we need to set aside the idea that anything parasitic is utterly bad. Let’s get to know them properly before we send them to extinction. (Not that hookworm is in danger of going extinct any time soon.)
I think we still have a lot to learn about our relationship with our parasites, especially our “old friends.”
Anybody who knows anything about malaria knows that one catches it from a mosquito bite. Mosquitoes don’t just physically carry the parasite from person to person: they are a required host for Plasmodium spp., the agents of malaria. In the mosquito, the parasites multiply sexually, producing tiny forms called sporozoites which are injected into the next person the mosquito bites.
Clearly, the mosquitoes are infected just as people are, but we seldom feel sorry for the poor mosquitoes because, well, we hate them for all sorts of reasons. The mosquito, however, does have an immune system which tries to fight off invading Plasmodium sp. parasites; Mosquitoes don’t mean to transmit these dangerous parasites.
Humans have had a long and costly battle with malaria which, so far, we have not won. Though not self-evident perhaps, it makes sense that we might be able to enlist the help of the lowly mosquito to our mutual benefit, and that’s what some researchers at Johns Hopkins University have done. Yuemei Dong et al. have genetically modified the immune system of a mosquito species, Anopheles stephensi, giving it an enhanced ability to fight off invading Plasmodium falciparum, the worst of the malaria parasites in humans.
In order for this research to prove useful in the real world, the modified mosquitoes would have to be released into the wild and allowed to breed with wild populations (and hopefully do better than the wild type). Aside from the obvious need for caution when releasing a genetically modified organism into the wild, at this point we still don’t know whether:
- the resistant mosquitoes will do as well in the wild, faced with different A. falciparum strains
- other Anopheles spp., also malaria vectors, can be similarly modified (there are about 40)
- Plasmodium falciparum will develop resistance to the mosquito resistance
- all other species of Plasmodium infecting humans can be targeted this way
This breakthrough is not the answer to the battle against malaria yet, but it may be part of the answer.
Read the paper:
Dong Y , Das S , Cirimotich C , Souza-Neto JA , McLean KJ , et al. 2011 “Engineered Anopheles Immunity to Plasmodium Infection” PLoS Pathog 7(12): e1002458. doi:10.1371/journal.ppat.1002458
The life cycle of Plasmodium spp., agents of malaria, is one of the harder ones for a parasitology student to grasp. It’s full of difficult words such as gametocyte and shizogony, and involves multiplication in both humans and mosquitoes – two hosts about as different from each other as one could imagine. Likewise, the immune system is so complex that most people can only achieve a basic understanding.
Recently, both of these things got more complicated as researchers discovered how malaria may evade the immune system and thereby survive for long periods and cause new bouts of illness later. Aha! Some old mysteries have been solved, but parasitology students will likely groan.
Two species of Plasmodium, P. vivax and P. ovale, have long been known to remain hidden away in the human liver after an initial episode of malaria, returning to the blood weeks, months, or even years later to start the infection all over again. Two other species, P. falciparum and P. malariae, do not stay within liver cells (hepatocytes) but can still mysteriously reappear after all parasites have disappeared from the blood. Where do these parasites, thought to multiply in humans only in red blood cells and hepatocytes, go? At last, we think we know.
A paper by Michelle N. Wykes et al reports that plasmodia can hide within dendritic cells—white cells that are an important part of the immune response intended to eliminate these parasites – in the spleen, multiply inside the cell and return to the bloodstream later to reinitiate malaria (“Rodent blood-stage Plasmodium survive in dendritic cells that infect naive mice.” PNAS 2011).
Plasmodium spp. are not the first parasites known to use the host’s immune system against it in this way: Leishmania sp. parasites invade macrophages, an immune cell intended to kill them, and multiply within the cell before bursting out and spreading to other cells in the body. Other parasites, such as the schistosomes and trypanosomes, trick the immune system in other ways.
This discovery will have implications for the treatment of malaria. Not only will it offer new possible targets for drug therapy or vaccine, it will oblige us to take these infected white cells in the spleen into account in treating infections. The authors suggest that parasites within the dentritic cells may be in a state of “arrested” development and thus able to live a long time before reappearing. I’m wondering what role these arrested parasites might have in the development of drug resistance in Plasmodium spp. parasites.
Adam Dunn, author of Rivers of Gold and The Big Dogs, has posted an interview with me on his website, dunnbooks.com. Dunn’s latest book deals with a different kind of “parasite:” the less than saintly financial gurus of Wall Street. My favourite review of The Big Dogs (for obvious reasons) is “Dunn’s writing is like the candiru fish. It squirms its way into one’s cerebral cortex & is quite difficult to dislodge.” (Col. Lee T. Guzofski, Chief Executive Officer, G2G Enterprises, Inc.)
It was a pleasure corresponding with Adam Dunn.
Babesia microti was first recognized as a potential cause of human infection in New England in 1969. Before this, human cases of babesiosis involving other Babesia species were recognized in other places, chiefly Europe. The appearance and persistence of Babesia microti have been associated with high deer populations, increased human contact with the deer tick, Ixodes scapularis, and the presence of Lyme disease.
In 2003, a paper published in the American Journal of Tropical Medicine and Hygiene noted “Human babesiosis generally is detected in sites where Ixodes ticks are endemic only after Lyme disease has become well established” (Krause et al, “Increasing Health Burden of Human Babesiosis in Endemic Sites,” 68(4)). Why?
It’s tempting to explain away the late appearance of babesiosis by saying, well, physicians aren’t familiar with it, no one is looking for it, and most cases are mild anyway, so it’s simply being missed. As well, no one’s collecting data on diagnosed cases, so the incidence is unknown.
A current article published on SouthCoastTODAY.com discusses the work of Stephen Rich at the University of Massachusetts Amherst’s Laboratory of Medical Zoology (Clark, “Much to Learn About Babesia’s Spread”). Rich’s research on Ixodes scapularis suggests that Babesia microti is spreading inland at a much slower rate than Borrelia burgdorferi, the organism that causes Lyme disease.
Rich’s work tells us that the organism truly is not well established in new locales – there’s not as much of it there. This likely explains why cases of babesiosis lag behind cases of Lyme disease, but it still raises a big question mark. If ticks and Lyme are spreading, why is Babesia not spreading just as quickly? The answer isn’t clear, but it appears that something is slowing down transmission of Babesia from host to host.
Rich doesn’t say that Babesia is absent in places where ticks and Lyme have appeared, he says there is a “much lower incidence” (qtd. in Clark). I suspect that incidence will rise over time – it may take years – and eventually make babesiosis a significant health concern over a much larger geographical area. I hope surveillance and medical knowledge stay ahead of it. If nothing else, the risk of contamination of the blood supply should fuel increased interest in this organism.