Archive for the ‘Parasites’ Category
A recent case of disseminated strongyloidiasis, reported by the New England Journal of Medicine highlighted a couple of intriguing features of this catastrophic disease: in the absence of an effective immune response, worms can mature in the lungs as well as the intestine, and, there’s something special about corticosteroid drugs that makes an unfortunate success of the worm.
Adult Strongyloides stercoralis in the Lungs
The case report of disseminated strongyloidiasis by Schroeder and Banaei describes adult worms, both rhabditiform and filarifom larvae, and ova containing active larvae in a tracheal aspirate. A similar case is reported by Bava et al. Typically, you’d find only filariform larvae in the lungs, and adults are almost never seen, even in the stool, because the adult females spend their time migrating through the tissues of the intestinal lining (and there are no parasitic males).
I assumed that the adults found in this case had actually matured in the lungs rather than migrating there from the intestine. A 2004 paper in Clinical Microbiology Reviews agrees. Keiser and Nutman write “…findings suggest that filariform larvae develop into adults in the lungs… This hypothesis is supported by… autopsy studies showing adult worms in lung tissue.” In this scenario, the parasite could be multiplying very rapidly with new worms originating not only in the intestine, but in the lungs as well. One can only imagine the numbers of parasites that could be present within a short period of time.
Corticosteroids and Strongyloides stercoralis
We know that corticosteroids can initiate disseminated strongyloidiasis. But do they just give the worms a green light by suppressing immune response, or do they actually favor the parasite? Corticosteroids prevent production of eosinophils and cause the rapid destruction of eosinophils that already exist; these cells are part of the body’s immune response to parasites. But it’s thought that corticosteroids actually contribute to the success of S. stercoralis in another way. Gary Simon writes in Medical Parasitology that “they may stimulate female worms to increase larval output and promote molting of rhabditiform larvae into the invasive filariform larvae.”
So it looks like giving corticosteroids to a patient with S. stercoralis expands the “territory” in which it can reproduce, hobbles the immune system’s attempts to control it, and boosts the worms’ fecundity and maturation. Given all of this, it’s easy to see why it might be difficult to save a patient suffering from disseminated strongyloidiasis, unless the problem is discovered quickly. It also sheds some light on why other types of immunosuppression are relatively less catastrophic.
Bava BAJ, Cecilia D et al. “Adult Female of Strongyloides stercoralis in Respiratory Secretions.”, Asian Pacific Journal of Tropical Biomedicine 3:4, April 2013, Pages 311–313
Castelletto ML, Massey HC Jr et al. “Morphogenesis of Strongyloides stercoralis Infective Larvae Requires the DAF-16 Ortholog FKTF-1.” , PLoS Pathogens 5(4): e1000370. doi:10.1371/journal.ppat.1000370
Schroeder L, and Banaei N. “Strongyloides stercoralis Embryonated Ova in the Lung.” New England Journal of Medicine: March 21, 2013; 368:e15 http://www.nejm.org/doi/full/10.1056/NEJMicm1204579
Simon, G. “Strongyloidiasis.” In: Medical Parasitology. Satoskar AR et al eds. Austin: Landes Bioscience; 2009, pg 31
Beauveria bassiana is a fungus that is well known for killing insects. Spores of B. bassiana adhere to the cuticle (the outer protective covering) of the insect, begin to grow, and work their way through to the inner tissues. There the fungal growth continues, taking nutrients from the host’s body until the insect dies. Because B. bassiana is lethal to many insects, including their larvae, it has been grown and distributed commercially for use in agricultural control of insect pests. It makes sense to wonder whether it could be used to control bedbugs as well.
Beauveria bassiana kills bedbugs
A study by Alexis Barbarin et al tested B. bassiana against bedbugs, and the results indicate that the fungus is lethal to the pests: not only does it kill virtually all bugs that come in contact with it, infected bugs can carry it back to daytime hiding places and pass it on to other bugs that have not been otherwise exposed. Barbarin el al propose that B. bassiana might rid a bedbug infested building of its bugs.
Bed bug traps using Beauveria bassiana
In their study, Barbarin et al exposed bedbugs to a mixture of oil and fungal spores on various surfaces, and found that jersey knit cotton transmitted the infection most effectively. Though further research is required, they propose that a fabric bed skirt impregnated with B. bassiana spores might be an efficient means of infecting a resident bedbug population. Presumably any trap designed so that all bedbugs climbing onto or leaving the bed would have to pass through it could be used to infect them with the fungus.
Is Beauveria bassiana safe for humans?
Beauveria bassiana is generally regarded as safe for humans and it’s already being used for insect control applications all over the world without dire consequences for human health. This fungus is already naturally occurring in the environment. However, there’s reason to be cautious with this approach. A study that tested fungi isolated from poultry barns found that B. bassiana has several virulence factors that potentially “increase [its] survival, growth, and propagation… in animal tissue.” Authors Taira el al comment, quite correctly, that otherwise harmless fungi can cause serious infections in people whose immune systems are already compromised. Such people include AIDs patients and organ donor recipients among others.
Cases of both deep tissue infection and skin infection caused by B. bassiana have been reported in the medical literature (Figueira et al). The possibility of skin infection, in particular, prompts second thoughts. Beauvaria bassiana does not wipe out bedbugs on contact: it takes time for the infection to kill. Therefore, bugs that have contacted the fungus will still visit the sleeping host to feed. And while feeding, they will create a break in the skin, often with severe irritation resulting, and possibly introduce fungal spores. This does not seem like a good plan.
Beyond the possibility of skin infection arising from contact with the bugs, a spore impregnated bed skirt would presumably contaminate a living space with fungal spores pretty thoroughly, and fungal spores are as hardy and as hard to eliminate as bed bugs are. Under the right conditions, they could remain viable for a very long time, possibly protecting against reinfestation by bed bugs, but also a potential hazard for the immunocompromised occupant of or visitor to the space.
Barbarin AM, Jenkins NE et al. “A Preliminary Evaluation of the Potential of Beauveria bassiana for Bed Bug Control.” Journal of Invertebrate Pathology 111 (2012) 82–85
Figueira L, Pinheiro D et al. “Beauveria bassiana Keratitis in Bullous Keratopathy: Antifungal Sensitivity Testing and Management.” European Journal of Ophthalmology 22:5 (2012) 814-818
Taira CL, Marcondes NR et al. “Virulence Potential of Filamentous Fungi Isolated From Poultry Barns in Cascavel, Paraná, Brazil.” Brazilian Journal of Pharmaceutical Sciences 47:1 Jan./Mar. 2011
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.
The tapeworm Echinococcus multilocularis normally spends its adult life in the intestine of a fox, usually an arctic or red fox. The fox acquires the worm by eating an infected rodent. In turn, the fox passes eggs in its feces, which rodents accidentally eat. In the intermediate host (the rodent or, sometimes, a human) the parasite occupies the liver rather than the intestine.
In the liver, the larva forms an alveolar cyst, a cyst composed of thin-walled chambers that multiply until the parasitic growth looks a bit like a mass of bubbles. These bubbles may break away and be carried to other parts of the body where they continue to grow. This is one reason why the alveolar cyst of E. multilocularis is often likened to a malignant tumor.
This is a nasty parasite and published accounts of the course of the disease in humans are rather horrifying. It spreads and is difficult to treat. It’s often fatal. This one, you never want to get. The literature and the media, meanwhile, lend the distinct impression that E. multilocualris is spreading and cases of alveolar echinococcosis in humans are becoming more common.
Distribution of Echinococcus multilocularis
A map in a 1984 parasitology text showing the global geographic distribution of E. multilocularis suggests that the worm has not broadened its horizons much in the last thirty years. In 1984, its range included most of Asia north of 40º latitude, Central and Eastern Europe, northern Canada, coastal Alaska, and a patch right in the middle of North America bisected by the Canada – US border and by 100º longitude. Today the distribution is marginally wider: more of Central Europe, parts of Western Europe, and the patch in the middle of North America has grown as well. Sporadic cases appear in other far flung regions: northern Africa, British Columbia in Canada.
So E. multilocularis is perhaps creeping rather than sweeping around the northern hemisphere. In truth, human infections are still extremely rare. Alveolar echinococcosisis, however, is “emerging” in humans in European locations, and there’s concern that it might do the same in parts of North America (most North American cases in the past have been in Alaska). In a recent paper in PLOS Neglected Tropical Diseases, Nahorski and others report that, in Poland, only two cases were known prior to 1980, compared with 121 cases diagnosed between 1990 and 2011.
Why is alveolar echinococcosis increasing?
Better diagnosis is certainly one reason for the increase, and Nahorski et al feel that many undiagnosed cases remain. They point to another possible cause however – a boom in the urban fox population. “In Poland,” they write, “the fox population increased from 67 000 in 1995 to 220 000 in 2006.” That’s a very significant increase, and many of the human cases came from provinces where the worm is especially common in foxes. The data led the authors to conclude that infected domestic dogs and cats are also important sources of the disease.
In order for a domestic animal to acquire the intestinal worm, the animal would have to eat an infected rodent. Cats, of course, are hunters, but according to the European Scientific Council Companion Animal Parasites (ESCCAP): “Cats, in contrast to dogs, are epidemiologically insignificant as sources of egg output as they are poor hosts for this worm.” Dogs are a different matter: they are good E. multilocularis hosts, and many domestic dogs do hunt. Many do not of course, especially urban dogs. One would have to know one’s dog to judge the relative likelihood that it would ever have E. multilocularis eggs in its feces, or on its fur.
Do foxes live in North American cities like they do in Europe? It’s true we don’t often read or hear about this, but they do: the city of Mississauga is one municipality that has addressed the issue of foxes in the city. And if those urban foxes have E. multilocularis, that could contribute to the emergence of alveolar echinococcosis in humans. But in North America, we have another canid that likes to live in cities, and it, too, can harbour E. multilocularis: the coyote. A study of urban coyotes in Chicago concluded that there are hundreds, perhaps thousands of coyotes living in that city, and those researchers believe that “the results likely apply to most major metropolitan areas in North America.”
So, while there’s no reason to be paranoid about this rare disease, awareness of it isn’t a bad thing. All the usual advice still applies: wash your hands often, keep your dog close, and provide your dog with good veterinary care including screening for intestinal parasites.
Beaver, Paul C., Jung, Rodney C., and Eddie W. Cupp. Clinical Parasitology 9th ed. Philadelphia: Lea & Febiger, 1984. Pg 534.
City of Mississauga. Animal Services: “Foxes.” 1995-2013
ESCCAP. “Worm Control in Dogs and Cats: ESCCAP Guideline 01 Second Edition.” September 2010
Nahorski WL, Knap JP, Pawłowski ZS, Krawczyk M, Polański J, et al. “Human Alveolar Echinococcosis in Poland: 1990–2011.” PLoS Negl Trop Dis 2013; 7(1): e1986. doi:10.1371/journal.pntd.0001986
Wagner, Holly. “On the Loose: Urban Coyotes Thrive in North American Cities.” Ohio State Research News. Last Updated 2005.
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
Naegleria fowleri: a protist that can be a cyst, an amoeba squelching along, or a whirling swimming flagellate; an organism found all over the world that loves warm water, a free living organism that can adopt a parasitic lifestyle; an organism that will almost certainly kill you if it gets into your brain. Beautiful. Fascinating. Deadly.
Every year during the sweltering days of summer we hear of deaths caused by the “brain eating amoeba.” This year a man died after teaching his daughter how to swim in an Indiana lake, and several children in other American states died after swimming in warm fresh water. Children have died after playing in bath water at home, and the use of neti pots to rinse the sinuses, or ritual inhalation of water into the sinuses, has resulted in deaths as well. The disease is called primary amoebic meningoencephalitis, or PAM.
Naegleria fowleri is just one of more than 20 Naegleria species found in the environment, but to date it is the only one found in human cases of PAM. What’s so special about N. fowleri? Perhaps it has something to do with N. fowleri being a thermophile – in other words it loves warmth. It can survive at temperatures as high as 45ºC, which would make it very comfortable at a normal human body temperature, and impervious to the highest fever. But many of the other species like high temperatures as well, so that’s not the whole answer.
Perhaps it’s important that N. fowleri adapts easily to axenic conditions – meaning that it doesn’t need a community of other organisms around to be happy; it can thrive all by itself. This does make it stand out from the other species, but living inside another organism isn’t exactly axenic, and strains of N. fowleri grown axenically in the lab lose their ability to produce disease. How this characteristic might help it invade the brain in the first place, then, and thrive there, is a tantalizing question – at least to me.
Studies have shown that N. fowleri isolated in the environment contain food vacuoles full of bacteria, whereas those isolated from cases of PAM contain vacuoles full of cell debris. So, when the organism is parasitic, it uses host cells as a food source instead of bacteria. It produces an enzyme that enables it to do this (Chang). This is clearly important, but do we know whether other Naegleria species produce a similar enzyme?
Perhaps it’s a combination of all these factors, and possibly others, that make N. fowleri uniquely equipped to be a “brain eating amoeba.” The question remains to be answered. What’s easier to understand is why it’s so rare, and yet so predictable. In order for N. Fowleri to get into a human brain, very warm water containing the organism must be inhaled into the nasal sinuses. This event is relatively uncommon, but can be expected to happen in the summer months when people – particularly young people – play in the water to cool off.
Chang SL. “Pathogenisis of Pathogenic Naegleria amoeba.” Folia Parasitol (Praha), 1979; (26)3:195-200.
De Jonckheere JF. “A Century of Reasearch on the Amoeboflagellate Genus Naegleria.” Acta Protozool, 2002; 41: 309-342.
Twenty-four small images of red blood cells appear on the screen. Your job is to click on any that have a malarial parasite inside, removing the image. When you’ve removed all the infected cells, click on “Label all Negative” and another twenty-four cells appear. At the end, you’ll get a score and some information about how many correct choices you made.
The game is called MOLT, and it was designed by the Ozcan Research Group at UCLA. Anyone can register and play. The idea is that anyone can be given some basic information about what malarial parasites look like in red blood cells and then be part of an accurate means of correctly diagnosing the disease without having to rely on experts in the field. This would be a huge improvement for malaria diagnosis in parts of the world where malaria kills millions each year and people skilled in diagnosis are rare.
A pilot study of the game using 20 gamers produced results that were within 1.25% of the accuracy of actual experts adept at recognizing malaria, which is pretty impressive. One can imagine an arrangement where someone puts a blood film on a microscope somewhere in Asia or Africa, the images are sent out electronically to potentially millions of gamers around the world, and the answer comes back, positive or negative, in a very short time. If the pilot is any indication, the answer would agree, most of the time, with what an expert would have said.
This has implications for lots of other things that are done by microscopy or other types of imagery: pap smears, fecal smears for parasites, pathology slides etc. It could be improved upon by adding automated scanning techniques and actual experts to the crowd of gamers. These things, plus a larger number of gamers would likely be even more accurate than the gamers used in the pilot. It’s exciting.
I’ve played the game – a number of times. I have lots of experience with reading blood films for malaria, and my biggest issue with the game is that the resolution – the sharpness – of the images is often not good enough
for me to feel completely comfortable with my choices. Platelets sitting on top of red blood cells can look like a parasite. So can debris on the slide. A red cell that’s damaged, or crunched up against another cell, or too darkly stained, or abnormal in some way, etc. etc., doesn’t look like it should to begin with.
I always want to look around a bit, see what the rest of the slide looks like, look for those particular features of a malarial parasite that leave no doubt. In other words, I have a very difficult time deciding whether something is positive or negative on the basis of only one cell (unless the resolution is very good).
My other complaint is with the scoring. I find it ambiguous. When they say “Correct Positive Diagnosis 91%” does that mean 91% of the cells marked as positive were actually positive (false positives), or 91% of positive cases were identified (false negatives). I think it means the latter, because it seems the fussier I am about calling something positive, the more my positive diagnosis score goes down. For anyone trying to improve at the game, clarification on this is important.
Of course I understand that the point is that people who are not experts, and not demanding in terms of excellent microscopic optics and parasite features, can still get the right answer if there are enough people providing input. From that perspective, I think the game is brilliant, and I hope it changes the world.
Play the game on Biogames
Read the paper:
Mavandadi S, Dimitrov S, Feng S, Yu F, Sikora U, et al. (2012) Distributed Medical Image Analysis and Diagnosis through Crowd-Sourced Games: A Malaria Case Study. PLoS ONE 7(5): e37245. doi:10.1371/journal.pone.0037245
We’ve known for years that Lyme disease is transmitted to humans by ticks. In Europe, it’s usually I. ricinus, the sheep tick, and any of a group of closely related organisms: Borrelia burgdorferi, B. garinii, or B. afzelii; while in my area it’s the deer tick, Ixodes scapularis, and B. burgdorferi. This is enough to worry about as the woods are full of deer and the deer are full of ticks. In some areas more than 30% of deer ticks carry Borrelia, and the ticks are not fussy: they’ll jump onto deer, dogs, cats, and people without hesitation. One hates to think that other biting arthropods could also be transmitting Lyme.
But studies going back as far as the 1980s, and perhaps even farther have found Borrelia in the guts of mosquitoes. Websites devoted to Lyme disease state that mosquitoes are transmitting the disease to humans. Why, then, does the CDC website say “There is no credible evidence that Lyme disease can be transmitted… from the bites of mosquitoes, flies, fleas, or lice” (Lyme Disease Transmission)?
It’s not a matter of a mosquito or tick sucking Borrelia out of one host and then simply injecting it into another like a flying (or crawling) syringe, not like pouring liquid from one glass to another with no change in the contents. Here we are dealing with interactions between living things. Research has shown that things happen in the tick, things that are important in transmission.
In the tick’s gut, Borrelia produces a protein that enables it to persist there for long periods of time, likely aiding survival until the tick feeds again. When the tick is feeding, the spirochete cuts back on this protein and produces a different one instead, one that enables it to invade the tick’s salivary gland and then be transmitted to the new host in the tick’s saliva.
Similarly, Borrelia is able to enhance a tick protein that protects both tick and spirochete from attack by the host immune system: “Borrelia burgdorferi, the Lyme disease agent, is critically dependent on the presence of the tick protein Salp15 when infecting the host” (Schwalie and Schultz). The extended time that a tick spends feeding (days) provides plenty of time for this interaction to take place.
In contrast, while Borrelia has been detected in mosquito guts and saliva, it doesn’t appear to survive there very long, probably because the proteins that support it in ticks don’t work in mosquitoes. Salp15, too, is a tick protein that won’t be available to help out in a mosquito, and mosquitoes take only minutes to obtain a blood meal, compared to days for a tick. Put simply, mosquitoes are not competent vectors of B. burgdorferi; they just don’t have the right stuff. While it’s not impossible that a mosquito bite could contain the spirochetes, it’s unlikely, and it’s even more unlikely Borrelia would succeed in setting up an infection. Mosquitoes are not significant vectors of Lyme disease.
Fontaine et al: Implication of haematophagous arthropod salivary proteins in host-vector interactions. Parasites & Vectors 2011 4:187 doi:10.1186/1756-3305-4-187
Hovius, JWR. Tick-host-pathogen interactions in Lyme borreliosis. Dissertation, Academic Medical Center, University of Amsterdam 2009
Kosik-Bogacka D, Bukowska K, Ku?na-Grygiel W. Detection of Borrelia burgdorferi sensu lato in mosquitoes (Culicidae) in recreational areas of the city of Szczecin. Annals of Agricultural and Environmental Medicine 2002, 9, 55–57
Schwalie PC, Schultz J. Positive Selection in Tick Saliva Proteins of the Salp15 Family. Journal of Molecular Evolution Volume 68, Number 2 (2009), 186-191, DOI: 10.1007/s00239-008-9194-1
Magnarelli LA, Anderson JF. Ticks and Biting Insects Infected with the Etiologic Agent of Lyme Disease, Borrelia burgdorferi. Journal of Clinical Microbiology Aug. 1988, p. 1482-1486
Reports this week of the death of Toola, a Toxoplasma gondii-infected sea otter who lived out her days at the Monterey Bay Aquarium, reminded me of the threat that T. gondii poses to marine mammals. Toola suffered from neurological damage thought to have been caused by the parasite and required daily anti-seizure medication. Among other things, she was the poster otter for legislation and other efforts to protect marine mammals from various health risks. And she was cute too.
My impression has been that the risk of acquiring T. gondii has been rising in marine mammals, and that this is likely to be the result of runoff – oocysts being washed off the land into coastal waters. This made sense to me when considering the number of feral and roaming domestic cats, and the quantity of cat feces that must be carried into coastal waters by runoff (this has actually been studied: “domestic feline faecal deposition in communities adjacent to Estero Bay was conservatively estimated at 107 metric tonnes/year, or 26 kg/ha:” Miller et al.) I was surprised; therefore, to read that the majority of California sea otters tested in the 2008 study reported by Miller et al had a unique strain (dubbed Type X) that is not typically found in domestic cats.
Rather, the paper by Miller et al. reports that Type X T. gondii was found in wild felids (mountain lion, bobcat) and foxes. While foxes might be doing relatively well in urban areas, the number of wild felids is down from what it must have been before humans covered the west coast of North America with concrete and asphalt. So if domestic cats aren’t to blame, why are there more infected marine mammals now than before?
One answer apparently lies in all that concrete and asphalt. Hardscaping of the coast reduces the amount of runoff that’s absorbed into the ground before it spills into the sea. In addition:
- Human development has reduced wetlands, which provide natural filtration for runoff.
- Bivalves such as mussels flourish near storm sewers and have been shown to filter organisms, including T. gondii oocycts out of the water and concentrate them in tissue.
- Sea otters feed on mussels and other bivalves, consuming at least 76 mussels each day.
Studies done on land mammals have shown that a single oocyst can potentially be the source of chronic toxoplasmosis. Given those odds, its not surprising that Toola, and lots of other California sea otters (and other marine mammals) are infected with T. gondii.
Read the paper:
Miller, M.A., W. A. Miller, P. A. Conrad et al. “Type X Toxoplasma gondii in a wild mussel and terrestrial carnivores from coastal California: New linkages between terrestrial mammals, runoff and toxoplasmosis of sea otters.” International Journal for Parasitology: 38(11), 2008
A paper in PLOS Medicine (January 24, 2012) reports that “sanitation is associated with a reduced risk of transmission of helminthiases to humans.” The authors looked at 36 previously published studies that measured prevalence of intestinal helminths (A. lumbricoides, large intestinal roundworm; T. trichiura, whipworm; and hookworm) compared to availability and use of sanitary facilities. They found that “people who either had or used a latrine were half as likely to be infected with a soil-transmitted helminth as people who neither had or used a latrine.”
I submit that there are no surprises here. One acquires hookworm by coming in contact with hookworm larvae from feces contaminating the soil. They penetrate skin. Trichuris trichiura and A. lumbricoides eggs, infective a week or so after being deposited in warm moist soil in feces, must be swallowed. Obviously if feces were deposited in a pit latrine, septic system or other sanitary arrangement, instead of on the ground, those eggs and larvae would not be available to infect new hosts.
The fact that intestinal helminthes are much less common, even rare, in developed countries is no mere accident of climate, especially for the tough A. lumbricoides. It is because the majority of people in developed countries don’t defecate outside on the ground.
The best point in this paper, though understated, is that periodically treating people for intestinal worms is perhaps not the best long term approach to getting rid of these parasites. Without good sanitation, people will quickly be reinfected due to contamination of their environment. Lets build toilets.
Read the paper:
Ziegelbauer K, Speich B, Mäusezahl D, Bos R, Keiser J, et al. (2012) “Effect of Sanitation on Soil-Transmitted Helminth Infection: Systematic Review and Meta-Analysis.” PLoS Med 9(1): e1001162. doi:10.1371/journal.pmed.1001162