Rosemary Drisdelle's Blog

Posted by Rosemary Drisdelle

A recent scientific paper details the results of a study that looked at twenty-five people with diagnosed Morgellons disease. The results are fascinating.

An unfortunate minority of people suffer from a group of symptoms including itching, and a sensation of something crawling on or under the skin; a belief in fibres or filaments that come out through the skin; a belief in a chronic parasitic infestation; and chronic skin lesions. These people are often passed off as delusional and encouraged to seek psychiatric help. To make matters worse, many do exhibit symptoms of emotional disturbance.

For those who think there may be more to it, a recent paper in the Journal of Medical Case Reports is a must-read (Harvey, Bransfield, Mercer et al). The researchers chose a study group of twenty-five people who fit their case definition of Morgellons, collected data on symptoms, and ran a battery of medical tests to see if they could find common abnormalities to help pinpoint the cause of the disease. They conclude that Morgellons is probably a “chronic infectious process.”

Abnormal findings in the study group included (among other things):

• Low blood pressure
• High resting pulse
• A decrease in NK (natural killer) cells, cells of the immune system
• Increased fasting insulin levels
• Increased TNF-alpha (tumor necrosis factor-alpha), which plays a role in inflammation
• Increased C-reactive protein, a protein that increases in inflammation

The researchers also noted a high level of certain autoimmune conditions. Patients with psychiatric diagnoses had been normal prior to developing physical symptoms of Morgellons, and the onset of symptoms frequently followed exposure to conditions of low sanitation.

These findings, the authors note, point to “a skin phenomenon, an immune deficiency state and a chronic inflammatory process.”

That should make a lot of people think (and Morgellons sufferers rejoice that someone is finally taking them seriously), but there are still a lot of questions to be answered:

• If Morgellons is an infection, what sort of infectious agent causes it?
• Which came first, the infection or the immune deficiency?
• What’s the relationship between delusional parasitosis (or delusions of parasitosis) and Morgellons?
• If exposure to unsanitary conditions is a risk factor, why isn’t there an epidemic of Morgellons in the Third World? Or is there?
• Is there any connection between the “hygiene hypothesis” and the rise of Morgellons in the industrialized world?

I hope these authors, and others, follow up with more research on Morgellons.

“Morgellons Disease; Illuminating an Undefined Illness: a Case Series.” Harvey, William T., Robert C. Bransfield, Dana E Mercer et al. Journal of Medical Case Reports 2009, 3:8243 (Open access at BioMed Central)

Posted by Rosemary Drisdelle

It’s long been suspected that various flukes play a role in the development of cancers in people who harbor the parasites. Schistosoma haematobium, Clonorchis sinensis, and Opisthorchis viverrini have all been implicated. Charlatans have capitalized on the association claiming that flukes are the cause of all cancers and offering treatment—a myth with barely a grain of truth: parasites account for a very small percentage of cancers (Parkin, 3030), and we are only beginning to learn how they might do it. A paper published in PLoS Pathogens (Smout, Laha, Mulvenna et al) reports on the detection of carcinogenic protein secreted by O. viverrini.

Millions of people in Southeast Asia, notably in Thailand and Laos harbor O. viverrini in the bile ducts of the liver, acquired from raw fish in the diet. A surprising number of those infected eventually develop liver cancer—theoretically the result of a combination of inflammation, dietary nitrosamines (found in foods that contain nitrates or nitrites), and a mitogen (something secreted by the fluke that causes cell division). Smout and colleagues think that they have found the mitogen.

Opisthorchis viverrini secretes a protein called granulin, which is then found both on and in the cells of the bile duct around the parasite. A similar protein found in humans is associated with cell division and the spread of cancer cells in a number of aggressive human cancers. Similarly, the granulin from the fluke causes cell proliferation, making it more likely that a tumor will form in the bile duct. The authors speculate that this cell proliferation might benefit the parasite either by providing it with additional food, or by helping to heal the damage feeding does to the bile duct.

The authors suggest that it might be possible to develop a vaccine to the granulin produced by O. viverrini to reduce the health impact of the parasite in areas where it is prevalent. Perhaps this discovery will lead to similar findings for other flukes associated with cancer.

“A Granulin-Like Growth Factor Secreted by the Carcinogenic Liver Fluke, Opisthorchis viverrini, Promotes Proliferation of Host Cells.” (2009) Smout MJ, Laha T, Mulvenna J, Sripa B, Suttiprapa S, et al. PLoS Pathogens 5(10): e1000611. doi:10.1371/journal.ppat.1000611

“The Global Health Burden of Infection-associated Cancers in the Year 2002.” (2006) Parkin, Donald Maxwell. International Journal of Cancer: 118, 3030–3044

Posted by Rosemary Drisdelle

Strongyloides stercoralis infestation is apparently very common in the aboriginal communities of Australia’s Northern Territory: in some communities 30 – 40 percent of residents may have the parasite. The local Health Department reportedly has a bad attitude toward dealing with S. stercoralis, claiming:

• People need not be treated unless they have symptoms (and therefore no testing is required in people with no symptoms).
• Hand washing, washing of vegetables and other foods, and excluding dogs from human dwellings is sufficient to control spread.
• The parasite will disappear as the socioeconomic situation in affected communities improves, those currently infected die, and contamination in the environment eases.

All of that sounds good, but it’s an approach that likely won’t work for a number of reasons:

• As many as half of infected people have no symptoms. Unfortunately, while they remain infected they are at risk of serious disease if their immune systems stop controlling the infection. (Among other things, malnutrition can compromise the immune response, and malnutrition is more common in communities with low socioeconomic status.)
• Chronically infected, asymptomatic people can continue to contaminate the environment with the parasite for many years. (Infections can last forty years or more).
• Washing hands and food is fine, but most infections occur when bare skin contacts contaminated soil – when people go barefoot or sit on the ground.
• Dogs pass on the parasite in their feces – keeping them out of houses will not prevent infected dogs from defecating outside and contaminating the soil.
• Preventing transmission of the parasite means good sanitation with a sanitary sewage system – and people who never resort to relieving themselves outside. This is as difficult to achieve as getting everyone to wear shoes all the time. Meanwhile infected dogs and other animals will continue to contaminate the soil.
• The parasite has a life cycle stage where adults reproduce in the soil, keeping the environment contaminated indefinitely.

It would be very difficult to eradicate S. stercoralis in an area where it is so well established that a third of the residents have it. An integrated approach would certainly be needed including screening and treatment of infected people and domestic animals, a sanitary sewage treatment system, cleanup of known contaminated areas, public education, and ongoing surveillance over a number of years.

Further Reading

Doctors Concerned Over Killer Parasite. Bolton, Katrina. ABC News. Oct 10, 2009.

Foundations of Parasitology 6^th Ed. Roberts, Larry S. and John Janovy Jr. Boston: McGraw Hill, 2000.

Posted by Rosemary Drisdelle

Gnathostomiasis is not for the squeamish. A recent report (Herman, Wall, Tulleken et al, 2009) describes a man with an immature Gnathostoma spinigerum larva that traveled from his groin up across his rib cage, around (or through) to his back after a possible detour down his right leg, over his shoulder and up his neck. After wandering about inside his face, the larva exited through the skin below his nose. Awful as this sounds, it wasn’t the larva’s behavior that was unusual, it was the fact that the man got it in Botswana. This is a parasite of Southeast Asia and Japan. Only a handful of human cases have been reported in Africa since 1994—in Zambia and Tanzania.

Has G. spinigerum spread to Africa, and if so, how did it do so? The adult worms live in the stomachs of carnivores and are usually acquired—by both carnivores and people—by eating raw fish, or other raw animal flesh. Many animals are paratenic hosts including… birds.

Nothing moves about the planet as famously as birds. Jonathan Elphick’s Atlas of Bird Migration (Firefly Books, 2007) confirms that some birds, notably birds of prey do migrate through Southeast Asia to the region of Africa that includes Tanzania, Zambia, and Botswana. And birds of prey eat fish, invertebrates, and small mammals. It makes sense that a migratory bird might bring G. spinigerum to southern Africa, fall prey to a carnivore there and start up a focus of the parasite. It has probably happened multiple times, but sporadically, and not often enough to establish the parasite permanently—or perhaps it is permanently established. If human cases in Africa increase, we will know.

This raises the question of why we don’t see sporadic cases in other regions that receive migrating birds from Southest Asia and Japan. One must remember that we are only likely to see human cases where people habitually eat raw fish and other animal flesh.

Read the Report of Recent Cases Acquired in Botswana:

"Gnathostomisasis Acquired by British Tourists in Botswana." Herman, Joanna S., Emma C. Wall, Christoffer van Tulleken et al. Emerging Infectious Diseases 2009; 15(4): 594-597.

Posted by Rosemary Drisdelle

A recent scientific paper titled “The Origin of Malignant Malaria” (see full reference below) sheds light on how one of the worst parasites to infect humans evolved. Reports in the media paraphrase the paper as saying that Plasmodium falciparum transferred from chimpanzees to humans between 5000 and 10,000 years ago, and speculate on why the parasite causes such serious disease. The authors of the paper, however, make no conclusions about either of these things.

Stephen M, Rich and others conclude that the parasite P. falciparum evolved from the closely related chimpanzee parasite P. reichenowi relatively recently, and that the transfer happened only once. Both conclusions are supported by the fact that P. reichenowi has considerable genetic diversity while P. falciparum has very little (indicating that the chimpanzee species has been evolving much longer).

On the subject of when the transfer occurred, the authors comment that “considerable time, …many tens or hundreds of thousands of years, may have elapsed” (p. 4 of 6). They discuss the previous work of others, which indicates P. falciparum expanded and began causing serious widespread disease after the introduction of agriculture—perhaps between 5000 and 10,000 years ago. Its increased success was probably due to a combination of factors including deforestation, climate change, and the development of malaria-carrying mosquitoes that preferred human blood. It’s not clear whether P. falciparum caused serious disease before the expansion, or whether it underwent a genetic change that favored success and spread as well.

Read the paper by Rich, Leendertz, Xu, and others:

“The Origin of Malignant Malaria.” Rich, Stephen. M., Fabian H. Leendertz, Guang Xu et al. Proceedings of the National Academy of Sciences of the United States of America (PNAS early edition). July 13, 2009.

Recent Blog Posts:

The Origin of Plasmodium falciparum. Where Did Malignant Malaria Come From?

Posted by Rosemary Drisdelle

In his book Who Gave Pinta to the Santa Maria (Norton, 1997) tropical disease specialist Robert Desowitz wrote that study of the DNA of Plasmodium falciparum proved the malaria parasite had leapt from birds to humans (p.61 – 2). I thought this a fascinating discovery, and one that answered several questions for me: Why does P. falciparum look so different from the three other species of Plasmodium that infect humans? And why is P. falciparum so much more dangerous than the other species?

That a bird parasite looks different from a monkey parasite is not too surprising. And because we are very different from birds, their Plasmodium sp. might have to co-evolve with humans for a long time before it became less dangerous to us.

I should, perhaps, have been more skeptical—it’s a big leap from a bird to a human, and its less likely P. falciparum in the wrong host—the human—would spread from person to person with such efficiency.

Now, twelve years later, we’re told that, based on genetic studies, P. falciparum came from chimpanzees, and it did so relatively recently—perhaps 5000 to 10000 years ago. Is that short time span an explanation for the severity of malignant malaria, infection with P. falciparum? Not necessarily. Scholars like Christopher Wills and Paul W. Ewald write that disease causing organisms only become less deadly (virulent) if that makes it easier for them to get from one person to another. In the case of P. falciparum, there’s another possibility: the parasite may have become more virulent when humans settled down in permanent settlements because the parasite spread faster among relative crowds when its victims were sicker and less able to ward off hungry mosquitoes.

I wonder, though, why the same thing didn’t happen with the other three Plasmodium spp. of humans?