Toxoplasma gondii - Andrew Alexander’s Terrifying Parasite

“I felt like Frankenstein,” Alice Smellie quotes Andrew Alexander in the MailOnline. The Downton Abbey star apparently picked up a “terrifying” parasite more than a year ago and waited months for a diagnosis. When that diagnosis came, it was disturbing, no doubt, but “terrifying” is a bit over the top. (Admittedly, the prevailing dramatic and negative response to anything parasitic could account for the terror.)

 

The series Downton Abbey is set in the early 1900s.
No one was worried about toxoplasmosis then, but
other parasites were much more common in England
  than they are today.
      Image by JB + UK_Planet; CC BY 2.0

Toxoplasma gondii, a Terrifying Parasite

Alexander had Toxoplasma gondii – often simply called toxoplasma. Smellie writes that the not-so-terrifying toxoplasmosis is actually “an incredibly common bacterial infection.” She’s right that it’s common; in fact, as many as a third of people living in the UK are infected with the parasite. But T. gondii is not a bacterium, it’s a protozoan.

What qualifies T gondii as a disturbing, and concerning, parasite? A handful of things:

• It lives in your tissues, including the brain, and once you have it, you have it forever. 
• A first exposure during pregnancy can have truly terrifying implications for the fetus. 
• If you have it and your immune system falters (with AIDS for instance), reactivation of the infection can be fatal. 
• There is evidence that T. gondii can change behavior, and it is implicated in some forms of mental illness. 
• Acute infection can make you look like Frankenstein. (Well, it can cause swollen lymph nodes but it usually doesn’t).

Andrew Alexander’s Forever Parasite

Most people who walk around with T. gondii in their tissues never know they have it. The acute infection is typically mild and goes undiagnosed. Perhaps one or two in ten infected people have more severe symptoms like Alexander: flu-like symptoms with fever, headache, sore throat, achy muscles, swollen lymph nodes. Within a few weeks, even these people usually feel better, though it can take much longer.

When good health returns, it means that the immune system has won the battle – at least for now. The parasite is no longer multiplying rapidly and spreading; it has formed tiny cysts and basically gone dormant. In the parasite’s perfect world, a carnivore eventually eats the host and the parasite gets to infect that carnivore next. I suspect, however, that Andrew Alexander’s bradyzoites have reached a dead end.

How Did Andrew Alexander Catch Toxoplasma gondii?

Most people catch T. gondii in one of two ways:

• By eating meat that is not fully cooked. Lots of people eat rare, or raw, meat; domestic and wild animals are often infected with T. gondii. The meat you buy from the butcher might well contain bradyzoites. 
• By swallowing infective oocysts that have been passed in cat feces. Cats are the only host in which T. gondii multiplies sexually, and during acute infection, a cat passes millions of oocysts.

Smellie’s article relates that Alexander became ill after returning from Africa. Did he catch T. gondii there? Possibly. But he could have picked it up just about anywhere. This parasite is ubiquitous. Where was he one to three weeks before becoming ill? That’s where he got it.

Further reading:

Drisdelle, Rosemary. Parasites: Tales of Humanity's Most Unwelcome Guests. University of California Press. 2010

Smellie, Alice. "I looked like Frankenstein... the cast gathered round as if I was about to expire: Downton's Andrew Alexander reveals his battle with a terrifying parasitic infection." MailOnline; Oct 12, 2013.

"Toxoplasmosis: Toxoplasma Infection." The Center for Food Security and Public Health, Institute for International Cooperation in Animal Biologics. May 2005

Elephantiasis and Wolbachia: The Bacteria Behind the Worms

Horrific parasites sometimes turn out to be mere vessels.

Filarial worms, nematodes that are transmitted by insects and live in the tissues, cause horrible disfigurement, disability, blindness. The common names for the diseases they cause are descriptive and apt: elephantiasis, and river blindness.

Wucheria bancrofti, and Brugia malayi nematode worms live in human lymph vessels. Prolonged presence of the worms there often results in the affected part – often a limb or the scrotum - becoming grossly enlarged and deformed. Microfilaria, the worm’s young, circulate in the blood.

Elephantiasis results in almost
unbelievable disfigurement of
various parts of the body.
Imagine living with this.
Tropenmuseum of the Royal
Tropical Institute (KIT)
CC BY-SA 3.0

Onchocerca volvulus adults live together in nodules in the skin. Their young migrate through the skin and, over the long term, can cause discoloration, aging, and sagging of the skin. Worse, microfilariae in the eyes cause blindness.

For a long time, we thought that the worms themselves, and the microfilariae, caused these terrible responses to infection – that the battle between the human body and the worms caused blindness and disfigurement. But now it’s becoming clear that the real culprit is not the worms, but a type of bacteria living inside the worms. The problem is Wolbachia pipientis.

Wolbachia and Filarial Worms

Wolbachia is best known for living in insects, where it is typically parasitic and sometimes causes fatal disease. In nematodes, the relationship is different. In nematodes, Wolbachia is a symbiont: the bacterium actually provides nutrients to the parasitic worm that the worm can’t otherwise get, and without the Wolbachia, the worm can’t survive.

Researchers now have compelling evidence that what the human immune system responds to is actually the Wolbachia, not the filariae or the microfilariae. It’s the Wolbachia that causes elephantiasis and river blindness.

Wolbachia, Filarial Nematodes’ Achilles Heel

Treatment of the diseases caused by filarial nematodes has proven difficult for many reasons, not the least of which is that few drugs kill the adult worms. The discovery of their reliance on Wolbachia reveals a weakness that may be the worm’s undoing: instead of finding a drug to kill the worms, we can use a drug to kill the Wolbachia.

Ironically, if it’s the Wolbachia that’s actually the culprit, the worms end up as collateral damage.

Schistosomes: The Snail, the Prawn, and the Dam

It’s a story that has played out in Africa all too often. A river is dammed to control flooding, or for hydroelectric power, or to create a water reservoir in case of drought (or all of the above at once). The dam, of course, creates a large lake and lots of good habitat along the shore for aquatic plants, which in turn support a large snail population.

Schistosome Life Cycle

People come to live near the water’s edge, to use the water and to fish. Generally, human contact with water is high, particularly for children and fishers. If schistosomes are present, along with the right snail species, escalating levels of schistosomiasis soon follow. This is how it works:

• People infected with schistosomes pass the eggs in urine or feces, and if those eggs find their way into fresh water, they hatch.

• The emerging larva seeks out an aquatic snail – only the right snail will do – and penetrates the snail, after which it multiplies asexually in the snail’s tissues.

• Larvae leave the snail host and, if a human enters the water, penetrate human skin, maturing to adult worms that reside in the tiny blood vessels around the bladder or intestine.

• Adult worms produce eggs which are passed in the urine or feces, and so on.

It makes perfect sense that water resource projects can result in rapidly increasing incidence of schistosomiasis because they bring together the two hosts of the parasites – the human and the snail – in circumstances ideal for transmission. We hardly need a more complicated explanation. It seems, however, that there’s at least one other factor that’s been left out: the African river prawn.

River Prawns and Schistosomes

River prawns are not small!
This is Macrobrachium carcinus (molt).
Clinton & Charles Robertson. CC BY 2.0

Fascinatingly, the adult river prawn lives in fresh water, but the young require brackish water – a mixture of river water and sea water – in order to survive. When we dam an African river, we cut off access to the river’s mouth where the water is brackish. Adult prawns cannot migrate downriver; young prawns cannot migrate upriver. The prawn population upstream of the dam is doomed. And what do prawns eat? Lots of things, but one of those things is snails.

So just as the dam provides beautiful habitat for the proliferation of snails, it also wipes out a key predator of those snails. Instead of tasty prawns, people living on the shores of the reservoir get schistosomiasis. That’s a bad deal.

At least one project – Project Crevette - is now rearing the prawns and releasing them into an affected river, effectively reducing the level of schistosomiasis and providing food and marketable prawns for the people in the area. That’s a good deal.

Michael B. New writes that postlarvae (the stage of prawn young that migrate upstream) of at least one species “can climb vertical surfaces and cross land, provided there is abundant moisture available” (Farming Freshwater Prawns: A Manual for the Culture of the Giant River Prawn Macrobrachium rosenbergeii. Food and Agriculture Organization of the United Nations, 2003, pg 10). One wonders how difficult it would be to re-establish the natural life cycle of the river prawn.