Wednesday, 29 March 2017

Pinworm – A Common Intestinal Worm

Have you ever had a pinworm infection? Probably. Infecting 400 million people, pinworm is the most common nematode parasite of humans. It owes its success largely to the simplicity of its life cycle.

Pinworm eggs can only be seen through a microscope.
Adapted from Susan A Secretariat Catalina Maya Rendón

Pinworm (sometimes called seatworm) infection is infestation with the tiny roundworm Enterobius vermicularis. The infection, called enterobiasis or oxyuriasis, is common in children because they tend to be careless about hand washing and often put fingers in their mouths. It is also more common in women than in men, probably because women spend more time caring for children and therefore come in contact with the worm more often.

The female pinworm is 8mm to 13mm long (five-sixteenths to half an inch), while the male is so tiny that he would be very difficult to see without a microscope.

The Life Cycle of Pinworm

Human infection with E. vermicularis usually begins when an infective egg is swallowed:
  • Eggs hatch in the duodenum (small intestine), releasing larvae.
  • Larvae mature to adult male and female worms, which are found in the greatest numbers in the cecum (at the beginning of the large intestine).
  • Male and female worms mate and each female produces five thousand to fifteen thousand microscopic eggs.
  • Females travel along the length of the large intestine, ultimately exiting the body via the anus.
  • The majority of eggs are deposited on the perianal skin, though eggs are also laid internally and are passed in stool.
  • Eggs are distributed to clothing, bedding, and towels, and spread via the hands to household objects such as doorknobs, handles and taps. They also become airborne and settle almost anywhere with dust.
  • At normal body temperature, a pinworm egg matures within about six hours and an active larva can be found within.
  • Infective eggs are swallowed or inhaled and the life cycle begins again.

Life cycle of Enterobius vermicularis CDC
Some human parasites, such as Ascaris lumbricoides, the large intestinal roundworm, are infective only after the eggs have spent time maturing in warm moist soil. Others, such as Taenia saginata, the beef tapeworm, must pass through another host before they can infect humans again. These requirements limit parasites to places where the climate is warm or the other host is available. Because E. vermicularis passes directly from person to person, however, it spreads unchecked through human populations all over the world.




Symptoms of Pinworm Infection

We hear anecdotal reports of pinworm infections that sound positively agonizing. But many infections (as many as a third) cause no symptoms or very mild discomfort. In rare cases enterobiasis has more serious consequences.

The most common and revealing symptom is itching in the perianal area, possibly a result of the movements of female worms. Sensitivity to the eggs is also thought to develop with repeated infection. Scratching in response to the itching leads to lesions, increased irritation, and possibly bacterial infection.

Many people with symptoms complain of abdominal pain, and small lesions may develop in the intestine causing inflammation and sometimes infection. Other general symptoms include insomnia, irritability, grinding the teeth during sleep, loss of appetite, nausea, and even vomiting. Female worms sometimes migrate away from the anus and invade the vulva or vagina. Very rarely, worms penetrate intestinal tissue with serious consequences.

Diagnosis and Treatment of Pinworm Infection

Enterobiasis is usually confirmed when adult female worms and/or eggs are recovered from the perianal skin. Stool samples for parasitology sometimes yield worms and eggs as well, but this is not the best specimen choice.

Antiparasitic drugs clear up enterobiasis. Consult a physician or pharmacist, however, before self-treating. Unfortunately, reinfection typically occurs because other family members are also infected and infective eggs remain in the house. Physicians generally recommend that all family members take the drug, with a repeat treatment two weeks later. Because eggs in the environment dry out fairly quickly and it takes about a month for a swallowed larvae to mature and produce eggs, the second treatment should prevent a recurrence.

Further reading about pinworm


Roberts, Larry S., and John Janovy Jr. 2009. Gerald D. Schmidt & Larry S. Roberts’ Foundations of Parasitology. Boston, McGraw Hill.

Thursday, 16 March 2017

Chiggers – Nasty Parasitic Mites

Chiggers create a tube called a stylostome,
through which they suck juices from host
tissues. Illustration by Bugboy52.40

The young of chigger mites prey on mammals and other animals. They occasionally bite humans, causing unbearably itchy lesions.

What Are Chigger Mites?

The group of mites collectively known as chigger mites includes a wide range of genera and species distributed over the tropical and temperate regions of the globe. In North America, the species most commonly encountered is Trombicula alfreddugesi. Like spiders and scorpions, mites are arachnids; adults have four pairs of legs. The adults of the various chiggers feed on invertebrates (worms, snails etc.) and are seldom noticed, but the larvae are parasitic on mammals, birds, reptiles, and amphibians, and cause great discomfort when they feed on humans.

How do People Get Chiggers?

Chigger mite larvae hatch from eggs deposited in the environment, usually in tall grasses, brushy areas, swamps and bogs, and other localities where plant growth is low and thick. The microscopic larvae wait in the low vegetation and climb onto any animal or human moving through the area near them. On people, the larvae tend to migrate to areas where the clothing is snug – under waistbands, under the tops of socks, or where a backpack presses against the skin, for example.

Chigger Bites

Chigger mites neither burrow under the skin nor suck blood. Instead, they attach to the skin and inject a substance that creates a pool of liquid nutrients by dissolving and liquefying the skin cells. The host’s immune system responds by trying to create a barrier between the affected cells and healthy cells. A tiny tubular hole called a stylostome forms in the skin with the larva in the center, still drawing liquefied food from the tissues below the bite as though sucking through a straw.

Chigger bites first appear as fluid-filled blisters,
but scab over later. They are notoriously itchy.
Image by Dick Culbert CC BY 2.0
Most people have no idea they’ve been invaded by microscopic mite larvae while out in the woods and fields. For the lucky few, there will be no aftereffects: not all chigger mites cause discomfort and not all individuals react to the bites. For many, however, days of suffering are just beginning. About twenty-four hours after the initial bite, a red raised lesion appears, often with a fluid blister-like center. The mite is still present; it will eventually drop off if allowed to finish its meal but many are killed at this stage when the host scratches. The intensely itchy bite progresses over the next few days, becoming larger, turning slightly bluish like a bruise and crusting over. Scratching may lead to secondary infection of the lesions.

The agony of chigger bites is usually limited to the unbearable discomfort and occasional secondary infection; however, some chiggers are known to carry diseases. Leptotrombidium sp. chiggers in Japan, Southeast Asia, and nearby countries carry an organism that causes scrub typhus, or tsutsugamushi disease, a serious infection that is occasionally fatal.

Chigger mites are often confused with another skin parasite: Tunga penetrans, the chigoe flea. The two pests are quite different however.

Further reading

Knutson, Roger M. Furtive Fauna: A Field Guide to the Creatures Who Live on Us. New York: Penguin Books, 1992.

Schmidt, Gerald D. and Larry S. Roberts. Foundations of Parasitology 6th Ed. Boston: McGraw Hill, 2000.

Wednesday, 1 March 2017

A Revised History of the African Trypanosomes


Human African trypanosomiasis (HAT), or African sleeping sickness, was a smoldering disease before European colonization of the African continent. The famous American explorer Henry Morton Stanley has been blamed for spreading it across the tse tse belt of Africa from west to east in the late 1800s, setting off a series of epidemics that have killed millions and continue to this day. Similarly, nagana, the related disease in animals has prevented the rearing of livestock in the tse tse belt.

The tse tse belt of Africa. Trypanosoma brucei and the tse tse
fly are confined to this region. Image by Mba123; CC BY-SA 3.0
The tse tse belt, named for the blood sucking fly that inhabits its ecosystems, is pivotal in the history of the parasite. Trypanosoma brucei must complete part of its life cycle in the fly and the fly cannot live outside the tse tse belt; therefore, the parasite cannot either. Early theories suggested that the trypanosomes were originally parasites of insects that later invaded vertebrate hosts when the insects began feeding on blood.

African sleeping sickness is caused by subspecies of a protozoan parasite, Trypanosoma brucei. In his book Forgotten People, Forgotten Diseases, Peter J. Hotez sums up the long-accepted breakdown of the species: “T. brucei gambiense (T. b. gambiense) is the cause of human sleeping sickness in West Africa.... T. brucei rhodesiense (T. b. rhodesiense) causes HAT in East Africa.... A third subspecies, T. brucei brucei (T. b. brucei), does not infect humans.” Trypanosoma b. gambiense, we are told, does not infect animals. Trypanosoma b. rhodesiense infects both animals and humans. Trypanosoma b. brucei is death to domestic livestock.

Untreated, HAT is almost invariably fatal. Trypanosoma b. rhodesiense acts quickly, invading the central nervous system and bringing death within months. Trypanosoma b. gambiense causes a more chronic illness that can last for years. Because of this relatively milder course of disease, and because T. b. gambiense is said to infect only humans, it has been theorized that we have had it for much longer and are better adapted to it.

Much of this is probably wrong.

Where Did African Sleeping Sickness Come From?

This tse tse fly is in the collection of the
American Museum of Natural History.
Image by Tam Nguyen. CC BY-SA 3.0

Today, genetic studies tell us that the African trypanosomes evolved in Africa, having diverged from T. cruzi, the agent of South American tryanosomiasis. Stevens et al date this divergence to about 100 million years ago, when the two continents separated. They write that the most likely scenario is that the ancient ancestors of these species were parasites of small early mammals, and later adapted to larger animals and the tse tse fly vector.

According to Stevens et al the ancestors of today's pigs and hippopotamuses were predominant in Africa until about 23 million years ago. “It is interesting,” they write “that several present-day trypanosome species are specific to pigs... and that analysis of tsetse blood meals indicates suids [pigs] to be a favourite food source.... The ecological requirements of tsetse and pigs (forest and thickets) are also very similar.” Perhaps HAT was a long-time disease of pigs that jumped to humans.

Investigators have found T. b. gambiense in various wild and domestic animals in the tse tse belt. Macleod et al, however, write that “the principal reservoir host for T. b. gambiense appears to be the domestic pig.” These findings lend further support to the idea that pigs may have been host to the parasite for thousands of years before humans were, and challenges the long-held belief that T. b. gambiense is an exclusively human parasite.

Subspecies of Trypanosoma brucei

Modern genetic analysis has revealed much about T. brucei. According to Balmer et al, the subspecies T. b. rhodesiense probably doesn't actually exist; rather, populations infective to humans are apparently populations of T. b. brucei that have acquired the serum resistance associated gene (SRA). Evidence suggests that this genetic mutation has evolved more than once and can be passed from one T. b. brucei population to another.

Meanwhile, T. b. gambiense apparently evolved resistance separately and shows less genetic diversity than T. b. brucei, suggesting that it infected humans and spread relatively recently. This again contradicts the idea that the subspecies has had a longer association with humans, which brings us back to the explorer Henry Morton Stanley.

Stanley and the Spread of African Sleeping Sickness

A map showing the main slave trade routes in Medieval times.
Runehelmet derived from Aliesin. CC BY-SA 3.0
Balmer et al don't suggest how recently T. b. gambiense might have spread, or where it started from. We know that HAT was present in northern Africa centuries before Stanley's expeditions: Arab slave traders from the 14th century left accounts of African slaves with typical symptoms. As well, Roberts and Janovy write that “swollen [lymph] nodes at the base of the skull were recognized by [European] slave traders as signs of certain death, and slaves who developed them were routinely thrown overboard...”

It appears, however, that HAT was not widespread in the tsetse belt, or at least it took few lives until after Stanley established shipping routes on the Congo River and helped the avaricious and brutal King Leopold II of Belgium to exploit the people and resources of what became the Congo Free State. If Stanley's exploits were the first steps toward epidemic HAT in the tsetse belt, Leopold's virtual genocide likely ensured that spreading trypanosomes upriver in human bloodstreams would precipitate disaster (even today, poverty and war in the tse tse belt bring epidemics of sleeping sickness).

 Stanley's last expedition started from the mouth of the Congo in 1887 and lasted about a year, but a 1904 New York Times article dates the beginnings of the HAT epidemic to about a decade after Stanley: “About six years ago,” the article states, “missionaries on the Congo began to write home of a mysterious disease which was ascending the river.” It was a wave of disease that would be “sure death to every person attacked by it.”

Further Reading About the History of African Trypanosomes

Alsan, M. (2012) "The Effect of the TseTse Fly on African Development." (2012)

Balmer O, Beadell JS. (2011) "Phylogeography and Taxonomy of Trypanosoma brucei." PLOS Neglected Tropical Diseases 5:2

Baumeister RF, and Tierney J. (2012) "Henry Morton Stanley's Unbreakable Will." Adapted from Willpower, by Roy F. Baumeister and John Tierney.
Cordon-Obras C, Berzosa P. et al. (2009) "Trypanosoma brucei gambiense in domestic livestock of Kogo and Mbini foci (Equatorial Guinea)." Tropical Medicine & International Health
14:5 535-541 doi:10.1111/j.1365-3156.2009.02271.x

Hoare CA. (1972) The Trypanosomes of Mammals. Blackwell, Oxford.

Hotez PJ. (2007) Forgotten People, Forgotten Places. Washington, DC: ASM Press

MacLeod A, Tait A et al. (2001) "The Population Genetics of Trypanosoma brucei and the origin of human infectivity." Philosophical Transactions of the Royal Society London 356, 1035-1044.

Yale University Genocide Studies Program. "Congo Free State 1885 – 1908." Yale University Genocide Studies Program. Accessed March, 2017.

Stevens JR, Noyes HA et al. (1999) "The Ancient and Divergent Origins of the Human Pathogenic trypanosomes, Trypanosoma brucei and T. cruzi." Parasitology 118: 107-116

Steverding D. (2008) "The History of African Trypanosomiasis." Parasites and Vectors 1:3

The New York Times. (1904) "Tens of Thousands Killed by a Tiny Fly." SM2