Consider the Carpaccio: Looking at Toxoplasmosis

A parasite that infects the human brain, subtly changing its personality and social behavior, and capable of passing from mother to infect an infant in utero? That is the essence of a body horror, but this little rascal isn’t fiction. And it gets better: this parasite is considered to be one of the most successful parasites in the world due to its widespread, global distribution as well as its capacity to infect nearly every type of body tissue in all warm-blooded vertebrates (a). Schedule a phone conference with Spielberg and Cruise ASAP, guys, we’ve got the next sci-fi-action blockbuster on our hands (brains?). We’re looking at the ubiquitous protozoa Toxoplasma gondii and research on its capacity to modulate human personality and behavior.

T. gondii is an obligate intracellular parasite that has a vast host distribution, capable of infecting all species of mammals. Domestic cats and other felines are, however, the definitive host for the parasite’s reproductive stage. As such, all other animals serve as intermediate hosts of this polyxenous parasite. Humans are usually infected through consumption of infected raw or undercooked meats that happen to be studded with tissue cysts, typically lamb or pork (a). Turns out that T. gondii infection, known as “toxoplasmosis”, is the most common food-borne parasitic infection that requires hospitalization, and the third most common food-borne illness overall (b). Indeed, a study in 2002 conducted in the United Kingdom examined commercial meat sold in grocery stores and found that 38% of samples were infected with T. gondii cysts (h).

Examples of Toxoplasma gondii transmission. Image: Nature Education. Click for source.

Humans can also acquire infection through contaminated water and contact with cat feces that contain oocysts. Depending upon one’s diet and exposure to cats, researchers estimate that up to 80% of the population may be infected with T. gondii (k). Unwelcome news for lovers of carpaccio and cats.

Acute toxoplasmosis includes symptoms very similar to a cold – fever, headache, sore throat and coughing – along with a few psychopathological features including depression, anxiety, apathy and paraesthesia (“pins and needles” sensation) (c). The parasites (in the form of tachyzoites, one stage of its life cycle) infect macrophages and are distributed throughout the body. Over time, parasite-containing cysts form as a response to the body’s acquired immunity and are commonly found in the brain, lymph nodes, lungs and liver (a). In 60% of cases, infection is asymptomatic and many people are unaware that they’re even infected (g). The parasite does its worst damage among immunocompromised patients, either as a primary infection or as a recrudescent infection, and is a dangerous complication for those who are HIV-positive. Congenital transmission in which a woman becomes infected during pregnancy is also of public health concern. A newborn exposed in utero may be born with profound neurological and ocular sequelae, such as microcephaly, deafness, retina damage and mental retardation (g). Spontaneous abortion or stillbirth may also be another heart-wrenching outcome of primary toxoplasmosis.

T. gondii oocysts in a fecal floatation. Image: CDC. Click for source

A great literature review by Pappas et al. examined worldwide seroprevalence levels to craft a global epidemiological picture of the disease. Click here to check out the map. Prevalence of the disease was found to be highest in Europe and South America and may be attributed to a greater consumption of undercooked meats (b). Most infectious diseases are geographically limited to specific locales due to their climatic requirements, access to intermediate hosts and other factors. The most interesting aspect of toxoplasmosis is that these little buggers can be found everywhere in pretty much every population group of humans studied! Toxoplasma is a remarkably adaptive and successful parasite, and not only because of its ubiquitousness – it also keeps its hosts alive (for the most part) instead of scrambling our brains by provoking an inflammatory immune response.

An intriguing hypothesis is that infection can bring about personality and behavior changes (k). T. gondii is neurotrophic and exhibits a particular preference for the glial cells that provide support to the brain’s neurons. That toxoplasmosis may modulate human behavior is fascinating in itself as it’s already been proven with rodents; rats infected with the parasite show behaviors associated with decreased anxiety and neophobia, as well as increased levels of aggressiveness (d). Such marked changes have been interpreted as the parasite increasing the rodent’s risk of cat predation, adapting to its intermediate rodent host by enhancing the likelihood of transmission to its definite feline host (d). The mechanism is unclear but many speculate that the parasite’s location in such a privileged spot in the brain may affect neuro-immunomodulation and neurotransmission (f). Sneaky stuff.

So consider this: Toxoplasma may also affect its human host’s behavior so as to enhance the parasite’s transition to its definite host in the cat. In other words, the parasite may be manipulating how we think and act to maximize the possibility … of our brain being eaten by our feline friends.

Of course no such thing happens. But indeed, there are a few studies that have found correlations between toxoplasmosis and changes in personality profiles. One such study conducted in 2000 by Flegr et al. used Cattel’s 16 Factor Questionnaire, a self-reported personality profile survey, to look at differences in personality traits amongst acute and latent toxoplasmosis patients. Both stages of the disease were correlated with increases in warmheartedness, outgoingness, easygoingness and high will-power in women, while the same factors were associated with decreases in men (d). Infected women are more likely to respect social rules, be amicable, attentive and loyal to others than women who are uninfected; infected men are more introspective, suspicious and have low self-esteem (g). Both women and men score higher for levels of anxiety than those uninfected (d)(g). Women seem to luck out with toxoplasmosis, whereas men turn into something like a jealous ex-boyfriend stalking you on Facebook.

Light micrograph of a cyst containing T. gondii parasites (stained red) in brain tissue. Thousands of resting parasites can be seen enveloped by the thin parasite cyst wall. Image: Science Photo Library. Click for source.

I read these results and am hesitate to fully endorse them. Don’t get me wrong, it’s a neat idea. Brain zombies? I’m totally there! But maybe this is the molecular biologist in me, reluctant to believe self-reporting psychological surveys. These ideas of behavior and personality modulation are also pretty controversial. And, of course, there’s the issue of correlation versus causation. Does toxoplasmosis cause a change in one’s personality or does a type of personality (say, a Brazilian cat-lover who is fond of undercooked pork) predispose one to infection with toxoplasmosis?

The researchers claim that the fact that identical personality changes can be seen in both the acute and latent cases serve as an indication of the persistence of the parasite’s effect. In another study by Flegr that looked at infected women over the course of fourteen years, he claimed that the high anti-Toxoplasma antibody titre seen in these patients reflects the long-term duration of the infection and can thusly be attributed to long-term personality shifts (d). However, IgG antibody levels typically level off in chronic infections due to a reduction in antigenic stimulation as the parasite settles down into its new human home (i). Does the parasite permanently change a person’s personality upon acute infection or does it continually modulate it over time? There’s a lot of questions raised in the paper but, as a thought experiment, it’s an interesting read.

In a similar vein is an article written by Kevin Lafferty that uses Flegr’s results. In “Can the common brain parasite, Toxoplasma gondii, influence human culture?” Lafferty speculates that the personality profiles resulting from toxoplasmosis, with increased feminine qualities in women and more masculine ones in men, may explain “greater differentiation of sex roles” in countries with rigid gender norms (e). The relationship between toxoplasmosis and the common personality profiles of a population may explain some aspects of the “personality” of a culture, in particular gender roles and expectations (e). You can find it here. More thought experiment stuff, really.

So. Brains. Toxo. What to make of it? There’s a wealth of research and reviews out in Pubmed-land that look at behavioral and mental disorders and the prevalence of toxoplasmosis infection. Schizophrenia and epilepsy are the two main neurological disorders that seem to continually be coincident with toxoplasmosis (g). Of course, everything will boil down to the boxing match between correlation vs. causation, as well as the incontrovertible fact that infection, mental disease, personality and the reason why people like cats (no, seriously, why?) result from a multitudinous array of factors – genetics, history, culture and culinary taste – that probably have nothing to do with this parasite. But maybe that steak should be more on the medium rare side, hmm? It’s food for (neuromodulated) thought!

Resources

T. gondii is one of those crazy protozoan parasites with complicated life cycles. I greatly simplified the details and you should go to the CDC site to get more info about the biology and such.

If you’re curious about that Cattel 16 Factor Questionaire, you can take a look at it here.

References

(a) Despommier, D, Gwadz RW, Hotez PJ and Knirsch CA. Parasitic Diseases. 5th ed. New York: Apple Trees Production, LLC. 2006
(b) Pappas G, Roussos N & Falagas ME. (2009) Toxoplasmosis snapshots: Global status of Toxoplasma gondii seroprevalence and implications for pregnancy and congenital toxoplasmosis. Int J for Parasitology. 39:1385–1394
(c) Flegr J, Zitková S, Kodym P, Frynta D. (1996) Induction of changes in human behaviour by the parasitic protozoan Toxoplasma gondii.  Parasitology. 113 (Pt 1):49-54
(d) Flegr J, Kodym P, Tolarová V. (2000) Correlation of duration of latent Toxoplasma gondii infection with personality changes in women. Biol Psychol. 53(1):57-68
(e) Lafferty KD (2006) Can the common brain parasite, Toxoplasma gondii, influence human culture? Proc Biol Sci. 273(1602): 2749-55
(f) Fekadu A, Shibre T, Cleare AJ.  (2010) Toxoplasmosis as a cause for behaviour disorders–overview of evidence and mechanisms.  Folia Parasitol (Praha). 57(2): 105-13
(g) da Silva RC, Langoni H. (2009) Toxoplasma gondii: host-parasite interaction and behavior manipulation. Parasitol Res. 105(4):893-8 Epub
(h) Aspinall TV, Marlee D, Hyde JE, Sims PFG. (2002) Prevalence of Toxoplasma gondii in commercial meat products as monitored by polymerase chain reaction—food for thought? Int J Epidemiol. 32:1193–1199
(i)Remington JS and R McLeod. Toxoplasmosis. Infectious Diseases in Medicine and Surgery (3rd Edition). J Bartlett, S. Gorbach, N Blacklow (Eds). Lippincott Williams & Wilkins: Philadelphia, 2003
(j) Daryani A,  Sharif M, Hosseini SH, Karimi A and Gholami S. (2010) Serological survey of Toxoplasma gondii in schizophrenia patients referred to Psychiatric Hospital, Sari City, Iran. Tropical Biomedicine. 27(3): 476–482

Flegr J, Kodym P, & Tolarová V (2000). Correlation of duration of latent Toxoplasma gondii infection with personality changes in women. Biological psychology, 53 (1), 57-68 PMID: 10876065

Blood Money: Hookworm Economics in the Postbellum South

In the early 20th century, the Rockefeller Foundation embarked upon a massive public-health campaign that radically changed the economic landscape of the Southeastern United States. A parasite, the hookworm Necator americanus, not only had been leeching Southerners of their blood and good health but also of their agricultural productivity and wealth.

There are two types of hookworm, Ancylostoma duodenale, known as the Old World hookworm, and Necator americanus, the New World hookworm. While both species may be found in Africa, Asia and the Americas, N. americanus is predominantly located in the Americas and Australia, while only A. duodenale is found in the Middle East, North Africa and southern Europe (a). The origin of the New World species in North America has been attributed to the Atlantic slave trade beginning in the 17th century, where infected African slaves brought the parasite to the Americas (b). The hookworm quickly adapted to the loamy soil, humid climate and rainfall patterns of the Southeast that mimicked that of the African continent (d). The socioeconomic conditions of the South and the treatment of slaves also facilitated the spread of the hookworm due to an absence of sanitary outhouses, widespread use of feces as fertilizer in fields (known as night-soil), and lack of footwear for children.

Geographic distribution of Necator americanus. Image: Palmer & Reeder. Click for source.

Infection begins when the soil-residing larval form penetrates human skin, typically a bare foot. It then embarks upon a multi-organ journey through the body, traveling through the blood vessels, the heart and the lungs to reach the trachea. The larva are then swallowed and reach their journey’s end in the small intestine. Upon maturation, the adult hookworm latches onto the mucosa of the small intestine and begin to blood-suck. An individual may harbor up to several hundreds of adult hookworms, which typically live for 1 to 2 years but in rare cases can live up to a jaw-dropping 20 years (i). Highly fertile females may churn out as many as five to twenty-five thousand eggs a day (e). Eggs exit the body with the feces and, upon finding themselves in environmentally friendly circumstances such as warm, moist soil, will mature into larva. And so the cycle continues.

The hookworm exacts a heavy toll on those infected but especially on those that are “poorly nourished, badly housed and equipped, and barefoot” (e). Symptoms include anemia, weight loss, fatigue, and impaired mental function; the heavier the worm burden, the greater the severity of symptoms. In fact, the weight loss, lethargy and reduced mental capacity brought about by severe hookworm infection earned the New World hookworm the title “the germ of laziness” (h). The popular image during the American Civil War of the lazy Southern redneck with “sallow skin, bare feet, scrawny neck, protuberant abdomen, retarded intelligence, and shiftless habits” undoubtedly derived from endemic hookworm infection and its debilitating symptoms (h).

Harvey Laforce of Woodbine, Whitley County, Kentucky revealing the characteristic symptoms of hookworm infection. Image: Rockefeller Archives Center 220H 220L1. Click for source.

As you can imagine, endemic disease amongst rural Southerners had a profound effect upon agricultural productivity and economic development in the region. The loamy soil found in the Southern coastal regions was ideal for farming but was also exceptionally well-suited to rearing hookworm larvae; what should have been the most successful agricultural region in the South was hampered by the hookworm’s presence in the guts of farmers (c). Hookworms had their heyday during the Civil War, when levels of infection exploded due to substandard living conditions, poor health and lack of sanitary infrastructure (j). Several studies have found negative correlations between agricultural income per capita and hookworm infection amongst rural families involved in subsistence farming prior immediately following the end of the Civil War and prior to the onset of the Rockefeller Commission (g)(j).

In 1910, the Rockefeller Sanitation Commission for the Eradication of Hookworm Disease set about investigating the state of the disease in the South and discovered that a staggering 40% of schoolchildren were infected, with an estimated roughly 7.5 million Southerners harboring the parasite (g). They immediately set about initiating a multi-pronged approach to tackling the disease. One million dollars was invested in a five-year program in eleven states that focused on the education of physicians, school children and the public on hookworm symptoms and transmission, along with construction of sanitary infrastructure and the creation of traveling medical dispensaries for diagnosing and treating hookworm infection (d). A pretty neat educational video by the campaign titled “Unhooking the Hookworm” can be found below,

Studies have found strong negative correlations between agricultural income per capita and hookworm infection amongst rural families involved in subsistence farming prior to the initiation of the Rockefeller Commission (g)(j). Following the campaign, those regions with the highest infection rates, particularly in Louisiana, Florida, Mississippi and Alabama, saw significant income expansion. The graph below shows the change in log earnings for exposed and unexposed cohorts depending on year of birth. This analysis of state-of-birth and average income suggests that those individuals that were young enough to benefit from the Rockefeller Commission, and thus experienced lower rates of hookworm infection post-treatment, subsequently enjoyed higher average incomes in adulthood (f). Zero or less exposure to the campaign’s activities during childhood effectively correlates with lower income (f).

Cohort-Specific Relationship Between Income & Pre-Eradication Hookworm. Image: Bleakley H. (2007) Disease and Development: Evidence from Hookworm Eradication in the American South. The Quarterly Journal of Economics 122 (1): 73-117.

Highly infected states saw greater increases in income. Image: Bleakley H. (2007) Disease and Development: Evidence from Hookworm Eradication in the American South. The Quarterly Journal of Economics 122 (1): 73-117.

At the time, the Rockefeller Commission constituted a major investment in human capital in its improvement of school-age children health. Studies of the intervention indicate that the campaign resulted in a general increase in enrollment, attendance, and literacy (f). Those regions with infection rates greater than 40% showed especially swift increases in these levels compared to regions with average or lower infection rates (f).

From a purely bureaucratic and economic perspective, poor health and high rates of disease retard productivity and limit capacity for growth. In this case, hookworm infection deleteriously affected the agricultural output and economic development of the postbellum South. Similar trends may be seen with influenza, malaria, dengue and a host of other infectious diseases that affect the global workforce and economic productivity; a Report of the Commission on Macroeconomics and Health chaired by Jeffrey Sachs in 2001 found that “poor health has particularly pernicious effects on economic development in sub-Saharan Africa, South Asia, and pockets of high disease and intense poverty elsewhere” (k).

Though hookworm has been eradicated from North America, it remains a serious burden in Africa and is responsible for significant morbidity, disability and premature mortality. It is the one of the most common chronic infections on the continent, affecting a third of its population, mostly children aged 5 to 14 years (l). Looking at the history of the postbellum South and the economic implications of hookworm treatment from a selection of data gives an idea of the gravity of endemic infection. Providing shoes, treatment and sanitation options could revolutionize the quality of life for those infected. For those who live in the South, myself included, this research serves as a reminder to cover those feet while putzing around in the backyard. Keep ‘em covered!

Resources

An exploration of the effect of poor health hookworm infected soldiers on the Civil War can be found here.

The supremely excellent online resource Imaging of Tropical Diseases has a more in-depth look at hookworm, its life cycle and pathologies here.

References

(a) Centers for Disease Control and Prevention (2009). Laboratory Identification of Parasites of Public Health Concern: Hookworm. Retrieved from http://www.dpd.cdc.gov/dpdx/html/hookworm.htm on April 18, 2011.
(b) Palmer PES & Reeder MM. The Imaging of Tropical Diseases: With Epidemiological, Pathological and Clinical Correla Correlation: Ancylostomiasis (Hookworm Disease). Birkhäuser, 2001. Accessed from http://tmcr.usuhs.mil/tmcr/chapter12/intro.htm on April 11, 2011
(c) Wilcox LS. (2008) Worms and Germs, Drink and Dementia: US Health, Society, and Policy in the Early 20th Century. Prev Chronic Dis. 5(4): A135.
(d) Nuwer DS. (2002) “The Importance of Wearing Shoes: Hookworm Disease in Mississippi”. Mississippi History Now. Accessed from http://mshistory.k12.ms.us/articles/241/hookworm-disease-in-mississippi:-the-importance-of-wearing-shoes on April 11, 2011.
(e) Palmer S. (2009) Migrant Clinics and Hookworm Science: Peripheral Origins of International Health, 1840–1920. Bulletin of the History of Medicine. 83(4): 676-709
(f) Bleakley H. (2007) Disease and Development: Evidence from Hookworm Eradication in the American South. The Quarterly Journal of Economics. 122 (1): 73-117.
(g) Brinkley, GL. The Economic Impact of Disease in the American South, 1860-1940 (PhD dissertation). University of California, Davis, 1994.
(h) Ettling J. The germ of laziness: Rockefeller philanthropy and public health in the New South. Cambridge (MA): Harvard University Press; 1981
(i) Despommier, D, Gwadz RW, Hotez PJ and Knirsch CA. Parasitic Diseases. 5th ed. New York: Apple Trees Production, LLC. 2006
(j)  Brinkley, GL. (1997) The Decline in Southern Agricultural Output, 1860-1880. The Journal of Economic History. 57(1): 116-138
(k) JD Sachs & the World Health Organization (2001) Macroeconomics and Health: Investing in Health for Economic Development. World Health Organization. Accessed whqlibdoc.who.int/publications/2001/924154550x.pdf
(l) Brooker S, Clements AC, Hotez PJ, Hay SI, Tatem AJ, Bundy DA &Snow RW (2006). The co-distribution of Plasmodium falciparum and hookworm among African schoolchildren. Malar J. 5:99

Bleakley, H. (2007). Disease and Development: Evidence from Hookworm Eradication in the American South* Quarterly Journal of Economics, 122 (1), 73-117 DOI: 10.1162/qjec.121.1.73
Brooker S, Clements AC, Hotez PJ, Hay SI, Tatem AJ, Bundy DA, & Snow RW (2006). The co-distribution of Plasmodium falciparum and hookworm among African schoolchildren. Malaria journal, 5 PMID: 17083720

Houston, We Mite Have a Problem

It’s getting to be summer time in the Northern Hemisphere and I’m starting to see more creepy-crawlies outside, inside and attacking my personal space. Spiders, mosquitoes and cockroaches are becoming an increasingly common, unpleasant sight. Finding these beasties in random corners of my house and ruthlessly killing them had me thinking about the human-insect relationship, in particular the special one we have with ectoparasites. Ectoparasites depend upon mammals for their survival but there are several that rely on humans specifically and have co-evolved over hundreds of years to inhabit our bodies. Examples include the sucking lice (body, head and crab), bed bugs, fleas and mites.

Naturally, I went to the internet to find pictures and to have an up-lifting, skin-crawling  session. There’s one notable ectoparasite that induced the greatest chills and hit all of the gross-out buttons – microscopic size, alien-like appearance, infestation fears and, of course, there’s not much you can do about them living within you. Allow me to introduce the follicle mites Demodex folliculorum and Demodex brevis!

Scanning electron micrograph of Demodex folliculorum mites (in blue) in skin follicles. Image: Science Photo Library. Click for source.

Human beings are the one and only host of this ubiquitous mite (a). In fact, these two mites are considered to be the most common ectoparasite of humans (d). Women tend to be the main beneficiary of these minute bugs, with a male:female ratio of 2:5 (c). Sorry, ladies. The rate of infestation seems to be correlated with age, with 84% of people at age 60 harboring mites and increasing to 100% in those 70 years and older (e). Whether those that are immunocompromised are more susceptible to higher infestation rates is unknown, though some studies indicate that AIDs and leukemia patients may be more prone to greater than average numbers (c).

The mites may be found in the scalp, face and upper chest area, with D. folliculorum exhibiting a predilection for the hair follicles and D. brevis for the sebaceous ducts and meibomian glands at the rim of the eyelids (the sebaceous ducts transfer the waxy sebum that lubricates the skin and hair from the sebum glands; the meibonmian glands are a special type of such gland) (b)(c). D. folliculorum are a communal bunch, tending to congregate in the follicle area of the hair or eyelashes with their posterior  ends protruding from the follicular pores. D. brevis, on the other hand, tend to be more solitary and will occupy the sebaceous glands singly (d). Both species are tiny, less than 0.4 mm, with elongated, clear bodies and four pairs of stout legs. D. brevis is usually a tad shorter, ~ 0.1 mm, than D. folliculorum. They both have ridged scales along their cephalothorax and sharp, piercing teeth (d).

Short-lived creatures, a mite’s life cycle from egg to larva to adult lasts from 14-18 days. Adults emerge from the follicles and ducts to reproduce at the surface of the skin where females will then deposit eggs in the sebaceous glands. Larva will mature via two nymphal stages in the glands until entering the follicles and ducts as adults to begin the cycle anew (d). It is hypothesized that both species of mites feed upon sebum as a primary food source but may also munch on follicular and glandular epithelia. They are obligate ectoparasites, incapble of living outside their human host.

Scanning electron micrograph of two D. folliculorum mites covered in cellular debris. Their ridged cephalothorax, four pairs of legs and sharp mouth-parts may be seen. Image: Science Photo Library. Click for source.

So what do Demodex mites do in our skin besides frolicking in our follicles and consuming cellular debris? For most people, mites live harmlessly in the skin as a result of either down-regulating host immunity or simply dodging host immune defenses (f). There is vociferous debate in the dermatology crowd as to whether or not they are the causative agents of such skin diseases as rosacea and blepharitis (inflammation of the eyelids). However, some studies have indicated that greater than average mite density, greater than five mites per cm2, certainly do play a role in these two diseases for some patients (d).

Researchers have suggested that blockage of the hair follicles and sebaceous ducts by mites may result in epithelial hyperplasia, elicit a phagocytic, granulomatous reaction or bring about an inflammatory response due to their waste products (d). Due to the fact that treatment with  certain antibiotics can reduce the severity of rosacea strongly suggests a microbial component to mite-related diseases. Indeed, in 2007, researchers isolated from D. folliculorum a bacterium Bacillus oleronium that provoked inflammatory responses in 73% of rosacea patients but only 29% of controls (f). These results suggest that patients with rosacea were sensitized to the bacteria and may be immunologically sensitive to the mites, bacteria or both (f).

Two antigenic proteins found on the bacterium’s cell surface in particular appeared to be responsible for the inflammatory response by stimulating peripheral blood mononuclear cell proliferation; one 83 kDa protein showed similarity with heat-shock proteins while the other 62 kDa protein shared amino acid sequence homology with a protease enzyme found to be involved signal transduction as well as carbohydrate metabolism (f). Stronger proof of the pathogenic role of B. oleroniusin rosacea may also be found in the sensitivity of the bacterium to many antibiotics proven to be effective in the treatment of rosacea, specifically tetracycline, doxycycline and minocycline (f).

Scanning electron micrograph of the posteriors of several D. folliculorum mites (in green) extending from a follicle containing a hair (in yellow). Image: Science Photo Library. Click for source.

Closely related species in the Demodex genus can cause mange in dogs and other mammals, and the reasoning that the two mite species that call humans “home” can cause disease as well may not be so farfetched. As such, more conclusive investigation into the role of Demodex in rosacea and blepharitis is needed. The latest research into B. oleronius and it’s immunoreactive antigens seems promising, especially upon consideration of the role of the bacterium Wolbachia in the inflammatory response of filariaisis. Bacteria that reside within medically important arthropods and nematodes are increasingly being seen as collaborative partners in pathology and B. oleronius seems to fit this pattern. Research into the function of B. oleronius in the mite’s biology should also be a priority.

For those of us content with our long-term, eight-legged guests, let us be thankful we don’t feel them and see them. And let this be a lesson to those who go image hunting on Google for ectoparasites.

Note: On April 30, 2012, the sentence “Women tend to be the greatest harbingers of these minute bugs” was changed to “Women tend to be the main beneficiary of these minute bugs”; the former incorrectly uses the word “harbinger”. Sorry for the mix up!

References

a) Kligman AM & Christensen MS. (2011) Demodex folliculorum: Requirements for Understanding Its Role in Human Skin Disease. Journal of Investigative Dermatology. 131: 8–10
b) Despommier, D, Gwadz RW, Hotez PJ and Knirsch CA. Parasitic Diseases. 5th ed. New York: Apple Trees Production, LLC. 2006
c) Hsu CK, Hsu MM, Lee JY. (2009) Demodicosis: a clinicopathological study.  J Am Acad Dermatol. 60(3): 453-62
d) Lacey N, Kavanagh K, Tseng SC. (2009) Under the lash: Demodex mites in human diseases. Biochem (Lond). 31(4): 2-6
e) Liua J, Sheha H, & Tsenga SCG. (2010) Pathogenic role of Demodex mites in blepharitis. Curr Opin Allergy Clin Immunol. 10(5): 505–510.
f) Lacey N, Delaney S, Kavanagh K, Powell FC. (2007) Mite-related bacterial antigens stimulate inflammatory cells in rosacea. Br J Dermatol. 157(3): 474-81

Lacey, N., Delaney, S., Kavanagh, K., & Powell, F. (2007). Mite-related bacterial antigens stimulate inflammatory cells in rosacea British Journal of Dermatology, 157 (3), 474-481 DOI: 10.1111/j.1365-2133.2007.08028.x