Everything You Didn’t Want to Know About Cockroaches

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Amongst its many epicurean, architectural and otherwise louche charms, New Orleans has another infamous, uncelebrated one: a problematically vibrant cockroach population. Every summer (oh, let’s be honest here: they’re here spring, summer and fall), the German brown cockroach can be seen snatching its way around your house, flitting on sidewalks at dusk, and intimidating the locals.

They fly down here in the Deep South, did you know?

One Saturday night back in August, one such creature dive-bombed into my cleavage. After one spilled G&T (Oh God, not my drink!) and many sputtered expletives, the critter was ousted and a friend graciously stomped it into a unrecognizable smear into the pavement.

And so with the impending cockroach population explosion coming any summer day now, I figure why not have a chat about what diseases they can harbor and spread on your tabletops. Hmmm? And lest you think that this article is a paean extolling their overlooked virtues – alas! – they really are as filthy as everyone thinks they are.

A colored scanning electron micrograph of Periplanta americana, the American cockroach, one of the smallest known species. Note the ubiquitous hairs covering the insect, allowing for microbes to be picked up during its feedings. Image: Dr. Biology, Arizona Board of Regents. Click for source.

I’ll try to make this as painless as possible.

Out of the 4000 species of cockroach that exist, there are three major species that plague humanity – Periplaneta americana, Blattella germanica and Blattella orientalis. They feed on just about anything, even their deceased brethren, but they do have a sweet tooth and prefer to eat sugary and starchy items such as sweets, cardboard and book-bindings (1). Included in their rather diverse diet is their consumption of human detritus such as feces, sputum, toe nails, and bodily residue on surgical swabs. These unseemly dietary choices lead to their contamination of food, utensils and surfaces for food prep and have direct consequences on human health in three interrelated ways – their arbitrary feeding habits, eating both human excrement and human food; their indiscriminate defecation habits; and the fact that they regurgitate digestive fluids in the process of eating (2). Endearing, no?

Roaches also serve as an important source of infectious pathogens. They serve as a sort of public transit for the busy microbiological world, a bus ferrying bacteria, viruses, fungi and parasites between filth and human comestibles; really, every buggy imaginable rides on this double-decker of an arthropod. Bacteria and viruses settle into the crevices and cracks between thorax and head, and begin to multiply. There are so many fissures and clefts and crannies on a cockroach. Everywhere there are hairs, but especially on the six legs that escort these scuttling creatures from one dark, humid hideaway to another. Microbes snatch a ride on these hairs or are accidentally consumed by the cockroach only to pass into the alimentary canal where they may multiple in number. In one study, the bacterium Pseudomonas aeruginosa was found to have increased multiple-fold over the course of 114 days in the gut of a cockroach (3).

Colored scanning electron micrograph (SEM) of Blattella germanica, the German cockroach, one of the smallest known species. This roach’s long antennae can be seen protruding from its head and its wings (blue) can be seen at lower left. The anatomy of the cockroach provides several areas for bacteria, viruses and parasitic eggs/cysts to settle into. Image: Volker Steger, Science Photo Library. Click for source.

In this regard, roaches are not so much vectors as they are reservoirs; a mosquito will squelch its proboscis in your ankle, inoculating you with malaria in their quest for blood but a cockroach indiscriminately contaminates anything lying around. Entomologists describe this process as “mechanical transmission”, indirectly transmitting disease to humans. It’s not personal, it’s just business. 

All types of passengers are welcome on this cockroach bus. Over 30 species of bacteria have been found on the cuticle and gut of roaches, including those of serious medical import such as E. coli, various species of Salmonella and Staphylcoccous, Pseudomonas aeruginosa and Klebsiella pneumoniae (4). These bacteria cause diseases such as urinary tract infections, dysentery, diarrhea, pneumonia, cholera, polio, septicemia and wound infections (5). One study that trapped cockroaches in order to measure their bacterial load found that number was as high as 14 million microbes found on the exterior of the bodies, and 7 million in their fecal droppings (5).

Viable eggs and dormant cysts of parasites also hitch a ride; the culprits include the ova of Ascaris lumbricoides (giant roundworm), Anchylostoma deodunale (hookworm), Trichuris trichura (whipworm), Enterobius vermicularis (pinworm) and Strongyloides stercoralis (threadworm), and the cysts of Entomoeba hystolitica, Balantidium coli, C. parvum, C. cayetenensis and Isospora belli (4). Even the virus that causes polio, poliomyelitis, has been found within the guts of cockroaches (6).

There are several documented cases of small outbreaks that pinpoint to cockroaches playing an indirect but prominent role in disease transmission. In one county in Northern Ireland in the late 1970s, fifteen food-handlers in various establishments fell ill to dysentery caused by the Shigella bacterium over the course of eight weeks (2). These restaurants had serious infestations, particularly in the kitchen and dining areas, and the stomach contents of trapped roaches showed viable Shigella dysenteriae serotype 7 bacteria, incriminating the arthropods in the spread of the disease.

Cockroaches were also suspected to be the cause of a hepatitis A outbreak in a Los Angeles housing project in the late 1950s. From 1956 to 1959, the Carmelitos Housing Project represented 39% of all cases of hepatitis A in Los Angeles County with numbers of the infected steadily increasing through the years (7). It was only until a full-scale cockroach control program employing a newly developed insecticide, the industrial silica aerogel Dri-Die 67, was the outbreak halted. Two years following the program, incidences of hepatitis A from the Housing Project dropped to 0.0% and cockroaches traversing between the sewage system and the Project were pinpointed as the source of the epidemic.

A colored scanning electron micrograph close-up of Periplaneta americana, the American cockroach, which can be found around the world. Image: Stephen Gschmeissner. Click for source.

Typhoid patients in Italy were found to have cockroaches harboring S. typhi in their homes in a study conducted in 1943 (2). Similarly, the same organism was found in cockroaches infesting a Belgian hospital’s children’s ward undergoing an epidemic of gastroenteritis in 1950 (2). Most recently, outbreaks of Klebsiella pneumoniae in neonatal units have been tied to cockroach infestations in hospitals in Ethiopia and South Africa (8)(9). These studies indicate that cockroaches may play an unappreciated role in the epidemiology of infections in both the home and hospital.

Though it’s difficult to say what part roaches play in small disease outbreaks, they are capable of harboring antibiotic-resistant bacteria. A 2012 study in Ethiopia looked at cockroaches trapped in a neonatal intensive care unit and found widespread multi-drug resistance among individual species of bacteria residing in the roaches. Reading the lists of antibiotics these bacteria were found to be resistant to is like a “who’s who” of the antibiotic world – ampicillin, augmentin, tetracycline, chloramphenicol, amoxicillin, doxycycline, and ciprofloxacin (8). An earlier study in South Korea found that cockroaches trapped in homes located 3 miles from a hospital harbored bacteria that were resistant to anywhere from 6 to 12 commonly used antibiotics (3). These medications are the mainstay for treating bacterial infections and the discovery that cockroaches in hospitals harbor bacteria no longer susceptible to them is discomfiting to say the least.

Bugs are such an inescapable component of our day-to-day living, whether we care to acknowledge them or not. They live their own buggy lives, spinning webs, squirming through our compost or draining picoliters of our blood. We pay little attention to them until they inconvenience us and spoil our clean, bleached perception of the world.

Cockroaches are especially gifted at this. They are the boldest creepy-crawlies, not only daring to openly traverse our homes and personal spaces but thriving in those environments. They need us for the waste and shelter we provide, and for that we despise them. And, sadly, the public opinion of them isn’t wrong. They really are gross – they serve as an efficient means for microbes of all kinds to traverse between sites of human waste and food preparation and consumption. Their traipsing through family dwellings, food establishments and hospitals compromises public health and may also contribute to the ongoing antibiotic-resistance in bacteria worldwide.

Check out the Resources below to see how you can prevent buggies and bacteria from getting a free ride into your kitchen. In the meantime, happy hunting!

Resources

The most recent cockroach-related outbreaks of disease have happened in developing countries that may lack adequate municipal sanitation and regular garbage disposal. Hospitals and multi-family dwellings that rely on old buildings may also suffer cockroach infestations due to shoddy construction or inevitable decay (3)(10). The WHO has a very helpful, fact-filled PDF here on how to protect your home from these little invaders.

Really wanna get in deep with Blattella germanica, the German cockroach? For only $326, this book could be yours. What a deal!  If you’re just into skimming, then you can check it out on Google here.

Cockroaches can dirty up human spaces but at least they have little friends that can keep their own bodies clean – mites!

From the ignominious Daily Mail, a collection of scanning electron micrograph images of the buggies that live in your home with you. More images can be found here but they’re sadly unlabeled.

References
(1) Rozendaal JA. October 1997. “Cockroaches.” Vector control: Methods for use by individuals and communities. World Health Organization. PDF of chapter is accessible here. Click here for access to the entire resource.
(2) Burgess NR & Chetwyn KN. (1981) Association of cockroaches with an outbreak of dysentery. Trans R Soc Trop Med Hyg. 75(2): 332-3
(3) Hsiu-Hua P et al. (2005) Isolation of bacteria with antibiotic resistance from household cockroaches (Periplaneta americana and Blattella germanica) Acta Tropica 93: 259–265  T
(4) Tatfeng YM et al. (2005) Mechanical transmission of pathogenic organisms: the role of cockroaches. J Vect Borne Dis. 42: 129–134
(5) Chaichanawongsaroj et al. (2004) Isolation of gram-negative bacteria from cockroaches trapped from urban environment. Southeast Asian J Trop Med Public Health. 35(3): 681-4
(6) Healing TD. (1993) Arthropod Pests as Disease Vectors. Proceedings of the First International Conference on Urban Pests. Accessible here.
(7) Tarshis IB. (1962) The cockroach–a new suspect in the spread of infectious hepatitis. Am J Trop Med Hyg 11: 705-11
(8) Tilahun et al. (2012) High load of multi-drug resistant nosocomial neonatal pathogens carried by cockroaches in a neonatal intensive care unit at Tikur Anbessa specialized hospital, Addis Ababa, Ethiopia. Antimicrobial Resistance and Infection Control. 1: 12
(9) Cotton MF et al. (2000) Invasive disease due to extended spectrum beta-lactamase-producing Klebsiella pneumoniae in a neonatal unit: the possible role of cockroaches. J Hosp Infect. 44(1): 13-7
(10) Fakoorziba MR et al. (2010) Cockroaches (Periplaneta americana and Blattella germanica) as potential vectors of the pathogenic bacteria found in nosocomial infections. Ann Trop Med Parasitol. 104(6): 521-8

ResearchBlogging.org
Pai, H., Chen, W., & Peng, C. (2005). Isolation of bacteria with antibiotic resistance from household cockroaches (Periplaneta americana and Blattella germanica) Acta Tropica, 93 (3), 259-265 DOI: 10.1016/j.actatropica.2004.11.006

Nobel Prizes, Tropical Medicine & One Nazi Sympathizer

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Nobel Prizes! We all want one, don’t we? While fantasizing about heavy gold medallions and the Swedish Nobel Assembly, I wondered how many of the Nobel Laureate prizes in Physiology and/or Medicine have gone towards scientists studying infectious diseases, immunology and the tropical medicine field. Snooze button alert, am I right? This is the product of a one-track mind so you have my apologies. But! If it’s any consolation, there’s a story hidden in this article of a Nobel Laureate Nazi sympathizer that infected mental patients with malaria to cure them of their psychoses. Science!

Let’s get down to numbers. As of 2011, this prize has been awarded 101 times to 199 scientists for their research in this field.  In recent years, the Nobel Prize has often been awarded jointly to two or three scientists for either collaborative research or for research that is similar in scope and specialty. Of those 101 occasions, 22 of these awards have been given to 39 researchers for their work in infectious diseases, virology, parasitology and/or immunology. Only one woman is on this list, Françoise Barré-Sinoussi, for her incredible work with Luc Montagnier in identifying HIV at the height of the HIV/AIDS epidemic in the 1980s.

The Nobel Medal for Physiology or Medicine is embossed with the Genius of Medicine "holding an open book in her lap, collecting the water pouring out from a rock in order to quench a sick girl's thirst". Description from NobelPrize. Click for image source.

(FYI, there have been nine years in which the Nobel Prize ceremony and awards did not occur due to the disruption of the two World Wars – in 1915 to 1918, 1921, 1925 and 1940 to 1942. Those Nazi’s again!)

So roughly one-fifth of the Nobel Prizes in medicine have gone to scientists making breakthroughs in the study of infectious diseases or in the immunological response to those diseases, indicating how crucial this particular field of medicine is to the scientific community. We’re not talking dermatology or podiatry here, folks.

In the early years, the Assembly awarded prizes for game-changing advances in the research of big killer diseases of the day – diptheria, tuberculosis and malaria, to name a few. The development of a yellow fever vaccine (1951), discoveries of vital antibiotics that are still used today globally (1939, 1945 and 1952), and the finding that HPV causes cervical cancer (2008) are just a few of the discoveries that the Nobel Assembly considered so revelatory to the field of medicine. Until the past century, how infectious diseases entered the body, their mechanisms of pathogenesis and even their treatment was largely unknown. Malaria is transmitted by mosquitoes? Not known till 1899 and Sir Ronald Ross’s discovery of the parasite hiding inside the stomach of an Anopheles mosquito was justly recognized by the Nobel Assembly in 1902. Lice transmit typhus? Charles Nicolle’s finding won him a good amount of money and worldwide recognition/obscurity in 1928. In 1954, a trio of American researchers were awarded the Nobel for identifying a method to culture the polio virus, launching the beginning of the end of polio’s affliction on humanity.

Many of the awarded discoveries laid the foundation for productive research that has led to profound advancements in disease and pest control, the emergence of the field of public health, development of the pharmaceutical industry and the industrial production of vaccines, antibiotics, and antivirals. Life-changing stuff, ya’ll. Flipping through this list is a reminder of how far we’ve come in the past century in establishing our domain over bacteria and viruses that previously wiped us out with shocking regularity. In fact, some of their findings and methods are so commonplace, hell! even banal, in today’s laboratories that it’s like stepping into a science time-warp reading about their discoveries. Thanks to these scientists, we possess the complex knowledge of genetics, immunology, antibiotics, vaccines and their respective methods to identify, culture and combat new diseases.

The list of winners is below and includes the year they were awarded, their country of origin and the award’s justification from the Nobel Assembly in quotes; those quotes come from the official website of the Nobel Prize. I’ve included in the list a few winners awarded for their work in immunology and antibiotics; while these are not strictly related to infectious diseases, their research laid a strong foundation for future infectious disease work and, well, they’re related and it’s important so get over it.

Scroll past this engrossing list that I’ve compiled for your disease-seeking pleasure.

1901
Emil Adolf von Behring (Germany) “for his work on serum therapy, especially its application against diphtheria, by which he has opened a new road in the domain of medical science and thereby placed in the hands of the physician a victorious weapon against illness and deaths”. Victorious weapon! I’d think the flowery language alone should do the trick. In any case, von Behring developed a diphtheria antitoxin, known as a “serum”, by repeatedly injecting a horse with diphtheria toxin.

"A Future Pharmacy". An editorial cartoon mocking Emil Adolf Von Behring and his discovery of serum therapy, in which a diphtheria antitoxin was developed by repeatedly exposing a horse to the diphtheria toxin. Click for source.

1902
Sir Ronald Ross (United Kingdom) for his discovery that malaria is transmitted by mosquitoes.

1905
Robert Koch (Germany) “for his investigations and discoveries in relation to tuberculosis”.

1907
Charles Louis Alphonse Laveran (France) “in recognition of his work on the role played by protozoa in causing diseases”.

1927
Julius Wagner-Jauregg (Austria) “for his discovery of the therapeutic value of malaria inoculation in the treatment of dementia paralytica”. In 1927, Wagner-Jauregg received the  Prize for his discovery of pyrotherapy, the treatment of mental disease by febrile diseases. Besides being a Nobel Laureate, Wagner-Jauregg was also a Nazi sympathizer, anti-semite and racial hygienist. A charmer of a man who forced sterilization upon the mentally ill and the criminal and the so-called “father of fever therapy”(1).

Mustachioed Wagner-Jauregg stands behind a mental patient receiving malarial pyrotherapy. Click for image source.

Since 1887, he had been investigating the phenomenon of how fever, as induced by tuberculosis or St. Anthony’s Fire, may reduce the effects of psychosis caused by tertiary syphilis. Bacterial infections didn’t seem to do the trick in terms of bringing about recurrent high fevers and so in 1917 Wagner-Jauregg turned to the malaria parasite. Turns out, malaria is an excellent specimen for this sort of thing and led to its usage as an established treatment for paralytic dementia and neurosyphilis. An application of quinine would end the fever therapy, eliminating the infection and leaving the patient free of his psychoses. For this hot discovery, Wagner-Jauregg is the only psychiatrist to have ever won the Nobel for investigative fieldwork on mental illness.

1928
Charles Jules Henri Nicolle (France) for his discovery that lice transmitted typhus. Nicholle was a master researcher of infectious diseases and made many discoveries regarding the pathology and epidemiology of brucellosis, leishmaniasis, measles, rinderpest, scarlet fever, Mediterranean spotted fever, toxoplasmosis, trachoma and tuberculosis. Nicholle’s typhus work was performed in Tunisia using chimpanzees and toque macaques (2).

Vials and tablets of prontosil, an industrial dye discovered to have antibacterial properties by Gerhard Domagk. Click for source.

1939
Gerhard Domagk (Germany) “for the discovery of the antibacterial effects of prontosil”. Prontosil was the first drug to be found effective against bacterial infections and Domagk made quick use of this fact – as a streptococcal infection threatened his daughter, his treatment with prontosil prevented the therapeutic amputation of her arm.

1945
Sir Alexander Fleming (United Kingdom), Sir Ernst Boris Chain (United Kingdom), and Howard Walter Florey (Australia) “for the discovery of penicillin and its curative effect in various infectious diseases”.

1951
Max Theiler Union (South Africa) “for his discoveries concerning yellow fever and how to combat it”. He had an enormous forehead. His award is the only one that has gone towards a virus vaccine.

1952
Selman Abraham Waksman (United States) for his discovery of streptomycin, the first antibiotic effective against tuberculosis”. Waksman coined the term “antibiotic”.

There's really no reason why I'm including this photo of Selman Waksman here aside from the fact that it's so gloriously Science!-y. Lab coat, check. Flask of something liquid, check. Mood lighting, check. Click for image source.

1954
John Franklin Enders, Thomas Huckle Weller and Frederick Chapman Robbins (all from the United States) “for their discovery of the ability of poliomyelitis viruses to grow in cultures of various types of tissue”. Their work laid the groundwork for Jonas Salk’s development of the polio vaccine.

1958
Joshua Lederberg (United States) “for his discoveries concerning genetic recombination and the organization of the genetic material of bacteria”.

1966
Peyton Rous (United States) “for his discovery of tumour-inducing viruses”. In 1911, Rous found that some cancers can be transmitted by viruses, known as retroviruses. Forty years later, he was awarded for his work.

1969
Max Delbrück, Alfred D. Hershey and Salvador E. Luria (all from the United States), “for their discoveries concerning the replication mechanism and the genetic structure of viruses”. The trio discovered that bacterial resistance to bacteriophages (viruses that infect bacteria) was a result of random mutations.

1972
Gerald M. Edelman (United States) and Rodney R. Porter (United Kingdom) used immunoglobins sourced from human blood to identify the chemical structure of antibodies.

1976
Baruch S. Blumberg and D. Carleton Gajdusek (United States) “for their discoveries concerning new mechanisms for the origin and dissemination of infectious diseases”. These guys were awarded for their research on kuru, a disease caused by human prions. Fun fact: Blumberg also discovered the hepatitis B virus and developed the diagnostic test and vaccine for it.

1984
Niels K. Jerne (Denmark), Georges J.F. Köhler (Federal Republic of Germany) and César Milstein (Argentina and the United Kingdom) “for theories concerning the specificity in development and control of the immune system and the discovery of the principle for production of monoclonal antibodies”.

1989
J. Michael Bishop and Harold E. Varmus (United States) “for their discovery of the cellular origin of retroviral oncogenes”.

1997
Stanley B. Prusiner (United States) “for his discovery of Prions – a new biological principle of infection”.

2005
Barry J. Marshall and J. Robin Warren (Australia) “for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease”. Marshall is famously known for downing culture medium loaded with H. pylori to directly prove that the bacterium is responsible for causing ulcers.

2006
Andrew Z. Fire and Craig C. Mello (United States) “for their discovery of RNA interference, [otherwise known as] gene silencing by double-stranded RNA”.

2008
Harald zur Hausen (Germany) “for his discovery of human papilloma viruses causing cervical cancer”, along with Françoise Barré-Sinoussi and Luc Montagnier (France) “for their discovery of the human immunodeficiency virus”.

Resources

The Nobel Prize website has a fleshed-out timeline for every Laureate and includes their biography, a short article about their research, the lecture they delivered to the Nobel Assembly and much much more.

References
(1) Howes OD et al (2009) Julius Wagner-Jauregg, 1857–1940. Am J of Psy. 166(4): 409.
(2) Schultz MG and Morens DM. (2009) Charles-Jules-Henri Nicolle. Emerg Infect Dis. 15(9): 1520-22. Accessed online.

ResearchBlogging.orgSchultz, M. (2009). Charles-Jules-Henri Nicolle Emerging Infectious Diseases, 1519-1522 DOI: 10.3201/eid1509.090891

Houston, We Mite Have a Problem

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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

ResearchBlogging.org
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