As research continues to reveal the many ways the human microbiome may affect human health, the potential role of Demodex mites in rosacea has come into sharper focus with new technology and may point to new approaches in patient care, according to experts at a roundtable on the clinical implications of Demodex in rosacea.
The controversy surrounding the role of Demodex mites in the pathophysiology of rosacea has been going on for over eight decades,” said Dr. James Del Rosso, adjunct clinical professor of dermatology at Touro University College of Osteopathic Medicine in Henderson, Nev. “We are now finally seeing more research using advanced technological methods to better evaluate and quantify the potential connections between Demodex mites, rosacea and other rosacea-form facial eruptions. This is great news for dermatologists and their patients!"
Demodex mites are a normal part of the human microbiome but have often been found in more than four times greater numbers on the facial skin of rosacea sufferers than in the normal population, according to Dr. Frank Powell, consultant dermatologist at Mater Misericordiae Hospital in Dublin and former president of the European Academy of Dermatology and Venereology.
“Researchers have more recently discovered that while Demodex folliculorum and D. brevis live in the hair follicles and sebaceous glands of the facial skin, D. folliculorum is also found in the meibomian (tear) glands of ocular rosacea patients,” he said. “In the mites’ brief life span of 14 days, they live and reproduce in the pilosebaceous units, subsisting on sebum and cellular contents, and emerge from the follicles primarily at night.”
He suggested that a genetic predisposition for rosacea may be reflected in a different skin type with specific lipid qualities that allows Demodex to flourish in greater numbers.
Recent research has identified a host of microscopic elements and interactions in the innate immune system that contribute to rosacea's development, involving such substances as kallikreins, cathelicidins and mast cells, said Dr. Diane Thiboutot, professor of dermatology and vice chair for research at Pennsylvania State University. Importantly, she noted, many of the triggers of rosacea – ultraviolet light damage or bacterial antigens, as well as Demodex, for example – have one thing in common: They have been shown to activate the enzyme toll-like receptor-2 (TLR-2) signaling, which initiates a cascade of events that leads to the inflammatory signs and symptoms of rosacea, including papules (bumps) and pustules (pimples).1 The challenge, however, is that TLR-2 activation is necessary to fight off pathogens, so wiping out its function would be counterproductive.
“The significance of the relationship between Demodex and rosacea has long been controversial, as it doesn’t fulfill certain traditional parameters for a causal association between a pathogen and a disease,” Dr. Thiboutot continued. “These parameters may have been superseded by more recent findings, and a recent review of 48 articles in the Archives of Dermatology concluded that the degree of Demodex infestation, as opposed to its simple presence, is an important factor in rosacea.”
Dr. Del Rosso stressed that Demodex may play a role in the pathophysiology of rosacea, at least in some patients, and may influence the type and severity of visible manifestations of rosacea in different individuals.
“The classic ‘subtypes’ of rosacea appear to reflect variations in inflammatory and immunologic responses which in some cases may be induced by Demodex mites,” he said. “For example, in one study, individuals with erythematotelangiectatic rosacea (subtype 1) were found to have higher facial counts of Demodex mites than those with papulopustular rosacea (subtype 2). It has been suggested that the higher Demodex counts lead to degradation of the follicular wall as the mites attempt to improve their survival. This loss of follicular wall integrity then triggers an immunologic response that reduces the number of Demodex mites, with papules and pustules subsequently emerging from the augmented perifollicular inflammation that occurs.”
Dr. Del Rosso noted that he has observed cases of patients with a more diffuse facial distribution of small papules, pustules and fine scaling than what is typical of rosacea. He has previously diagnosed these cases as demodicosis, as skin scrapings of the facial lesions have easily revealed multiple Demodex mites on light microscopy.
The roundtable participants agreed that further studies should be conducted to improve understanding of the presence of Demodex and its potential actions and interactions with other pathogenic factors in rosacea. The roundtable was sponsored by the National Rosacea Society with funding from Galderma Laboratories.
1. Murillo N, Aubert J, Raoult D. Microbiota of Demodex mites from rosacea patients and controls. Microb Pathog 2014; 71-72:37-40.