Observation of the arachnid, Demodex folliculorum, has been reported since 1840. This hair follicle mite is the only metazoan organism commonly found in the pilosebaceous components of the eyelid of humans. Coston "opened the eyes" of ophthalmologists when he described 22 patients with demodectic eyelid signs and symptoms. 
D folliculorum (all stages) is found in small hair follicles and eyelash hair follicles. In all forms, immature and adult, it consumes epithelial cells, produces follicular distention and hyperplasia, and increases keratinization leading (in eyelashes) to cuffing, which consists of keratin and lipid moieties. Demodex brevis (all stages) is present in the eyelash sebaceous glands, small hair sebaceous glands, and lobules of the meibomian glands. Adults and immature forms consume the gland cells in all of these loci and, when infestations are heavy, can affect the formation of the superficial lipid layer of the tear film coacervate. Demodectic mites produce histologically observable tissue and inflammatory changes, epithelial hyperplasia, and follicular plugging.
Infestation of the eyelash hair follicle results in easier epilation and more brittle cilia. These mites also serve as vectors of infective elements and interrupt tissue integrity. They have been implicated in meibomian granulomas and are associated with certain dermatologic changes. All reported histologic sections of lid follicles infested with D folliculorum show distention and thickening. Coston claims that less than one half of the specimens he observed showed perifollicular lymphocytic infiltration. 
Follicular inflammation produces edema and results in easier epilation of the eyelashes. It also affects cilia construction, and lashes are observed to be more brittle in the presence of demodicosis. Madarosis (loss of lashes) is associated with abundant mites, the loss of eyelashes as a result of intercellular edema in the hair shaft, and loss of hair resiliency. Although epithelial hyperplasia associated with follicular plugging is often encountered, dermal changes seldom extend beyond the perifollicular epidermal area. Once believed to be mite excreta, this plugging is now known to be epithelial hyperplasia with interspersed layers of lipid. The formation of a collar of tissue around the base of the lashes is observed clinically. This occurs significantly more often in follicles infected with D folliculorum. The epithelial hyperplasia is hypothesized to be most likely a product of the abrasive action of the mite's claws.
Accumulation of waste material of the follicle mite may occur in affected follicles or sebaceous glands. Electron micrographs of the mite surface and feces show bacterial, viral, and rickettsial elements. Specific reports have revealed that both species pierce epithelial cells and consume cytoplasm. Only D brevis has been observed with channels burrowed to the germinal epithelium in the sebaceous glands.
Demodex species-induced pathologic changes have been implicated in dry eye conditions. When follicular plugging involves the meibomian gland (D brevis) or the gland of Zeis (D folliculorum or D brevis), reduction of the superficial lipid layer of the tear film occurs. The effect of D brevis on the meibomian structure has been implicated in chalazion formation. Chalazia are granulomatous inflammation of the meibomian glands, made of an organized core of epithelioid cells and histocytes surrounded by fibroblasts, lymphocytes, and plasma cells. These defense cells encircle particles too large for normal macrophages to engulf. D brevis has been observed in the center of these meibomian granulomas. Lid infestation by the Demodex species may or may not accompany dermatologic changes of the nose, the cheek, or the forehead.
D folliculorum has been suggested as a factor in pityriasis folliculorum. This dermal inflammation manifests itself as a diffuse erythema of the affected areas; scaly, dry skin; and, in certain cases, rosacealike lesions. The dry skin cycle described by Ayres is initiated when the demodectic mite plugs the follicle and reduces the sebaceous outflow, which leads to scaling as well as rough and dry skin texture.  Sebaceous outflow is further reduced when patients inadvertently decide to apply facial cream. The mite flourishes in this environment of oily additives, leading to an increase in the population of the mites and a continuation of the dry skin cycle.
Several individuals have attempted to estimate the prevalence of D folliculorum in the eyelash follicles. The initial report in 1961 suggested a prevalence of 95%. 
Madarosis (loss of lashes) may result from untreated demodicosis.
No racial predilection has been observed.
Infestation by these parasites is equal in males and females. Infestation is correlated to the number of sebaceous glands but not to the density of the hair follicles.
Post reported that D folliculorum was observed in 84% of the sample population with a mean age of 61 years and in 100% of those older than 70 years.  Liang L et al  reported in 2010 that ocular demodicosis should be considered as a potential cause of pediatric (2.5-11 years) refractory blepharoconjunctivitis.
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