Demodex

D. folliculorum and D. brevis

D. folliculorum and D. brevis are typically found on humans. D. folliculorum was first described in 1842 by Simon; D. brevis was identified as separate in 1963 by Akbulatova. D. folliculorum is found in hair follicles, while D. brevis lives in sebaceous glands connected to hair follicles. Both species are primarily found in the face, near the nose, the eyelashes, and eyebrows, but also occur elsewhere on the body.

The adult mites are only 0.3–0.4 mm (0.012–0.016 in) long, with D. brevis slightly shorter than D. folliculorum. Each has a semitransparent, elongated body that consists of two fused segments. Eight short, segmented legs are attached to the first body segment. The body is covered with scales for anchoring itself in the hair follicle, and the mite has pin-like mouthparts for eating skin cells and oils (sebum) which accumulate in the hair follicles. The mites can leave the hair follicles and slowly walk around on the skin, at a speed of 8–16 cm per hour, especially at night, as they try to avoid light. The mites are transferred between hosts through contact with hair, eyebrows, and the sebaceous glands of the face.

Females of D. folliculorum are larger and rounder than males. Both male and female Demodex mites have a genital opening, and fertilization is internal. Mating takes place in the follicle opening, and eggs are laid inside the hair follicles or sebaceous glands. The six-legged larvae hatch after three to four days, and the larvae develop into adults in about seven days. The total lifespan of a Demodex mite is several weeks.

Research about human infection by Demodex mites is ongoing, with several preliminary studies suggesting an association between mite infection and rosacea.

Older people are much more likely to carry the mites; about a third of children and young adults, half of adults, and two-thirds of elderly people carried them. The lower rate in children may be because children produce less sebum. Recently, a study of 29 adults (18 and over) in North Carolina, USA, found that 70% of those 18 years of age carried mites, and that all adults over 18 (n = 19) carried them. This study (using a DNA detection method, more sensitive than traditional sampling and observation by microscope), along with several studies of cadavers, suggests that previous work may have underestimated the mites' prevalence. However, the small sample size and small geographical area involved prevent drawing broad conclusions from these data.

In the vast majority of cases, the mites go unobserved, without any adverse symptoms, but in certain cases (usually related to a suppressed immune system, caused by stress or illness), mite populations can dramatically increase, resulting in a condition known as demodicosis or Demodex mite bite, characterised by itching, inflammation, and other skin disorders. Blepharitis (inflammation of the eyelids) can also be caused by Demodex mites. Evidence of a correlation between Demodex infection and acne vulgaris exists, suggesting it may play a role in promoting acne. The zoonosis caused by Demodex is called Demodicosis.

D. canis

The natural host of D. canis is the domestic dog. Although it can temporarily infect humans, D. canis mites cannot survive on the human skin and therefore will die shortly after exposure and are considered to not be zoonotic. Naturally, the D. canis mite has a commensal relationship with the dog and therefore under normal conditions does not produce any clinical signs or disease. The escalation of a commensal D. canis infestation into one requiring clinical attention usually involves complex immune factors. Under normal health conditions the mite can live within the dermis of the dog without causing any harm to the animal. However, whenever an immunosuppressive condition is present and the dog's immune system (which naturally ensures that the mite population cannot escalate to an infestation that can damage the dermis of the host) is compromised, it allows the mites to proliferate. As they continue to infest the host, clinical signs begin to become apparent and demodicosis/demodectic mange/red mange is diagnosed. Demodicosis can manifest as lesions of two types: squamous, which causes dry alopecia and thickening of the skin, and pustular, which is the more severe form, causing secondary infection (usually by Staphylococcus), resulting in the characteristic numerous red pustules and wrinkling of the skin. Demodicosis can follow immunosuppressive conditions or treatments, or may be related to a genetic immune deficiency. Also, certain breeds—such as the Dalmatian, the American Bulldog, and the American Pit Bull Terrier—appear to be more susceptible.

Since D. canis is a part of the natural fauna on a canine's skin, the mite is not considered to be contagious. All dogs receive an initial exposure from their mother during nursing. The immune system of the animal under most all healthy conditions keeps the population of the mite in check and therefore subsequent exposure to dogs possessing clinical demodectic mange does not increase an animal's chance of developing demodicosis. Since demodicosis is usually the result of an immune deficiency, it is not uncommon for subsequent infestations after treatment to occur.

Ivermectin:

Ivermectin is an avermectin and a fermentation product of Streptomyces avermitilis (also see Macrocyclic Lactones). It acts as a GABA agonist, causing paralysis in susceptible arthropods and nematodes. It is used in small animals for treatment of Sarcoptes scabiei, Otodectes cynotis, Cheyletiella blakei, C yasguri, and Demodex canis; in cattle for psoroptic mange, lice, and Hypoderma larvae; in horses for equine filarial dermatitis from Onchocerca cervicalis; and in swine for Sarcoptes scabiei.

In small animals, all use for skin conditions is extra-label in the USA. For Demodex, the dosage is 0.3–0.6 mg/kg/day, PO, until two negative skin scrapings 1 mo apart. For Sarcoptes, Otodectes, and Cheyletiella, the dosage is 0.3 mg/kg, PO, repeated in 2 wk. In cattle, 0.2 mg/kg is given as a single SC injection for Psoroptes and lice. In horses, 0.2 mg/kg, PO, kills microfilariae but not adult Onchocerca cervicalis, so relapse may be noted within 2 mo of treatment. In swine, the dosage is 0.3 mg/kg, SC, repeated in 2 wk, or 0.1–0.2 mg/kg in feed for 7 days.

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Some dog breeds (Collies, Shetland Sheepdogs, Old English Sheepdogs, Australian Collies, and their crosses) have an abnormality in the blood-brain barrier associated with a mutation of the multiple drug resistance gene MDR1, which allows increased ivermectin into the CNS and results in toxicity. Dogs that are homozygous for the mutation produce a severely truncated P-glycoprotein (<10% of the normal amino acid sequence) and will develop ivermectin toxicity at any of the dosages used to treat demodicosis. The critical point seems to be 120–150 mcg/kg, at which transient, nonfatal clinical signs (mydriasis, ataxia, tremors) are seen. At higher dosages, collapse, coma, and respiratory collapse may develop. Similar idiosyncratic reactions may develop in any breed, so a gradually increasing dose (daily progression of 50, 100, 150, 200, then 300 mcg/kg) should be given to identify susceptible individuals. Administration should be stopped if any adverse effects are seen.[16]