Scabies

Scabies is a highly pruritic skin infestation caused by the mite Sarcoptes scabiei var. hominis. It is transmitted through prolonged direct skin to skin contact, with brief, casual contact generally insufficient for transmission.

A distinct, more severe variant, crusted (Norwegian) scabies, occurs in significantly immunocompromised or neurologically impaired individuals unable to mount an adequate scratching response. It carries substantially greater infectivity given the vastly increased mite burden.

Recognition of this distinction is required given its important implications for both individual treatment intensity and the scale of contact tracing and infection control measures required.

Pathophysiology

• Female mites burrow into the epidermis, laying eggs within the resulting burrow.
• The characteristic intense pruritus reflects a delayed type hypersensitivity response to mite antigens, faeces and eggs.
• This explains the typical delay of several weeks between initial infestation and symptom onset in a first, previously unsensitised infestation. Reinfestation in an already sensitised individual causes much more rapid onset (within days).
• Crusted scabies reflects an impaired host immune and scratching response. This occurs in advanced HIV infection, other significant immunosuppression, neurological conditions limiting normal scratching behaviour, and cognitive impairment or learning disability affecting recognition of and response to itching.
• The impaired response permits massive, largely unchecked mite proliferation. The resulting hyperkeratotic, crusted skin lesions contain extremely high numbers of mites, in marked contrast to the relatively low mite burden (typically only ten to fifteen mites) of ordinary scabies.

• Intense pruritus, characteristically worse at night, comes with a widespread excoriated papular rash. Characteristic sites are the finger webs, wrists, axillae, periumbilical area, buttocks and, in men, the genitalia.
• The face and scalp are typically spared in adults. These sites can be affected in infants and young children, which is relevant to examination in this age group.
• Burrows are thin, greyish, linear or serpiginous tracks representing the mite's tunnel within the epidermis. They are the pathognomonic finding where identified, though may be difficult to visualise because excoriation and secondary eczematous change from scratching frequently obscure them.
• Crusted scabies presents with widespread, thick, hyperkeratotic, scaly and crusted plaques, often affecting the hands, feet, scalp and nails.
• Pruritus in crusted scabies is characteristically less prominent or even absent, reflecting the underlying impaired immune or scratching response. This is potentially misleading: the apparent absence of significant itching might lower clinical suspicion for what is in fact a far more heavily infested and infectious presentation than ordinary scabies.
• Secondary bacterial infection (impetiginisation) from scratching is common, particularly in heavily excoriated or crusted lesions.
• In some endemic settings it can contribute to post streptococcal complications including glomerulonephritis, given the association between scabies associated skin breakdown and secondary streptococcal skin infection.

• Diagnosis is generally clinical, based on the characteristic distribution and appearance of the rash together with a compatible history of intense, often nocturnal, pruritus and relevant close contact exposure.
• Dermoscopy, where available, can improve visualisation of burrows and the characteristic mite itself (visible as a small, delta wing shaped structure at the end of the burrow).
• Skin scraping with microscopic examination for mites, eggs or faecal pellets provides definitive confirmation where diagnostic certainty is required.
• This is particularly relevant for confirming crusted scabies, where the substantially higher mite burden typically makes microscopic identification more straightforward.
• Obtain a careful history of close contacts, including household members and, where relevant, sexual partners. All relevant close contacts need concurrent treatment regardless of whether they are currently symptomatic, given the delayed symptom onset characteristic of first infestation.

• Standard first line treatment is topical permethrin 5 percent cream, applied to the entire body from the neck down, including under fingernails and in all skin folds.
• In infants and young children, apply it additionally to the face and scalp, given the different distribution pattern in this age group.
• Leave it on for eight to fourteen hours before washing off. Repeat the application after seven days to eliminate any mites hatching from eggs that survived the initial treatment.
• Oral ivermectin 200 micrograms per kg, given as a single dose repeated after one to two weeks, is an effective alternative. It is particularly useful where topical treatment is not feasible or has failed, and in widespread outbreak settings (institutional settings such as care homes, where treating large numbers of residents and staff with topical preparations may be impractical).
• Treat all household members and other close contacts simultaneously with the affected individual, regardless of whether currently symptomatic.
• Delayed symptom onset in first infestation means an asymptomatic contact may already be infested and capable of ongoing transmission or subsequent symptomatic relapse if left untreated.
• Crusted scabies requires more intensive treatment given the vastly higher mite burden. Typically combine topical permethrin (applied more frequently, sometimes daily for the first week, then reducing frequency) with oral ivermectin.
• Ivermectin is given in multiple doses, typically on days one, two, eight, nine and fifteen, with further doses according to clinical response and repeat skin scraping to confirm mite clearance.
• Add keratolytic agents to help remove the thick hyperkeratotic crust and improve topical treatment penetration. Specialist dermatology input is generally required given the complexity and intensity of treatment.
• Crusted scabies requires strict contact and additional environmental infection control precautions in the healthcare or institutional setting, given the potential for environmental mite survival from heavily shed skin scales.
• Broader contact tracing is needed given the substantially increased infectivity of this presentation. It can cause outbreaks even following relatively brief or casual contact that would be insufficient for transmission of ordinary scabies.
• Pruritus can persist for several weeks following successful treatment, reflecting ongoing hypersensitivity to residual mite antigen even after all live mites have been eliminated. It should not be misinterpreted as treatment failure or reinfestation.
• Symptomatic relief uses emollients, oral antihistamines and, where significant post scabetic eczematous change is present, a short course of topical corticosteroid.
• Wash clothing and bedding used in the days preceding treatment at high temperature, or seal in a plastic bag for a period sufficient to ensure mite death (mites generally surviving no more than two to three days away from the host in ordinary environmental conditions).
• This is a reasonable adjunctive environmental measure. It is of less critical importance than direct treatment of the affected individual and their close contacts, because the mite survives poorly away from the host.