Diagnosis

At present there is no accurate means of diagnosing scabies in various clinical settings. Presumptive diagnosis is often made on the basis of clinical signs, and a history of contact with other scabies cases [9]. In practice (especially in resource poor settings), identifying scabies mite from patient’s skin is challenging, and a negative result by even experienced clinical staff, does not rule out scabies. A positive response to therapy cannot exclude the spontaneous disappearance of a skin condition other than scabies, and a negative response to the first-line treatment option does not exclude scabies, especially with growing resistance among scabies mites [9]. Recent findings in this field, e.g. serodiagnosis [10] shows promising potential; however, more research is required to evaluate its efficiency in tropical clinical settings.

Treatments

Most treatments (Table 2) are potentially hazardous and are associated with moderate to severe side effects (e.g. secondary eczematisation, oedema, erosions and/or pyoderma) [17–22]. The most frequent complication of topical scabicides is persisting post-scabies eczema (generalised eczematous dermatitis) resulting from irritant effects of the various formulations [23]. These may escalate xerosis and worsen delayed-type eczema. Further, it may be difficult to treat patients with secondary eczematisation, erosions or ulcers using currently available topical scabicidal agents such as permethrin, lindane, benzoyl peroxide and sulphur, as they can cause serious cutaneous and systemic side-effects in addition to the problem of compliance, resulting in poor treatment uptake [24].

Oral ivermectin is not widely available and has not been approved for the management of scabies in many countries [8]. At present, there is some observational evidence of its effectiveness in controlling scabies outbreaks in institutional settings including nursing homes [5]. However; the safety or efficacy of ivermectin, the sole oral therapy available, has not been well-established in the elderly, patients with impaired liver function (potential for toxicity resulting from long elimination half-life [36 h]), children (aged <5 years) and pregnant women, where the blood–brain barrier is incompletely developed in the foetus, raising the potential for neurotoxicity [12]. Because of the drug’s lipophilicity, ivermectin may be poorly distributed in the asteototic stratum corneum of the elderly compared to younger patients, leading to mediocre therapeutic responses in the former patient cohort and requiring combination therapy with topical scabicides [12]. Ivermectin is not ovicidal, does not adequately penetrate the thick egg shell of the scabies mite, and is also ineffective against the younger stages of the parasite (whose nervous system is poorly developed), resulting in delayed therapeutic response [25].

Mass drug administration (MDA) programs have been attempted to use ivermectin to control scabies in endemic communities around the world [26]. However, such programs’ superiority over alternative topical treatment is questionable [27, 28]. Ivermectin is indicated in Australia only for crusted scabies or cases of typical scabies when prior topical treatment has failed or has been contraindicated [29]. It is generally recommended that for maximum absorption ivermectin must be given in empty stomach [30], which is a challenge in community-based programs. Ivermectin administration can be labour-intensive since the weight of all patients and the pregnancy status of all women of childbearing age must be determined. Paradoxically, its use is not recommended in those under 5 years of age when these are the most vulnerable group (particularly among Aboriginal and Torres Strait Islander children) [29, 30]. Institutional outbreaks of scabies in aged care centres, prisons, hospital wards and kindergartens are not uncommon developed counties. In Australia it is neither given to contacts of index cases, nor to households in heavily infected large communities, as the prescribing information does not support ivermectin administration to contacts of index cases [31].

Permethrin resistance is widespread in other ectoparasites [32]. Evidence of increasing acaricide resistance leading to treatment failures has been reported (Table 1) [33–37]. In vitro sensitivity data of scabies mites from the last 10 years (Australian data) indicate that median survival times to leading acaricides (ivermectin and permethrin) have increased 2–3 fold [33, 34]. Treatment failure of permethrin as a scabicide in Indigenous communities in Australia (following MDA) and elsewhere has been documented and it is the slowest-acting acaricide (in vitro) in the Northern Territory, Australia [33, 38]. Permethrin resistance to scabies mites has been confirmed in an animal model and its likely resistance mechanism has also been documented [37, 39]. Since the first documented case in Australia in 1994 [40], there have been reports of resistance of Sarcoptes scabiei to ivermectin in vitro and in vivo, including treatment failure in clinical trials [30, 34, 41–43]. MDAs programs that encounter poor compliance increase the risk of developing resistance and targeted treatment of index cases and contacts may be a better approach [44].