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Seminar

Scabies
Jrg Heukelbach, Hermann Feldmeier

Summary
Scabies is a neglected parasitic disease that is a major public health problem in many resource-poor regions. It causes substantial morbidity from secondary infections and post-infective complications such as acute post-streptococcal glomerulonephritis. Disease control requires treatment of the aected individual and all people they have been in contact with, but is often hampered by inappropriate or delayed diagnosis, poor treatment compliance, and improper use of topical compounds such as permethrin, lindane, or benzyl benzoate. In addition to concerns over toxicity with such compounds, parasite resistance seems to be increasing. Oral ivermectin is an alternative that has been used successfully in community control programmes. Plant derivatives such as turmeric, neem, and tea tree oil are also promising future treatments. The disease is strongly associated with poverty and overcrowding, and the associated stigma can ostracise aected individuals. Treatment of scabies in poor countries needs to integrate drug treatment programmes with eorts to improve the socioeconomic conditions and education programmes to reduce stigma. We expect the future to bring more sensitive and specic clinical and laboratory-based diagnostic methods, as well as new therapeutic strategies. In 1687, the Italian physician Giovan Cosimo Bonomo and the apothecary Diacinto Cestoni described the causal relation between the scabies mite and the typical skin lesions seen after infestation. They showed for the rst time that a disease can be caused by a microorganism.1 Scabies is caused by the mite Sarcoptes scabiei, and at 0305 mm adult female S scabiei are at the limit of visibility.2,3 Away from their hosts, mites are able to survive and remain capable of infestation for 2436 h at 21C and 4080% relative humidity.4,5 Lower temperatures and higher humidities prolong survival.3 For example, at 10C and 97% relative humidity, mites remain capable of infestation for about one week.3,4 However, at temperatures below 20C, they are unable to move and cannot penetrate the skin.2 At 34C, mites survive for fewer than 24 h, irrespective of environmental humidity. The mites infectivity decreases the longer they are o their host.3,4 Several mammals other than humans can be aected by S scabiei.6,7 Sarcoptic mange causes considerable morbidity in both domestic and wild animals, and can lead to large economic losses in livestock.79 There is general agreement that S scabiei is a single species that has evolved to be able to infect various mammalian hosts, with limited cross-infectivity between dierent host species.3,7,10,11 However, S scabiei from animals occasionally infest humans. Companion dogs are the most common cause of human infestation, and small outbreaks caused by scabies mites from dogs and other animals have been reported.10,12,13 In infestation with animal scabies mites, compared with those from other humans, the incubation period is shorter, and the topographic distribution of the lesions is dierent, with lesions mainly occurring on areas that have been in contact with the animal. In addition, the infestation tends to be self-limiting, often needing no treatment.3,6,7,10,14 skin for an unfertilised female.2,15 Female mites live for 46 weeks and produce 24 eggs per day, which are deposited in the burrowed tunnel.2 Larvae hatch 24 days after the eggs have been laid, and adult mites develop 1014 days later.2,3,16 In a key experiment in the UK in 1940, Mellanby2,17 showed that transmission occurs by body contact and that under normal conditions fomites (inanimate objects that transmit an infection from person to person) are unlikely to play a role. In the study, volunteers climbed nude into warm beds just vacated by infested patients. Only four cases (133%) resulted from 300 attempts when patients had fewer than 20 mites. This number rose to 45 (15%) when patients carried more than 50 infective mites. The parasite burden of individuals with scabies is usually low. An average burden of 1012 mites has been determined for the rst 3 months of infestation.2,18 However, hundreds of mites can be found in neglected children in underprivileged communities, and millions in patients with crusted scabies.2,19 Mites dislodged from an infested individual use odour and heat to nd a new host. For these stimuli to be intense enough, individuals must be in close skin contact, for example during sexual intercourse or when children sleep in the same bed or hammock more or less undressed. However, bedding and clothing can act as fomites, especially when used by patients with a high parasite load such as in crusted (Norwegian) scabies.
Search strategy and selection criteria MEDLINE, LILACS, and COCHRANE searches using the keywords parasitic skin disease, scabies, sarna, escabiose and galle were used as a primary source of reference. Reference lists found in Spanish, Portuguese, and French language textbooks on dermatology, parasitic diseases, and tropical medicine were also used. The inclusion or exclusion of individual manuscripts was based on the originality of the data and a robust study design.
Lancet 2006; 367: 176774 Department of Community Health, School of Medicine, Federal University of Cear, Brazil (Prof J Heukelbach MD); and Department of Medical Microbiology and Immunology of Infection, Charit Medical School, Campus Benjamin Franklin, Berlin, Germany (Prof H Feldmeier MD) Correspondence to: Prof Hermann Feldmeier hermann.feldmeier@charite.de

Parasite lifecycle and transmission


Once on human skin, female mites burrow into the epidermis for about 30 mins.4 The male mite explores the
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Epidemiology
Scabies can occur both epidemically and endemically. Sporadic cases are typically seen in industrialised countries, where epidemics usually occur in institutional settings or in socially deprived groups. Within a community, scabies is unevenly distributed, and prevalence in the general population is usually low.14,2022 However, the frequency of infested individuals can be 4080% in some high risk groups, as studies in dermatology patients in sub-Saharan Africa, Indigenous communities in Australia and New Zealand, and homeless or displaced children have shown.2327 The role of poor hygiene has been overestimated. Mites burrowed in the epidermis are resistant to water and soap, and continue to be viable even after daily hot baths.28 The more crowded the living conditions, the higher the prevalence of scabies in the population.25 In a study in Brazil, scabies was twice as prevalent in a densely populated urban slum than in a shing community where families lived in larger spaces.29 Data obtained from countries in temperate zones indicate that the incidence is higher in winter than in summer, probably due to increased physical crowding of individuals during the cold season and because mites can survive away from the host for longer in lower temperatures.20,3036 Although the occurrence of scabies peaked in the cold and dry season in the East African highlands, no seasonal variation was found in Bangladesh, The Gambia, or Brazilareas with little variation of air temperature throughout the year.23,29,37,38

For a few years, S scabiei cDNA libraries and expressed sequence tag (EST) databases have been available.7,4245 Fischer and colleagues45 used an EST approach to identify homologues of dust mite allergens in S scabiei.45 Several homologues have been cloned in the meanwhile.4648 Thousands of cDNA clones have been sequenced, and molecules with possible immunodiagnostic or immunostimulating properties have been identied.7

Clinical aspects
Scabies can mimic a broad range of skin diseases. Once a female mite has identied a suitable place on the skin, it rapidly penetrates into the epidermis and burrows more or less parallel to the corneal layers at a rate of 055 mm per day. The resulting tunnel is rarely visible. Clinically visible burrows, which can be seen after several days, probably occur when there is a local host reaction around the tunnel. The burrow looks like a short wavy line, and is most commonly seen on the ngers, wrists, and penis. Papules are small and erythematous. They can be sparse, or numerous and close-set. Over time papules can change into vesicles and bullae. The face and neck are often aected in infants and children, but rarely in other age groups.6,14,29 Papules and vesicles frequently develop into secondary scabies lesions: excoriations, eczematisations, secondary infections, and crusts. Primary and secondary lesions generally coexist on the same patient. Scratching frequently leads to denudation of the lesion, and secondary infection; in this case the clinical picture is often similar to pyoderma. Nodules develop at sites such as the elbows, anterior axillary folds, penis, and scrotum. These are rm, dull red or brownish masses that can persist for months. In contrast to burrows and papules, they do not necessarily indicate active infestation. Crusted scabies is a hyperinfestation with thousands of mites present in exfoliating scales as a result of the hosts insucient immune response. The condition occurs usually in individuals with underlying immunosuppression, such as infection with HIV, human T-cell lymphotropic virus 1, or leukaemia, but has also been seen in patients with healthy immune systems.19,49 This highly contagious form of scabies has been most often seen in institutionalised elderly people and in Australian Aborigines.19,50 Clinically, crusted scabies is a hyperkeratotic skin disease resembling psoriasis. Other atypical presentations, including scabies incognito, bullous scabies, nodular scabies, and hidden scabies, have been reviewed by Cestari and Martignago.51

Immune response
The signs and symptoms of scabies are the result of an adaptive immune response and only occur after sensitisation. This explains the delayed onset of symptoms in primary infestations. When patients are infested for a second time, hypersensitivity develops within a day.16 Protective immunity could explain why experimental re-infestation is dicult in sensitised patients, and why parasite load is usually lower in individuals with a second infestation compared with those being infested for the rst time.39 Raised systemic interleukin 4 has been recorded in patients with crusted scabies.7 In rodent scabies, an increased synthesis of interleukin 4 and a reduced release of IFN- also indicated a Th2 immune response.39 Histopathological examination of skin biopsy samples has shown that mites are surrounded by inammatory cell inltrates comprising eosinophils, lymphocytes, and histiocytes. Peripheral immunoglobulin E levels are usually raised in patients with crusted scabies.19,40

Associated pathology
Pruritus, the result of a hypersensitive reaction to components of the saliva, eggs, and faecal material of the mites, typically worsens at night and can prevent patients from sleeping well. Breaks in the epidermis, scratching, and subsequent excoriations serve as an entry point for
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Molecular biology
The absence of an animal model and in vitro methods for research for S scabiei has hampered research on the biology of the parasite and its relation with the host.7,41
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pathogenic bacteria. In the tropics, scabies is frequently associated with secondary bacterial infection of the lesions, and staphylococci or streptococci are common.5256 Pyoderma is therefore a typical complication, particularly when patients have many lesions.55 Substantial evidence indicates that scabies is a risk factor for developing acute post-streptococcal glomerulonephritis (APSGN): within a country the spatial distributions of areas with a high prevalence of scabies and a high incidence of APSGN overlap;57 a rising prevalence of scabies over time was paralleled by an increasing incidence of APSGN;5658 seasonal variation in the occurrence of scabies was followed by similar patterns in patients newly diagnosed with APSGN;5960 and epidemics of scabies coincided with epidemics of APSGN in the same population.52,6163 In Trinidad, the number of nephritogenic strains of streptococci isolated increased with a rise in the occurrence of scabies and APSGN in the general population.52,56,63 The existence of nephritogenic streptococci in an area is probably the main prerequisite for APSGN. Lawrence and colleagues64 have shown that signs of APSGN are greatly reduced after mass treatment with ivermectin. Currie and Brewster65 suggested that the high burden of group A streptococci on the skin of Australian Aboriginals contributes to the exceptionally high incidence of acute rheumatic fever recorded in this population. The role of scabies in this context remains to be shown.53 In crusted scabies, a generalised lymphadenopathy is common and secondary sepsis can lead to death.53,66 In addition, pyoderma is the predominant source of group A streptococcal invasive disease.53

high equipment cost means the techniques are accessible only in well-resourced settings. We propose a practical approach for the diagnosis of scabies that includes the presence of papules, vesicles, pustules, itching (especially at night), and a positive family history.29 Nearly all pruritic dermatoses have to be considered as dierential diagnoses. The probability of a certain dierential diagnosis varies according to the age of the patient and the local setting. In industrialised countries, scabies is often mistaken for eczema, tinea, and atopic dermatitis. In developing countries, particularly in children, pyoderma without scabies is the most common dierential diagnosis.71 In some cases, scabies can mimic systemic lupus erythematosus,72 bullous pemphigoid,73 Langerhans cell histiocytosis,74 urticaria pigmentosa,75 and seborrhaeic dermatitis.76 Crusted scabies can also resemble psoriasis.77

Case management
Immediate treatment of the patient with an eective drug and rigorous treatment of close contacts remains the mainstay in case management. Since individuals can be infested without showing symptoms, people they have been in contact with should be treated independently whether clinical symptoms are present or not.78 Surprisingly, few controlled studies have been done to compare the eectiveness of topical compounds on the market.79 As a result, treatment recommendations vary from one country to another, and the selection of a drug is often based on the personal preference of the physician, local availability and cost, rather than on medical evidence. For example, the low cost of benzyl benzoate cream or lotion (10% or 25%) means it is commonly used as the rst line drug in developing countries, whereas permethrin cream (5%) is the standard treatment in the USA, UK, and Australia.80 Other topical treatments in use are monosulram (25%), malathion (05%), lindane (031%), crotamiton (10%), and sulphur in petrolatum (210%).7,8184 Benzyl benzoate was rst known as a component of balsam of Peru. In the 1930s, successful treatment of thousands of scabies cases with topical benzyl benzoate was reported from Denmark.85 The ecacy of benzyl benzoate (25%) as a cream or lotion is high. However, it requires repeated applications (twice a day for 23 days, and then this must be repeated again after 10 days), irritates the skin, and can produce a burning sensation, greatly reducing compliance. Permethrin, a synthetic pyrethoid, is used in many countries as rst-line therapy and it is judged to have low toxicicity.86 Since permethrin is adulticidal and ovicidal, it is highly eective after a single application. In a study in 467 patients, a single application of 5% permethrin was as eective as 1% lindane, and it has been successfully used in outbreaks of lindane-resistant scabies.8789 However, after in-vitro tests, Walton and colleagues7,90
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Diagnosis
In primary infestation, signs and symptoms only develop after 34 weeks. A clinical diagnosis can be made when a burrow is detected at a typical predilection site and the lesion is severely itching. In this case, even a single burrow is pathognomonic. In practice, however, burrows are often obliterated by bathing, scratching, formation of crusts, or superinfection. In severely aected communities in developing countries and in Australia, burrows are rarely seen (Heukelbach J, unpublished).7 Individuals are suspected of having scabies if another member of the household shows similar lesions. Dermatology textbooks say the diagnosis of scabies requires the microscopic detection of the mite, ova, or faecal pellets. In reality, however, the sensitivity of skin scrapings is so low that its diagnostic usefulness is questionable. This method is very specic, though, and a mite or eggs seen in the microscope are diagnostic. Epiluminescence microscopy and high-resolution videodermatoscopy seem to be promising diagnostic methods,6770 but there have been no robust studies to compare the sensitivity and specicity of clinical diagnosis and microscopic examinations of the skin. The
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raised concerns about increasing permethrin resistance in Australia (they noted that some strains were totally resistant to permethrin). Pyrethroids applied in a thermolabile foam formulation seem to be better tolerated than the cream form, and reduce itching quicker.91 For years, lindane was the rst-line medication for scabies. But reported toxic eects have prompted debate over its use since the 1970s. Adverse events are especially common when the medication is ingested or when the manufacturers instructions are not followed rigorously, such as application on broken skin or using it more often than recommended.9295 Toxic eects are mainly neurotoxic symptoms such as numbness of skin, restlessness, anxiety, tremor, and convulsions.83,92,93,96,97 Accidental oral ingestion can lead to nervous system damage and death.83,93,97 Several researchers have reported parasitic resistance to the treatment.87,88 Because of its high toxicity and increasing resistance, it is contraindicated in children younger than 3 years and is considered, at least in the USA, as a second-line drug only.98 Since most scabies drugs are potentially toxic, treatment in pregnancy and infancy requires special attention. Sulphur in petrolatum has been used for centuries, and is still the treatment of choice in some resource-poor settings.14,83 Both sulphur in petrolatum and permethrin are safe for pregnant women and young children.99,100 Crotamiton is safe for use in children and infants, but its ecacy is questionable. Benzyl benzoate at 10% is commonly used in pregnancy and childhood in the developing world. The treatment of clothing and bed linen (washing at 60C, treatment with a scabicide lotion, or putting it in a hermetically sealed bag for several days) is recommended.101 However, this practice should be restricted to patients with crusted scabies, since the risk of a re-infestation through fomites is negligible in other forms of scabies. Presumably, most relapses are due to the lack of adherence to treatment protocols and a low compliance. Often, patients do not apply the drug to all aected body parts, with the head, the genitals, and the periungual area frequently left untreated. Re-infestation increases the risk of development of resistance and cumulative toxicity as a consequence of repeated applications. In crusted scabies, 57 doses of oral ivermectin in combination with topical permethrin and keratolytic therapy is recommended.19 Since many scabicides are potentially hazardous, much eort is being invested in the development of less toxic alternatives.102 Essential oils have shown an impressive eect against mites in vitro as well as in eld studies. For example, tea tree oil (Melaleuca alternifolia) is highly eective in vitro,90,103 and a paste made from extracts of neem (Azadirachta indica) and turmeric (Curcuma longa) cured 790 (97%) patients with scabies.104 In a clinical trial in Nigeria, bush tea (Lippia multiora) essential oil showed similarly high cure rates.105 A randomised control
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study in Brazil showed a commercially available repellent containing coconut oil and jojoba was highly eective (Heukelbach J, unpublished). The treatment of scabies with oral ivermectin, a macrolytic lactone with a good safety prole, has opened a new area in the treatment of ectoparasitosis.106108 Ivermectin has been available since the mid 1980s, and millions of individuals have been treated with it for onchocerciasis and lymphatic lariasis control programs in Africa and South America. The ecacy and eectiveness of oral ivermectin is equivalent to, or better than, that of topically applied lindane,109,110 benzyl benzoate,111113 and permethrin.114 Adverse events are rare, of minor severity, and transient. Barkwell and Shields115 reported three deaths 6 months after treating elderly individuals with ivermectin. However, whether the deaths were causally related to ivermectin is unclear, and the signicance of the report has been questioned subsequently.116120 At present, oral ivermectin isexcept in a few countries such as France and Brazilonly approved for the treatment of nematode infections. However, o-label use for parasitic skin diseases is common worldwide. It is judged to be particularly useful in institutional outbreaks of scabies, for the treatment of crusted scabies, and in immunocompromised patients.121125 In developing countries, ivermectin has been used to control scabies in the community, and to reduce associated morbidity.64,126,127 In addition, the simultaneous elimination of the most common intestinal nematodes and of other ectoparasites benets patients in developing countries who are typically polyparasitised.127,128 So far, resistance to oral ivermectin has been reported in two cases. These patients had received 3058 doses of the drug over 4 years, indicating that resistance can be induced by repetitive treatment.129

Scabies in the developing world


Unlike in industrialised countries, scabies is a major public health threat in the developing world. Scabies is common in resource-poor urban and rural communities, with prevalence reaching up to 10% in the general population and 50% in children.6,23,29,37,130133 In an urban slum in Bangladesh, the incidence in children younger than 6 years was 952 per 1000 per year, meaning that nearly all children had had at least one S scabiei infection per year.37 The belief that scabies in young single adults stems mainly from sexual contacts and that in families it starts with the children might be valid in industrialised countries, but clearly does not pertain to the developing world where the relation between low socioeconomic status, overcrowding, risk behaviour, proportion of individuals infested, and the spread of S scabiei is complex (gure 1). Poverty with its typical consequences inadequate living conditions, overcrowding, and a low level of educationseems to be a major driving force for
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maintaining a high incidence and prevalence of the disease.25,37,53,133 The best evidence for the predominant role of poverty in determining the occurrence of scabies in a community comes from Bangladesh. Compared with households without scabies, families with scabies were signicantly less likely to own their house, as well as being less likely to have constant electricity, and were more likely to live in a house constructed from waste material, and to have a lower monthly income.37 Drug shortages can also contribute to a high prevalence of infestation in the community.52 Presumably, existing treatment options (mainly benzyl benzoate and sulphur compounds) are responsible for poor adherence to treatment protocols.128 Economically disadvantaged people usually have restricted access to health care, which delays diagnosis and treatment, and thus increases the number of individuals spreading the infestation for a protracted period. In an urban squatter settlement in Dhaka, for example, 375 (49%) of infested children were not treated for up to 44 weeks after the characteristic signs and symptoms had developed.37 Even the provision of health care free of charge, as in Brazil, cannot guarantee that patients with scabies will be identied and treated appropriately. In a primary health-care setting in Northeast Brazil, clinically apparent scabies went unnoticed by doctors in 52% of patients.134 Controlling scabies at the community level in resource-poor settings has rarely been attempted. A few successful examples show that prolonged reduction of prevalence can be achieved by mass therapy in combination with public health education and training of health-care providers.25,55,64,89,126,127,131,135 Parallel to the reduction of scabies, the occurrence and severity of strepotoccoal pyoderma decreased signicantly. Health education should also address the stigma attached to diseases such as scabies.128 In the tropics, the topographic distribution of scabies lesions is dierent from that in the developed world, and often include the face, neck, scalp, and post-auricular fold.7,29 Thus, mass treatment with topical drugs can be dicult since the whole body surface has to be covered with the compoundwhich does not go unnoticed by other individuals, thereby reinforcing stigmatisation. Oral treatment with ivermectin is more easily accepted and administration can be directly supervised by auxiliary personnel.119,127,128 We are sceptical that a sustained reduction of scabies in the developing world can be achieved by drug treatment alone. However, what is needed is an integrated approach that combines treatment with the amelioration of the socioeconomic situation of people at risk. Although it is dicult to disentangle the causal web that makes scabies so prevalent in resource-poor communities, the consequences of the ectoparasitosis in these settings are well known (gure 2). Pyoderma is so consistently associated with scabies and other parasitic
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Presence of vulnerable groups -(homeless) children -young adults -the elderly

Core transmitters (crusted scabies) Infestation of family members

Behaviour -disease perception -health-care seeking -sleeping habits

Poverty -overcrowding -poor living conditions -limited access to water -low level of education

Restricted access to health care

Prevalence of scabies in the community

Delayed diagnosis and treatment

Favourable climate -temperature -humidity

Persistent infestation

Treatment failure -poor or no compliance

Decient public-health care -wrong or missed diagnosis -shortage of drugs

Poor sensitivity of laboratory tests

Figure 1: Factors contributing to a high prevalence of scabies in resource-poor communities

skin diseases that it is rare to nd a patient with an ectoparasitosis without superinfected lesions.52,53,55,56 Hence, sequels of group A streptococcal skin infection are common.

The future
A better understanding of factors associated with infestation and severe disease is of pivotal importance. The molecular characterisation of mites isolated from infested individuals could help to track the spread of S scabieieg, in a nursery, kindergarten, or resource-poor community. The identication of behavioural and environmental risk factors in dened sociocultural settings will provide the rationale to target control measures to the most vulnerable groups. An ELISA for the detection of antibodies in pigs and dogs now is commercially available and an immunoassay for human scabies is likely to follow soon.7,136 An initial

Disturbance of sleep or alteration of mood

Consequences of scabies

Stigmatisation or ostracisation

Other parasitic skin diseases

Pyoderma

Scabetic dogs with (nephritogenic) streptococci

Rheumatic heart disease

Septicaemia

APSGN

Figure 2: Eects of scabies in resource-poor settings

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study has shown that DNA from scabies mites can be amplied, and that diagnostic PCR from skin material is highly specic, indicating the possible use of PCR in the future in clinically non-apparent cases.137 Since cDNA libraries and Expressed Sequence Tag (EST) databases have become available, new achievements in immunodiagnostics are to be expected. Existing therapeutic options are insucient, especially for the treatment of young children, pregnant and breast-feeding women, and immunocompromised individuals. Plant-based compounds such as turmeric and tea tree oil seem to have great therapeutic potential and need to be explored systematically in dierent settings. There is reason for hope that treatment of scabies with such compounds will increase both the compliance and the eectiveness of treatment protocols. Without doubt, considerably more commitment is needed from health-care providers and the research community to improve the knowledge of this parasitic skin disease and to better care for those aected or at risk.
Acknowledgments We thank Richard Speare and Wayne Melrose for critically reviewing the manuscript, and Michi Feldmeier for secretarial assistance. Jrg Heukelbach holds an Endeavour Australia Postgraduate and Postdoctoral Research Scholarship, and Hermann Feldmeier acknowledges travel support from DAAD, Bonn, Germany. Conict of interest statement We declare that we have no conict of interest. References 1 Ramos-e-Silva M. Giovan Cosimo Bonomo 16631696: discoverer of the etiology of scabies. Int J Dermatol 1998; 37: 62530. 2 Mellanby K. Biology of the parasite. In: Orkin M, Maibach HI, eds. Cutaneous infestations and insect bites. New York: Marcel Dekker; 1985: 918. 3 Arlian LG. Biology, host relations, and epidemiology of Sarcoptes scabiei. Annu Rev Entomol 1989; 34: 13961. 4 Arlian LG, Runyan RA, Achar S, Estes SA. Survival and infectivity of Sarcoptes scabiei var. canis and var. hominis. J Am Acad Dermatol 1984; 11: 21015. 5 Arlian LG, Vyszenski-Moher DL, Pole MJ. Survival of adults and development stages of Sarcoptes scabiei var. canis when o the host. Exp Appl Acarol 1989; 6: 18187. 6 Chakrabarti A. Some epidemiological aspects of animal scabies in human population. Int J Zoonoses 1985; 12: 3952. 7 Walton SF, Holt DC. Scabies: new future for a neglected disease. Adv Parasitol 2004; 57: 30976. 8 Rehbein S, Visser M, Winter R, et al. Productivity eects of bovine mange and control with ivermectin. Vet Parasitol 2003; 114: 26784. 9 Pence DB, Ueckermann E. Sarcoptic mange in wildlife. Rev Sci Tech 2002; 21: 38598. 10 Fain A. Epidemiological problems of scabies. Int J Dermatol 1978; 17: 2030. 11 Arlian LG, Runyan RA, Estes SA. Cross infestivity of Sarcoptes scabiei. J Am Acad Dermatol 1984; 10: 97986. 12 Morsy TA, Bakr ME, Ahmed MM, Kotb MM. Human scabies acquired from a pet puppy. J Egypt Soc Parasitol 1994; 24: 30508. 13 Mitra M, Mahanta SK, Sen S, Ghosh C, Hati AK. Sarcoptes scabiei in animals spreading to man. Trop Geogr Med 1993; 45: 14243. 14 Burgess IF. Sarcoptes scabiei and scabies. Adv Parasitol 1994; 33: 23592. 15 Heilesen B. Studies on Acarus scabiei and scabies. Acta Derm Venereol 1946; 26: 2630.

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