Journal of Hospital Infection (2007) 65, 9e14

www.elsevierhealth.com/journals/jhin

REVIEW

Nosocomial scabies
R. Vorou a, H.D. Remoudaki b, H.C. Maltezou b,*
a

Department of Epidemiological Surveillance, Hellenic Centre for Disease Control and

Prevention, Athens, Greece
b
Office for Nosocomial Infections, Microbe Resistance, and Rational Use of Antibiotics,
Hellenic Centre for Disease Control and Prevention, Athens, Greece
Available online 30 November 2006

KEYWORDS
Scabies; Nosocomial;
Hospital-acquired;
Outbreak; Epidemics

Summary Scabies is a parasitic dermatosis with a worldwide distribution.

This infestation affects millions of people annually and may cause large
nosocomial outbreaks with considerable morbidity among patients and
healthcare workers. Immunocompromised or elderly institutionalized
patients admitted with unrecognized crusted scabies are the main source
of nosocomial transmission. Factors that facilitate the development of
hospital-acquired scabies and nosocomial epidemics are: poor knowledge
of scabies epidemiology, unfamiliarity of healthcare workers with atypical
presentations, long incubation period, diagnostic delay and incomplete
monitoring. Within hospitals, containment of an outbreak relies on the
strict implementation of appropriate infection control measures and
treatment administration to contacts. It is associated with a considerable
working and economic burden.
2006 The Hospital Infection Society. Published by Elsevier Ltd. All rights
reserved.

Introduction
Scabies is a contagious, parasitic dermatosis with
worldwide distribution that affects 300 million
individuals annually, encompassing all age groups,
races and social classes. It is associated with
* Corresponding author. Address: Office for Nosocomial Infections, Microbe Resistance, and Rational Use of Antibiotics,
Hellenic Centre for Disease Control and Prevention, 54, 3rd
Septemvriou Street, Athens, Greece. Tel.: 30 210 8899 219;
fax: 30 210 8899 330.
E-mail address: helen-maltezou@ath.forthnet.gr

considerable morbidity among specific groups of

patients and in endemic tropical and subtropical
communities. Epidemics occur during war and as
a result of poverty, poor hygiene, overcrowding,
institutionalization, malnutrition and sexual
promiscuity.1e9
Scabies outbreaks have been reported in various
well-confined settings, including long-termcare facilities, nursing homes and acute care
facilities.5,10e15 Within hospitals, immunocompromised patients or elderly, institutionalized patients
admitted with unrecognized crusted (Norwegian)
scabies constitute the main source for spread of

0195-6701/$ - see front matter 2006 The Hospital Infection Society. Published by Elsevier Ltd. All rights reserved.
doi:10.1016/j.jhin.2006.08.012

10
scabies to other patients and healthcare workers
(HCWs).16e31 Nosocomial scabies represents a challenge as HCWs may not be familiar with atypical
presentations, and its containment is associated
with a considerable working and economic
burden.16,17,21,23,32 The aim of this article is to
review nosocomial scabies, focusing on its epidemiology and control.

Epidemiology
Scabies is caused by Sarcoptes scabiei var. hominis,
an obligate human parasite. The parasite is not
a vector of infectious agents. The fertilized
female lays two to three eggs daily in tunnels
burrowed in the epidermis, which mature to mites
17 days later. The males die after a short time but
the females live for up to six weeks.3,4,6
Scabies is transmitted through skin-to-skin
contact, and transmission through sexual contact
is also common. In classic scabies, the estimated
number of mites per patient is 10e15 compared
with two million per patient in crusted scabies.3e5
The numerous mites found in crusted scabies
facilitate transmission through the environment
and explain why it is highly contagious.33 Patients
with crusted scabies serve as a reservoir for the
mite. The crusts flake off and contaminate the
environment, and mites survive in the environment
for up to three days.4,6 In classic scabies, the
environment plays a minor role in transmission;
transmission through household contact may result
in family clusters.5 Canine mites may cause
transient infestation of humans that is terminated
by animal treatment.4
The prevalence of scabies is underestimated,
since it is not a notifiable disease in most countries. Few studies presenting prevalence data are
present in the literature. In Europe, the highest
prevalence (4.2%) was noted in a village in Spain.34
In the Lower Silesia region of Poland, the prevalence of scabies ranged from 7.9 to 80 per
100 000 people between 1990 and 1997.35 In most
European studies, scabies is more frequent among
children, young adults, women, family members,
and during autumn and winter.34e38 In Central
Poland, the prevalence of scabies is higher in rural
areas; in contrast, in the UK, the prevalence is
higher in urban areas.36,38 During the last decade,
the prevalence of scabies has decreased in Poland,
whereas increasing trends have been noted in the
UK.35,38
In developing countries, scabies represents a
serious public health problem, with prevalence
ranging from 3.8% to 8.8%.1,9,39,40 In the Solomon

R. Vorou et al.
Islands and in Aboriginal populations in Australia,
prevalence rates of 25% have been reported in
children.2,8 In the latter population, crusted
scabies represents the most common form,
without any known immunosuppression.5 In
poorly-resourced communities, scabies is frequently associated with superinfection caused by
Streptococcus pyogenes or Staphylococcus aureus,
which may be associated with increased morbidity
and occasionally fatal outcome.1,2,7,8 Superinfection is also common in patients with acquired
immunodeficiency syndrome (AIDS) and homeless
people.18,41e43
Crusted scabies develops in immunocompromised patients, including patients infected with
human immunodeficiency virus (HIV)/AIDS and/or
human T-lymphotropic virus-I (HTLV-I), patients on
topical or systemic steroid therapy, organtransplant recipients, leukaemic patients, and
elderly institutionalized or debilitated individuals.4,5,23,33,44e48 Among HIV/AIDS patients, the
correlation with scabies is stronger when CD4
counts are low.49e52 In areas where HTLV-I
infection is endemic, crusted scabies constitutes
a marker for HTLV-I infection, and adversely,
HTLV-I infection affects the clinical course of scabies.53 In immunocompromised patients, crusted
scabies may be complicated by staphylococcal
sepsis with increased morbidity and mortality.54e56
Homeless people frequently seek medical
care for dermatological problems, with scabies
accounting for a significant proportion.41,42,57,58
In a study conducted in 1996 in France, 56.5% of
189 homeless people were infested with scabies
as a result of poor hygiene, close contact within
shelters and deficient medical care.41,42,57 When
homeless people seek medical care, HCWs should
consider the possibility of infestation.
Among elderly people, those living in nursing
homes are prone to develop scabies.10e14,59 Treatment failure is common in elderly people on immunosuppressive therapy and may contribute to the
onset of outbreaks.14 In a survey of 130 chronic
healthcare institutions in Canada, 25% reported
cases of scabies among their residents during a
one-year period. HCWs were also infested in 11%
of these institutions. The size of the institution,
in terms of the number of residents and the number of staff, was a risk factor for the development
of scabies.10
Nosocomial scabies is not uncommon. The authors identified 19 outbreaks in 16 hospitals in the
literature.16e31 The mean duration was 14.5 weeks
(range 4e52 weeks).16e27,29,31 In all outbreaks, the
source concerned immunocompromised patients,
mainly HIV/AIDS patients or elderly people residing

Nosocomial scabies
in institutions, on long-term steroid treatment or
with chronic diseases. Most source cases came
from the community. All but one had crusted
scabies that was unrecognized at admission. Most
HIV/AIDS patients were misdiagnosed with seborrhoeic dermatitis or eczema, and scabies was
suspected when no response occurred following
treatment.17,19 In outbreaks where elderly people
were the sources of infestation, investigation for
scabies began when HCWs developed intense
pruritus.21,23,25,31
The mean number of infested patients per
outbreak was 18 (range 3e82),16,18e23,26,28
with a mean attack rate of 12.9% (range
4e40%).18,20,23,26,28 The mean number of infested
HCWs was 39 (range 6e278),16e31 with a mean attack rate of 34.6% (range 6.95e88%).18,20,23,25,27e31
Most of the infested HCWs were nurses due to
their close contact with patients. In an outbreak
that occurred in a large US hospital, risk factors
for developing scabies among HCWs were working
with AIDS patients and being a nurse, a physical
therapist, or an HCW with extensive contact
with infected patients.18 In a nosocomial outbreak that occurred in Brazil, 22.5% of 200 laundry workers were infested because of ignorance
regarding preventive measures.29 All infected
HCWs developed classic scabies.5,11,12,23,25,29 It is
noteworthy that 11.1% of 5606 work-related infections reported by HCWs to occupational disease networks in the UK between 2000 and 2003
concerned scabies, second only to diarrhoeal
disease.60 The unfamiliarity of HCWs with atypical
presentations, misdiagnosis of cases, and intensive contact with patients facilitates the transmission of scabies.17e20,23,25
Within hospitals, the control of scabies
outbreaks requires a considerable amount of
work. The cost and inconvenience for tracing all
contacts is underlined in a large US nosocomial
outbreak, where 981 people received treatment.18
The burden is even heavier for poorly-resourced
countries with high community prevalence of
scabies. Infested asymptomatic HCWs, patients
and members of the community may contribute
to the spread of infestation throughout hospitals,
as occurred in an outbreak where 112 people
were infested during a 12-month period in three
waves; the second and third waves were caused
by a treated asymptomatic contact of the previous
waves.23 This suggests that therapeutic failures
due to resistance or re-infestation may contribute
to the prolongation of an outbreak.22,23,25
Nosocomial outbreaks of scabies are associated
with a high economic burden due to additional
medications, working hours, prolongation of

11
hospitalization, and ward closures. Estimated
costs for the containment of two outbreaks in
Canada were Canadian $20 000 and $100 000,
respectively, whereas the cost of an outbreak in
Brazil was US$ 50 000.21,29,32 Estimations were
made in 1992.
In conclusion, factors that facilitate the onset
and prolongation of nosocomial outbreaks of
scabies include the fact that it is not a notifiable
disease, unknown community epidemiology in
developed countries, admission of unrecognized
cases, increasing numbers of immunocompromised
patients, long incubation period, unfamiliarity of
HCWs with atypical presentations, diagnostic delay,
therapeutic failures, and incomplete surveillance
following intervention.

Clinical manifestations
Classic scabies
Scabies has a long incubation period. Symptoms
develop three to four weeks after initial
infestation, and one to three days following
re-infestation.5,6
Classic scabies manifests as generalized intensive pruritus with nocturnal predominance.3e6,43
Lesions appear as burrows or erythaematous
papules. Burrows are slightly elevated lines, often
with crusts sited on the hands, wrists, elbows,
genitalia, axillae, umbilicus, buttocks and
nipples.4,13,18,44 In adults and older children, the
head, palms and soles are spared, whereas these
sites are often involved in young children and
immunocompromised patients.4e6

Atypical presentations
Crusted scabies is a scaly dermatosis with mild or
no pruritus, occasionally accompanied by generalized lymphadenopathy. Nails are commonly
involved. Crusted scabies may also manifest as an
erythematous eruption.3,5,23 Nodular scabies manifests with a few pruritic lesions that are mainly
located in the groin, axillary regions and male
genitalia. Nodules appear after prolonged infestation and may persist for weeks or months after
successful therapy.4,46 Bullous scabies mimics
bullous pemphigoid eruptions in patients over 65
years of age.4,5 Elderly people may have nonspecific pruritic lesions attributed to senile
pruritus or anxiety.5,23,46 Subsequent long-term
local corticosteroid application may lead to
crusted scabies.21,30,31,43

12

Diagnosis
A compatible presentation and a family history,
residence or working in a nursing home, or a cluster
of non-specific pruritic rashes among HCWs should
raise the suspicion for scabies. In case of strong
clinical suspicion but in the absence of laboratory
confirmation, diagnosis may be established by the
patients response to appropriate treatment.
An oil preparation of a skin scraping or material
retrieved from underneath the nails enables visualization of mites, eggs or faeces. Microscopy may
be difficult in classic scabies due to the small
number of mites found.4e6,46 Epiluminescence
microscopy is an in vivo technique with high sensitivity that allows rapid diagnosis without patient
inconvenience.61

Infection control
Prompt recognition of scabies followed by immediate implementation of preventive measures is
the mainstay for the containment of a nosocomial
outbreak. All HCWs involved in the management of
a case should be educated, with emphasis on the
aforementioned topics.23,26,46
Patients with scabies should be isolated for 24 h
following treatment. Infection control measures
differ between classic and crusted scabies. In
classic scabies, disposable gloves should be used
during contact and for 24 h following treatment.
Patients with crusted scabies should be hospitalized for treatment. When a case of crusted scabies
is suspected, contact precautions should be
strictly implemented, including the use of disposable gloves, gowns and shoe covers. A course of
treatment should follow any skin-to-skin contact
with the patient. Testing for scabies should be
repeated when the patient becomes asymptomatic
and two to four weeks after treatment completion.5,16e18,23,46 Patients with crusted scabies
should be cared for by the minimum number of
HCWs.5,16e18,23,46 In outpatient settings, homeless
people suspected to have scabies should be
treated.41,42 AIDS patients with a pruritic rash
should be tested for scabies and managed accordingly while awaiting the results.17e19,24
Fomites should only be handled by people wearing gloves. Clothing and linens should be machine
washed in hot water and dried thoroughly or
ironed.4,5,13 Carpets and furniture should be vacuumed. Items that that cannot be washed should
be treated with insecticidal powder such as chloramine 5%, and stored in plastic bags for 10 days or in
a freezer at 20  C for 72 h.4,5,13,46

R. Vorou et al.
During an outbreak, attempts should be made to
confirm the diagnosis in contact cases. Diagnosis
can be established on clinical grounds alone.
Suspect cases should be isolated until results are
known, and cohorting of diagnosed cases is an
additional option. Selective admissions should be
postponed. Contacts should be treated simultaneously, regardless of symptoms, and provided
with written instructions.5,16e18,23

Treatment
Scabies can be treated with local or oral agents.
Patients should be aware that pruritus may persist
for one to two weeks following treatment. It is
recommended that local agents should be applied
twice, one week apart.5
Local treatments include 5% permethrin cream,
1% lindane (gamma benzene hexachloride) lotion,
6% precipitated sulphur and crotamiton. Ivermectin
is the only oral treatment available. In published
nosocomial outbreaks, 5% permethrin cream, applied overnight on two occasions, one week apart,
has been the standard treatment. Permethrin
cream is suitable for patients aged over two
months. Adverse effects include contact and irritant dermatitis.4,5,46 Lindane lotion 1% is a cheap
alternative; its major adverse effect is neurotoxicity, so it is used as an alternative for cases that are
resistant to other agents.4,18,32,46,62 Lindane should
not be applied to pregnant, lactating women, children and highly damaged skin.4,5 Resistance to
lindane has been reported from the American continent, Asia and Spain.5,22 Precipitated sulphur
can be used in children aged less than two months
and pregnant women. Crotamiton is not sufficiently
effective for scabies, but it is applied for the alleviation of itching.46 In AIDS patients, local scabicidals
should be used with a topical steroid in order to
prevent the onset of seborrhoeic eczema.17 In this
patient group, lindane may be more effective
when applied twice daily three times weekly, and
accompanied by a keratolytic; alternatives are
permethrin and crotamiton.16
Ivermectin is indicated for crusted scabies at
one to three doses of 200 mg/kg each.46 This agent
is 100% effective with rare relapses and it is cost
comparable with local agents; for immunocompromised patients, ivermectin is recommended along
with local scabicides and keratolytics.4,18,63e65
Ivermectin is also indicated for debilitated
patients, in institutional outbreaks and in cases
with severe lesions.5,54,66 Regarding safety, six
million people have received ivermectin worldwide
for various parasitic infections with no serious

Nosocomial scabies
adverse effects.66 Initial reports on increased
death rates among elderly patients treated with
ivermectin were not confirmed by subsequent
studies.64,65,67 Ivermectin should not be administered to pregnant, lactating women or young
children.5,65
In a systemic review of 11 randomized trials
comparing the effectiveness of various agents, no
differences in clinical cure rates or adverse events
were demonstrated.68 Permethrin may be preferable to lindane or crotamiton based on traditional
reviews, professional opinions and small studies,68
or on published experience with nosocomial
outbreaks.18,20e22,24

Conclusions
The onset of a nosocomial outbreak of scabies is
associated with considerable morbidity and
economic burden. Prompt recognition of cases,
immediate implementation of infection control
measures, simultaneous treatment of all contacts,
and prolonged monitoring after the outbreak are
of principal importance for its control.

References
1. Heukelbach J, Wilcke T, Winter B, Feldemeier H. Epidemiology and morbidity of scabies and pediculosis capitis in
resource-poor communities in Brazil. Br J Dermatol 2005;
153:150e156.
2. Lawrence G, Leafasia J, Sheridan J, et al. Control of
scabies, skin sores and haematuria in children in the Solomon Islands: another role for ivermectin. Bull World Health
Organ 2005;8:34e42.
3. Mathieu ME, Brounstein Wilson B. Scabies. In: Mandell GL,
Bennet JE, Dolin R, editors. Principles and practice of infectious diseases. Philadelphia: Churchill Livingstone; 2001.
p. 2974e2976.
4. Angel TA, Nigro J, Levy ML. Infestations in the pediatric
patient. Pediatr Clin North Am 2000;47:921e935.
5. Chosidow O. Scabies and pediculosis. Lancet 2000;355:
819e826.
6. McCarthy JS, Kemp DJ, Walton SF, Currie BJ. Scabies:
more than just an irritation. Postgrad Med J 2004;80:
382e387.
7. Davis JS, Currie BJ, Fisher DA, et al. Prevention of opportunistic infections in immunosuppressed patients in the
tropical top end of the Northern Territory. Commun Dis
Intell 2003;27:526e532.
8. Carapetis JR, Connors C, Yarmirr D, Krause V, Currie BJ.
Success of a scabies control program in an Australian aboriginal community. Pediatr Infect Dis J 1997;16:494e499.
9. Hegazy AA, Darwish NM, Abdel-Hamid IA, Hammad SM.
Epidemiology and control of scabies in an Egyptian village.
Int J Dermatol 1999;3:291e295.
10. Holness DL, DeKoven JG, Nethercott JR. Scabies in
chronic health care institutions. Arch Dermatol 1992;
128:1257e1260.

13
11. Chan LY, Tang WY, Ho HH, Lo KK. Crusted (Norwegian)
scabies in two old-age home residents. Hong Kong Med J
2000;6:428e430.
12. Burns DA. An outbreak of scabies in a residential home. Br J
Dermatol 1987;117:359e361.
13. Andersen BM, Haugen H, Rasch M, Heldal Haugen A,
Tageson A. Outbreak of scabies in Norwegian nursing homes
and home care patients: control and prevention. J Hosp
Infect 2000;45:160e164.
14. Moberg SAW, Lowhagen GBE, Hersle KS. An epidemic of
scabies with unusual features and treatment resistance in
a nursing home. J Am Acad Dermatol 1984;11:242e244.
15. Johnsen C, Bellin E, Nadal E, Simone V. An outbreak of
scabies in a New York City jail. Am J Infect Control 1991;
19:162e163.
16. Sirera G, Rius F, Romeu J, et al. Hospital outbreak of
scabies stemming from two AIDS patients with Norwegian
scabies. Lancet 1990;335:1227.
17. Moss VA, Salisbury J. Scabies in an AIDS hospice unit. Br J
Clin Pract 1991;45:35e36.
18. Obasanjo OO, Wu P, Conlon M, et al. An outbreak of scabies
in a teaching hospital: lessons learned. Infect Control Hosp
Epidemiol 2001;22:13e18.
19. Scalzini A, Barni C, Bertelli D, Sueri L. A hospital outbreak of
scabies. J Hosp Infect 1992;22:167e168.
20. Larrosa A, Cortes-Blanco M, Martinez S, et al. Nosocomial
outbreak of scabies in a hospital in Spain. Euro Surveill
2003;8:199e203.
21. Bannatyne RM, Patterson TA, Wells BA, MacMillan SA,
Cunningham GA, Tellier R. Hospital outbreak traced to
a case of Norwegian scabies. Can J Infect Control 1992;7:
111e113.
22. Boix V, Sanchez-Paya J, Portilla J, Merino E. Nosocomial
outbreak of scabies clinically resistant to lindane. Infect
Control Hosp Epidemiol 1997;18:677.
23. Jimenez-Lucho VE, Fallon F, Caputo C, Ramsey K. Role of
prolonged surveillance in the eradication of nosocomial
scabies in an extended care veterans affairs medical center.
Am J Infect Control 1995;23:44e49.
24. Zafar AB, Beidas SO, Sylvester LK. Control of transmission
of Norwegian scabies. Infect Control Hosp Epidemiol
2002;23:278e279.
25. Lerche NW, Currier RW, Juranek DD, Baer W, Dubay NJ.
Atypical crusted Norwegian scabies: report of nosocomial
transmission in a community hospital and an approach to
control. Cutis 1983;31:637e642, 668, 684.
26. Clark J, Friesen DL, Williams WA. Management of an
outbreak of Norwegian scabies. Am J Infect Control 1992;
20:217e220.
27. Corbett EL, Crossley I, Holton J, Levell N, Miller R, De
Cock KM. Crusted (Norwegian) scabies in a specialist
HIV unit: successful use of ivermectin and failure to
prevent nosocomial transmission. Genitourin Med 1996;
72:115e117.
28. Lempert KD, Baltz PS, Welton WA, Whittier FC. Pseudouremic pruritus: a scabies epidemic in a dialysis unit. Am J
Kidney Dis 1985;5:117e119.
29. Pasternak J, Richtmann R, Ganme AP, et al. Scabies
epidemic: price and prejudice. Infect Control Hosp
Epidemiol 1994;15:540e542.
30. Voss A, Wallrauch C. Occupational scabies in healthcare
workers. Infect Control Hosp Epidemiol 1995;16:4.
31. Danchaivijitr S, Suthipinittharm P, Srihapol N. An outbreak
of Norwegian scabies in a surgical ward. J Med Assoc Thai
1995;78(Suppl. 2):S99eS101.
32. Jack M. Scabies outbreak in an extended care unit e a
positive outcome. Can J Infect Control 1993;8:11e13.

14
33. Kolar KA, Rapini RP. Crusted (Norwegian) scabies. Am Fam
Physician 1991;44:1317e1321.
34. Reid HF, Thorne CD. Scabies infestation: the effect of intervention by public health education. Epidemiol Infect 1990;
105:595e602.
35. Lonc E, Okulewiz A. Scabies and head-lice infestations in
different environmental conditions of Lower Silesia,
Poland. J Parasitol 2000;86:170e171.
36. Buczek A, Pabis B, Bartosik K, Stanislawek IM, Salata M,
Rabis A. Epidemiological study of scabies in different
environmental conditions in central Poland. Ann Epidemiol
2006;16:423e428.
37. Otero L, Varela JA, Espinosa E, et al. Sarcoptes scabiei in
a sexually transmitted infections unit: a 15-year study.
Sex Transm Dis 2004;31:761e765.
38. Downs AM, Harvey I, Kennedy CT. The epidemiology of
head lice and scabies in the UK. Epidemiol Infect 1999;
122:471e477.
39. Henderson C. Community control of scabies. Lancet 1991;
337:1548.
40. Ogunbiyi AO, Owoaje E, Ndahi A. Prevalence of skin disorders in school children in Ibadan, Nigeria. Pediatr Dermatol
2005;22:6e10.
41. Arfi C, Dehen L, Benassaia E, et al. Dermatologic consultation in a precarious situation: a prospective medical
and social study at the Hopital Saint-Louis in Paris. Ann
Dermatol Venereol 1999;126:682e686.
42. Raoult D, Foucault C, Brouqui P. Infections in the homeless.
Lancet Infect Dis 2001;1:77e84.
43. Almond DS, Green CJ, Geurin DM, Evans S. Lesson of the
week: Norwegian scabies misdiagnosed as an adverse drug
reaction. BMJ 2000;320:35e36.
44. Bergman JN, Dodd WA, Trotter MJ, Oger JJ, Dutz JP.
Crusted scabies in association with human T-cell lymphotropic virus 1. J Cutan Med Surg 1999;3:148e152.
45. Adedayo O, Grell G, Bellot P. Hospital admissions for human
T-cell lymphotropic virus 1 (HTLV-1) associated diseases in
Dominica. Postgrad Med J 2003;79:341e344.
46. Scheinfeld N. Controlling scabies in institutional settings:
a review of medications, treatment models, and implementation. Am J Clin Dermatol 2004;5:31e37.
47. Wong SS, Woo PC, Yuen KY. Unusual laboratory findings in
a case of Norwegian scabies provided a clue to diagnosis.
J Clin Microbiol 2005;43:2542e2544.
48. Bonomo RA, Jacobs M, Jacobs G, Graham R, Salata RA.
Norwegian scabies and a toxic shock syndrome toxin
1-producing strain of Staphylococcus aureus endocarditis in
a patient with trisomy 21. Clin Infect Dis 1998;27:645e646.
49. Munoz-Perez MA, Rodriguez-Pichardo A, CamachoMartinez F. Sexually transmitted diseases in 1161 HIVpositive patients: a 38-month prospective study in southern
Spain. J Eur Acad Dermatol Venereol 1998;11:221e226.
50. Josephine M, Issac E, George A, Ngole M, Albert SE. Patterns
of skin manifestations and their relationships with CD4
counts among HIV/AIDS patients in Cameroon. Int J
Dermatol 2006;45:280e284.

R. Vorou et al.
51. Brites C, Weyll M, Pedrose C, Badaro R. Severe and Norwegian scabies and strongly associated with rertoviral
(HIV-1/HTLV-1) infections in Bahia, Brazil. AIDS 2002;16:
1292e1293.
52. Ambroise-Thomas P. Parasitic diseases and immunodeficiencies. Parasitology 2001;122(Suppl.):S65eS71.
53. Gotuzzo E, Arango C, de Queiroz-Campos A, Isturiz RE.
Human T-cell lymphotropic virus-I in Latin America. Infect
Dis Clin North Am 2000;14:211e239.
54. Sadick N, Kaplan MH, Pahwa SG, Sarngadharan MG.
Unusual features of scabies complicating human
T-lymphotropic virus type III infection. J Am Acad
Dermatol 1986;15:482e486.
55. Hall JC, Brewer JH, Appl BA. Norwegian scabies in patient
with acquired immune deficiency syndrome. Cutis 1989;
43:325e329.
56. Glover A, Young L, Goltz AW. Norwegian scabies in acquired
immunodeficiency syndrome: report of a case resulting in
death from associated sepsis. J Am Acad Dermatol 1987;
16:396e399.
57. Moy JA, Sanchez MR. The cutaneous manifestations of
violence and poverty. Arch Dermatol 1992;128:829e839.
58. Badiaga S, Menard A, Tissot Dupont H, Raoult D. Prevalence
of skin infections in sheltered homeless. Eur J Dermatol
2005;15:382e386.
59. Tsutsumi M, Nishiura H, Kobayashi T. Dementia-specific risks
of scabies: retrospective epidemiologic analysis of an
unveiled nosocomial outbreak in Japan from 1989e90.
BMC Infect Dis 2005;5:85.
60. Turner S, Lines S, Chen Y, Hussey L, Agius R. Work-related
infectious disease reported to the Occupational Disease
Intelligence Network and The Health and Occupation
Reporting network in the UK (2000e2003). Occup Med
(Lond) 2005;55:275e281.
61. Argenziano G, Fabbrocini G, Delfino M. Epiluminescence
microscopy. A new approach to in vivo detection of
Sarcoptes scabiei. Arch Dermatol 1997;133:751e753.
62. Franz TJ, Lehman PA, Franz SF, et al. Comparative percutaneous absorption of lindane and permethrin. Arch Dermatol
1996;132:901e905.
63. Meinking TL, Taplin D, Hermida JL, Pardo R, Kerdel FA. The
treatment of scabies with ivermectin. N Engl J Med 1995;
333:26e30.
64. del Giudice P, Marty P. Ivermectin: a new therapeutic
weapon in dermatology? Arch Dermatol 1999;135:705e706.
65. Fawcett R. Ivermectin use in scabies. Am Fam Physician
2003;68:1089e1092.
66. Heukelbach J, Winter B, Wilcke T, et al. Selective mass
treatment with ivermectin to control intestinal
helminthiases and parasitic skin diseases in a severely
affected population. Bull World Health Organ 2004;82:
563e571.
67. Barkwell R, Shields S. Deaths associated with ivermectin
treatment of scabies. Lancet 1997;349:1144e1145.
68. Walker GJA, Johnstone PW. A systematic review of the
treatment of scabies. Arch Dermatol 2000;136:387e389.