Journal of Infection (2016) 72, S61eS67

www.elsevierhealth.com/journals/jinf

Impetigo and scabies e Disease burden

and modern treatment strategies
Daniel K. Yeoh a, Asha C. Bowen a,b, Jonathan R. Carapetis a,b,*
a
b

Princess Margaret Hospital for Children, Perth, Western Australia, Australia

Telethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia

Available online 11 May 2016

KEYWORDS
Scabies;
Skin sores;
Impetigo;
Pyoderma;
Children;
Paediatrics

Summary Impetigo and scabies both present different challenges in resource-limited

compared with industrialised settings. Severe complications of these skin infections are common in resource-limited settings, where the burden of disease is highest. The microbiology,
risk factors for disease, diagnostic approaches and availability and suitability of therapies also
vary according to setting. Taking this into account we aim to summarise recent data on the
epidemiology of impetigo and scabies and describe the current evidence around approaches
to individual and community based treatment.
2016 Published by Elsevier Ltd on behalf of The British Infection Association.

Introduction

Impetigo

Both impetigo and scabies are common infections of the

skin with a large global burden.1,2 In the industrialised
world, significant complications from impetigo and scabies
are rare whilst in resource-poor settings and certain marginalised communities, their collective impact is much
greater. There are several effective options for the treatment of both impetigo and scabies. Despite this, challenges
remain in addressing the burden of disease on a community
level in regions where infection is endemic.

Background
Impetigo is a common superficial skin infection which
predominantly affects young children.3,4 It is estimated
that more than 162 million children are suffering from
impetigo at any one time.2 The burden of disease is highest
in low-income countries and within marginalised populations in developed nations.2 Infection is caused by invasion
of the epidermis by bacteria colonising the skin following

* Corresponding author. Telethon Kids Institute, University of Western Australia, West Perth, Western Australia 6872, Australia.
Tel.: 61 894897777.
E-mail addresses: daniel.yeoh@health.wa.gov.au (D.K. Yeoh), Asha.Bowen@menzies.edu.au (A.C. Bowen), Jonathan.Carapetis@
telethonkids.org.au (J.R. Carapetis).
http://dx.doi.org/10.1016/j.jinf.2016.04.024
0163-4453/ 2016 Published by Elsevier Ltd on behalf of The British Infection Association.

S62
minor trauma. Autoinoculation is common and the infection
is highly transmissible. Hot and humid climatic conditions,
poor access to water and possibly overcrowding are factors
which play a role in frequent impetigo transmission in
endemic areas.4
The bacterial aetiology of impetigo varies according to
region and continues to change over time. In tropical
climates Streptococcus pyogenes (Group A Streptococcus
or GAS) remains the major pathogen3,4 and co-infection
with Staphylococcus aureus is common.5 In temperate climates S. aureus has largely replaced S. pyogenes as the
predominant pathogen in impetigo6 and community acquired methicillin resistant S. aureus (CA-MRSA) is of
increasing importance worldwide.6e8

Clinical manifestation, complications and diagnosis

Impetigo can present as bullous lesions or non-bullous,
papular lesions that go on to form a crust. Bullous impetigo
is caused by S. aureus whilst non-bullous lesions are associated with both S. pyogenes and S. aureus as described
above. Ecthyma is a deep form of impetigo in which ulceration extends into the dermis. In the developed world
impetigo is a common reason for presentations to primary
health care providers but it is generally a self-limiting condition in this setting.9 In resource-limited settings severe
disease
and
complications
of impetigo
remain
problematic3,4,10
Invasive infections such as erysipelas (involving the
dermis and lymphatics), cellulitis (involving subcutaneous
tissue), osteomyelitis, septic arthritis and bacteraemia can
all complicate impetigo. S. pyogenes bacteraemia and
streptococcal toxic shock syndrome are commonly preceded by skin and soft tissue infection.11,12 S. aureus bacteraemia carries a high mortality and skin infection is an
important risk factor in settings where impetigo is
common.8,13
Where S. pyogenes is the predominant pathogen, impetigo can also lead to significant immune-mediated complications. In endemic settings most cases of acute poststreptococcal glomerulonephritis (APSGN) are preceded by
impetigo.14,15 Individuals with a history of APSGN in childhood are at increased risk of developing ongoing albuminuria and chronic kidney disease in later life.16,17 There is
also a plausible link between S. pyogenes skin infection
and acute rheumatic fever.18 This hypothesis is supported
by the presence of very high rates of rheumatic fever and
rheumatic heart disease in Aboriginal populations in
Australia wherein impetigo is pervasive and S. pyogenes
throat infection is uncommon.19
The diagnosis of impetigo is generally made clinically.
The use of clinical algorithms may aid in the identification
and treatment of impetigo in resource-limited settings. For
example, the WHO Integrated Management of Childhood
Illness (IMCI) skin algorithm has been assessed in Fiji and
demonstrated improvement in the clinical recognition of
impetigo.20 Elsewhere, flipcharts using high quality photographs and clinical descriptions are used to train health
care workers in diagnosing impetigo.21 Gram stain and culture of skin swabs to confirm the aetiological agent are
often recommended22 but adequate laboratory resources

D.K. Yeoh et al.

are not always available in resource-limited settings and
treatment of typical cases without microbiology is
empiric.22 Nonetheless, in the current milieu of increasing
antimicrobial resistance,6 regional data on causative bacteriological agents and their antibiotic sensitivity profiles
remain vital to best direct empiric therapy and to monitor
for changing patterns of resistance.4

Treatment
When determining impetigo treatment, there are several
important factors including the extent of disease, community wide prevalence, likely adherence to treatment and
known antimicrobial resistance. Most of the clinical trials
for impetigo treatment relate to limited or uncomplicated
impetigo, defined as fewer than 5 lesions. Where, impetigo
is extensive (greater than 5 lesions) or community prevalence is high, refer to the treatment section on extensive
impetigo.
Limited or uncomplicated impetigo
A Cochrane systematic review concluded that topical
antibiotics are the most effective treatment for limited
impetigo.23 This review included 68 randomised control trials representing 5578 participants,23 finding that mupirocin, fusidic acid and retapamulin were all superior to
placebo and there was no difference demonstrated between the most commonly studied topical agents: mupirocin and fusidic acid. In addition, there was no significant
difference found in 7-day cure rates between topical and
oral antibiotics (excluding erythromycin which is inferior
to topical mupirocin) and topical antibiotic use was associated with fewer adverse events.23 The review also cited a
lack of supportive evidence for the use of disinfectant solutions in the treatment of impetigo.23
There are several factors to consider when selecting a
topical antibiotic. Resistance to mupirocin and fusidic acid
among S. aureus isolates is increasing in association with
increased use of these agents.6,24 Although retapamulin
has demonstrated good in vitro activity against methicillin
resistant S. aureus (MRSA), its efficacy in clinical trials
against MRSA infections has been variable25,26 and it is
not approved for the treatment of MRSA infections. Moreover, S. aureus isolates with elevated minimum inhibitory
concentrations (MICs) to retapamulin have been described,
although the clinical significance of this is uncertain.27
There are calls to restrict the use of topical fusidic acid
in order to preserve the oral formulation as a useful agent,
in combination with rifampicin, for difficult-to-treat MRSA
infections.24 Topical fusidic acid is not available for use in
the USA and this is reflected in the Infectious Diseases Society of America (IDSA) guidelines for skin and soft tissue
infection which recommend topical retapamulin or mupirocin for uncomplicated impetigo.22
Extensive impetigo
Determining the optimal treatment of extensive impetigo,
particularly in resource-limited settings where the burden
of disease is highest, remains a challenge.4 It is generally
accepted that the use of systemic antibiotics for extensive
disease is practical and appropriate, yet there are limited

Impetigo and scabies

data comparing therapies for this indication4,23 and this is a
clear limitation of the Cochrane review on treatment of
impetigo.23 Furthermore the demonstrated frequency of
co-infection of S. pyogenes with S. aureus and the emergence of CA-MRSA present additional challenges in selecting
appropriate therapy.5,6 Antibiotic treatment of affected individuals leads to resolution of impetigo lesions which likely
reduces transmission. Studies to date have not explored the
effect of antibiotics on rarer endpoints such as invasive
infection or APSGN due to the large sample size required.
Further work is needed to understand the full benefits of
treatment of extensive impetigo, and the potential risk of
inducing more widespread antimicrobial resistance if antibiotics are widely dispensed in highly-endemic
communities.
The available systemic treatment options for impetigo
have some limitations. Benzathine penicillin G (BPG) has
been widely used however it is poorly accepted in some
settings due to its intramuscular (IM) route of administration and its efficacy has been questioned with the emergence of S. aureus as a pathogen in impetigo.4 Empiric
therapy with S. aureus cover is recommended for extensive
impetigo however oxacillins and first generation cephalosporins lack activity against MRSA and may not be appropriate in settings where methicillin-resistance is
common.22 Amongst oral agents with activity against
MRSA, tetracyclines are contraindicated for use in children
and liquid formulations of lincosamides are unpalatable for
this age group. Co-trimoxazole (TMPeSMX) is an attractive
option in that it is cheap, licenced for use in children and
is available in a palatable liquid formulation. Although
the conventional wisdom is that TMPeSMX lacks activity
against S. pyogenes there are both in vitro25 and in vivo28
data to challenge this perception.29
A recent large clinical trial demonstrated non-inferiority
of oral co-trimoxazole compared to IM BPG in the treatment
of impetigo in Indigenous children in Northern Australia.10
The majority of participants (72%) had extensive disease
and S. pyogenes and S. aureus were isolated from 90%
and 81% of participants respectively. Clearance of S. pyogenes (but not S. aureus) was associated with clinical resolution of sores, highlighting the primary role of S. pyogenes
in impetigo pathogenesis in this setting.10 The only other
study that has clear findings for this context compared
oral amoxicillin with oral erythromycin for treatment of
impetigo. Treatment success was achieved in 89% of both
groups, although microbiology was not available.30 Presumably the high success rate seen in this study was also due to
the dominance of S. pyogenes in the microbiology of
impetigo.
Community treatment and prevention
Community based drug administration in certain scenarios
may reduce the burden of disease associated with impetigo
particularly in the setting of APSGN outbreaks and in
communities where scabies infestation is widespread. A
review of observational studies of such outbreaks in Northern Australia concluded that targeted treatment of children
with skin sores and household contacts of cases using BPG
was warranted.31 In communities where scabies is endemic,
targeted or mass community treatment of scabies has also
been shown to reduce the prevalence of impetigo.32,33

S63
Bacterial decolonisation may play a role in the management of patients with recurrent skin infections, the prevention of post-surgical infections and in hospital based
MRSA control,22,34,35 however the utility of decolonisation
in the prevention of impetigo on a community level is unclear. Recent randomised controlled trials in military cohorts
assessing
nasal
mupirocin36
and
topical
chlorhexidine37 respectively failed to demonstrate any
reduction in S. aureus skin and soft tissue infections. In
addition to the practical issues of implementing ongoing
topical decolonisation measures on a community level,
the widespread community use of mupirocin and/or chlorhexidine could result in the increased circulation of S.
aureus strains resistant to these agents and thus limit their
effectiveness.27,38,39 Recommendations for the use of
chemoprophylaxis to decolonise household contacts of
cases of invasive S. pyogenes disease vary and clear evidence of efficacy in preventing invasive disease is lacking.12,40 The role of broader community based S.
pyogenes decolonisation in the prevention of skin disease
has not been assessed.
It is clear that the greatest burden of impetigo and its
complications is borne by resource-limited populations,
where it is critical to focus on disease prevention. There
is ongoing work in the development of a vaccine against
GAS which could offer a cost-effective and practical avenue
for disease prevention, although a vaccine is not imminent.41 In the interim, advocacy to improve access to
health services, sanitation and housing and to reduce overcrowding in areas where impetigo is highly prevalent should
be a major focus in disease prevention. There is some evidence that greater access to swimming pools42,43 and a
combination of hand-washing and daily bathing44 can
reduce the burden of impetigo. On a broader scale, as evidenced in the industrialisation of Asian countries such as
Singapore, complications such as APSGN can be virtually
eliminated in the setting of improved socioeconomic status,
housing and health services.45

Scabies
Background
Scabies is an infection of the skin caused by the mite Sarcoptes scabiei var hominis. The adult mites burrow into
the epidermis and reproduce. In the epidermis, the mites
and their excreta produce a delayed hypersensitivity reaction which is responsible for the rash and pruritus associated
with
scabies
infestation.
Transmission
is
predominantly via prolonged skin-to-skin contact and
most commonly occurs between members of a household.46
Unsurprisingly scabies infection is associated with overcrowding and socioeconomic disadvantage4,46,47 and children carry the highest burden of disease.48 The
prevalence of scabies was found to range from 0.2% to
71.4% in a recent systematic review of population based
studies.48 The highest prevalence is seen in tropical regions, such as Central America, the Pacific islands and
Northern Australia.48 In developed countries prevalence is
generally low but outbreaks amongst populations in institutionalised care are well described.47

S64

Clinical manifestations, complications and

diagnosis
During primary infection, the appearance of symptoms is
delayed until 4 weeks following initial contact.46 Patients
present with a papular or vesicular eruption which is
intensely pruritic, usually worse at night. The mites are
most often found in web spaces of the fingers, on the
wrists, in the axillae, around the umbilicus and in the groin
or the popliteal fossa. Other family members may also have
pruritus. The distribution of infestation is different in infants with involvement of the palms, soles and scalp.49
Scabies infestation is associated with significant complications related to secondary infection with bacteria. Bacterial infection, particularly with S. pyogenes and S.
aureus, is a well-recognised complication of scabies infestation.1,4,5,13 The presence of scabies is associated with
complications of impetigo including invasive bacterial
infection and post-streptococcal glomerulonephritis.11,13,14
As discussed earlier, in endemic settings the treatment of
scabies at a community level has been shown to reduce
the prevalence and severity of skin sores32 and
haematuria.33
Crusted scabies is a severe form of scabies where the
host immune system fails to control the number of mites.50
It is characterised by crusted, hyperkeratotic lesions with
mite numbers reaching millions in some patients.50 Cases
classically occur in immunosuppressed patients and those
in institutional care although, in particular communities,
patients with no underlying risk factors are also affected.50
Because of the high mite burden, contacts of patients with
crusted scabies are at high risk of infestation themselves51
and this may drive community outbreaks.
Diagnosis of scabies is predominantly based on the
clinical findings of intense pruritus and a typical distribution of papules. Skin scrapings occasionally reveal mites,
ova or faeces, however microscopy is time consuming, of
low-yield and may be impractical in resource-limited
settings.46,52 While dermatoscopy is a potentially useful
diagnostic tool, the cost of equipment and the reliance
on appropriate training are limitations.52,53 As with impetigo, clinical algorithms designed for use in resourcelimited settings have shown promise in increasing case
identification and warrant further evaluation.20 Certainly
comparison between studies examining prevalence and
treatment outcomes is hindered by the lack of consensus
criteria for the diagnosis of scabies.48,49 Further research
in designing simple and accurate diagnostic tests for scabies
is ongoing.

Treatment
Individual treatment
There are various topical therapies utilised in the treatment of scabies. In a Cochrane review of randomised
control trials comparing scabies therapies, permethrin
was found to be the most effective topical therapy (superior to lindane and crotamiton).49 Benzyl benzoate is
another effective topical therapy that is preferred in
some resource-limited settings due to the relatively high
cost of permethrin, but is less well tolerated.46,54 The

D.K. Yeoh et al.

application of topical scabies therapies can result in skin reactions and tolerability may be further reduced in humid
tropical climates.49
Ivermectin is an oral scabicide which was previously
reserved for cases of scabies refractory to topical therapy
but is increasingly seen as a useful agent for both individual
and community based treatment.55 As ivermectin is not
ovicidal a second dose is recommended 8e15 days following
the initial dose to prevent recrudescence.47 The efficacy of
oral ivermectin is superior to placebo and topical lindane
whilst trials comparing oral ivermectin to topical benzyl
benzoate have demonstrated mixed results.49,54 In the Cochrane review of scabies therapies, topical permethrin
was found to be superior to oral ivermectin although the
length of follow up in included trials ranged from 1 to 2
weeks only.49
Although ivermectin is an effective and well-tolerated
agent in the treatment of scabies there remain some
limitations to its use. Resistance is a potential concern
particularly in endemic communities.56 Also, there are
limited data demonstrating safety and tolerability of ivermectin in infants57 and it is not yet licensed for the treatment of uncomplicated scabies in many regions.
Community treatment and prevention
The treatment of the close contacts of patients with
scabies is recommended in order to prevent re-infection
and further transmission although there is a lack of data
supporting this strategy.55 Topical permethrin is considered
first-line therapy,47 however poor compliance amongst contacts has been identified as a barrier to the efficacy of this
approach.58 Oral ivermectin is an alternative agent for the
treatment of contacts which may prove effective and more
acceptable than topical therapies but this has yet to be assessed in comparative trials.46,47 There is a clear need for
further research in this area with a recent Cochrane review
failing to identify any well-designed randomised trials assessing prophylactic measures to prevent the transmission
of scabies.59
Mass drug administration (MDA) may be an alternative
approach to scabies control in settings where scabies is
endemic.46,55 This strategy has been explored as a control
measure using permethrin60,62 and ivermectin33,61,62
respectively with promising results. Notably, a recently
published randomised trial assessing the effectiveness of
scabies MDA in Fiji compared ivermectin MDA and
permethrin MDA with standard care (i.e. permethrin
treatment of cases and contacts) in three separate island
communities.62 There was a significant and sustained
reduction in scabies and impetigo in all three groups with
the most marked effect in the ivermectin group followed
by the permethrin MDA group.62 A significant reduction in
the community prevalence of scabies has previously been
demonstrated following the implementation of an ivermectin MDA program for the treatment of lymphatic filariasis in Tanzania.63 This study highlights the potential for
collaborative research in assessing the effects of MDA programmes on a number of neglected tropical diseases
including scabies.64
As with impetigo, the long-term control of scabies in
endemic settings is greatly dependent on addressing the
social determinants of health within these populations.

Impetigo and scabies

Crusted scabies treatment
It is recommended that patients with crusted scabies be
treated with a combination of topical permethrin and oral
ivermectin.47,51 Keratolytic agents should also be applied to
skin crusts to increase the efficacy of the topical scabicide.47,51 As yet there are no randomised control trials
comparing treatment regimens for patients with crusted
scabies. With regards to community control, active case
identification and treatment of core transmitters with
crusted scabies within a population is a potential adjuvant
approach in endemic settings.51

Conclusions
The significant impact of scabies and impetigo on the
health of people in resource-limited settings has in the
past been under-recognised. Promisingly, there is growing
interest and advocacy concerning scabies and skin sores as
demonstrated by the recent formation of the International
Alliance for the Control of Scabies55 and the inclusion of
scabies on the WHO list of neglected tropical diseases in
2013. There is advocacy for impetigo to be included on
this list as well.2
There are safe and efficacious treatments available for
these common skin infections, yet in many areas where
disease burden is highest, little has changed with regards to
control. Ongoing research exploring risk factors and aetiology, improved methods for diagnosis and approaches to
both individual and community based treatment is
required. Arguably, addressing the environmental and socioeconomic factors which serve to perpetuate the high
rates of skin disease in certain communities is of chief
importance. Whilst in the industrialised world scabies and
impetigo are often considered trivial, ongoing efforts to
address the major impact of these infections in the
developing world remain extremely important.

Conflict of interest
The authors have no conflict of interest to declare.

References

1. Romani L, Koroivueta J, Steer AC, Kama M, Kaldor JM,

Wand H, et al. Scabies and impetigo prevalence and risk factors in Fiji: a national survey. PLoS Negl Trop Dis 2015;9(3):
e0003452.
2. Bowen AC, Mahe A, Hay RJ, Andrews RM, Steer AC, Tong SY,
et al. The global epidemiology of impetigo: a systematic review of the population prevalence of impetigo and pyoderma.
PLoS One 2015;10(8):e0136789.
3. Carapetis JR, Steer AC, Mulholland EK, Weber M. The global
burden of group A streptococcal diseases. Lancet Infect Dis
2005;5(11):685e94.
4. Mahe A, Hay RJ. Epidemiology and management of common
skin diseases in children in developing countries. Geneva:
World Health Organisation; 2005.
5. Bowen AC, Tong S, Chatfield MD, Carapetis JR. The microbiology of impetigo in Indigenous children: associations between Streptococcus pyogenes, Staphylococcus aureus,
scabies, and nasal carriage. BMC Infect Dis 2014;14(1):3854.

S65
6. Bangert S, Levy M, Hebert AA. Bacterial resistance and impetigo treatment trends: a review. Pediatr Dermatol 2012;
29(3):243e8.
7. Tong SY, Varrone L, Chatfield MD, Beaman M, Giffard PM. Progressive increase in community-associated methicillin-resistant Staphylococcus aureus in Indigenous populations in
northern Australia from 1993 to 2012. Epidemiol Infect
2015;143(7):1519e23.
8. Tong SY, Davis JS, Eichenberger E, Holland TL, Fowler Jr VG.
Staphylococcus aureus infections: epidemiology, pathophysiology, clinical manifestations, and management. Clin Microbiol Rev 2015;28(3):603e61.
9. Koning S, Mohammedamin RS, van der Wouden JC, van Suijlekom-Smit LW, Schellevis FG, Thomas S. Impetigo: incidence
and treatment in Dutch general practice in 1987 and 2001 e
results from two national surveys. Br J Dermatol 2006;
154(2):239e43.
10. Bowen AC, Tong SY, Andrews RM, OMeara IM, McDonald MI,
Chatfield MD, et al. Short-course oral co-trimoxazole versus
intramuscular benzathine benzylpenicillin for impetigo in a
highly endemic region: an open-label, randomised, controlled,
non-inferiority trial. Lancet 2014;384(9960):2132e40.
11. Gear RJ, Carter JC, Carapetis JR, Baird R, Davis JS. Changes in
the clinical and epidemiological features of group A streptococcal bacteraemia in Australias Northern Territory. Trop
Med Int Health TM IH 2015;20(1):40e7.
12. Boyd R, Patel M, Currie BJ, Holt DC, Harris T, Krause V. High
burden of invasive group A streptococcal disease in the Northern Territory of Australia. Epidemiol Infect 2016;144(5):
1018e27.
13. Skull SA, Krause V, Coombs G, Pearman JW, Roberts LA. Investigation of a cluster of Staphylococcus aureus invasive infection in the top end of the Northern Territory. Aust N Z J
Med 1999;29(1):66e72.
14. Currie BJ, Carapetis JR. Skin infections and infestations in
Aboriginal communities in northern Australia. Australas J Dermatol 2000;41(3):139e43. quiz 44e5.
15. Marshall CS, Cheng AC, Markey PG, Towers RJ, Richardson LJ,
Fagan PK, et al. Acute post-streptococcal glomerulonephritis
in the Northern Territory of Australia: a review of 16 years
data and comparison with the literature. Am J Trop Med
Hyg 2011;85(4):703e10.
16. Hoy WE, White AV, Tipiloura B, Singh G, Sharma SK,
Bloomfield H, et al. The multideterminant model of renal disease in a remote Australian Aboriginal population in the
context of early life risk factors: lower birth weight, childhood post-streptococcal glomerulonephritis, and current
body mass index influence levels of albumi. Clin Nephrol
2015;83(7 Suppl. 1):75e81.
17. Hoy WE, White AV, Dowling A, Sharma SK, Bloomfield H,
Tipiloura BT, et al. Post-streptococcal glomerulonephritis is
a strong risk factor for chronic kidney disease in later life.
Kidney Int 2012;81(10):1026e32.
18. McDonald M, Currie BJ, Carapetis JR. Acute rheumatic fever:
a chink in the chain that links the heart to the throat? Lancet
Infect Dis 2004;4(4):240e5.
19. McDonald MI, Towers RJ, Andrews RM, Benger N, Currie BJ,
Carapetis JR. Low rates of streptococcal pharyngitis and
high rates of pyoderma in Australian aboriginal communities
where acute rheumatic fever is hyperendemic. Clin Infect
Dis e Off Publ Infect Dis Soc Am 2006;43(6):683e9.
20. Steer AC, Tikoduadua LV, Manalac EM, Colquhoun S,
Carapetis JR, Maclennan C. Validation of an Integrated Management of Childhood Illness algorithm for managing common
skin conditions in Fiji. Bull World Health Organ 2009;87(3):
173e9.
21. Project. East Arnhem regional healthy skin project e recognising and treating skin conditions. 2009.

S66
22. Stevens DL, Bisno AL, Chambers HF, Dellinger EP,
Goldstein EJ, Gorbach SL, et al. Practice guidelines for the
diagnosis and management of skin and soft tissue infections:
2014 update by the Infectious Diseases Society of America.
Clin Infect Dis e Off Publ Infect Dis Soc Am 2014;59(2):
e10e52.
23. Koning S, van der Sande R, Verhagen AP, van SuijlekomSmit LW, Morris AD, Butler CC, et al. Interventions for impetigo. Cochrane Database Syst Rev 2012;1:CD003261.
24. Howden BP, Grayson ML. Dumb and dumber e the potential
waste of a useful antistaphylococcal agent: emerging fusidic
acid resistance in Staphylococcus aureus. Clin Infect Dis e
Off Publ Infect Dis Soc Am 2006;42(3):394e400.
25. Tanus T, Scangarella-Oman NE, Dalessandro M, Li G,
Breton JJ, Tomayko JF. A randomized, double-blind, comparative study to assess the safety and efficacy of topical retapamulin ointment 1% versus oral linezolid in the treatment of
secondarily infected traumatic lesions and impetigo due to
methicillin-resistant Staphylococcus aureus. Adv Skin Wound
Care 2014;27(12):548e59.
26. Yang LP, Keam SJ. Retapamulin: a review of its use in the
management of impetigo and other uncomplicated superficial
skin infections. Drugs 2008;68(6):855e73.
27. McNeil JC, Hulten KG, Kaplan SL, Mason EO. Decreased susceptibilities to Retapamulin, Mupirocin, and Chlorhexidine
among Staphylococcus aureus isolates causing skin and soft
tissue infections in otherwise healthy children. Antimicrob
Agents Chemother 2014;58(5):2878e83.
28. Miller LG, Daum RS, Creech CB, Young D, Downing MD,
Eells SJ, et al. Clindamycin versus trimethoprimsulfamethoxazole for uncomplicated skin infections. N Engl
J Med 2015;372(12):1093e103.
29. Bowen AC, Lilliebridge RA, Tong SY, Baird RW, Ward P,
McDonald MI, et al. Is Streptococcus pyogenes resistant or susceptible to trimethoprim-sulfamethoxazole? J Clin Microbiol
2012;50(12):4067e72.
30. Faye O, Hay RJ, Diawara I, Mahe A. Oral amoxicillin vs. oral
erythromycin in the treatment of pyoderma in Bamako,
Mali: an open randomized trial. Int J Dermatol 2007;46(Suppl.
2):19e22.
31. Johnston F, Carapetis J, Patel MS, Wallace T, Spillane P. Evaluating the use of penicillin to control outbreaks of acute poststreptococcal glomerulonephritis. Pediatr Infect Dis J 1999;
18(4):327e32.
32. 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(5):494e9.
33. Lawrence G, Leafasia J, Sheridan J, Hills S, Wate J, Wate C,
et al. Control of scabies, skin sores and haematuria in children
in the Solomon Islands: another role for ivermectin. Bull
World Health Organ 2005;83(1):34e42.
34. Cookson B, Bonten MJ, Mackenzie FM, Skov RL, Verbrugh HA,
Tacconelli E. Meticillin-resistant Staphylococcus aureus
(MRSA): screening and decolonisation. Int J Antimicrob
Agents 2011;37(3):195e201.
35. Simor AE. Staphylococcal decolonisation: an effective strategy for prevention of infection? Lancet Infect Dis 2011;
11(12):952e62.
36. Ellis MW, Griffith ME, Dooley DP, McLean JC, Jorgensen JH,
Patterson JE, et al. Targeted intranasal mupirocin to prevent
colonization and infection by community-associated methicillin-resistant Staphylococcus aureus strains in soldiers: a
cluster randomized controlled trial. Antimicrob Agents Chemother 2007;51(10):3591e8.
37. Whitman TJ, Herlihy RK, Schlett CD, Murray PR,
Grandits GA, Ganesan A, et al. Chlorhexidine-impregnated
cloths to prevent skin and soft-tissue infection in Marine recruits: a cluster-randomized, double-blind, controlled

D.K. Yeoh et al.

38.

39.

40.

41.

42.

43.

44.

45.

46.

47.
48.

49.
50.

51.

52.

53.

54.

55.

effectiveness trial. Infect Control Hosp Epidemiol 2010;

31(12):1207e15.
Batra R, Cooper BS, Whiteley C, Patel AK, Wyncoll D,
Edgeworth JD. Efficacy and limitation of a chlorhexidinebased decolonization strategy in preventing transmission of
methicillin-resistant Staphylococcus aureus in an intensive
care unit. Clin Infect Dis e Off Publ Infect Dis Soc Am 2010;
50(2):210e7.
Riley TV, Carson CF, Bowman RA, Mulgrave L, Golledge CL,
Pearman JW, et al. Mupirocin-resistant methicillin-resistant
Staphylococcus aureus in Western Australia. Med J Aust
1994;161(6):397e8.
Prevention of invasive group A streptococcal disease among
household contacts of case patients and among postpartum
and postsurgical patients: recommendations from the Centers
for Disease Control and Prevention. Clin Infect Dis e Off Publ
Infect Dis Soc Am 2002;35(8):950e9.
Moreland NJ, Waddington CS, Williamson DA, Sriskandan S,
Smeesters PR, Proft T, et al. Working towards a group A streptococcal vaccine: report of a collaborative Trans-Tasman
workshop. Vaccine 2014;32(30):3713e20.
Lehmann D, Tennant MT, Silva DT, McAullay D, Lannigan F,
Coates H, et al. Benefits of swimming pools in two remote
Aboriginal communities in Western Australia: intervention
study. BMJ 2003;327(7412):415e9.
Hendrickx D, Stephen A, Lehmann D, Silva D, Boelaert M,
Carapetis J, et al. A systematic review of the evidence that
swimming pools improve health and wellbeing in remote
Aboriginal communities in Australia. Aust N Z J Public Health
2015;40(1):30e6.
Luby SP, Agboatwalla M, Feikin DR, Painter J, Billhimer W,
Altaf A, et al. Effect of handwashing on child health: a randomised controlled trial. Lancet 2005;366(9481):225e33.
Yap HK, Chia KS, Murugasu B, Saw AH, Tay JS, Ikshuvanam M,
et al. Acute glomerulonephritis e changing patterns in
Singapore children. Pediatr Nephrol (Berlin, Germany) 1990;
4(5):482e4.
Hay RJ, Steer AC, Engelman D, Walton S. Scabies in the developing worldeits prevalence, complications, and management. Clin Microbiol Infect e Off Publ Eur Soc Clin
Microbiol Infect Dis 2012;18(4):313e23.
Currie BJ, McCarthy JS. Permethrin and ivermectin for
scabies. N Engl J Med 2010;362(8):717e25.
Romani L, Steer AC, Whitfeld MJ, Kaldor JM. Prevalence of
scabies and impetigo worldwide: a systematic review. Lancet
Infect Dis 2015;15(8):960e7.
Strong M, Johnstone P. Interventions for treating scabies. Cochrane Database Syst Rev 2007;(3):CD000320.
Roberts LJ, Huffam SE, Walton SF, Currie BJ. Crusted scabies:
clinical and immunological findings in seventy-eight patients
and a review of the literature. J Infect 2005;50(5):375e81.
Lokuge B, Kopczynski A, Woltmann A, Alvoen F, Connors C,
Guyula T, et al. Crusted scabies in remote Australia, a new
way forward: lessons and outcomes from the East Arnhem
Scabies Control Program. Med J Aust 2014;200(11):644e8.
Walton SF, Currie BJ. Problems in diagnosing scabies, a global
disease in human and animal populations. Clin Microbiol Rev
2007;20(2):268e79.
Walter B, Heukelbach J, Fengler G, Worth C, Hengge U,
Feldmeier H. Comparison of dermoscopy, skin scraping, and
the adhesive tape test for the diagnosis of scabies in a
resource-poor setting. Arch Dermatol 2011;147(4):468e73.
Ly F, Caumes E, Ndaw CA, Ndiaye B, Mahe A. Ivermectin
versus benzyl benzoate applied once or twice to treat human
scabies in Dakar, Senegal: a randomized controlled trial. Bull
World Health Organ 2009;87(6):424e30.
Engelman D, Kiang K, Chosidow O, McCarthy J, Fuller C,
Lammie P, et al. Toward the global control of human scabies:

Impetigo and scabies

56.

57.

58.

59.

60.

introducing the International Alliance for the Control of

Scabies. PLoS Negl Trop Dis 2013;7(8):e2167.
Mounsey KE, Holt DC, McCarthy JS, Currie BJ, Walton SF. Longitudinal evidence of increasing in vitro tolerance of scabies
mites to ivermectin in scabies-endemic communities. Arch
Dermatol 2009;145(7):840e1.
Becourt C, Marguet C, Balguerie X, Joly P. Treatment of scabies
with oral ivermectin in 15 infants: a retrospective study on
tolerance and efficacy. Br J Dermatol 2013;169(4):931e3.
La Vincente S, Kearns T, Connors C, Cameron S, Carapetis J,
Andrews R. Community management of endemic scabies in
remote aboriginal communities of northern Australia: low
treatment uptake and high ongoing acquisition. PLoS Negl
Trop Dis 2009;3(5):e444.
FitzGerald D, Grainger RJ, Reid A. Interventions for preventing the spread of infestation in close contacts of people
with scabies. Cochrane Database Syst Rev 2014;2:CD009943.
Andrews RM, Kearns T, Connors C, Parker C, Carville K,
Currie BJ, et al. A regional initiative to reduce skin infections
amongst aboriginal children living in remote communities of

S67

61.

62.

63.

64.

the Northern Territory, Australia. PLoS Negl Trop Dis 2009;

3(11):e554.
Haar K, Romani L, Filimone R, Kishore K, Tuicakau M,
Koroivueta J, et al. Scabies community prevalence and mass
drug administration in two Fijian villages. Int J Dermatol
2014;53(6):739e45.
Romani L, Whitfield MJ, Koroivueta J, Andrews R, Calder JM,
Steer AC, et al. Mass drug administration for scabies control in
a population with endemic disease. N Engl J Med 2015;
373(24):2305e13.
Mohammed KA, Deb RM, Stanton MC, Molyneux DH. Soil transmitted helminths and scabies in Zanzibar, Tanzania following
mass drug administration for lymphatic filariasis e a rapid
assessment methodology to assess impact. Parasit Vectors
2012;5:299.
Engelman D, Martin DL, Hay RJ, Chosidow O, McCarthy JS,
Fuller LC, et al. Opportunities to investigate the effects of
ivermectin mass drug administration on scabies. Parasit Vectors 2013;6:106.