Centr Journal of Dermatology and

al Clinical Research
Review Article *Corresponding author

Impetigo in the
Patty Ghazvini, FAMU College of Pharmacy and
Pharmaceutical Sciences, #349 New Pharmacy
Building, Tallahassee, Florida, USA, Tel: 850-599-

Pediatric
3636; Email:
Submitted: 23 November 2016
Accepted: 04 February 2017

Population Published: 07 February 2017

Copyright
2017 Ghazvini et al.
Patty Ghazvini*, Phillip Treadwell, Kristen Woodberry, Edouard
OPEN ACCESS
Nerette Jr, and Hermn Powery II
FAMU College of Pharmacy and Pharmaceutical Sciences, Florida, USA Keywords
Impetigo
Non-bullous impetigo
Abstr Bullous impetigo
act Pediatric population
Impetigo is an endemic bacterial skin infection most commonly Staphylococcus aureus
Group-A -hemolytic streptococci (GABHS)
associated with the pediat- ric population; it is seen in more than an
Topical antibiotics
estimated 162 million children between the ages of
Systemic antibiotics
2 and 5 years old. Geographically, this infection is mostly found in Oral antibiotics
tropical areas around the globe. Impetigo has the largest increase in
incidence rate, as compared to other various skin infections seen in
children. The major characteristic observed in this infection is lesions.
They first appear as bullae that eventually form a honey-colored, thick
crust that may cause pruritus. There are three forms of impetigo: bullous,
non-bullous and ecthyma. The primary causative organisms for impetigo
include Staphylococcus aureus and Group-A -hemolytic streptococci
(GABHS). Most impetigo infections resolve without requiring medication;
however, to reduce the duration and spread of the disease, topical and
oral antibiotic agents are utilized. A positive prognosis as well as minimal
complications are associated with this disease state.

ABBREVIATIONS from the disease. The study showed that these children tend to
reside in low-income countries located in tropical regions [4,6-8].
SSTI: Skin and Soft Tissue Infection; GABHS: Group-A
-hemolytic Streptococci; SSSS: Staphylococcal Scalded Skin PATHOPHYSIOLOGY
Syndrome; CA-MRSA: Community-Acquired Methicillin-Resistant
Skin serves as the first line of defense between humans and
Staphylococcal aureus; PVL: Panton-Valentine-Leucodin; PSGN:
their environment [9]. An imbalance of homeostasis between the
Postreptococcal Glomerulonephritis

INTRODUCTION
The evolution of bacteria and the widespread distribution
of antibiotic-resistance have continued to increase and further
validate the inevitable post-antibiotic era that has penetrated
the consciousness of the healthcare world. Skin and soft tissue
(SSTI) infections are a clinical priority, in part, because of the
disproportionate effect that they have on the most vulnerable
populations [1]. Impetigo is a highly communicable superficial
skin infection commonly caused by gram-positive bacteria that
includes either Staphylococcus aureus or a Group-A -hemolytic
streptococci (GABHS), such as Streptococcus pyogenes. Both
organisms have been influential in the pervasive spread of
bacterial resistance [2,3]. It is predominantly a pediatric
infection that tends to occur in environments with hot, humid
weather [4,5]. A global study on the population prevalence of
impetigo concluded that more than an estimated 162 million
children between the ages of two and five years old have suffered
Cite this article: Ghazvini P, Treadwell P, Woodberry K, Nerette E Jr, Powery H II (2017) Impetigo in the Pediatric Population. J Dermatolog Clin Res 5(1):
1092.
skins microbiome and host has been associated with disease.
Different factors responsible for the unique variability of the
skin microbiome are only partly understood, but results suggest
that host genetic and environmental influences play a major role
[10,11]. Naturally, skin is colonized by a diverse assortment of
bacteria [12]. Infections resulting from high concentrations of
bacteria are rare due to the skins own natural protective
abilities. The human bodys natural resistance to infection is due
to both the skin and subcutaneous tissues low pH of
approximately
5.6, as well as sebaceous fluids that hydrolyze to form free fatty
acids that strongly inhibit the growth of many bacteria and fungi,
and skin possessing its own normal flora, helping to prevent
the colonization of other pathogenic organisms [13]. Bacterial
antimicrobial peptides, also called bacteriocins, are thought to be
produced by many or most bacteria found in normal flora and
Cite this article: Ghazvini P, Treadwell P, Woodberry K, Nerette E Jr, Powery H II (2017) Impetigo in the Pediatric Population. J Dermatolog Clin Res 5(1):
1092.
plays a Major beneficial role in the relationship between bacteria
and the skin. Bacteriocins do not protect against infection in the
traditional sense; they contribute to the survival of individual
bacterial cells by killing other bacteria that might compete for
nutrients in the same environment [14,15]. Another example of
a beneficial relationship between bacteria and the skin involves
the innate capacity of the epithelium to detect microorganisms
with Toll-like receptors (TLRs). Stimulation of TLRs induces
distinct patterns of gene expression that lead to activation of
a variety of immune responses. Traditionally, these immune
responses were considered to be exclusively pro-inflammatory
and designed to defend against the microbe causing infection
[16]. However, under certain conditions pathogens can penetrate
the integumentary barrier of a susceptible host and may cause
tissue damage that may stimulate an inflammatory response.
Conditions that may predispose a patient to the development

Central
of skin infections include chickenpox, herpes simplex, insect
bites, pediculosis, radiation therapy, scabies, scratching, surgery,
thermal burns, trauma, high concentrations of bacteria, excessive
moisture of the skin, an inadequate blood supply, the availability
of bacterial nutrients, and damage to the corneal layer allowing
for bacterial penetration [5,17-19]. The development of impetigo
is dependent on the following three factors: bacterial adherence
to host cells, invasion of tissue with evasion of host defenses,
and the dissemination of toxins [13]. Bacterial invasion occurs
initially in low numbers, with teichoic acid mediating adhesion
in either of the impetigo causing microorganisms [20,21].
However, fibronectin, a cell adhesion molecule that allows for
bacterial cells such as Streptococcus pyogenes (GABHS), to
attach to collagen and invade disrupted skin surfaces is required
in order to colonize skin [13]. In contrast, Staphylococcus aureus
colonizes the nasal epithelium first and from this reservoir,
colonization of the skin occurs [22]. As bacteria increase in
number where the integumentary barrier is disrupted, invasion
by these colonizing bacteria ensues and impetigo may develop.
With the majority of SSTIs resulting from the dismantling of
normal host defenses by processes such as skin puncture,
abrasion, or underlying diseases, it must be understood that the
nature and severity of the infection depends on both the type of
microorganism present and the site of inoculation [9,17,19].
Etiology & Epidemiology
In general, the main causative pathogens of impetigo are
Staphylococcus aureus and Group-A -hemolytic streptococci
(GABHS) [23]. Less common pathogens associated with
impetigo include Group C streptococci, Group G streptococci,
and anaerobic bacteria [23,24]. When focusing on the different
types of impetigo however, there is a clear delineation of which
pathogens predominate, as impetigo can be separated into non-
bullous impetigo and bullous impetigo.
Non-bullous impetigo, also known as impetigo contagiosa
[24,25] or pyoderma [23], is currently caused mostly by S.
aureus. Following S. aureus are mixed infections of staphylococci
and streptococci, and then streptococci alone. However, this has
not always been the case. Over time the main causative agent has
alternated between S. aureus and GABHS. According to Koning
S et al., in moderate climates, S. aureus was the predominant
causative organism in the 1940s and 1950s, after which GABHS
became more prevalent; in the past two decades, S. aureus has
become more common again. S. aureus alone or in combination
with GABHS is responsible for about 80% of impetigo cases
[25,26]. To further validate the higher prevalence of S. aureus,
according to data from the Dermatology Department of Heim
Pa l Childrens Hospital Budapest, more than 70% of the cases
are caused by S. aureus, 20-25% are caused by a mixed infection
of staphylococci and streptococci, and 5-10% of the cases are
caused only by streptococci [27]. In contrast, there are instances
when streptococcal infection is more common, such as in
warmer, more humid climates [24,25].
Bullous impetigo is almost exclusively caused by strains of
S. aureus that produce exfoliative toxins that cause a loss of cell
adhesion in the superficial epidermis by targeting desmoglein1
[23,28,29]. The specific toxin is exfoliative toxin A, as opposed
to exfoliative toxin B, which is produced by S. aureus in
J Dermatolog Clin Res 5(1): 1092 (2017)
Ghazvini et al. (2017)
Email:
Staphylococcal Scalded Skin Syndrome (SSSS) [26]. There are a
small percentage of infections caused by GABHS [26].
Ecthyma, which is described either as a deeper form of
impetigo [30], or as a separate but similar type of infection [31],
extends through the epidermis and reaches the deep dermis.
Similar to bullous impetigo, the primary pathogen is S. aureus
[32], but streptococci may sometimes be the cause [27,31].
The presence of MRSA as the causative agent of community-
acquired impetigo is considered unusual and heterogeneous
[26]. Staphylococcal induced impetigo is usually caused by S.
aureus strains that possess the exfoliative toxin gene.
Community- acquired methicillin-resistant Staphylococcal
aureus (CA-MRSA) do not possess the exfoliative toxin gene, but
instead have the Panton-Valentine-Leucodin (PVL) gene.
Staphylococci that possess PVL usually cause abscesses and
furuncles; therefore, concern of MRSA should be less in cases of
impetigo [26]. Furthermore, no studies have identified a problem
with MRSA- related impetigo in adults or children, but cultures
may still be useful in some settings [24]. However, if present,
MRSA that is associated with impetigo is usually seen in the non-
bullous form [29].
CLINICAL PRESENTATION
Non-bullous impetigo may occur as a primary or secondary
bacterial infection. Primary infection occurs via direct bacterial
invasion of intact healthy skin [24]. Secondary infection, which
is more common, occurs via bacterial infection of disrupted
skin caused by trauma, eczema, insect bites, scabies, herpetic
outbreaks, or other diseases [24]. Regardless of its primary
or secondary nature, non-bullous impetigo initially presents
as a maculopapular lesion that becomes a thin-walled vesicle
located on an erythematous base. The vesicles tend to be <0.5cm
as opposed to the bullae seen in bullous impetigo, which are
typically >0.5cm [29]. Upon rupturing, the subsequent superficial
ulceration is covered with purulent discharge that dries as a
yellowish or honey colored crust [24,26]. The infection tends
to occur in exposed areas, especially on the limbs and the face
(e.g., nares, perioral region). Satellite lesions, caused by self-
inoculation, are frequent; and regional lymphadenopathy is
common [23,26]. However, systemic symptoms are unlikely [23-
25] although fever can occur in severe cases [26]. Non-bullous
impetigo tends to heal without scarring, and if left untreated, it
may resolve spontaneously in 2-3 weeks [24-26].
Bullous impetigo initially starts as small vesicles, which
become localized flaccid bullae or blisters measuring about 2cm
in diameter; the blisters contain clear content that later becomes
purulent [26]. These blisters do not rupture as easily as the
vesicles seen in non-bullous impetigo, and may persist for
several days [25]. Once the blister ruptures, the wet,
erythematous base can be seen. Regional enlarged lymph nodes
are usually absent, and systemic symptoms are uncommon but
can include fever, diarrhea, and weakness [24,26].The evidence
supporting the presence of regional lymphadenopathy in
bullous impetigo is conflicting. Some articles state that
lymphadenopathy rarely occurs in bullous impetigo [26,33],
while others do not mention lymphadenopathy in regards to
bullous impetigo [24,25]. In contrast, one source states that
lymphadenopathy is more
2/5
 Central
common in bullous impetigo than non-bullous impetigo [34].
The infection tends to occur on the trunk; the intertriginous
regions such as the diaper area, axillae, and neck; and the
extremities. However, other cutaneous areas can be affected as
well [24,26]. As with the other form of impetigo, the infection
generally resolves within 2-3 weeks without scarring [24].
Ecthyma is characterized by vesicles that rupture to produce
circular, erythematous ulcers with adherent brown-black crusts.
There is usually surrounding erythematous edema [30-32].
Itching is common and scratching can spread the infection [32].
Ecthyma mainly occurs on the legs and gluteus after a trauma
or when insect bites have been scratched open [27]. In addition,
unlike impetigo ecthyma heals with scarring.
DIAGNOSIS
Diagnosis of impetigo or ecthyma is typically completed via
visual observation and clinical findings [29,32]. Gram stains and
culture of the pus or exudates from skin lesions and ecthyma
are recommended to help identify whether S. aureus and/or
GABHS is the cause; treatment without these studies however, is
reasonable in typical cases [31]. In addition, in patients
suspected of having acute glomerulonephritis following
impetigo, analysis of elevated anti-DNase B levels can provide
supporting evidence of previous streptococcal infection [23].
When diagnosing impetigo, it must be remembered that
there can be other disorders that present with similar clinical
manifestations. With non-bullous impetigo, diagnostic confusion
can occur with a variety of skin disorders including shingles, cold
sores, cutaneous fungal infections, and eczema [25]. With
bullous impetigo, diagnostic confusion can occur with
thermal burns, blistering disorders such as bullous
pemphigoid, and Stevens Johnson syndrome [25].
THER
APY
There are various treatment options that may be utilized
in the treatment of impetigo. Depending on the severity of the
condition, the options range from topical disinfectants to topical
and oral antibiotics. For uncomplicated impetigo, it has been
observed that the infection is self-limiting and will resolve within
a few weeks without scarring [29]. Because impetigo is highly
contagious, it is best to treat with medications as opposed to
only observation.
For local wound care, it is recommended that lesions are
gently cleansed, remove the crusts of non-bullous impetigo us-
ing antibacterial soap and a washcloth, and frequent application
of wet dressings to the affected areas [26]. Topical disinfect-
ants are a good option for prevention of recurrence and serve
as a great alternative to topical antibiotics for treatment. It has
been demonstrated in studies that sodium hypochlorite baths
have been effective at eradicating multiple community-acquired
MRSA strains [35]. Although topical disinfectants are effective for
prophylaxis, this option is not recommended for the treatment of
impetigo in its active form. It is not recommended that this
option be used in active disease.
In a review performed by the Cochrane Database of Systemic
Reviews, it was noted that topical antibiotics showed better
cure rates than topical placebo [25]. Topical mupirocin has
demonstrated superior efficacy to the oral agent erythromycin
and has been proven to be a viable option in patients with
erythromycin-resistant strains of Staphylococcus aureus. In
other comparisons, cure rates between topical and oral agents
show no significant difference [25]. According to Infectious
Diseases Society of America guidelines, non-bullous and bullous
impetigo can be treated with oral or topical antimicrobials for a
duration of five to seven days, but oral therapy is recommended
in patients with numerous lesions or outbreaks affecting several
people to help mitigate the transmission of infection [31].
TOPICAL ANTIBIOTICS
Topical antibiotics are a viable option for limited impetigo
disease. They are less likely to promote bacterial resistance and
have less side effects. For infants, children, and adolescents in
the United States, mupirocin and retapamulin are the two topical
agents most commonly used (Table 1) [14,29].Mupirocin inhibits
bacterial protein synthesis by reversibly and specifically binding
to transfer-RNA synthetase. It has tolerable side effects such as
application site reactions (pruritus and stinging of skin) [14].
Retapamulin exhibits its action by inhibiting bacterial protein
synthesis at the 50S ribosomal unit [14].Due to the risk of
epistaxis, retapamulin should not be used on the nasal mucosa
[36]. Fusidic acid is also a common topical agent used worldwide,
but it is not FDA approved in the United States.
Over-the-counter: Triple antibiotics (bacitracin-neomycin-
polymixin) have some activity against the organisms, but they
are not as effective for treatment [37]. Bacitracin and neomycin
have also been known to cause contact dermatitis. These agents
are not recommended for the treatment of impetigo.
SYSTEMIC ANTIBIOTICS
For lesions that are widespread, it is recommended
that patients use oral antibiotics. Preferred agents for
pediatric population include different types of penicillins and
cephalosporins (Table 1); both of these classes inhibit bacterial
cell wall synthesis. Dicloxacillin and cephalexin are used in
infants, children, and adolescents (Table 1). If MRSA is suspected
or confirmed by a culture and sensitivity test, the preferred
antibiotics are clindamycin, doxycycline, or trimethoprim-
sulfamethoxazole. Doxycycline is a tetracycline that exerts
its function by inhibiting bacterial protein synthesis. It is not
recommended in children less than 8 years of age due to teeth
discoloration. Neonatal patients with bullous form of impetigo
can be treated with nafcillin, oxacillin, or clindamycin.
Erythromycin, a macrolide, is the drug of choice for neonates
with non-bullous impetigo (Table 1). Intravenous vancomycin
is recommended for MRSA cases [29]. Systemic antimicrobial
agents are indicated when there is involvement of deep tissue
structures, fever, lymphadenopathy, pharyngitis, infections near
the oral cavity, and infections on the scalp and/or numerous
lesions [26].
COMPLICATIONS
Complications are rare, but local and systemic spread of
infection may result in cellulitis, lymphangitis, septicemia,
guttate psoriasis, scarlet fever, and postreptococcal
glomerulonephritis (PSGN) [25]. PSGN is one of the most
serious complications
 Central
Table 1: Pediatric Impetigo Treatment Regimens.
Medications Age
Topical Agents
Mupirocin 2% Ointment (Bactroban) Children 2 mo:
Retapamulin 1% Ointment (Altabax) Children 9 mo:
Systemic Agents
Infants < 3 mo:
Amoxicillin-Clavulanic Acid (Augmentin) Children 3 mo and < 40 kg
Children 40 kg
Infants and children 3 mo-12y
Cefuroxime Children 12 yr
(Ceftin, Zinacef) Adolescents
Cephalexin (Keflex) Children 1 yr:
Neonates
Dicloxacillin Children < 40 kg Children
Children 40 kg
Erythromycin (E.E.S. 400, E.E.S.
Granules, Ery-tab, EryPed 200, EryPed Weight Based
400, Erythrocin Stearate)
and tends to occur as a result of streptococcal impetigo more
commonly than streptococcal throat infection [25,26,32]. PSGN
can occur in up to 5% of patients with non-bullous impetigo and
tends to manifest approximately 2 weeks after infection [24,29].
Symptoms can include swelling in the face, especially around the
eyes, oliguria, hematuria, and increased blood pressure. Most
patients tend to recover without permanent kidney damage, but
PSGN can lead to chronic kidney disease [29]. Currently there
is no data to indicate that treating impetigo has any effect on
preventing the development of acute PSGN [23-26,29]; however,
treatment does reduce the dissemination of nephritogenic
strains in the human population [23,25,26].
PROGNOSIS
Impetigo generally heals within 2-3 weeks, even without
treatment. In randomized trials, it was demonstrated that in
the placebo arms approximately 13% to 52% had spontaneous
resolution within 7 to 10 days[14]. However, a higher cure rate
is seen with the use of medications and it reduces the risk of
spreading the infection[25,38].
PREVENTION
Proper hygiene is essential in the prevention of impetigo;
washing hands with warm water and antibacterial soap and
bathing regularly should help reduce chance of infection. Nails
should be kept clipped and filed in order to avoid auto-
inoculation by scratching sores. Patients infected with impetigo
should use clean towels and washcloths every time [29].
Children may return to school 24 hours after beginning an
effective antibiotic regimen, and draining lesions should be kept
covered [39]. To limit the contamination of fomites, parents or
guardians should wash childrens toys and use disinfectant wipes
on hard surfaces.
Directions
Apply to lesions 2-3 times daily for 7-10 days
Apply to affected areas twice daily for 5 days
30 mg/kg/day po divided q12h x 10 days
30 -90 mg/kg/day po divided q8-12h x 10 days
250-500 mg po divided q8h or 875 mg q12h x 10 days
30 mg/kg/day (max 1 g/day) divided q12h x 10 days (suspension)
250 mg q12h x 10 days (tablet)
250-500 mg q12h x 10 days (tablet)
25-100 mg/kg/day in divided doses every 6-8 x 10 days; Max 4 g/day
Not recommended
12.5-100 mg/kg/day divided q6h x 5-7 days
125-250 mg q6h x 5-7 days
Erythromycin base: 30-50 mg/kg/day in 2-4 divided doses x 5-7
days; Max 2 g/day
Erythromycin ethylsuccinate: 30-50 mg/kg/day in 2-4 divided doses
x 5-7 days; Max 3.2 g/day
Erythromycin base stearate: 30-50 mg/kg/day in 2-4 divided doses x
5-7 days; Max 2 g/day
Also, parents should follow-up with a primary care physician if
they notice that the lesion is continuing to spread, the sore is not
beginning to heal, or the child is developing systemic symptoms
[29].
DISCUSSION & CONCLUSION
Impetigo is a highly contagious bacterial infection that mainly
affects children between the ages of 2 to 5; however, people of
any age can acquire the infection. Impetigo is principally caused
by Staphylococcus aureus, and Streptococcus pyogenes (GABHS).
Diagnosis is generally made through visual observation of clinical
manifestations; cultures may be drawn to tailor treatment.
Limited infection is treated with topical antibiotics such as
Mupirocin or Retapamulin, while more extensive disease is
treated with oral or IV antibiotics. Although rare, complications
are possible; however, most cases of impetigo resolve completely
without complications.
REFERENCES
1. Hay RJ, Johns NE, Williams HC, Bolliger IW, Dellavalle RP, Margolis DJ,
et al. The Global Burden of Skin Disease in 2010: An Analysis of the
Prevalence and Impact of skin conditions. J Clin Investig Dermatol.
2014; 134: 1527-1534.
2. Fish DN. Chapter 42. Skin and soft tissue infections. In: Wofford MR,
Posey LM, Linn WD, OKeefe ME, eds. Pharmacotherapy in Primary
Care. New York, NY: McGraw-Hill; 2009.
3. Mahe AH, Hay RJ. Epidemiology and Management of Common Skin
Diseases in Children in Developing Countries. Geneva: World Health
Organization; 2005.
4. Steer AC, Jenney AWJ, Kado JH, Batzloff MR, La Vincente S,
Waqatakirewa L, et al. High Burden of Impetigo and Scabies in a
Tropical Country. Lancet Infect Dis. 2009; 3.
 Central
5. RothRR, James WD. Microbial Ecology of the Skin. Anna Rev Microbial.
1988; 42: 441-464.
6. Bowen AC, Mahe AH, 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.
7. Carapetis JR, Steer AC, Mulholland EK, Weber MW. The Global Burden
of Group A Streptococcal Diseases. Lancet Infect Dis. 2005; 5: 685-
694.
8. Andrews RM, McCarthy JS, Carapetis JR, Currie BJ. Skin disorders,
including pyoderma, scabies, and tinea infections. Pediatr Clin North
Am. 2009; 56: 1421-1440.
9. Cogen AL, Nizet V, Gallo RL. Skin Microbiota: A Source of Disease or
Defence? Br J Dermatol. 2008; 158: 442-455.
10. Human Microbiome Project Consortium Structure, function and
diversity of the healthy human microbiome. Nature. 2012; 486: 207-
214.
11. Costello EK, Lauber CL, Hamady M, Fierer N, Gordon JI, Knight R.
Bacterial community variation in human body habitats across space
and time. Science. 2009; 326: 1694-1697.
12. Hancock RE, Lehrer R. Cationic peptides: a new source of antibiotics.
Trends Biotechnol. 1998; 16: 82-88.
13. McAdam AJ, Sharpe AH: Infectious diseases bacterial infections. In:
Kumar V, Abbas AK, Fausto N, editors. Robbins & Cotran Pathologic
Basis of Disease. Philadelphia: Elsevier Inc; 2005; 371-396.
14. Klaenhammer TR. Bacteriocins of lactic acid bacteria. Biochimie.
1988; 70: 337-349.
15. Riley MA. Molecular mechanisms of bacteriocin evolution. Annu Rev
Genet. 1998; 32: 255-278.
16. Lai Y, Di Nardo A, Nakatsuji T, Leichtle A, Yang Y, Cogen AL, et al.
Commensal bacteria regulate Toll- like receptor 3-dependent
inflammation after skin injury. Nat Med. 2009; 15: 1377-1382.
17. Gould D. Skin flora: Implications for nursing. Nurs Stand. 2012; 26:
48-56.
18. Granato PA. Pathogenic and Indigenous Microorganisms of Humans.
In: Murray PR, Baron EJ, Jorgensen JH, et al., eds. Manual of Clinical
Microbiology, 9th ed. Washington, DC: ASM Press 2007; 46-56.
19. Reichel M, Heisig P, Kampf G. Identification of Variables for Aerobic
Bacterial Density at Clinically Relevant Skin Sites. J Hosp Infect. 2011;
78: 5-10.
20. Weidenmaier C, A Peschel. Teichoic Acids and Related Cell-Wall
Glycopolymers in Gram-Positive Physiology and Host Interactions.
Nat Rev Microbiol. 2008; 6: 276-287.
21. Sutcliffe IC, N Shaw. Atypical Lipoteichoic Acids of Gram-Positive
Bacteria. J Bacteriol. 1991; 173: 7065-7069.
22. Darmstadt GL, Lane AT. Impetigo: an overview. Pediatr Dermatol.
1994; 11: 293-303.
23. Stevens DL, Bryant AE. Impetigo, Erysipelas and Cellulitis. 2016 Feb
10. In: Ferretti JJ, Stevens DL, Fischetti VA, editors. Streptococcus
pyogenes: Basic Biology to Clinical Manifestations [Internet].
Oklahoma City (OK): University of Oklahoma Health Sciences Center;
2016.
24. Hartman-Adams H, Banvard C, Juckett G. Impetigo: diagnosis and
treatment. Am Fam Physician. 2014; 90: 229-235.
25. Koning S, van der Sande R, Verhagen AP, van Suijlekom-Smit LW,
Morris AD, Butler CC, et al. Interventions for impetigo. Cochrane
Database Syst Rev. 2012; 1.
26. Pereira LB. Impetigo-review. An Bras Dermatol. 2014; 89: 293-299.
27. Zita s E , Me sza ros J. The most common childhood skin diseases. Our
Dermatol Online. 2016; 7: 213-218.
28. Amagai M, Matsuyoshi N, Wang ZH, Andl C, Stanley JR. Toxin in
bullous impetigo and staphylococcal scalded-skin syndrome targets
desmoglein1. Nat Med. 2000; 6: 1275-1277.
29. Sahraoui S, Akiyode O. Impetigo in Children and Adolescents. US
Pharm. 2013; 38: 68-71.
30. Davis S. Impetigo: a review with a focus on retapamulin. S Afr Pharm
J. 2015; 82: 22-25.
31. 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. 2014; 59: 10-
52.
32. Behesti M, Ghotbi Sh. Impetigo, a brief review. Shiraz E-Medical
Journal. 2007; 8: 138-141.
33. Dagan R. Impetigo in childhood: changing epidemiology and new
treatments. Pediatric Annals. 1993; 22: 235-240.
34. NHS. Health A-Z. Impetigo. Overview.
35. Fisher RG, Chain RL, Hair PS, Cunnion KM. Hypochlorite killing of
community-acquired methicillin-resistant Staphylococcus aureus.
Pediatr Infect Dis J. 2008; 27: 934-935.
36. Altabax (retapamulin) ointment. FDA Medwatch. September 2010.
37. Bass JW, Chan DS, Creamer KM, Thompson MW, Malone FJ, Becker
TM, et al. Comparison of oral cephalexin, topical mupirocin and
topical bacitracin for treatment of impetigo. Pediatr Infect Dis J.
1997; 16:
708-710.
38. George A, Rubin G. A systematic review and meta-analysis of
treatments for impetigo. Br J Gen Pract. 2003; 53: 480-487.
39. Baddour. Impetigo. Up to Date.
40. Impetigo Treatment & Management. Medscape.
 Cite this article
Ghazvini P, Treadwell P, Woodberry K, Nerette E Jr, Powery H II (2017) Impetigo in the Pediatric Population. J Dermatolog Clin Res 5(1): 1092.

ABSTRAK
Impetigo adalah infeksi kulit bakteri endemik yang paling sering dikaitkan dengan populasi anak-

Journal
anak; Hal ini terlihat di lebih dari ofanak
sekitar 162 juta Dermatology
yang berusia antara 2 danand
5 tahun.Clinical
Secara geografis,

Research
infeksi ini banyak ditemukan di daerah tropis di seluruh dunia. Impetigo memiliki tingkat kejadian insidensi
terbesar, dibandingkan dengan berbagai infeksi kulit lainnya yang terlihat pada anak-anak. Karakteristik
utama yang diamati pada infeksi ini adalah lesi. Lesi pertama kali muncul sebagai bullae yang akhirnya
membentuk krusta berwarna madu dan tebal yang bisa menyebabkan pruritus. Ada tiga bentuk impetigo:
bullous, non-bullous dan ecthyma. Organisme penyebab utama impetigo yaitu Staphylococcus aureus dan
streptokokus -hemolitik Grup-A (GABHS). Sebagian besar infeksi impetigo sembuh tanpa memerlukan
pengobatan; Namun, untuk mengurangi durasi dan penyebaran penyakit, digunakan agen antibiotik topikal
dan oral. Prognosis positif dan komplikasi minimal pada penyakit ini.
SINGKATAN
SSTI: Skin and Soft Tissue Infection; GABHS: Group-A -hemolytic Streptococci; SSSS: Staphylococcal
Scalded Skin Syndrome; CA-MRSA: Community-Acquired Methicillin-Resistant Staphylococcal aureus;
PVL: Panton-Valentine-Leucodin; PSGN: Postreptococcal Glomerulonephritis

PENGANTAR
Evolusi bakteri dan meluasnya penyebaran resistansi antibiotik yang terus meningkat. Infeksi kulit
dan jaringan lunak (SSTI) merupakan prioritas klinis, sebagian, karena efek yang tidak proporsional
terhadap populasi yang paling rentan [1]. Impetigo adalah infeksi kulit superfisial yang sangat menular yang
umumnya disebabkan oleh bakteri gram positif yang mencakup Staphylococcus aureus atau streptokokus B
hemolitik Grup -A- (GABHS), seperti Streptococcus pyogenes. Kedua organisme tersebut telah berpengaruh
dalam meluasnya penyebaran resistensi bakteri [2,3]. Infeksi pediatrik terutama diderita oleh orang-orang
yang cenderung terjadi di lingkungan dengan cuaca panas dan lembab [4,5]. Sebuah studi global mengenai
prevalensi populasi impetigo menyimpulkan bahwa lebih dari kira-kira 162 juta anak-anak berusia antara
dua dan lima tahun menderita penyakit ini. Studi tersebut menunjukkan bahwa anak-anak ini cenderung
tinggal di negara berpenghasilan rendah yang berada di daerah tropis [4,6-8].
PATOFISIOLOGI
Kulit berfungsi sebagai garis pertahanan pertama antara manusia dan lingkungannya [9].
Ketidakseimbangan homeostasis antara mikrobioma dan host kulit telah dikaitkan dengan penyakit. Faktor
yang berbeda bertanggung jawab atas variabilitas unik dari Mikrobiom kulit hanya sebagian dipahami,
namun hasil menunjukkan bahwa pengaruh genetik dan lingkungan host yang memainkan peran besar
[10,11]. Alaminya, kulit dijajah oleh beragam bakteri. [12]. Infeksi akibat tingginya konsentrasi bakteri
jarang terjadi karena kemampuan kulit memiliki pelindung alami. Resistensi alami pada tubuh manusia
terhadap infeksi disebabkan oleh pH kulit dan jaringan subkutan yang rendah sekitar 5,6, serta cairan
sebaceous tersebut yang menghidrolisis membentuk asam lemak bebas yang sangat kuat menghambat
pertumbuhan bakteri dan jamur, dan kulit yang memiliki flora normal, yang membantu mencegah kolonisasi
organisme patogen lainnya [13]. Peptida antimikroba bakteri, juga disebut bakteriosin, yang diproduksi oleh
banyak atau kebanyakan bakteri yang ditemukan di flora normal yang memainkan peran besar dan
menguntungkan dalam hubungan antara bakteri dan kulit. Bakteriosin tidak melindungi agen infeksi secara
sederhananya; bakteriosin berkontribusi terhadap bertahannya suatu individu sel bakteri dengan membunuh
bakteri lain yang mungkin bersaing untuk mendapatkan nutrisi di lingkungan yang sama [14,15]. Contoh
lain dari hubungan yang menguntungkan antara bakteri dan kulit yaitu melibatkan kapasitas epitel untuk
mendeteksi mikroorganisme dengan reseptor seperti Tol (TLRs). Stimulasi TLRs menginduksi pola ekspresi
gen yang berbeda yang menyebabkan aktivasi berbagai respon imun. Secara sederhana, respon imun ini
dianggap secara eksklusif bersifat pro-inflamasi dan dirancang untuk bertahan melawan infeksi mikroba
yang menyebabkan infeksi [16].
Namun, dalam kondisi tertentu, patogen dapat menembus penghalang integumen dari hospes yang
rentan dan dapat menyebabkan kerusakan jaringan yang dapat merangsang respons inflamasi. Kondisi yang
dapat mempengaruhi pasien terhadap perkembangan infeksi kulit meliputi cacar air, herpes simpleks, gigitan
serangga, pedikulosis, terapi radiasi, kudis, goresan, operasi, luka bakar termal, trauma, konsentrasi bakteri
yang tinggi, berlebihan, Kelembaban kulit, suplai darah yang tidak adekuat, ketersediaan nutrisi bakteri, dan
kerusakan pada lapisan korneum yang melakukn penetrasi bakteri [5,17-19]. Perkembangan impetigo
bergantung pada tiga faktor berikut: kepatuhan bakteri terhadap sel inang, invasi jaringan dengan
penghindaran dari pertahanan host, dan penyebaran toksin [13]. Invasi bakteri terjadi pada awalnya dalam
jumlah rendah, dengan adhesi memediasikan asam techoic di salah satu impetigo yang menyebabkan
mikroorganisme [20,21]. Namun, fibronektin, sebuah sel molekul adhesi yang memungkinkan sel bakteri
Seperti Streptococcus pyogenes (GABHS) untuk menempel pada kolagen dan menyerang permukaan kulit
yang diperlukan terganggu untuk mengkolonisasi kulit [13]. Sebaliknya, Staphylococcus aureus
mengkolonisasi epitus nasal pertama dan dari reservoir ini, kolonisasi kulit terjadi [22]. Seiring
bertambahnya jumlah bakteri dimana Hambatan integumen terganggu, invasi bakteri penjajah ini terjadi
kemudian dan impetigo dapat terjadi. Dengan mayoritas SSTI yang dihasilkan dari pembongkaran
pertahanan host normal melalui proses seperti tusukan, abrasi, atau pembedahan kulit. Harus dipahami
bahwa sifat dan tingkat keparahan infeksi tergantung pada kedua jenis mikroorganisme yang ada dan tempat
inokulasi [9,17,19].

ETIOLOGI & EPIDEMIOLOGI

Secara umum, patogen penyebab utama impetigo adalah Staphylococcus aureus dan streptokokus -
hemolitik Grup-A (GABHS) [23]. Patogen yang kurang umum yang terkait dengan impetigo meliputi
streptokokus Grup C, streptokokus Grup G, dan bakteri anaerobik [23,24]. Ketika memfokuskan pada
berbagai jenis impetigo, ada penggambaran yang jelas tentang patogen mana yang mendominasi, karena
impetigo dapat dipisahkan menjadi impetigo nonbullous dan impetigo bulosa.
Impetigo non-bulosa, juga dikenal sebagai impetigo contagiosa [24,25] atau pyoderma [23], saat ini
sebagian besar disebabkan oleh S. aureus. S. aureus merupakan campuran infeksi staphylococci dan
streptococci, dan kemudian streptococci saja. Namun, ini tidak selalu terjadi. Seiring waktu, agen penyebab
utama bergantian antara S. aureus dan GABHS. Menurut Koning S et al., Pada iklim sedang, S. aureus
adalah organisme penyebab utama pada tahun 1940an dan 1950an, setelah itu GABHS menjadi lebih umum;
Dalam dua dekade terakhir, S. aureus telah menjadi lebih umum lagi. S. aureus sendiri atau dikombinasikan
dengan GABHS sekitar 80% kasus impetigo [25,26]. Untuk lebih memvalidasi prevalensi S. aureus yang
lebih tinggi, menurut data dari Departemen Dermatologi Rumah Sakit Anak Heim Pl Budapest, lebih dari
70% kasus tersebut disebabkan oleh S. aureus, 20-25% disebabkan oleh infeksi campuran Staphylococci
dan streptococci, dan 5-10% kasus hanya disebabkan oleh streptokokus [27]. Sebaliknya, ada kejadian
ketika infeksi streptokokus lebih umum terjadi, seperti di iklim yang lebih hangat dan lembab [24,25].
Impetigo bulosa hampir secara eksklusif disebabkan oleh strain S. aureus yang menghasilkan toksin
eksfoliatif yang menyebabkan hilangnya adhesi sel di epidermis superfisial dengan menargetkan
desmoglein1 [23,28,29]. Toksin spesifik adalah toksin eksfoliatif A, berlawanan dengan toksin eksfoliatif B,
yang diproduksi oleh S. aureus dalam Staphylococcal Scalded Skin Syndrome (SSSS) [26]. Ada sedikit
persentase infeksi yang disebabkan oleh GABHS [26].
Ecthyma, yang digambarkan sebagai bentuk impetigo yang lebih dalam [30], atau sebagai jenis infeksi yang
terpisah namun serupa [31] meluas melalui epidermis dan mencapai dalam dermis. Serupa dengan impetigo
bulosa, patogen utamanya adalah S. aureus [32], namun streptokokus kadang-kadang menjadi penyebabnya
[27,31]. Kehadiran MRSA sebagai agen penyebab impetigo communityaquinta dianggap tidak biasa dan
heterogen [26]. Staphylococcal induced impetigo biasanya disebabkan oleh strain S. aureus yang memiliki
gen toksin exfoliative. Komunikator Staphylococcal aureus yang resisten terhadap methicillin (CA-MRSA)
tidak memiliki gen toksin exfoliative, namun memiliki gen Panton-Valentine-Leucodin (PVL).
Staphylococci yang memiliki PVL biasanya menyebabkan abses dan furuncle; Oleh karena itu,
kekhawatiran terhadap MRSA harus kurang dalam kasus impetigo [26]. Selanjutnya, tidak ada penelitian
yang mengidentifikasi masalah dengan impetigo MRSA terkait pada orang dewasa atau anak-anak, namun
budaya mungkin masih berguna dalam beberapa situasi [24]. Namun, jika ada, MRSA yang terkait dengan
impetigo biasanya terlihat dalam bentuk non-bullous [29].
MANIFESTASI KLINIS
Impetigo non-bullous dapat terjadi sebagai infeksi bakteri primer atau sekunder. Infeksi primer
terjadi melalui invasi bakteri langsung pada kulit sehat yang utuh [24]. Infeksi sekunder, yang lebih umum
terjadi, terjadi melalui infeksi bakteri pada kulit yang terganggu akibat trauma, ekzema, gigitan serangga,
kudis, wabah herpetik, atau penyakit lainnya [24]. Terlepas dari sifat primer atau sekundernya, impetigo
non-bulosa awalnya hadir sebagai lesi makulopapular yang menjadi vesikel berdinding tipis yang terletak di
dasar eritematosa. Vesikel cenderung <0,5cm dibandingkan dengan bullae yang terlihat pada impetigo
bulosa, yang biasanya berukuran> 0,5cm [29]. Setelah pecah, ulserasi dangkal berikutnya ditutupi dengan
cairan purulen yang mengering seperti kerak berwarna kekuning-kuningan atau kekuningan [24,26]. Infeksi
cenderung terjadi di daerah yang terpapar, terutama pada anggota badan dan wajah (misalnya, nares, daerah
perioral). Lesi satelit, yang disebabkan oleh selfinoculation, sering terjadi; Dan limfadenopati regional
umum [23,26]. Namun, gejala sistemik tidak ada [23-25] meskipun demam dapat terjadi pada kasus yang
parah [26]. Impetigo non-bulosa cenderung sembuh tanpa bekas luka, dan jika tidak diobati, bisa sembuh
secara spontan dalam 2-3 minggu [24-26].
Impetigo bulosa awalnya dimulai sebagai vesikula kecil, yang menjadi lepuhan lokal berukuran
sekitar 2cm; Lepuh mengandung kandungan yang jelas yang kemudian menjadi purulen [26]. Lepuh ini
tidak pecah semudah vesikula yang terlihat pada impetigo non-bulosa, dan mungkin bertahan selama
beberapa hari [25]. Begitu blister pecah, basis basah dan eritematosa dapat terlihat. Daerah pembesaran
kelenjar getah bening biasanya tidak ada, dan gejala sistemik jarang terjadi tapi bisa termasuk demam, diare,
dan kelemahan [24,26]. Bukti pendukung adanya limfadenopati regional pada impetigo bulosa saling
bertentangan. Beberapa artikel menyatakan bahwa limfadenopati jarang terjadi pada impetigo bulosa
[26,33], sementara yang lain tidak menyebutkan limfadenopati terkait impetigo bulosa [24,25]. Sebaliknya,
satu sumber menyatakan bahwa limfadenopati lebih sering terjadi pada impetigo bulosa daripada impetigo
non-bulosa [34]. Infeksi cenderung terjadi pada tubuh ; Daerah intertriginous seperti daerah, axillae, dan
neck; dan ekstremitas. Namun, daerah kutaneous lainnya juga bisa terkena dampaknya [24,26]. Seperti
bentuk impetigo lainnya, infeksi umumnya sembuh dalam waktu 2-3 minggu tanpa jaringan parut [24].
Ecthyma ditandai oleh vesikula yang pecah menghasilkan ulkus melingkar dan eritematosa dengan
krusta coklat hitam . Biasanya ada eritema edema di skeitarnya [30-32]. Rasa gatal biasa terjadi dan
menggaruk bisa menularkan infeksi [32]. Ecthyma terutama yang terjadi pada kaki dan gluteus setelah
trauma atau saat gigitan serangga mempunyai goresan yang terbuka [27]. Selain itu, tidak seperti impetigo,
ecthyma sembuh meninggalkan jaringan parut.

DIAGNOSA
 Diagnosis impetigo atau ecthyma biasanya diselesaikan melalui pengamatan visual dan temuan
klinis [29,32]. Pewarnaan Gram dan kultur nanah atau eksudat dari lesi kulit dan ektima dianjurkan untuk
membantu mengidentifikasi apakah penyebabnya S. aureus dan / atau GABHS;[31]. Selain itu, pada pasien
yang dicurigai mengalami glomerulonefritis akut termasuk impetigo, analisis kadar anti-DNase B yang
meningkat dapat memberikan bukti pendukung infeksi streptokokus sebelumnya [23].
Saat mendiagnosis impetigo, harus diingat bahwa ada kelainan lain yang hadir dengan manifestasi
klinis serupa. Dengan impetigo non-bullous, kebingungan diagnostik dapat terjadi dengan berbagai kelainan
kulit termasuk ruam, cold sores, infeksi kulit berupa jamur, dan eksim [25]. Dengan impetigo bulosa,
kebingungan diagnostik dapat terjadi dengan luka bakar termal, gangguan yang melepuh seperti pemfigoid
bulosa, dan sindrom Stevens Johnson [25].

TERAPI
Ada berbagai pilihan pengobatan yang bisa digunakan dalam pengobatan impetigo. Bergantung pada
tingkat keparahan kondisinya, pilihannya berkisar dari desinfektan topikal hingga antibiotik topikal dan oral.
Untuk impetigo tanpa komplikasi, telah di amati bahwa infeksi itu akan sembuh sendiri dalam beberapa
minggu tanpa jaringan parut [29]. Karena impetigo sangat menular, yang terbaik adalah mengobati dengan
obat-obatan yang bertentangan dengan hanya pengamatan.

Untuk perawatan luka lokal, dianjurkan agar lesi dibersihkan dengan lembut, lepaskan krusta krusta
impetigo non-bulosa menggunakan sabun antibakteri dan lap , dan sering melakukan perban basah ke
daerah yang terkena dampak [26]. Desinfektan topikal adalah pilihan tepat untuk pencegahan kekambuhan
dan menjadi alternatif untuk terapi antibiotik topikal. Telah ditampilkan dalam penelitian bahwa mandi
dengan sodium hipoklorit telah efektif dalam memberantas beberapa strain MRSA pada masyarakat [35].
Meskipun desinfektan topikal efektif untuk profilaksis, pilihan ini tidak dianjurkan untuk pengobatan
impetigo dalam bentuk aktifnya. Tidak disarankan agar pilihan ini digunakan pada penyakit aktif.
Dalam tinjauan yang dilakukan oleh Database Cochrane of Systemic Reviews, diketahui bahwa
antibiotik topikal menunjukkan tingkat kesembuhan yang lebih baik daripada plasebo topikal [25].
Mupirocin topikal telah menunjukkan khasiat yang superior dari pada eritromisin oral dan telah terbukti
menjadi pilihan tepat bagi pasien dengan strain Staphylococcus aureus yang resisten terhadap eritromisin.
Dalam perbandingan lainnya, tingkat kesembuhan antara agen topikal dan oral tidak menunjukkan
perbedaan yang signifikan [25]. Menurut pedoman Infectious Diseases Society of America, impetigo non-
bullous dan bullous dapat diobati dengan antimikroba oral atau topikal selama lima sampai tujuh hari,
namun terapi oral direkomendasikan pada pasien dengan banyak lesi atau wabah yang menyerang beberapa
orang untuk membantu mengurangi Penularan infeksi [31].

ANTIBIOTIK TOPIKAL
 Antibiotik topikal adalah pilihan tepat untuk penyakit impetigo terbatas. Antibiotik topical
cenderung tidak meningkatkan resistensi bakteri dan memiliki lebih sedikit efek samping. Untuk bayi, anak-
anak, dan remaja di Amerika Serikat, mupirocin dan retapamulin adalah dua agen topikal yang paling umum
digunakan (Tabel 1) [14,29]. Mupirocin menghambat sintesis protein bakteri secara reversibel dan mengikat
secara khusus untuk transfer-RNA synthetase. Ini memiliki efek samping yang dapat ditoleransi seperti
pruritus dan stinging kulit [14]. Retapamulin kerjanya dengan menghambat sintesis protein bakteri pada unit
ribosom 50S [14]. Karena risiko epistaksis, retapamulin tidak boleh digunakan pada mukosa hidung [36].
Asam fusidat juga merupakan agen topikal yang umum digunakan di seluruh dunia, namun FDA tidak
disetujui di Amerika Serikat.
Over-the-counter: Triple antibiotik (bacitracin-neomycinpolymixin) memiliki beberapa aktivitas
melawan organisme, namun tidak efektif untuk pengobatan [37]. Bacitracin dan neomisin juga diketahui
menyebabkan dermatitis kontak. Agen ini tidak dianjurkan untuk pengobatan impetigo.
Table 1: Pediatric Impetigo Treatment Regimens.
Medications Age Directions
Topical Agents
Mupirocin 2% Ointment (Bactroban) Children 2 mo: Apply to lesions 2-3 times daily for 7-10 days
Retapamulin 1% Ointment (Altabax) Children 9 mo: Apply to affected areas twice daily for 5 days
Systemic Agents
Infants < 3 mo: 30 mg/kg/day po divided q12h x 10 days
Amoxicillin-Clavulanic Acid (Augmentin) Children 3 mo and < 40 kg 30 -90 mg/kg/day po divided q8-12h x 10 days
Children 40 kg 250-500 mg po divided q8h or 875 mg q12h x 10 days

Infants and children 3 mo-12y

30 mg/kg/day (max 1 g/day) divided q12h x 10 days (suspension)
Cefuroxime Children 12 yr
250 mg q12h x 10 days (tablet)
(Ceftin, Zinacef) Adolescents
250-500 mg q12h x 10 days (tablet)

Cephalexin (Keflex) Children 1 yr: 25-100 mg/kg/day in divided doses every 6-8 x 10 days; Max 4 g/day

Neonates Not recommended

Dicloxacillin Children < 40 kg Children 12.5-100 mg/kg/day divided q6h x 5-7 days
Children 40 kg 125-250 mg q6h x 5-7 days

Erythromycin base: 30-50 mg/kg/day in 2-4 divided doses x 5-7

Erythromycin (E.E.S. 400, E.E.S.
Granules, Ery-tab, EryPed 200, EryPed
400, Erythrocin Stearate)
days; Max 2 g/day
Erythromycin ethylsuccinate: 30-50 mg/kg/day in 2-4 divided doses
Weight Based
x 5-7 days; Max 3.2 g/day
Erythromycin base stearate: 30-50 mg/kg/day in 2-4 divided doses x
5-7 days; Max 2 g/day

ANTIBIOTIK SISTEMIK
 Untuk lesi yang meluas, dianjurkan agar pasien menggunakan antibiotik oral. Agen pilihan untuk
populasi anak-anak mencakup berbagai jenis penisilin dan sefalosporin (Tabel 1); Kedua kelas ini
menghambat sintesis dinding sel bakteri. Dicloxacillin dan cephalexin digunakan pada bayi, anak-anak, dan
remaja (Tabel 1). Jika MRSA dicurigai atau dikonfirmasi dengan tes kultur dan sensitivitas, antibiotik
pilihannya adalah klindamisin, doksisiklin, atau trimetoprimsulfamethoxazole. Doxycycline adalah
tetrasiklin yang fungsinya dengan menghambat sintesis protein bakteri. Obat tersebut tidak dianjurkan pada
anak-anak berusia di bawah 8 tahun karena perubahan warna gigi. Pasien neonatal dengan bentuk impetigo
bulosa dapat diobati dengan nafcillin, oxacillin, atau clindamycin. Eritromisin, makrolida, adalah obat
pilihan untuk neonatus dengan impetigo non-bulosa (Tabel 1). Vankomisin intravena direkomendasikan
untuk kasus MRSA [29]. Agen antimikroba sistemik ditunjukkan saat ada keterlibatan struktur jaringan
dalam, demam, limfadenopati, faringitis, infeksi di dekat rongga mulut, dan infeksi pada kulit kepala dan /
atau banyak lesi [26].

KOMPLIKASI
Komplikasi jarang terjadi, namun penyebaran infeksi lokal dan sistemik dapat menyebabkan
selulitis, limfangitis, septikemia, psoriasis guttate, demam scarlet, dan glomerulonefritis postreptococcal
(PSGN) [25]. PSGN adalah salah satu komplikasi yang paling serius dan cenderung terjadi sebagai akibat
impetigo streptokokus lebih sering dari pada infeksi tenggorokan streptokokus [25,26,32]. PSGN dapat
terjadi pada 5% pasien dengan impetigo non-bulosa dan cenderung muncul sekitar 2 minggu setelah infeksi
[24,29]. Gejalanya bisa meliputi pembengkakan di wajah, terutama di sekitar mata, oliguria, hematuria, dan
peningkatan tekanan darah. Sebagian besar pasien cenderung pulih tanpa kerusakan ginjal permanen, namun
PSGN dapat menyebabkan penyakit ginjal kronis. Saat ini tidak ada data yang menunjukkan bahwa
mengobati impetigo memiliki efek pada pencegahan perkembangan PSGN akut [23-26,29]; Namun,
pengobatan mengurangi penyebaran jenis nephritogenic pada populasi manusia [23,25,26].

PROGNOSA
Impetigo umumnya sembuh dalam 2-3 minggu, bahkan tanpa pengobatan. Dalam uji coba secara
acak, ditunjukkan bahwa pada kelompok plasebo sekitar 13% sampai 52% memiliki resolusi spontan dalam
waktu 7 sampai 10 hari [14]. Namun, tingkat kesembuhan yang lebih tinggi terlihat dengan penggunaan
obat-obatan dan mengurangi risiko penyebaran infeksi [25,38].

PENCEGAHAN
Kebersihan yang tepat sangat penting dalam pencegahan impetigo; Mencuci tangan dengan air
hangat dan sabun antibakteri dan mandi secara teratur membantu mengurangi kemungkinan infeksi. Kuku
jangan panjang dan dimasukkan agar terhindar dari auto-inokulasi dengan menggores luka. Pasien yang
terinfeksi impetigo harus menggunakan handuk bersih dan lap setiap kali [29]. Anak-anak dapat kembali ke
sekolah 24 jam setelah memulai regimen antibiotik yang efektif, dan mengeringkan lesi harus terus ditutupi
[39]. Untuk membatasi kontaminasi fomites, orang tua atau wali harus mencuci mainan anak-anak dan
menggunakan desinfektan pada permukaan yang keras. Juga, orang tua harus menindaklanjuti dengan
dokter pelayanan primer jika mereka memperhatikan bahwa lesi terus menyebar, sakitnya tidak mulai
sembuh, atau anak tersebut menunjukkan gejala sistemik [29].

PEMBAHASAN & KESIMPULAN

Impetigo adalah infeksi bakteri yang sangat menular yang terutama menyerang anak-anak berusia
antara 2 sampai 5 tahun; Namun, orang-orang dari segala usia bisa terkena infeksi. Impetigo pada
prinsipnya disebabkan oleh Staphylococcus aureus, dan Streptococcus pyogenes (GABHS). Diagnosis
umumnya dilakukan melalui pengamatan visual manifestasi klinis; kultur dapat menentukan ke pengobatan
khusus. Infeksi terbatas diobati dengan antibiotik topikal seperti Mupirocin atau Retapamulin, sementara
penyakit yang lebih luas diobati dengan antibiotik oral atau IV. Meski jarang, komplikasi bisa terjadi;
Namun, sebagian besar kasus impetigo sembuh total tanpa komplikasi.