Central Journal of Dermatology and Clinical Research

Review Article *Corresponding author

Patty Ghazvini, FAMU College of Pharmacy and

Impetigo in the Pediatric Pharmaceutical Sciences, #349 New Pharmacy

Building, Tallahassee, Florida, USA, Tel: 850-599-3636;

Population
Email:
Submitted: 23 November 2016
Accepted: 04 February 2017
Patty Ghazvini*, Phillip Treadwell, Kristen Woodberry, Edouard Published: 07 February 2017
Nerette Jr, and Hermn Powery II Copyright
FAMU College of Pharmacy and Pharmaceutical Sciences, Florida, USA 2017 Ghazvini et al.

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

ABBREVIATIONS
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
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 from the
disease. The study showed that these children tend to reside in
low-income countries located in tropical regions [4,6-8].
PATHOPHYSIOLOGY
Skin serves as the first line of defense between humans and
their environment [9]. An imbalance of homeostasis between the
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
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
Pl 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
J Dermatolog Clin Res 5(1): 1092 (2017)
Ghazvini et al. (2017)
Email:
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
3/5

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.
J Dermatolog Clin Res 5(1): 1092 (2017)
Ghazvini et al. (2017)
Email:
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. Mah 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.
4/5

Central
5. RothRR, James WD. Microbial Ecology of the Skin. Anna Rev Microbial.
1988; 42: 441-464.
6. Bowen AC, Mah 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.
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.
J Dermatolog Clin Res 5(1): 1092 (2017)
Ghazvini et al. (2017)
Email:
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. Zits , Mszros 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.
5/5
 Journal of Dermatology and Clinical
Email:
Research
Ghazvini et al. (2017)

ABSTRAK
Impetigo adalah infeksi kulit bakteri endemik yang paling sering dikaitkan dengan populasi anak-
anak; Hal ini terlihat di lebih dari sekitar 162 juta anak yang berusia antara 2 dan 5 tahun. Secara geografis,
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
J Dermatolog Clin Res 5(1): 1092 (2017)
6/5
 Ghazvini et al. (2017)
Email:

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
J Dermatolog Clin Grup
Res 5(1):C,
1092streptokokus
(2017) Grup G, dan bakteri anaerobik [23,24]. Ketika memfokuskan 7/5
pada
 Ghazvini et al. (2017)
Email:

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,
J Dermatolog Clin Resatau penyakit
5(1): 1092 (2017) lainnya [24]. Terlepas dari sifat primer atau sekundernya, impetigo non-bulosa
8/5
 Ghazvini et al. (2017)
Email:

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.
J Dermatolog Clin Dengan impetigo
Res 5(1): 1092 (2017) non-bullous, kebingungan diagnostik dapat terjadi dengan berbagai kelainan
9/5
 Ghazvini et al. (2017)
Email:

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
J Dermatolog Clin[14]. Retapamulin
Res 5(1): 1092 (2017) kerjanya dengan menghambat sintesis protein bakteri pada unit ribosom10/
50S
5
 Ghazvini et al. (2017)
Email:

[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.

ANTIBIOTIK SISTEMIK
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

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
J Dermatologadalah klindamisin,
Clin Res 5(1): 1092 (2017)
11/
doksisiklin, atau trimetoprimsulfamethoxazole. Doxycycline adalah tetrasiklin
5
 Ghazvini et al. (2017)
Email:

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
J Dermatolog Clin Res 5(1): 1092 (2017)
12/
5
 Ghazvini et al. (2017)
Email:

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.

J Dermatolog Clin Res 5(1): 1092 (2017)

13/
5