Impetigo – Patofizjologia i mechanizm

Impetigo
Patofizjologia i mechanizm

Impetigo to ostra, wysoce zakaźna bakteryjna infekcja powierzchownych warstw naskórka, najczęściej wywoływana przez Staphylococcus aureus (około 80% przypadków niepęcherzowej postaci) oraz Streptococcus pyogenes (GAS). W klimacie umiarkowanym dominującym patogenem jest S. aureus, natomiast w tropikach przeważa GAS. Impetigo dzieli się na niepęcherzowe (70% przypadków) i pęcherzowe (30%), z których pęcherzowe jest niemal wyłącznie wywoływane przez S. aureus produkujące toksyny eksfoliatywne (A, B, D), które hydrolizują desmogleinę-1, prowadząc do utraty adhezji keratynocytów i powstawania pęcherzy. Patogeneza obejmuje również produkcję superantygenów, które masowo aktywują limfocyty T i indukują cytokiny prozapalne (IL-1, IL-6, TNF-α), co może skutkować poważnymi objawami ogólnoustrojowymi. Szczepy MRSA, często zawierające leukocydynę Panton-Valentine, wykazują zwiększoną zjadliwość i oporność na leczenie.

Impetigo – patogeneza i mechanizm rozwoju zakażenia

Impetigo (liszajec zakaźny) to ostra, wysoce zakaźna bakteryjna infekcja powierzchownych warstw naskórka, najczęściej występująca u dzieci w wieku 2-5 lat, choć może również dotykać starsze dzieci i dorosłych. Jest to jedna z najczęstszych bakteryjnych infekcji skórnych u dzieci.¹² Impetigo można klasyfikować jako pierwotne (infekcja wcześniej nieuszkodzonej skóry) lub wtórne (infekcja w miejscu wcześniejszego uszkodzenia skóry).³⁴

Czynniki etiologiczne

Główne bakterie odpowiedzialne za rozwój impetigo to:⁵⁶

Staphylococcus aureus (gronkowiec złocisty) – obecnie najczęstszy patogen, odpowiedzialny za około 80% przypadków niepęcherzowej postaci impetigo
Streptococcus pyogenes (paciorkowiec grupy A – GAS) – może występować samodzielnie lub w połączeniu z S. aureus
Coraz częściej notuje się również przypadki wywołane przez metycylinooporny Staphylococcus aureus (MRSA)

Częstość występowania poszczególnych patogenów może się różnić w zależności od regionu geograficznego. W klimacie tropikalnym GAS jest uważany za główny patogen, podczas gdy w klimacie umiarkowanym S. aureus zastąpił w dużej mierze GAS jako dominujący patogen.⁷⁸

Mechanizm kolonizacji skóry

Nieuszkodzona, zdrowa skóra zazwyczaj wykazuje odporność na kolonizację bakteryjną dzięki takim czynnikom jak:⁹¹⁰

Integralność bariery skórnej z jej kwaśnym pH
Obecność wydzieliny łojowej (kwasy tłuszczowe, szczególnie kwas oleinowy)
Lizozym
Produkcja defensyn
Odpowiedni stan odżywienia

Do zakażenia dochodzi, gdy bakterie przenikają przez barierę skórną. Bakterie mogą wnikać przez:¹¹¹²

Przerwanie ciągłości skóry (zadrapania, skaleczenia)
Ukąszenia owadów
Urazy
Poparzenia
Wcześniejsze zmiany skórne (atopowe zapalenie skóry, świerzb, ospa wietrzna)

Każde naruszenie bariery skórnej prowadzi do ekspozycji receptorów fibronektyny, których potrzebują zarówno GAS, jak i S. aureus do kolonizacji.¹³ Kwas teichoowy odgrywa kluczową rolę w początkowym przyleganiu bakterii do komórek gospodarza.¹⁴¹⁵ Kolonizacja wymaga fibronektyny – cząsteczki adhezji komórkowej, która umożliwia takim bakteriom jak Streptococcus pyogenes przyłączanie się do kolagenu i wnikanie w uszkodzone powierzchnie skóry.¹⁶

Patogeneza impetigo niepęcherzowego

Niepęcherzowe impetigo (impetigo contagiosa) stanowi około 70% wszystkich przypadków impetigo.¹⁷ W przypadku tej postaci choroby:¹⁸

Staphylococcus aureus jest zaangażowany w prawie 80% przypadków
Paciorkowce grupy A również przyczyniają się do patogenezy, albo samodzielnie, albo w połączeniu z S. aureus
Bakterie produkują toksyny, które działają jako superantygeny
Dochodzi do aktywacji limfocytów T i produkcji IL-1, IL-6 i TNF-α
Prowadzi to do eksfoliatywnych zmian skórnych i rozwoju impetigo

W przypadku zakażenia paciorkowcami, białko M (szczególnie szczepy D i E) działa jako czynnik zjadliwości dla paciorkowców grupy A.¹⁹²⁰ Białko to nadaje GAS zdolność do szybkiego namnażania się w świeżej ludzkiej krwi i inicjowania chorób, a także zapewnia oporność na fagocytozę przez neutrofile.

Patogeneza impetigo pęcherzowego

Impetigo pęcherzowe, stanowiące około 30% przypadków, jest wywoływane niemal wyłącznie przez S. aureus.²¹²² Kluczowy mechanizm patogenezy to:²³²⁴

Produkcja toksyn eksfoliatywnych (eksfoliatyny A, B i D) przez szczepy S. aureus
Toksyny te są proteazami serynowymi, które selektywnie hydrolizują desmogleina-1 (Dsg1) – białko obecne w desmosomach keratynocytów warstwy ziarnistej naskórka
Eksfoliatyny rozpoznają i przecinają Dsg1 w jednym specyficznym miejscu – po reszcie kwasu glutaminowego 381, między pozakomórkowymi domenami 3 i 4
Prowadzi to do utraty adhezji komórkowej w powierzchownej warstwie naskórka
W rezultacie następuje tworzenie się pęcherzy i złuszczanie skóry

W przeciwieństwie do niepęcherzowego impetigo, zmiany w impetigo pęcherzowym występują na nieuszkodzonej skórze.²⁵ Toksyny eksfoliatywne są najważniejszym czynnikiem zjadliwości S. aureus w tym typie impetigo, powodując dysocjację komórek naskórka i tworzenie pęcherzy.²⁶²⁷

Rola superantygenów i odpowiedź immunologiczna

Kluczowym czynnikiem zjadliwości infekcji jest zdolność bakterii do produkcji krążących toksyn, które działają jako superantygeny.²⁸²⁹ Superantygeny te:

Mogą pomijać pewne etapy odpowiedzi immunologicznej
Prowadzą do masowej aktywacji limfocytów T
Stymulują produkcję różnych limfokin, takich jak interleukina 1 i 6 oraz czynnik martwicy nowotworów alfa
Ta odpowiedź może prowadzić do powstawania złuszczającej wysypki skórnej, wymiotów, niedociśnienia, a nawet wstrząsu

Większość szczepów MRSA nabytych w środowisku zawiera leukocydynę Panton-Valentine (P-VL), wysoce zjadliwy egzotoksyna tworzący pory, który powoduje martwicę skóry i ma działanie cytolityczne na neutrofile i monocyty.³⁰ Niszczenie leukocytów przez P-VL jest jednym z powodów, dla których MRSA jest bardziej skłonny do wywoływania infekcji klinicznych.

Czynniki ryzyka i szerzenie się zakażenia

Impetigo szerzy się przez bezpośredni kontakt ze zmianami skórnymi osoby zakażonej lub przez przedmioty, których dotykała, takie jak ubrania, pościel, ręczniki czy zabawki.³¹³² Choroba staje się zakaźna po 4-10 dniach od początkowej ekspozycji na bakterie i przestaje być zakaźna po 48 godzinach od rozpoczęcia leczenia.³³

Czynniki zwiększające podatność na rozwój impetigo obejmują:³⁴³⁵³⁶

Niedożywienie
Immunosupresję
Uczęszczanie do żłobka/przedszkola
Przeludnienie
Cukrzycę
Słabą higienę
Wysoką temperaturę lub wilgotność
Współistniejące choroby skóry
Młody wiek
Wcześniejsze leczenie antybiotykami

Związek z infekcjami współistniejącymi

Istnieje interesujący związek między impetigo a świerzbem w środowiskach tropikalnych. Wykazano, że wymazy ze zmian skórnych pobrane podczas epizodów z jednoczesnym rozpoznaniem świerzbu częściej wskazywały na zakażenie S. pyogenes (OR 2,2, 95% CI 1,1-4,4, p=0,03).³⁷ Silniejszy związek S. pyogenes (niż S. aureus) z obecnością świerzbu potwierdza wcześniejsze prace, które łączyły epidemie świerzbu z późniejszymi epidemiami poinfekcyjnego kłębuszkowego zapalenia nerek.³⁸

Warto zauważyć, że nie wykazano pozytywnej korelacji między nosicielstwem S. aureus w nosie a występowaniem S. aureus w zmianach impetigo, ani związku między nasileniem impetigo a występowaniem S. pyogenes, S. aureus lub obu patogenów.³⁹

Powikłania impetigo

Chociaż impetigo jest zwykle samoograniczającą się infekcją, nieleczone może prowadzić do poważnych powikłań:⁴⁰⁴¹⁴²

Ostre poinfekcyjne kłębuszkowe zapalenie nerek (PSGN) – wynik odpowiedzi immunologicznej wywołanej infekcją paciorkowcową grupy A
Gorączka reumatyczna – nowe dowody sugerują, że może występować jako powikłanie po infekcjach skórnych wywołanych przez paciorkowce grupy A, w tym impetigo
Zapalenie tkanki łącznej – rozprzestrzenianie się infekcji na głębsze warstwy skóry
Posocznica – szczególnie w przypadku zakażeń S. aureus
Zespół oparzonej skóry (SSSS) – ciężkie powikłanie spowodowane przez te same toksyny, które wywołują impetigo pęcherzowe, ale z ogólnoustrojowym rozprzestrzenianiem się toksyn

Warto podkreślić, że roczna zachorowalność na inwazyjne zakażenia S. aureus jest 10-krotnie wyższa w populacji pediatrycznej rdzennych mieszkańców w porównaniu z nierdzenną zamieszkującą tereny endemiczne impetigo.⁴³

Leczenie i oporność na antybiotyki

Leczenie impetigo obejmuje stosowanie antybiotyków miejscowych lub ogólnoustrojowych.⁴⁴⁴⁵ Spektrum działania wybranego antybiotyku musi obejmować zarówno gronkowce, jak i paciorkowce, zarówno w przypadku impetigo pęcherzowego, jak i niepęcherzowego.⁴⁶ Ze względu na zdolność S. aureus i GAS do szybkiego rozwoju oporności na leki, mogą one ograniczać skuteczność obecnych metod leczenia.⁴⁷

W przypadku podejrzenia infekcji MRSA, zaleca się początkowe leczenie trimetoprimem/sulfametoksazolem, klindamycyną lub tetracykliną (doksycyklina lub minocyklina) w oczekiwaniu na wyniki hodowli.⁴⁸ Warto zaznaczyć, że mupirocyna działa poprzez hamowanie syntezy białek bakteryjnych przez wiązanie się z enzymem syntetazy izoleucylo-tRNA, zapobiegając w ten sposób włączeniu izoleucyny do łańcuchów białkowych.⁴⁹

Retapamulina jest nowatorskim antybiotykiem pleuromutylowym i pierwszym nowym miejscowym antybiotykiem od prawie 20 lat, który może stanowić alternatywę w leczeniu impetigo.⁵⁰

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Materiały źródłowe

#1 Impetigo: Diagnosis and Treatment | AAFP
https://www.aafp.org/pubs/afp/issues/2014/0815/p229.html
Impetigo is the most common bacterial skin infection in children two to five years of age. There are two principal types: nonbullous (70% of cases) and bullous (30% of cases). Nonbullous impetigo, or impetigo contagiosa, is caused by Staphylococcus aureus or Streptococcus pyogenes, and is characterized by honey-colored crusts on the face and extremities. Impetigo primarily affects the skin or secondarily infects insect bites, eczema, or herpetic lesions. Bullous impetigo, which is caused exclusively by S. aureus, results in large, flaccid bullae and is more likely to affect intertriginous areas. […] Impetigo is a common bacterial skin infection caused by Staphylococcus aureus, group A beta-hemolytic Streptococcus pyogenes, a combination of the two, or less commonly, anaerobic bacteria. […] Other factors that predispose to impetigo are skin trauma; hot, humid climates; poor hygiene; day care settings; crowding; malnutrition; and diabetes mellitus or other medical comorbidities.
#2 Chapter 4: Impetigo
https://themedicalxchange.com/en/review/2511_chapter-4-impetigo/
Impetigo is a common bacterial infection of the superficial skin that most commonly occurs among children. […] Non-bullous impetigo, or impetigo contagiosa, is the more common of the two types and is characterized by yellowish crusty lesions. […] Bullous impetigo, as the name suggests, is characterized by large, flaccid bullae that are prone to rupture and ooze yellow fluid. […] Highly contagious, impetigo is associated with overgrowth of bacteria introduced from the environment which transiently colonize healthy skin. […] For nonbullous impetigo, Group A streptococcus is the most common pathogen. For bullous impetigo, S. aureus infection accounts for most cases. […] There are several risk factors for bacterial overgrowth, including poor hygiene, diminished immune defenses, high temperature or humidity, comorbid dermatoses, and young age.
#3 Impetigo – StatPearls – NCBI Bookshelf
https://www.ncbi.nlm.nih.gov/books/NBK430974/
Impetigo can be classified as either primary or secondary. Primary impetigo involves previously normal skin affected by direct bacterial invasion. Secondary impetigo involves infection forming at a previous skin wound site. […] Any disturbance of the skin barrier leads to access to fibronectin receptors by GABHS and S aureus which require fibronectin for colonization. Trauma, cuts, insect bites, surgery, atopic dermatitis, burns, and varicella are common mechanisms of skin breakdown. Once a lesion is present, self-inoculation to other sites is very common. Malnutrition, immunosuppression, daycare attendance, overcrowding, diabetes, and poor hygiene make one more susceptible to impetigo. […] Triggers that breakdown skin and increase susceptibility to impetigo include: Varicella, Herpes, Scratching, Lice, Burns, Trauma, Insect bites.
#4 Impetigo | NHS inform
https://www.nhsinform.scot/illnesses-and-conditions/infections-and-poisoning/impetigo/
Impetigo occurs when the skin becomes infected with bacteria, usually either Staphylococcus aureus or Streptococcus pyogenes. […] The bacteria can infect the skin in 2 main ways: through a break in otherwise healthy skin such as a cut, insect bite or other injury this is known as primary impetigo […] through skin damaged by another underlying skin condition, such as head lice, scabies or eczema this is known as secondary impetigo. […] The bacteria can be spread easily through close contact with someone who has the infection, such as through direct physical contact, or by sharing towels or flannels. […] As the condition doesn’t cause any symptoms until 4 to 10 days after initial exposure to the bacteria, it’s often easily spread to others unintentionally. […] Impetigo stops being infectious after 48 hours of treatment starting or after the sores have stopped blistering or crusting.
#5
https://pmc.ncbi.nlm.nih.gov/articles/PMC4008061/
Impetigo is a common cutaneous infection that is especially prevalent in children. Historically, impetigo is caused by either group A -hemolytic streptococci or Staphylococcus aureus. Currently, the most frequently isolated pathogen is S. aureus. […] Host factors, such as integrity of the skin barrier with its acidic pH, presence of sebaceous secretion (fatty acids, particularly oleic acid), lysozyme and production of defensins and adequate nutritional status, play an important role in resistance to infection. […] A crucial factor to the infection virulence is the ability of these bacteria to produce circulating toxins that act as superantigens. Superantigens are able to skip certain steps of the immune response and promote massive activation of T lymphocytes and also the production of various lymphokines such as interleukin 1 and 6 and tumor necrosis factor alpha. This response may lead to the formation of exfoliative cutaneous eruption, vomiting, hypotension and shock.
#6 Impetigo: Practice Essentials, Background, Pathophysiology
https://emedicine.medscape.com/article/965254-overview
Impetigo is an acute, highly contagious gram-positive bacterial infection of the superficial layers of the epidermis. […] These bacteria can be introduced from the environment and only transiently colonize the cutaneous surface. […] The teichoic acid adhesions for GABHS and S aureus require the epithelial cell receptor component, fibronectin, for colonization. […] Factors that can modify the usual skin flora and facilitate transient colonization by GABHS and S aureus include high temperature or humidity, preexisting cutaneous disease, young age, or recent antibiotic treatment. […] Common mechanisms for disruption of skin that can facilitate bacterial colonization or infection include the following: Scratching, Atopic dermatitis, Dermatophytosis, Varicella, Herpes simplex, Scabies, Pediculosis, Thermal burns, Surgery, Trauma, Radiation therapy, Insect bites.
#7 Intolerable Burden of Impetigo in Endemic Settings: A Review of the Current State of Play and Future Directions for Alternative Treatments
https://www.mdpi.com/2079-6382/9/12/909
Impetigo (school sores) is a common superficial bacterial skin infection affecting around 162 million children worldwide, with the highest burden in Australian Aboriginal children. […] Impetigo is caused by the Gram-positive bacteria Staphylococcus aureus, Streptococcus pyogenes (group A beta-haemolytic streptococcus, GAS), or a combination of these two bacteria. […] The bacteria may invade the healthy (primary infection) or injured skin (secondary infection), such as atopic dermatitis, insect bites, or scabies, which disrupt the healthy skin barrier and facilitate the entry of pathogenic bacteria into patientâs blood. […] The bacterial aetiology of impetigo varies according to climatic regions, and continues to evolve over time. […] In tropical climatic regions, GAS is considered as the major pathogen and co-infection with S. aureus is common, while S. aureus has largely replaced GAS as the predominant pathogen in temperate climates.
#8 The microbiology of impetigo in Indigenous children: associations between Streptococcus pyogenes, Staphylococcus aureus,scabies, and nasal carriage | BMC Infectious Diseases | Full Text
https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-014-0727-5
Impetigo is caused by both Streptococcus pyogenes and Staphylococcus aureus; the relative contributions of each have been reported to fluctuate with time and region. […] However, few studies have utilised high quality microbiological culture methods to confirm this assumption. […] Skin sore swabs taken during episodes with a concurrent diagnosis of scabies were more likely to culture S. pyogenes (OR 2.2, 95% CI 1.1 4.4, p=0.03). […] While clearance of S. pyogenes is the key determinant of treatment efficacy, co-infection with S. aureus warrants consideration of treatment options that are effective against both pathogens where impetigo is severe and prevalent. […] Impetigo is strongly associated with scabies infestation in tropical environments, but the influence of scabies on the microbiology of impetigo has not previously been described.
#9
https://pmc.ncbi.nlm.nih.gov/articles/PMC4008061/
Impetigo is a common cutaneous infection that is especially prevalent in children. Historically, impetigo is caused by either group A -hemolytic streptococci or Staphylococcus aureus. Currently, the most frequently isolated pathogen is S. aureus. […] Host factors, such as integrity of the skin barrier with its acidic pH, presence of sebaceous secretion (fatty acids, particularly oleic acid), lysozyme and production of defensins and adequate nutritional status, play an important role in resistance to infection. […] A crucial factor to the infection virulence is the ability of these bacteria to produce circulating toxins that act as superantigens. Superantigens are able to skip certain steps of the immune response and promote massive activation of T lymphocytes and also the production of various lymphokines such as interleukin 1 and 6 and tumor necrosis factor alpha. This response may lead to the formation of exfoliative cutaneous eruption, vomiting, hypotension and shock.
#10 SciELO Brazil – Impetigo – review Impetigo – review
https://www.scielo.br/j/abd/a/cpm9SxPg4rwGjq7Qf679Ffq/?lang=en
Impetigo is a common cutaneous infection that is especially prevalent in children. Historically, impetigo is caused by either group A -hemolytic streptococci or Staphylococcus aureus. Currently, the most frequently isolated pathogen is S. aureus. This article discusses the microbiologic and virulence factors of group A -hemolytic streptococci and Staphylococcus aureus, clinical characteristics, complications, as well as the approach to diagnosis and management of impetigo. […] Host factors, such as integrity of the skin barrier with its acidic pH, presence of sebaceous secretion (fatty acids, particularly oleic acid), lysozyme and production of defensins and adequate nutritional status, play an important role in resistance to infection. […] A crucial factor to the infection virulence is the ability of these bacteria to produce circulating toxins that act as superantigens. Superantigens are able to skip certain steps of the immune response and promote massive activation of T lymphocytes and also the production of various lymphokines such as interleukin 1 and 6 and tumor necrosis factor alpha. This response may lead to the formation of exfoliative cutaneous eruption, vomiting, hypotension and shock.
#11 Impetigo: MedlinePlus Medical EncyclopediaLock
https://medlineplus.gov/ency/article/000860.htm
Impetigo is caused by streptococcus (strep) or staphylococcus (staph) bacteria. Methicillin-resistant staph aureus (MRSA) is an increasing cause. […] When there is a break in the skin, bacteria can enter the body and grow there. This causes inflammation and infection. Breaks in the skin may occur from injury or trauma to the skin or from insect, animal, or human bites. […] Impetigo may also occur on the skin, where there is no visible break. […] In adults, it may occur following another skin problem. It may also develop after a cold or other virus. […] Impetigo can spread to others. You can catch the infection from someone who has it if the fluid that oozes from their skin blisters touches an open area on your skin.
#12 Impetigo – Symptoms & causes – Mayo Clinic
https://www.mayoclinic.org/diseases-conditions/impetigo/symptoms-causes/syc-20352352
Impetigo is caused by bacteria, usually staphylococci organisms. […] You might be exposed to the bacteria that cause impetigo when you come into contact with the sores of someone who’s infected or with items they’ve touched such as clothing, bed linen, towels and even toys. […] The bacteria that cause impetigo often enter the skin through a small cut, insect bite or rash.
#13 Impetigo – StatPearls – NCBI Bookshelf
https://www.ncbi.nlm.nih.gov/books/NBK430974/
Impetigo can be classified as either primary or secondary. Primary impetigo involves previously normal skin affected by direct bacterial invasion. Secondary impetigo involves infection forming at a previous skin wound site. […] Any disturbance of the skin barrier leads to access to fibronectin receptors by GABHS and S aureus which require fibronectin for colonization. Trauma, cuts, insect bites, surgery, atopic dermatitis, burns, and varicella are common mechanisms of skin breakdown. Once a lesion is present, self-inoculation to other sites is very common. Malnutrition, immunosuppression, daycare attendance, overcrowding, diabetes, and poor hygiene make one more susceptible to impetigo. […] Triggers that breakdown skin and increase susceptibility to impetigo include: Varicella, Herpes, Scratching, Lice, Burns, Trauma, Insect bites.
#14 Impetigo: Practice Essentials, Background, Pathophysiology
https://emedicine.medscape.com/article/965254-overview
Impetigo is an acute, highly contagious gram-positive bacterial infection of the superficial layers of the epidermis. […] These bacteria can be introduced from the environment and only transiently colonize the cutaneous surface. […] The teichoic acid adhesions for GABHS and S aureus require the epithelial cell receptor component, fibronectin, for colonization. […] Factors that can modify the usual skin flora and facilitate transient colonization by GABHS and S aureus include high temperature or humidity, preexisting cutaneous disease, young age, or recent antibiotic treatment. […] Common mechanisms for disruption of skin that can facilitate bacterial colonization or infection include the following: Scratching, Atopic dermatitis, Dermatophytosis, Varicella, Herpes simplex, Scabies, Pediculosis, Thermal burns, Surgery, Trauma, Radiation therapy, Insect bites.
#15 Impetigo in the Pediatric Population
https://www.jscimedcentral.com/jounal-article-info/Journal-of%C2%A0Dermatology%C2%A0and-Clinical-Research/Impetigo-in-the-Pediatric–Population-8660
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. […] 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. […] Bacterial invasion occurs initially in low numbers, with teichoic acid mediating adhesion in either of the impetigo causing microorganisms. […] 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. […] As bacteria increase in number where the integumentary barrier is disrupted, invasion by these colonizing bacteria ensues and impetigo may develop. […] The nature and severity of the infection depends on both the type of microorganism present and the site of inoculation.
#16 Impetigo in the Pediatric Population
https://www.jscimedcentral.com/jounal-article-info/Journal-of%C2%A0Dermatology%C2%A0and-Clinical-Research/Impetigo-in-the-Pediatric–Population-8660
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. […] 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. […] Bacterial invasion occurs initially in low numbers, with teichoic acid mediating adhesion in either of the impetigo causing microorganisms. […] 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. […] As bacteria increase in number where the integumentary barrier is disrupted, invasion by these colonizing bacteria ensues and impetigo may develop. […] The nature and severity of the infection depends on both the type of microorganism present and the site of inoculation.
#17 Impetigo: Diagnosis and Treatment | AAFP
https://www.aafp.org/pubs/afp/issues/2014/0815/p229.html
Impetigo is the most common bacterial skin infection in children two to five years of age. There are two principal types: nonbullous (70% of cases) and bullous (30% of cases). Nonbullous impetigo, or impetigo contagiosa, is caused by Staphylococcus aureus or Streptococcus pyogenes, and is characterized by honey-colored crusts on the face and extremities. Impetigo primarily affects the skin or secondarily infects insect bites, eczema, or herpetic lesions. Bullous impetigo, which is caused exclusively by S. aureus, results in large, flaccid bullae and is more likely to affect intertriginous areas. […] Impetigo is a common bacterial skin infection caused by Staphylococcus aureus, group A beta-hemolytic Streptococcus pyogenes, a combination of the two, or less commonly, anaerobic bacteria. […] Other factors that predispose to impetigo are skin trauma; hot, humid climates; poor hygiene; day care settings; crowding; malnutrition; and diabetes mellitus or other medical comorbidities.
#18 Impetigo pathophysiology – wikidoc
https://www.wikidoc.org/index.php/Impetigo_pathophysiology
Bullous impetigo is caused by exfoliative toxins which are released by Stapphylococcus aureus. The exfoliative toxins can hydrolyze desmoglein 1 and thus weaken the desmosomes. The toxins are of two types, A and B, and lead to the production of bullae in the superficial layer of epidermis. These bullae are flaccid and can rupture easily. […] The pathogenesis of non-bulbous impetigo involves: Staphylococcus aureus is involved in almost 80% cases. Group A streptococci also contribute in the pathogenesis either alone or in combination with Staphylococcus aureus. Toxins are produced by the bacteria which act as superantigens. Activation of T-lymphocytes and the production of IL-1, IL-6 and TNF-a is mediated by the toxins. These lead to exfoliative skin changes and thus impetigo.
#19 Impetigo pathophysiology – wikidoc
https://www.wikidoc.org/index.php/Impetigo_pathophysiology
Impetigo, the infection of epidermis, can either be primary or secondary to scratches, injuries, bites or conditions that lead to a break in the continuity of the skin. The breaks in the continuity are potential sites for the pathogens to enter and infect. […] The D and E strains of emm protein act as a virulence factor for group A streptococci. […] Group A Streptococci have great invasive potential. They can be isolated from the skin 10 days before an infection and from the oropharynx, 2-3 weeks after the appearance on the skin. […] Staphylococci cause toxin mediated impetigo in the following way: Staphylococci produce toxins that act as superantigens. These superantigens can activate T-lymphocytes. The exfoliative toxins produced can hydrolyze desmoglein 1 and thus weaken the desmosomes. They can also produce IL-1 and IL-6 and tumor necrosis factor alpha (TNF-a). These lymphokines can act on the skin producing bullous impetigo.
#20 Current Microbiological, Clinical and Therapeutic Aspects of Impetigo
https://clinmedjournals.org/articles/cmrcr/clinical-medical-reviews-and-case-reports-cmrcr-5-205.php
Impetigo is a highly contagious infection of the epidermis, seen especially among children, and transmitted through direct contact. Two bacteria are associated with impetigo: S. aureus and GAS. […] The aim of this review is to present the current microbiological knowledge of the two organisms mentioned with the relevant virulence factors that enable to initiate skin diseases and how they contribute to the clinical presentation, as well as to show the clinical presentation itself. […] The major somatic virulence factor of GAS is protein M. This protein is known to confer resistance to phagocytosis by PMNs. It also gives GAS the ability to multiply quickly in fresh human blood and to initiate diseases. […] Initiation of various skin infections is done through ETA and ETB which are active serine proteases produced by some strains of S. aureus. While ETA is encoded on a prophage, ETB is encoded on a large penicillinase-type plasmid. ETA and ETB lead to epidermal cleavage, through the effect on desmogelin-1 which is a desmosomal cadherin. This cleavage is directly responsible for the clinical manifestation of the blistering skin disease: Pemphigus neonatorum and/or generalized staphylococcal scalded skin syndrome (SSSS) in neonates, and bullous impetigo in young children and adults.
#21 Impetigo – Wikipedia
https://en.wikipedia.org/wiki/Impetigo
Impetigo is primarily caused by Staphylococcus aureus, and sometimes by Streptococcus pyogenes. […] Both bullous and nonbullous are primarily caused by S. aureus, with Streptococcus also commonly being involved in the nonbullous form. […] The infection is spread by direct contact with lesions or with nasal carriers. The incubation period is 1-3 days after exposure to Streptococcus and 4-10 days for Staphylococcus. […] Impetigo is usually diagnosed based on its appearance. It generally appears as honey-colored scabs formed from dried sebum and is often found on the arms, legs, or face. […] If a visual diagnosis is unclear a culture may be done to test for resistant bacteria. […] Without treatment, individuals with impetigo typically get better within three weeks. […] Complications may include cellulitis or poststreptococcal glomerulonephritis.
#22 Impetigo: Diagnosis and Treatment | AAFP
https://www.aafp.org/pubs/afp/issues/2014/0815/p229.html
Impetigo is the most common bacterial skin infection in children two to five years of age. There are two principal types: nonbullous (70% of cases) and bullous (30% of cases). Nonbullous impetigo, or impetigo contagiosa, is caused by Staphylococcus aureus or Streptococcus pyogenes, and is characterized by honey-colored crusts on the face and extremities. Impetigo primarily affects the skin or secondarily infects insect bites, eczema, or herpetic lesions. Bullous impetigo, which is caused exclusively by S. aureus, results in large, flaccid bullae and is more likely to affect intertriginous areas. […] Impetigo is a common bacterial skin infection caused by Staphylococcus aureus, group A beta-hemolytic Streptococcus pyogenes, a combination of the two, or less commonly, anaerobic bacteria. […] Other factors that predispose to impetigo are skin trauma; hot, humid climates; poor hygiene; day care settings; crowding; malnutrition; and diabetes mellitus or other medical comorbidities.
#23 Impetigo: Practice Essentials, Background, Pathophysiology
https://emedicine.medscape.com/article/965254-overview
After initial infection, new lesions may be seen in areas with no apparent break in the skin. […] Bullous impetigo is commonly due to exfoliative toxins of S aureus termed exfoliatins A and B. […] These exotoxins cause a loss of cell adhesion in the superficial dermis, which, in turn, causes blisters and skin sloughing by cleaving of the granular cell layer of the epidermis. […] One of the target proteins for exotoxin A is desmoglein I, which maintains cell adhesion. […] Unlike nonbullous impetigo, the lesions of bullous impetigo occur on intact skin. […] Most strains of community-acquired MRSA contain Panton-Valentine leucocidin (P-VL), a highly virulent, pore-forming exotoxin that causes dermal necrosis and has cytolytic activity against neutrophils and monocytes. […] Destruction of leukocytes by P-VL is one of the reasons that MRSA is more likely to produce clinical infection.
#24
https://www.jci.org/articles/view/15766
The pathophysiologic basis of this specificity has been a mystery for over 30 years, even though recent crystal structure and amino acid sequences of ETA and ETB have suggested that they are atypical glutamate-specific serine proteases. […] Very recently, we identified a relevant substrate of ETA, ETB, and ETD to be desmoglein 1 (Dsg1), a transmembrane glycoprotein of desmosomes in the cadherin gene superfamily. […] Here we demonstrate that ETA, ETB, and ETD act as glutamic acid-specific serine proteases with unusually focused specificity that results in a single cleavage of Dsg1, leading to its functional inactivation. […] The observations that substitution of serine 195 with both cysteine and alanine inhibit cleavage, and that the mutant ETs still specifically bind Dsg1, demonstrate that serine 195 is necessary for efficient catalytic cleavage of Dsg1.
#25 Impetigo: Practice Essentials, Background, Pathophysiology
https://emedicine.medscape.com/article/965254-overview
After initial infection, new lesions may be seen in areas with no apparent break in the skin. […] Bullous impetigo is commonly due to exfoliative toxins of S aureus termed exfoliatins A and B. […] These exotoxins cause a loss of cell adhesion in the superficial dermis, which, in turn, causes blisters and skin sloughing by cleaving of the granular cell layer of the epidermis. […] One of the target proteins for exotoxin A is desmoglein I, which maintains cell adhesion. […] Unlike nonbullous impetigo, the lesions of bullous impetigo occur on intact skin. […] Most strains of community-acquired MRSA contain Panton-Valentine leucocidin (P-VL), a highly virulent, pore-forming exotoxin that causes dermal necrosis and has cytolytic activity against neutrophils and monocytes. […] Destruction of leukocytes by P-VL is one of the reasons that MRSA is more likely to produce clinical infection.
#26
https://pmc.ncbi.nlm.nih.gov/articles/PMC4008061/
S. aureus produces exfoliative toxins, which are proteases that selectively hydrolyze one of the intracellular adhesion molecules, desmoglein-1, present in the desmosomes of keratinocytes located in the epidermic granular layer. Toxins are the greatest virulence factor of S. aureus, causing dissociation of epidermal cells with blister formation. […] Bullous impetigo is almost universally caused by a single organism, S. aureus, mainly belonging to group II (80%); phage type 71 (60% of cases). […] The presence of MRSA as impetigo’s causative agent in non-hospitalized patients is considered unusual and with heterogeneous distribution. Staphylococcal impetigo is usually caused by S. aureus strains that possess the exfoliative toxin gene. […] The spectrum of the selected antibiotic must cover staphylococci and streptococci, both for bullous impetigo as well as for crusted impetigo. Thus, benzathine penicillin or those sensitive to penicillinases are not indicated in the treatment of impetigo.
#27 SciELO Brazil – Impetigo – review Impetigo – review
https://www.scielo.br/j/abd/a/cpm9SxPg4rwGjq7Qf679Ffq/?lang=en
Bullous impetigo is almost universally caused by a single organism, S. aureus, mainly belonging to group II (80%); phage type 71 (60% of cases). […] S. aureus produces exfoliative toxins, which are proteases that selectively hydrolyze one of the intracellular adhesion molecules, desmoglein-1, present in the desmosomes of keratinocytes located in the epidermic granular layer. Toxins are the greatest virulence factor of S. aureus, causing dissociation of epidermal cells with blister formation. […] The presence of MRSA as impetigo’s causative agent in non-hospitalized patients is considered unusual and with heterogeneous distribution. Staphylococcal impetigo is usually caused by S. aureus strains that possess the exfoliative toxin gene. […] The spectrum of the selected antibiotic must cover staphylococci and streptococci, both for bullous impetigo as well as for crusted impetigo. Thus, benzathine penicillin or those sensitive to penicillinases are not indicated in the treatment of impetigo.
#28
https://pmc.ncbi.nlm.nih.gov/articles/PMC4008061/
Impetigo is a common cutaneous infection that is especially prevalent in children. Historically, impetigo is caused by either group A -hemolytic streptococci or Staphylococcus aureus. Currently, the most frequently isolated pathogen is S. aureus. […] Host factors, such as integrity of the skin barrier with its acidic pH, presence of sebaceous secretion (fatty acids, particularly oleic acid), lysozyme and production of defensins and adequate nutritional status, play an important role in resistance to infection. […] A crucial factor to the infection virulence is the ability of these bacteria to produce circulating toxins that act as superantigens. Superantigens are able to skip certain steps of the immune response and promote massive activation of T lymphocytes and also the production of various lymphokines such as interleukin 1 and 6 and tumor necrosis factor alpha. This response may lead to the formation of exfoliative cutaneous eruption, vomiting, hypotension and shock.
#29 SciELO Brazil – Impetigo – review Impetigo – review
https://www.scielo.br/j/abd/a/cpm9SxPg4rwGjq7Qf679Ffq/?lang=en
Impetigo is a common cutaneous infection that is especially prevalent in children. Historically, impetigo is caused by either group A -hemolytic streptococci or Staphylococcus aureus. Currently, the most frequently isolated pathogen is S. aureus. This article discusses the microbiologic and virulence factors of group A -hemolytic streptococci and Staphylococcus aureus, clinical characteristics, complications, as well as the approach to diagnosis and management of impetigo. […] Host factors, such as integrity of the skin barrier with its acidic pH, presence of sebaceous secretion (fatty acids, particularly oleic acid), lysozyme and production of defensins and adequate nutritional status, play an important role in resistance to infection. […] A crucial factor to the infection virulence is the ability of these bacteria to produce circulating toxins that act as superantigens. Superantigens are able to skip certain steps of the immune response and promote massive activation of T lymphocytes and also the production of various lymphokines such as interleukin 1 and 6 and tumor necrosis factor alpha. This response may lead to the formation of exfoliative cutaneous eruption, vomiting, hypotension and shock.
#30 Impetigo: Practice Essentials, Background, Pathophysiology
https://emedicine.medscape.com/article/965254-overview
After initial infection, new lesions may be seen in areas with no apparent break in the skin. […] Bullous impetigo is commonly due to exfoliative toxins of S aureus termed exfoliatins A and B. […] These exotoxins cause a loss of cell adhesion in the superficial dermis, which, in turn, causes blisters and skin sloughing by cleaving of the granular cell layer of the epidermis. […] One of the target proteins for exotoxin A is desmoglein I, which maintains cell adhesion. […] Unlike nonbullous impetigo, the lesions of bullous impetigo occur on intact skin. […] Most strains of community-acquired MRSA contain Panton-Valentine leucocidin (P-VL), a highly virulent, pore-forming exotoxin that causes dermal necrosis and has cytolytic activity against neutrophils and monocytes. […] Destruction of leukocytes by P-VL is one of the reasons that MRSA is more likely to produce clinical infection.
#31 Impetigo – Symptoms & causes – Mayo Clinic
https://www.mayoclinic.org/diseases-conditions/impetigo/symptoms-causes/syc-20352352
Impetigo is caused by bacteria, usually staphylococci organisms. […] You might be exposed to the bacteria that cause impetigo when you come into contact with the sores of someone who’s infected or with items they’ve touched such as clothing, bed linen, towels and even toys. […] The bacteria that cause impetigo often enter the skin through a small cut, insect bite or rash.
#32 Impetigo | NHS inform
https://www.nhsinform.scot/illnesses-and-conditions/infections-and-poisoning/impetigo/
Impetigo occurs when the skin becomes infected with bacteria, usually either Staphylococcus aureus or Streptococcus pyogenes. […] The bacteria can infect the skin in 2 main ways: through a break in otherwise healthy skin such as a cut, insect bite or other injury this is known as primary impetigo […] through skin damaged by another underlying skin condition, such as head lice, scabies or eczema this is known as secondary impetigo. […] The bacteria can be spread easily through close contact with someone who has the infection, such as through direct physical contact, or by sharing towels or flannels. […] As the condition doesn’t cause any symptoms until 4 to 10 days after initial exposure to the bacteria, it’s often easily spread to others unintentionally. […] Impetigo stops being infectious after 48 hours of treatment starting or after the sores have stopped blistering or crusting.
#33 Impetigo | NHS inform
https://www.nhsinform.scot/illnesses-and-conditions/infections-and-poisoning/impetigo/
Impetigo occurs when the skin becomes infected with bacteria, usually either Staphylococcus aureus or Streptococcus pyogenes. […] The bacteria can infect the skin in 2 main ways: through a break in otherwise healthy skin such as a cut, insect bite or other injury this is known as primary impetigo […] through skin damaged by another underlying skin condition, such as head lice, scabies or eczema this is known as secondary impetigo. […] The bacteria can be spread easily through close contact with someone who has the infection, such as through direct physical contact, or by sharing towels or flannels. […] As the condition doesn’t cause any symptoms until 4 to 10 days after initial exposure to the bacteria, it’s often easily spread to others unintentionally. […] Impetigo stops being infectious after 48 hours of treatment starting or after the sores have stopped blistering or crusting.
#34 Impetigo – StatPearls – NCBI Bookshelf
https://www.ncbi.nlm.nih.gov/books/NBK430974/
Impetigo can be classified as either primary or secondary. Primary impetigo involves previously normal skin affected by direct bacterial invasion. Secondary impetigo involves infection forming at a previous skin wound site. […] Any disturbance of the skin barrier leads to access to fibronectin receptors by GABHS and S aureus which require fibronectin for colonization. Trauma, cuts, insect bites, surgery, atopic dermatitis, burns, and varicella are common mechanisms of skin breakdown. Once a lesion is present, self-inoculation to other sites is very common. Malnutrition, immunosuppression, daycare attendance, overcrowding, diabetes, and poor hygiene make one more susceptible to impetigo. […] Triggers that breakdown skin and increase susceptibility to impetigo include: Varicella, Herpes, Scratching, Lice, Burns, Trauma, Insect bites.
#35 Impetigo: Practice Essentials, Background, Pathophysiology
https://emedicine.medscape.com/article/965254-overview
Impetigo is an acute, highly contagious gram-positive bacterial infection of the superficial layers of the epidermis. […] These bacteria can be introduced from the environment and only transiently colonize the cutaneous surface. […] The teichoic acid adhesions for GABHS and S aureus require the epithelial cell receptor component, fibronectin, for colonization. […] Factors that can modify the usual skin flora and facilitate transient colonization by GABHS and S aureus include high temperature or humidity, preexisting cutaneous disease, young age, or recent antibiotic treatment. […] Common mechanisms for disruption of skin that can facilitate bacterial colonization or infection include the following: Scratching, Atopic dermatitis, Dermatophytosis, Varicella, Herpes simplex, Scabies, Pediculosis, Thermal burns, Surgery, Trauma, Radiation therapy, Insect bites.
#36 Impetigo: Diagnosis and Treatment | AAFP
https://www.aafp.org/pubs/afp/issues/2014/0815/p229.html
Impetigo is the most common bacterial skin infection in children two to five years of age. There are two principal types: nonbullous (70% of cases) and bullous (30% of cases). Nonbullous impetigo, or impetigo contagiosa, is caused by Staphylococcus aureus or Streptococcus pyogenes, and is characterized by honey-colored crusts on the face and extremities. Impetigo primarily affects the skin or secondarily infects insect bites, eczema, or herpetic lesions. Bullous impetigo, which is caused exclusively by S. aureus, results in large, flaccid bullae and is more likely to affect intertriginous areas. […] Impetigo is a common bacterial skin infection caused by Staphylococcus aureus, group A beta-hemolytic Streptococcus pyogenes, a combination of the two, or less commonly, anaerobic bacteria. […] Other factors that predispose to impetigo are skin trauma; hot, humid climates; poor hygiene; day care settings; crowding; malnutrition; and diabetes mellitus or other medical comorbidities.
#37 The microbiology of impetigo in Indigenous children: associations between Streptococcus pyogenes, Staphylococcus aureus,scabies, and nasal carriage | BMC Infectious Diseases | Full Text
https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-014-0727-5
Impetigo is caused by both Streptococcus pyogenes and Staphylococcus aureus; the relative contributions of each have been reported to fluctuate with time and region. […] However, few studies have utilised high quality microbiological culture methods to confirm this assumption. […] Skin sore swabs taken during episodes with a concurrent diagnosis of scabies were more likely to culture S. pyogenes (OR 2.2, 95% CI 1.1 4.4, p=0.03). […] While clearance of S. pyogenes is the key determinant of treatment efficacy, co-infection with S. aureus warrants consideration of treatment options that are effective against both pathogens where impetigo is severe and prevalent. […] Impetigo is strongly associated with scabies infestation in tropical environments, but the influence of scabies on the microbiology of impetigo has not previously been described.
#38 The microbiology of impetigo in Indigenous children: associations between Streptococcus pyogenes, Staphylococcus aureus,scabies, and nasal carriage | BMC Infectious Diseases | Full Text
https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-014-0727-5
The stronger association of S. pyogenes (than S. aureus) with scabies presence concurs with earlier work that linked scabies outbreaks with subsequent epidemics of post-streptococcal glomerulonephritis. […] We also found no positive correlation between nasal carriage of S. aureus and recovery of S. aureus from impetigo lesions, and no association between the severity of impetigo and recovery of either S. pyogenes, S. aureus or both. […] We thus provide robust evidence to refute earlier observational data in patients with impetigo where the association of co-infection with a more severe phenotype was suspected but not confirmed. […] Our findings are in keeping with those reported from Fiji and confirm that impetigo in tropical contexts continues to be driven by S. pyogenes. […] However, we have demonstrated that co-infection with both S. pyogenes and S. aureus is likely. […] We have also concluded that in the context of impetigo, there is no association between nasal colonisation and skin infection with S. aureus.
#39 The microbiology of impetigo in Indigenous children: associations between Streptococcus pyogenes, Staphylococcus aureus,scabies, and nasal carriage | BMC Infectious Diseases | Full Text
https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-014-0727-5
The stronger association of S. pyogenes (than S. aureus) with scabies presence concurs with earlier work that linked scabies outbreaks with subsequent epidemics of post-streptococcal glomerulonephritis. […] We also found no positive correlation between nasal carriage of S. aureus and recovery of S. aureus from impetigo lesions, and no association between the severity of impetigo and recovery of either S. pyogenes, S. aureus or both. […] We thus provide robust evidence to refute earlier observational data in patients with impetigo where the association of co-infection with a more severe phenotype was suspected but not confirmed. […] Our findings are in keeping with those reported from Fiji and confirm that impetigo in tropical contexts continues to be driven by S. pyogenes. […] However, we have demonstrated that co-infection with both S. pyogenes and S. aureus is likely. […] We have also concluded that in the context of impetigo, there is no association between nasal colonisation and skin infection with S. aureus.
#40 Impetigo, Contagious Skin Infection: Causes, Treatment & Prevention
https://my.clevelandclinic.org/health/diseases/15134-impetigo
Complications are rare. Certain strains of strep bacteria that cause impetigo can also cause glomerulonephritis. This inflammatory kidney disease can produce high blood pressure and blood in your pee (hematuria). Other complications of impetigo may include: The rash spreading to deeper skin layers. […] Impetigo treatment includes antibiotics. A provider may prescribe topical antibiotics to put directly on your childs skin. Impetigo treatments may also include an oral antibiotic (a liquid or pill taken by mouth) if the impetigo covers a large area of your childs skin or multiple body parts. […] With treatment, your child usually isnt contagious after 48 hours. The sores may take some time to heal completely, but the infection rarely leaves scars.
#41 Impetigo: Types, Symptoms, Causes, Diagnosis, Treatment and More
https://www.health.com/impetigo-overview-7494686
A third type of impetigo, called ecthyma, may develop if impetigo is left untreated. This type of impetigo involves deep layers of the skin and causes painful, ulcer-like sores surrounded by red, inflamed skin. These lesions can leave scars on your skin. Ecthyma typically develops on the ankles, buttocks, feet, and legs. […] The gold standard for impetigo treatment is topical or oral antibiotics. The treatment you receive will depend on the severity of your infection. […] Common diagnostic tests for impetigo include: Skin swab: A fluid sample from the blister or sore is collected and sent to the lab to identify the type of bacteria causing the infection. […] Impetigo is highly contagious and spreads easily to other people and body parts. Preventing impetigo involves practicing good hygiene and avoiding skin-to-skin contact with others with the infection. […] Most cases of impetigo heal without scarring and complications. However, untreated impetigo can lead to complications, such as: Post-streptococcal glomerulonephritis (PGSN): Streptococcus, a type of bacteria that can cause impetigo, can sometimes lead to complications as your body fights impetigo.
#42 Clinical Guidance for Group A Streptococcal Impetigo | Group A Strep | CDC
https://www.cdc.gov/group-a-strep/hcp/clinical-guidance/impetigo.html
Impetigo (also called pyoderma) is a superficial bacterial skin infection caused by either S. pyogenes or S. aureus. This page focuses solely on infections caused by S. pyogenes, which are also called group A Streptococcus (group A strep bacteria). […] Antibiotic treatment should target both group A strep and S. aureus. […] PSGN is thought to be the result of an immune response that is triggered by the group A strep infection. […] However, new evidence suggests that acute rheumatic fever can occur as a complication after group A strep skin infections, including impetigo.
#43 Intolerable Burden of Impetigo in Endemic Settings: A Review of the Current State of Play and Future Directions for Alternative Treatments
https://www.mdpi.com/2079-6382/9/12/909
The clinical appearances of impetigo forms may be dependent on the type of disease causing bacteria or aetiologic agent; however, the histopathology of both forms appear to be similar and mainly characterised by the formation of intraepidermal pustules. […] In impetigo elicited by S. aureus, local and systemic spread of infection could result in cellulitis, lymphangitis, or septicaemia. […] The annual incidence of invasive S. aureus is 10 times higher in the Indigenous paediatric population compared with the non-Indigenous counterparts living in impetigo endemic settings. […] The ARF occurs after a latency period of 2â3 weeks post streptococcal infection. […] Given the S. aureus and GAS species tendency to quickly develop resistance to drugs, they are likely to limit the potency of the current treatments, clearly showing the urgent need for new and effective impetigo treatments options. […] Given the enormous burden of impetigo in Australian aboriginal children, this review aims to explore the potential of promising alternative selections for impetigo treatment.
#44 JMIR Dermatology – From the Cochrane Library: Interventions for Impetigo
https://derma.jmir.org/2021/2/e33433
Impetigo is a contagious, superficial skin infection, most commonly affecting children, caused by Staphylococcus aureus, group A beta-hemolytic streptococcus (Streptococcus pyogenes), or both pathogens in combination. Bacteria infect the epidermis, leading to itchy or painful, yellow-crusted, erythematous plaques. If blisters are present, the infection is referred to as bullous impetigo. […] While untreated impetigo is often self-limited, treatment is important for symptom control, limiting the spread of infection and minimizing the risk of developing life-threatening complications. Due to the prevalence and risks associated with impetigo, evidence-based research to inform treatment guidelines is critical to decreasing its disease burden. […] Topical antibiotics (mupirocin, retapamulin, fusidic acid) were found to be more effective than the placebo and preferable to oral antibiotics for limited impetigo. Topical antibiotics were also superior to disinfection methods.
#45 JMIR Dermatology – From the Cochrane Library: Interventions for Impetigo
https://derma.jmir.org/2021/2/e33433/
Impetigo is a contagious, superficial skin infection, most commonly affecting children, caused by Staphylococcus aureus, group A beta-hemolytic streptococcus (Streptococcus pyogenes), or both pathogens in combination. Bacteria infect the epidermis, leading to itchy or painful, yellow-crusted, erythematous plaques. If blisters are present, the infection is referred to as bullous impetigo. While untreated impetigo is often self-limited, treatment is important for symptom control, limiting the spread of infection and minimizing the risk of developing life-threatening complications. Due to the prevalence and risks associated with impetigo, evidence-based research to inform treatment guidelines is critical to decreasing its disease burden. […] Current treatment options for impetigo, summarized in Table 1, include topical and systemic antibiotics, as well as topical disinfectants. A 2012 Cochrane review, Interventions for Impetigo, assessed 68 randomized controlled trials (26 oral treatments and 24 topical treatments for the management of primary impetigo). Specifically, various management strategies were evaluated: watchful waiting, topical disinfectants (saline, hexachlorophene, povidone-iodine, chlorhexidine), topical antibiotics (neomycin, bacitracin, polymyxin B, gentamycin, fusidic acid, mupirocin, retapamulin, topical steroid/antibiotic combination), and systemic antibiotics (penicillin, [flu]cloxacillin, amoxicillin/clavulanic acid, erythromycin, cephalexin). Primary outcome measures included an assessment of clearance of crusts, blisters, and redness, as well as resolution of associated symptoms.
#46
https://pmc.ncbi.nlm.nih.gov/articles/PMC4008061/
S. aureus produces exfoliative toxins, which are proteases that selectively hydrolyze one of the intracellular adhesion molecules, desmoglein-1, present in the desmosomes of keratinocytes located in the epidermic granular layer. Toxins are the greatest virulence factor of S. aureus, causing dissociation of epidermal cells with blister formation. […] Bullous impetigo is almost universally caused by a single organism, S. aureus, mainly belonging to group II (80%); phage type 71 (60% of cases). […] The presence of MRSA as impetigo’s causative agent in non-hospitalized patients is considered unusual and with heterogeneous distribution. Staphylococcal impetigo is usually caused by S. aureus strains that possess the exfoliative toxin gene. […] The spectrum of the selected antibiotic must cover staphylococci and streptococci, both for bullous impetigo as well as for crusted impetigo. Thus, benzathine penicillin or those sensitive to penicillinases are not indicated in the treatment of impetigo.
#47 Intolerable Burden of Impetigo in Endemic Settings: A Review of the Current State of Play and Future Directions for Alternative Treatments
https://www.mdpi.com/2079-6382/9/12/909
The clinical appearances of impetigo forms may be dependent on the type of disease causing bacteria or aetiologic agent; however, the histopathology of both forms appear to be similar and mainly characterised by the formation of intraepidermal pustules. […] In impetigo elicited by S. aureus, local and systemic spread of infection could result in cellulitis, lymphangitis, or septicaemia. […] The annual incidence of invasive S. aureus is 10 times higher in the Indigenous paediatric population compared with the non-Indigenous counterparts living in impetigo endemic settings. […] The ARF occurs after a latency period of 2â3 weeks post streptococcal infection. […] Given the S. aureus and GAS species tendency to quickly develop resistance to drugs, they are likely to limit the potency of the current treatments, clearly showing the urgent need for new and effective impetigo treatments options. […] Given the enormous burden of impetigo in Australian aboriginal children, this review aims to explore the potential of promising alternative selections for impetigo treatment.
#48 Impetigo: Diagnosis and Treatment | AAFP
https://www.aafp.org/pubs/afp/issues/2014/0815/p229.html
The incidence of MRSA-related skin and soft tissue infections was increasing, but more recent studies show it may be declining. […] If MRSA infection is suspected, initial treatment with trimethoprim/sulfamethoxazole, clindamycin, or a tetracycline (doxycycline or minocycline) is recommended pending culture results.
#49
https://pmc.ncbi.nlm.nih.gov/articles/PMC4008061/
Mupirocin acts by inhibiting bacterial protein synthesis, by binding with isoleucyl-tRNA synthetase enzyme, thus preventing the incorporation of isoleucine into protein chains. It is highly effective against Staphylococcus aureus, Streptococcus pyogenes and all other species of streptococci except those of group D.
#50 Impetigo: Diagnosis and Treatment | AAFP
https://www.aafp.org/pubs/afp/issues/2014/0815/p229.html
The highly contagious nature of impetigo also allows spread from patients to close contacts. […] Bullous impetigo is caused only by S. aureus and is characterized by large, fragile, flaccid bullae that can rupture and ooze yellow fluid. These larger bullae form because of exfoliative toxins produced by S. aureus strains that cause loss of cell adhesion in the superficial epidermis. […] The number of possible causes, incidence, and clinical severity of acute poststreptococcal glomerulonephritis have decreased, because the causative organism of impetigo has shifted from S. pyogenes to S. aureus. […] The ideal treatment should be effective, be inexpensive, have limited adverse effects, and should not promote bacterial resistance. […] Retapamulin is a novel pleuromutilin antibacterial and the first new topical antibacterial in nearly 20 years.