Ropień skóry – Patofizjologia i mechanizm

Ropień skóry
Patofizjologia i mechanizm

Ropień skóry to zlokalizowane zbiorowisko ropy powstające w odpowiedzi na zakażenie bakteryjne, głównie przez Staphylococcus aureus, który odpowiada za około 75% przypadków. Szczepy metycylinooporne (MRSA) stanowią rosnące zagrożenie kliniczne. Patogeneza ropnia obejmuje naruszenie bariery skórnej, aktywację układu odpornościowego, migrację neutrofili i formowanie ropy oraz kapsuły włóknikowej. Neutrofile odgrywają kluczową rolę, uwalniając peptydy przeciwdrobnoustrojowe, reaktywne formy tlenu i azotu oraz proteazy. S. aureus produkuje liczne czynniki wirulencji, takie jak alfa-hemolizyna, leukocydyna Panton-Valentine (PVL) i modulin rozpuszczalny w fenolu (PSM), które uszkadzają tkanki i modulują odpowiedź immunologiczną. Czynniki koagulujące (koagulaza, białko wiążące czynnik von Willebranda, ClfA) uczestniczą w tworzeniu kapsuły włóknikowej, co sprzyja utrzymaniu ropnia i ochronie bakterii przed układem odpornościowym.

Patogeneza ropnia skóry

Ropień skóry to zlokalizowane zbiorowisko ropy, które powstaje jako odpowiedź organizmu na zakażenie bakteryjne lub obecność ciała obcego w skórze. Stanowi mechanizm obronny organizmu, którego celem jest ograniczenie i ostateczne wyeliminowanie patogenu, zapobiegając rozprzestrzenianiu się infekcji do sąsiednich zdrowych tkanek¹². Proces ten jednak, mimo swojej funkcji ochronnej, przyczynia się do zniszczenia tkanek i powstawania charakterystycznych objawów klinicznych ropnia.

Czynniki etiologiczne

Staphylococcus aureus jest głównym patogenem odpowiedzialnym za powstawanie ropni skórnych, występującym w około 75% przypadków³⁴. Coraz częściej identyfikowane są szczepy metycylinooporne S. aureus (MRSA), szczególnie w Stanach Zjednoczonych i innych częściach świata⁵. Inne bakterie wywołujące ropnie skórne obejmują paciorkowce beta-hemolizujące (w tym Streptococcus pyogenes), które w niektórych badaniach były odpowiedzialne za prawie trzy czwarte przypadków rozlanego zapalenia tkanki łącznej⁶.

W przypadku ropni umiejscowionych w okolicach krocza (pachwinowych, pośladkowych, okołoodbytniczych i sromowo-pochwowych) często identyfikuje się liczne beztlenowe bakterie jelitowe, szczególnie Bacteroides⁷. W ropniach okolic okołoodbytniczych dominuje mieszana flora beztlenowa i tlenowa jelit oraz skóry okolicy odbytu, w tym S. aureus, S. pyogenes, Bacteroides, Peptococcus, Peptostreptococcus, Porphyromonas, Fusobacterium, Clostridium, Escherichia coli, Pseudomonas aeruginosa, Klebsiella, Proteus i enterokoki⁸.

Mechanizm powstawania ropnia

Proces powstawania ropnia skóry rozpoczyna się od naruszenia bariery ochronnej skóry, co umożliwia wniknięcie bakterii⁹¹⁰. Bakterie mogą przedostać się przez:

Przerwanie ciągłości skóry (skaleczenia, zadrapania, rany kłute)
Mieszki włosowe lub gruczoły skórne
Miejsca po iniekcjach
Rany operacyjne
Ugryzienia zwierząt lub owadów

¹¹¹²

Po przeniknięciu bakterii do skóry, układ odpornościowy gospodarza aktywuje się w celu zwalczenia infekcji¹³. Proces ten przebiega następująco:

Rozpoznanie patogenu – Wzorce molekularne związane z patogenami (MAMPs) bakterii są rozpoznawane przez receptory rozpoznające wzorce (PRRs), co prowadzi do aktywacji układu obronnego gospodarza¹⁴.
Aktywacja odpowiedzi zapalnej – Uwolnienie cytokin prozapalnych powoduje miejscową reakcję immunologiczną i rekrutację fagocytów do miejsca zakażenia¹⁵¹⁶.
Migracja neutrofili – Leukocyty wielojądrzaste (neutrofile) przechodzą przez ściany naczyń krwionośnych do obszaru zakażenia i gromadzą się w uszkodzonej tkance. Stanowią one główny komórkowy mechanizm obronny przeciwko zakażeniom S. aureus i są głównym składnikiem ropni¹⁷¹⁸.
Formowanie się ropy – W trakcie tego procesu tworzy się ropa, która jest mieszaniną żywych i martwych krwinek białych, obumarłej tkanki, bakterii i innych substancji obcych¹⁹.
Tworzenie kapsuły – Sąsiadujące zdrowe komórki formują ścianę lub kapsułę ropnia w celu utrzymania ropy i zapobieżenia infekcji sąsiednich struktur²⁰.

Rola neutrofili w powstawaniu ropnia

Neutrofile odgrywają kluczową rolę zarówno w tworzeniu, jak i rozwiązywaniu ropni²¹. Po przybyciu do miejsca zakażenia, uwalniają szereg substancji przeciwdrobnoustrojowych, w tym:

Peptydy przeciwdrobnoustrojowe
Reaktywne formy tlenu (ROS)
Reaktywne formy azotu
Proteazy
Lizozym

²²

W centrum ropnia znajduje się ostry wysięk zapalny składający się z wielu żywych i martwych neutrofili, pozostałości tkanek, włóknika i żywych bakterii²³. Gromadzenie się i utrzymywanie neutrofili, a następnie nekrotyczne rozpuszczanie komórek, przyczyniają się do ogólnej patologii zakażeń skóry i tkanek miękkich wywołanych przez S. aureus²⁴.

W miarę powiększania się ropnia, może on uciskać zewnętrzne naczynia krwionośne, powodując zakrzepicę i martwicę na swojej drodze²⁵. Jeśli ropień nie zostanie zdrenowany przez interwencję chirurgiczną lub nie przedostanie się wzdłuż płaszczyzn tkankowych, makrofagi zaczynają zastępować neutrofile jako dominująca populacja komórek w obrębie błony ropnej²⁶.

Czynniki wirulencji S. aureus w patogenezie ropnia

S. aureus wytwarza liczne czynniki wirulencji, które odgrywają istotną rolę na każdym poziomie interakcji gospodarz-patogen, w tym cząsteczki umożliwiające unikanie układu odpornościowego gospodarza²⁷. Te czynniki wirulencji można podzielić na kilka kategorii według ich funkcji.

Toksyny cytolityczne

S. aureus wytwarza szereg toksyn, które przyczyniają się do uszkodzenia tkanek i formowania ropni:

Alfa-hemolizyna (Hla) – Zdolność Hla do powodowania cytolizy komórek gospodarza (i tym samym destabilizacji skóry właściwej) oraz wywoływania rekrutacji neutrofili prawdopodobnie odgrywa kluczową rolę w patogenezie zakażeń skóry i tkanek miękkich²⁸.
Leukocydyna Panton-Valentine (PVL) – Początkowo uważano, że zwiększona wirulencja CA-MRSA opiera się głównie na zdolności bakterii do unikania zabijania przez fagocyty dzięki PVL, toksynie tworzącej pory zabijające komórki odpornościowe²⁹. PVL jest produkowana przez prawie wszystkie szczepy CA-MRSA, co wyjaśnia przewagę ropnych zakażeń skóry jako klinicznych manifestacji zakażeń CA-MRSA³⁰.
Moduliny rozpuszczalne w fenolu (PSM) – W mysim modelu zakażenia skórnego S. aureus wykazano, że już 4 godziny po infekcji napływ neutrofili był całkowicie zależny od rodziny bakteryjnych toksyn S. aureus zwanych modulinami rozpuszczalnymi w fenolu³¹.

Koagulazy i czynniki związane z krzepnięciem

S. aureus produkuje czynniki, które przyczyniają się do formowania kapsuły włóknikowej otaczającej ropień:

Koagulaza (Coa) i białko wiążące czynnik von Willebranda (vWbp) – Te białka powodują krzepnięcie osocza poprzez aktywację protrombiny i konwersję fibrynogenu do fibryny³². Znaczenie Coa i vWbp w tworzeniu ropni S. aureus najlepiej ilustrują ostatnie badania nad szczepionkami, w których aktywna i bierna immunizacja przeciwciałami przeciwko Coa i vWbp znacząco zmniejszyła liczbę zmian w mysim modelu ropnia nerki³³.
Czynnik zlepiający A (ClfA) – ClfA jest białkiem powierzchniowym, które przyczynia się do tworzenia ropni w modelach zakażenia skóry i tkanek miękkich³⁴³⁵.

Badania na królikach wykazały, że wszystkie trzy czynniki (Coa, vWbp i ClfA) przyczyniają się do tworzenia ropni S. aureus w doświadczalnym modelu zakażenia³⁶. Osadzanie fibryny jest procesem krytycznym dla tworzenia ropnia i przyczynia się do obrony gospodarza przed inwazyjnym S. aureus³⁷.

Lipoproteiny i kwas tejchojowy ściany komórkowej

Lipoproteiny (Lpp) S. aureus, mimo że są głównym czynnikiem bakteryjnym alarmującym układ odpornościowy człowieka, odgrywają słabo poznaną rolę w zakażeniach skóry. Badania wykazały, że:

Lpp indukują zapalenie skóry i promują tworzenie ropni, co chroni bakterie przed zabijaniem przez układ odpornościowy³⁸.
Podskórne wstrzyknięcie oczyszczonych Lpp S. aureus wywołało zapalenie skóry za pośrednictwem TLR2 z szybkim napływem leukocytów do tkanki skórnej, co prowadziło do zaburzenia lokalnej hemostazy w kierunku stanu prozakrzepowego³⁹.
Ekspresja Lpp w S. aureus zwiększyła ciężkość zakażeń skóry i obciążenie bakteryjne w lokalnych tkankach⁴⁰.

Również polimer cukrowy ściany komórkowej – kwas tejchojowy ściany (WTA) – odgrywa rolę w rozwoju zakażeń skóry. Wykazano, że:

Zwitterjonowy WTA indukuje proliferację limfocytów T CD4+ w sposób zależny od MHCII, co z kolei moduluje tworzenie ropni w mysim modelu zakażenia skóry⁴¹.
Szczepy CA-MRSA mogą zmieniać swoją zewnętrzną otoczkę komórkową, wprowadzając zwiększone ilości długołańcuchowego polimeru cukrowego (WTA), co powoduje zmianę reakcji immunologicznej w przypadku zakażeń skóry i zwiększa zdolność tych agresywnych bakterii do wywoływania szczególnie ciężkich zakażeń skóry⁴².

Mechanizmy unikania układu odpornościowego przez S. aureus

S. aureus rozwija różne strategie, aby przetrwać w organizmie gospodarza i uniknąć eliminacji przez układ odpornościowy:

Unikanie opsonofagocytozy

W środowisku pozakomórkowym S. aureus musi przezwyciężyć opsonizację przez dopełniacz i przeciwciała, które bezpośrednio lub pośrednio prowadzą do zabicia S. aureus lub pochłonięcia przez fagocyty poprzez receptory Fc lub receptory dopełniacza. S. aureus unika opsonofagocytozy poprzez ekspresję na swojej powierzchni⁴³:

Otoczki
Czynnika zlepiającego A
Białka A
Inhibitorów dopełniacza

Te czynniki inaktywują lub zapobiegają wiązaniu się opsonin gospodarza do bakterii lub ukierunkowują ją na zniszczenie.

Obrona przed reaktywnymi formami tlenu

Obrona przed ROS w S. aureus jest zapośredniczona przez rozmieszczenie dużej liczby enzymów przeciwutleniających, które neutralizują ROS i reaktywne formy azotu⁴⁴.

Hamowanie rekrutacji i funkcji neutrofili

Jako środek zapobiegawczy, S. aureus przeciwdziała, wydzielając specyficzne toksyny, które lizują neutrofile⁴⁵. S. aureus wyraża dużą liczbę toksyn dwuskładnikowych, z których wiele wykazuje specyficzność dla komórek ludzkich, ale nie mysich; dlatego wiele z ich funkcji nie zostało scharakteryzowanych⁴⁶.

Tworzenie biofilmu

Tworzenie biofilmu to kolejny mechanizm wirulencji o znaczeniu klinicznym, który pozwala S. aureus przetrwać na tworzywach sztucznych i opierać się obronie gospodarza lub antybiotykom⁴⁷. Tworzenie biofilmu rozpoczyna się od przyłączenia bakterii do powierzchni, wytworzenia macierzy pozakomórkowej i rozpadnięcia biofilmu w celu rozprzestrzenienia się do innych miejsc⁴⁸.

Czynniki ryzyka rozwoju ropnia skóry

Istnieje szereg czynników, które zwiększają ryzyko rozwoju ropni skórnych:

Czynniki związane ze skórą

Naruszenie bariery skórnej – skaleczenia, otarcia, ukłucia, ugryzienia zwierząt/owadów⁴⁹
Grzybica międzypalcowa stóp⁵⁰
Skóra wysuszona lub uszkodzona przez przewlekłe choroby skóry⁵¹
Nadmierna suchość skóry prowadząca do nierównowagi w powierzchniowym ekosystemie⁵²
Wysoka wilgotność i temperatura sprzyjające zwiększeniu obciążenia bakteryjnego na skórze⁵³

Czynniki związane z gospodarzem

Obrzęk tkanek⁵⁴
Niewydolność żylna⁵⁵
Immunosupresja – wszystkie stany immunodepresji, czy to wrodzone, nabyte czy jatrogenne, sprzyjają infekcjom skórnym⁵⁶⁵⁷
Otyłość⁵⁸
Cukrzyca⁵⁹
Nosicielstwo S. aureus lub kolonizacja MRSA⁶⁰

Czynniki środowiskowe

Narażenie zawodowe lub przemysłowe na czynniki prowokujące⁶¹
Suboptymalna higiena (np. dzielenie się zanieczyszczonymi przedmiotami higienicznymi, takimi jak maszynki do golenia)⁶²
Gorący i wilgotny klimat⁶³

Implikacje kliniczne i terapeutyczne

Zrozumienie patogenezy ropni skórnych ma kluczowe znaczenie dla opracowania skutecznych strategii terapeutycznych:

Aktualny stan terapii

Głównym postępowaniem w leczeniu ropni skórnych jest nacięcie i drenaż⁶⁴. Antybiotyki nie są rutynowo stosowane, ale są wskazane jako terapia uzupełniająca, jeśli ropień jest głęboki, ropnie są mnogie, występuje znaczące zapalenie tkanki łącznej wokół ropnia lub gdy jego wielkość przekracza 2 cm⁶⁵.

Antybiotyki skierowane przeciwko S. aureus, oprócz nacięcia i drenażu, powinny być podawane, jeśli istnieją dowody na ogólnoustrojowy zespół zapalny⁶⁶. Ze względu na rosnącą częstość występowania MRSA, antybiotyki, gdy są stosowane, powinny być skuteczne przeciwko MRSA, w oczekiwaniu na wyniki posiewu i antybiogramu⁶⁷.

Nowe podejścia terapeutyczne

Naukowcy opracowują nowe strategie walki z zakażeniami S. aureus, w tym:

Szczepionki – Ostatnie odkrycia podkreśliły, że limfocyty T produkujące interleukinę-17 odgrywają szczególnie ważną rolę w odpowiedzi immunologicznej na zakażenie skóry S. aureus, sugerując, że strategie szczepionek specjalnie ukierunkowane na te typy limfocytów T mogą być korzystne w leczeniu zakażeń skóry i tkanek miękkich wywołanych przez S. aureus⁶⁸.
Strategie anty-wirulencyjne – Odkrycie mechanizmów molekularnych leżących u podstaw modyfikacji osłony komórkowej S. aureus otwiera możliwość celowego zapobiegania procesowi modyfikacji w poważnych zakażeniach skóry wywołanych przez szczepy CA-MRSA. Takie podejście terapeutyczne dałoby ludzkiemu układowi odpornościowemu szansę na bardziej efektywne zwalczanie infekcji⁶⁹. W przeciwieństwie do klasycznego leczenia antybiotykami, strategia anty-wirulencyjna powinna prowadzić do niższych wskaźników oporności, ponieważ komórka bakteryjna nie jest zabijana ani hamowana w swoim wzroście, jest więc poddana mniejszej presji ewolucyjnej⁷⁰.

Zrozumienie roli poszczególnych czynników wirulencji w patogenezie ropni skórnych jest kluczowe dla opracowania skutecznych strategii terapeutycznych. Badania sugerują, że specyficzne odpowiedzi immunologiczne mogą mieć większe znaczenie w różnych miejscach zakażenia, co oznacza, że wymagania dla szczepionki mogą być dostosowane do rodzaju zakażenia, któremu ma zapobiegać⁷¹.

Patogeneza ropnia skóry – kluczowe elementy

Ropień skóry stanowi złożony proces patofizjologiczny, który rozpoczyna się od naruszenia bariery skórnej i wniknięcia bakterii. Głównymi elementami tego procesu są:

Inicjacja – Wniknięcie bakterii (głównie S. aureus) przez naruszenie bariery skórnej.
Rozpoznanie patogenu – Aktywacja układu odpornościowego gospodarza w odpowiedzi na obecność bakterii.
Reakcja zapalna – Rekrutacja neutrofili do miejsca zakażenia i uwalnianie mediatorów zapalnych.
Formowanie ropnia – Tworzenie zbiorowiska ropy składającego się z żywych i martwych neutrofili, bakterii i martwej tkanki.
Kapsułkowanie – Otaczanie ropnia przez włóknistą kapsułę w celu ograniczenia zakażenia.

Na każdym etapie tego procesu S. aureus wykorzystuje różnorodne czynniki wirulencji, które przyczyniają się do uszkodzenia tkanek, rekrutacji neutrofili i tworzenia kapsuły włóknikowej, jednocześnie rozwijając mechanizmy unikania układu odpornościowego gospodarza. Zrozumienie tych mechanizmów otwiera drogę do opracowania nowych strategii terapeutycznych, które mogą uzupełnić lub zastąpić klasyczne leczenie antybiotykami, co jest szczególnie ważne w obliczu rosnącej oporności na antybiotyki wśród szczepów S. aureus.

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Materiały źródłowe

#1 Abscess – Wikipedia
https://en.wikipedia.org/wiki/Abscess
An abscess is a defensive reaction of the tissue to prevent the spread of infectious materials to other parts of the body. […] Organisms or foreign materials destroy the local cells, which results in the release of cytokines. The cytokines trigger an inflammatory response, which draws large numbers of white blood cells to the area and increases the regional blood flow. […] The final structure of the abscess is an abscess wall, or capsule, that is formed by the adjacent healthy cells in an attempt to keep the pus from infecting neighboring structures. However, such encapsulation tends to prevent immune cells from attacking bacteria in the pus, or from reaching the causative organism or foreign object.
#2 Pathogenesis of Staphylococcus aureus Abscesses
https://pmc.ncbi.nlm.nih.gov/articles/PMC4450319/
The pyogenic abscess begins as a localized host acute inflammatory response to bacterial infection. […] As an abscess forms, it acquires several characteristic features. The center of the abscess contains an acute inflammatory exudate composed of many viable and necrotic PMNs, tissue debris, fibrin, and live bacteria. […] Abscess formation is a mechanism used by the host to contain and ultimately eliminate the pathogen. […] Indeed, some SSTIs resolve spontaneously in the absence of treatment. Notably, PMNs play a prominent role in the formation and resolution of abscesses. […] The accumulation and persistence of PMNs, followed by necrotic cell lysis, contribute to the overall pathology of S. aureus SSTIs. […] Staphylococcus aureus produces an array of potential virulence factors that play an important role on every level of host-pathogen interactions, including immune evasion molecules that allow bacteria to circumvent host innate and adaptive immunity.
#3 Bacterial Skin Abscess | IntechOpen
https://www.intechopen.com/chapters/71743
Patients with skin and soft tissue infections may appear with the abscess. […] Risk for developing skin abscess factors includes disruption of the skin barrier, edema, venous insufficiency, and immune suppression. […] The most common microbiologic cause of abscess, a commonly group Streptococcus or Streptococcus pyogenes; Staphylococcus aureus (including methicillin-resistant strains) is a notable but less common cause. […] The most common cause of abscess skin is Staphylococcus aureus (either methicillin or midwife to methicillin. Staphylococcus aureus aureus), occurring in up to 75% of cases; many patients infected with MRSA do not have risk factors. […] The abscess can also be fatal in rare cases, such as when it is in an area where pressure on vital organs such as the trachea in the case of abscess in the neck area.
#4 Abscesses – Infectious Diseases – Merck Manual Professional Edition
https://www.merckmanuals.com/professional/infectious-diseases/biology-of-infectious-disease/abscesses
Numerous organisms can cause abscesses, but the most common is Staphylococcus aureus. […] Organisms may enter the tissue via direct implantation (eg, penetrating trauma with a contaminated object), a surgical site, spread from an established, contiguous infection, dissemination via lymphatic or hematogenous routes from a distant site, or migration from a location where there are resident flora into an adjacent, normally sterile area because natural barriers are disrupted (eg, by perforation of an abdominal viscus causing an intra-abdominal abscess). […] Abscesses may begin in an area of cellulitis or in compromised tissue where leukocytes accumulate. Progressive dissection by pus or necrosis of surrounding cells expands the abscess. Highly vascularized connective tissue may then surround the necrotic tissue, leukocytes, and debris to wall off the abscess and limit further spread.
#5 Bacterial Skin Abscess | IntechOpen
https://www.intechopen.com/chapters/71743
While the main cause is pathogenic bacteria, fungi or parasites, the most common cause is methicillin-resistant Staphylococcus aureus in the United States and other parts of the world. […] The main barrier against microbial invasion is the skin. […] The development of molecular techniques to identify and quantify microorganisms has revolutionized our view of the world Microbial. […] The emergence of new sequencing technologies (such as pyrosequencing) is to increase productivity significantly while reducing the cost of sequencing. […] The secretions of fluid from the abscess and ulcers are the common features of bacterial abscesses. […] The delay is known in the final revision of the soft tissue infections is considered one of the most important risk factor for death. […] The main question that arises from the study is the relationship between the strict response and abscess formation.
#6 Skin and Soft Tissue Infections | AAFP
https://www.aafp.org/pubs/afp/issues/2015/0915/p474.html
Most SSTIs occur de novo, or follow a breach in the protective skin barrier from trauma, surgery, or increased tissue tension secondary to fluid stasis. […] The infection may also originate from an adjacent site or from embolic spread from a distant site. […] S. aureus and streptococci are responsible for most simple community-acquired SSTIs. […] In one prospective study, beta-hemolytic streptococcus was found to cause nearly three-fourths of cases of diffuse cellulitis. […] S. aureus, P. aeruginosa, enterococcus, and Escherichia coli are the predominant organisms isolated from hospitalized patients with SSTIs. […] MRSA infections are characterized by liquefaction of infected tissue and abscess formation; the resulting increase in tissue tension causes ischemia and overlying skin necrosis.
#7 A guide to abscesses in the skin
https://www.contemporarypediatrics.com/view/guide-abscesses-skin
The principal pathogens of abscesses vary with the location of the lesion, however. Most abscesses of the perineal region (inguinal, buttocks, perirectal, and vulvovaginal) contain many anaerobic stool organisms, particularly Bacteroides, although anaerobes occasionally appear to act alone to cause the abscess. […] In general, the causative organism(s) should be identified whenever a neonate or an immunocompromised individual has an abscess. Identificationalso is called for when the abscess is recurrent or recalcitrant to standard therapy, requires surgical treatment, or is unusually severe and associated with complications such as local or systemic extension of infection. […] A furuncle, commonly known as a boil, is a cutaneous abscess that develops around a hair follicle. […] Epidemiology and etiology. These abscesses may or may not be preceded by folliculitis. The most common sites are hair-bearing areas on the face, neck, axillae, buttocks, and groin. Furuncles are almost always caused by S aureus, though other bacteria or fungi occasionally may be culprits.
#8 A guide to abscesses in the skin
https://www.contemporarypediatrics.com/view/guide-abscesses-skin
Hidradenitis suppurativa probably is initiated when the apocrine gland ducts become plugged with keratinous debris. Bacterial infection, particularly with S aureus, Streptococcus milleri, Escherichia coli, and possibly anaerobic streptococci, appears to be important in the progressive dilatation below the obstruction. […] Perirectal abscess appears to be initiated by a break in the mucosal barrier or occlusion of anal crypts. […] The organisms in perirectal abscesses are predominantly mixed anaerobic and aerobic flora of the intestine and skin of the anal verge, including S aureus and S pyogenes as well as Bacteroides, Peptococcus, Peptostreptococcus, Porphyromonas, Fusobacterium, Clostridium, E coli, P aeruginosa, Klebsiella, Proteus, and enterococci. […] An abscess in the breast, or in the scalp, develops exclusively in the neonate, while a rectal abscess also may be found in older infants.
#9 Cutaneous Abscess – Dermatologic Disorders – Merck Manual Professional Edition
https://www.merckmanuals.com/professional/dermatologic-disorders/bacterial-skin-infections/cutaneous-abscess
Bacteria causing cutaneous abscesses are typically indigenous to the skin of the involved area. […] Pathogens reflect flora of the involved area (eg, S. aureus and streptococci in the trunk, axilla, head, and neck). […] Culture abscesses to identify MRSA.
#10 Skin abscess
https://www.nhs.uk/conditions/skin-abscess/
Skin abscesses are usually caused by an infection. […] However, bacteria can sometimes get into your skin, for example through a cut or along a hair follicle. This can cause pus to form, creating an abscess.
#11 Skin and Soft Tissue Infections | AAFP
https://www.aafp.org/pubs/afp/issues/2015/0915/p474.html
Most SSTIs occur de novo, or follow a breach in the protective skin barrier from trauma, surgery, or increased tissue tension secondary to fluid stasis. […] The infection may also originate from an adjacent site or from embolic spread from a distant site. […] S. aureus and streptococci are responsible for most simple community-acquired SSTIs. […] In one prospective study, beta-hemolytic streptococcus was found to cause nearly three-fourths of cases of diffuse cellulitis. […] S. aureus, P. aeruginosa, enterococcus, and Escherichia coli are the predominant organisms isolated from hospitalized patients with SSTIs. […] MRSA infections are characterized by liquefaction of infected tissue and abscess formation; the resulting increase in tissue tension causes ischemia and overlying skin necrosis.
#12 Overview of Bacterial Skin Infections – Skin Disorders – MSD Manual Consumer Version
https://www.msdmanuals.com/home/skin-disorders/bacterial-skin-infections/overview-of-bacterial-skin-infections
Bacterial skin infections develop when bacteria enter through hair follicles or through small breaks in the skin that result from scrapes, punctures, surgery, burns, sunburn, animal or insect bites, wounds, and pre-existing skin disorders. […] Skin that is inflamed or damaged is more likely to become infected. In fact, any break in the skin predisposes a person to infection. […] Abscesses should be cut open by a doctor and allowed to drain, and any dead tissue must be surgically removed.
#13 Abscess: Types, Symptoms, Causes & Treatment
https://my.clevelandclinic.org/health/diseases/22876-abscess
Bacterial infections usually cause abscesses. […] When bacteria enter your body, your immune system sends white blood cells to go fight the infection. This process causes inflammation, and the tissue nearby dies. When this happens, a pocket forms and fills with pus, creating an abscess. […] The outlook for internal abscesses depends on the location and treatment.
#14 Staphylococcus aureus lipoproteins promote abscess formation in mice, shielding bacteria from immune killing | Communications Biology
https://www.nature.com/articles/s42003-021-01947-z
Despite being a major bacterial factor in alerting the human immune system, the role of Staphylococcus aureus (S. aureus) lipoproteins (Lpp) in skin infections remains largely unknown. […] Our data suggest that S. aureus Lpp induce skin inflammation and promote abscess formation that protects bacteria from innate immune killing. This suggests an intriguing bacterial immune evasion mechanism. […] During staphylococcal skin infection, microbe-associated molecular patterns (MAMPs) of S. aureus are recognized by pattern recognition receptors (PRRs), leading to activation of the host defense system. As a result, a local immune reaction with the production of proinflammatory cytokines is initiated and recruitment of phagocytes to the local infection site is induced, thus giving rise to the local formation of skin abscesses or skin necrosis.
#15 Abscess – Wikipedia
https://en.wikipedia.org/wiki/Abscess
An abscess is a defensive reaction of the tissue to prevent the spread of infectious materials to other parts of the body. […] Organisms or foreign materials destroy the local cells, which results in the release of cytokines. The cytokines trigger an inflammatory response, which draws large numbers of white blood cells to the area and increases the regional blood flow. […] The final structure of the abscess is an abscess wall, or capsule, that is formed by the adjacent healthy cells in an attempt to keep the pus from infecting neighboring structures. However, such encapsulation tends to prevent immune cells from attacking bacteria in the pus, or from reaching the causative organism or foreign object.
#16 Molecular Pathogenesis of Staphylococcus aureus Infection | Pediatric Research
https://www.nature.com/articles/pr2009125
Infections occur frequently as a consequence of S. aureus inoculation into an open wound. Alternatively, in the upper airway, viral infection damages mucosal linings and predisposes the host to S. aureus pneumonia, which classically presents a week after onset of influenza infection. […] Initial exposure of S. aureus to host tissues beyond the mucosal surface or skin is thought to trigger up-regulation of virulence genes. For the host, resident phagocytes and epithelial cells in the skin or mucosal tissue respond to either bacterial products or tissue injury by activation of the immune system. S. aureus peptidoglycan and lipoprotein are sensed by host pattern recognition molecules; hyaluronan breakdown products and endogenous toll-like receptor ligands released by necrotic tissues during infection further augment proinflammatory signaling leading to local immune cell activation and neutrophil and macrophage recruitment.
#17 Pathogenesis of Staphylococcus aureus Abscesses
https://pmc.ncbi.nlm.nih.gov/articles/PMC4450319/
Staphylococcus aureus causes many types of human infections and syndromes most notably skin and soft tissue infections. Abscesses are a frequent manifestation of S. aureus skin and soft tissue infections and are formed, in part, to contain the nidus of infection. Polymorphonuclear leukocytes (neutrophils) are the primary cellular host defense against S. aureus infections and a major component of S. aureus abscesses. […] By comparison, S. aureus produces several molecules that also contribute to the formation of abscesses. Such molecules include those that recruit neutrophils, cause host cell lysis, and are involved in the formation of the fibrin capsule surrounding the abscess. […] Herein, we review our current knowledge of the mechanisms and processes underlying the formation of S. aureus abscesses, including the involvement of polymorphonuclear leukocytes, and provide a brief overview of therapeutic approaches.
#18 Abscess: MedlinePlus Medical EncyclopediaLock
https://medlineplus.gov/ency/article/001353.htm
Abscesses occur when an area of tissue becomes infected and the body’s immune system tries to fight and contain it. White blood cells (WBCs) move through the walls of the blood vessels into the area of the infection and collect in the damaged tissue. During this process, pus forms. Pus is the buildup of fluid, living and dead white blood cells, dead tissue, and bacteria or other foreign substances. […] Abscesses may be caused by bacteria, parasites, and foreign substances.
#19 Abscess: MedlinePlus Medical EncyclopediaLock
https://medlineplus.gov/ency/article/001353.htm
Abscesses occur when an area of tissue becomes infected and the body’s immune system tries to fight and contain it. White blood cells (WBCs) move through the walls of the blood vessels into the area of the infection and collect in the damaged tissue. During this process, pus forms. Pus is the buildup of fluid, living and dead white blood cells, dead tissue, and bacteria or other foreign substances. […] Abscesses may be caused by bacteria, parasites, and foreign substances.
#20 Abscess – Wikipedia
https://en.wikipedia.org/wiki/Abscess
An abscess is a defensive reaction of the tissue to prevent the spread of infectious materials to other parts of the body. […] Organisms or foreign materials destroy the local cells, which results in the release of cytokines. The cytokines trigger an inflammatory response, which draws large numbers of white blood cells to the area and increases the regional blood flow. […] The final structure of the abscess is an abscess wall, or capsule, that is formed by the adjacent healthy cells in an attempt to keep the pus from infecting neighboring structures. However, such encapsulation tends to prevent immune cells from attacking bacteria in the pus, or from reaching the causative organism or foreign object.
#21 Pathogenesis of Staphylococcus aureus Abscesses
https://pmc.ncbi.nlm.nih.gov/articles/PMC4450319/
The pyogenic abscess begins as a localized host acute inflammatory response to bacterial infection. […] As an abscess forms, it acquires several characteristic features. The center of the abscess contains an acute inflammatory exudate composed of many viable and necrotic PMNs, tissue debris, fibrin, and live bacteria. […] Abscess formation is a mechanism used by the host to contain and ultimately eliminate the pathogen. […] Indeed, some SSTIs resolve spontaneously in the absence of treatment. Notably, PMNs play a prominent role in the formation and resolution of abscesses. […] The accumulation and persistence of PMNs, followed by necrotic cell lysis, contribute to the overall pathology of S. aureus SSTIs. […] Staphylococcus aureus produces an array of potential virulence factors that play an important role on every level of host-pathogen interactions, including immune evasion molecules that allow bacteria to circumvent host innate and adaptive immunity.
#22 Molecular Pathogenesis of Staphylococcus aureus Infection | Pediatric Research
https://www.nature.com/articles/pr2009125
S. aureus has been generally recognized to survive well both inside and outside of host cells. In the extracellular milieu, S. aureus must overcome opsonization by complement and antibodies, which directly or indirectly leads to killing of S. aureus or uptake by phagocytes through Fc or complement receptors. S. aureus avoids opsonophagocytosis by expressing on its surface a capsule, clumping factor A, protein A, and a number of complement inhibitors, all of which inactivate or prevent host opsonins from binding or targeting the bacterium for destruction. […] Upon arriving at the infection site, neutrophils unleash a battery of antimicrobial substances, including antimicrobial peptides, reactive oxygen species (ROS), reactive nitrogen species, proteases, and lysozyme. Defense against ROS is mediated in S. aureus by deployment of a large number of antioxidant enzymes that neutralize ROS and reactive nitrogen species.
#23 Pathogenesis of Staphylococcus aureus Abscesses
https://pmc.ncbi.nlm.nih.gov/articles/PMC4450319/
The pyogenic abscess begins as a localized host acute inflammatory response to bacterial infection. […] As an abscess forms, it acquires several characteristic features. The center of the abscess contains an acute inflammatory exudate composed of many viable and necrotic PMNs, tissue debris, fibrin, and live bacteria. […] Abscess formation is a mechanism used by the host to contain and ultimately eliminate the pathogen. […] Indeed, some SSTIs resolve spontaneously in the absence of treatment. Notably, PMNs play a prominent role in the formation and resolution of abscesses. […] The accumulation and persistence of PMNs, followed by necrotic cell lysis, contribute to the overall pathology of S. aureus SSTIs. […] Staphylococcus aureus produces an array of potential virulence factors that play an important role on every level of host-pathogen interactions, including immune evasion molecules that allow bacteria to circumvent host innate and adaptive immunity.
#24 Pathogenesis of Staphylococcus aureus Abscesses
https://pmc.ncbi.nlm.nih.gov/articles/PMC4450319/
The pyogenic abscess begins as a localized host acute inflammatory response to bacterial infection. […] As an abscess forms, it acquires several characteristic features. The center of the abscess contains an acute inflammatory exudate composed of many viable and necrotic PMNs, tissue debris, fibrin, and live bacteria. […] Abscess formation is a mechanism used by the host to contain and ultimately eliminate the pathogen. […] Indeed, some SSTIs resolve spontaneously in the absence of treatment. Notably, PMNs play a prominent role in the formation and resolution of abscesses. […] The accumulation and persistence of PMNs, followed by necrotic cell lysis, contribute to the overall pathology of S. aureus SSTIs. […] Staphylococcus aureus produces an array of potential virulence factors that play an important role on every level of host-pathogen interactions, including immune evasion molecules that allow bacteria to circumvent host innate and adaptive immunity.
#25 Pathogenesis â Primary Care Notebook
https://primarycarenotebook.com/pages/dermatology/abscess/pathogenesis
An abscess starts around a bacterial focus. The origin of the infective agent is extremely varied e.g. puncture wounds of the skin, haematogenous spread from a primary infection, perforation of the gastrointestinal tract. […] The inflammatory response is initiated. Neutrophils are attracted to the area by chemotactic products. They are overwhelmed by infection, die, and release proteolytic enzyme products. […] Within the abscess cavity, destruction of cells and proteolysis of the products leads to the production of more chemotactic factors. Consequently, more neutrophils and macrophages ingress into the centre of the abscess where liquefactive necrosis is occurring. […] If the abscess does not drain by surgical intervention or tracking along tissue planes, macrophages begin to replace neutrophils as the dominant population of cells within the pyogenic membrane. […] An increasingly large abscess can press on external blood vessels causing thrombosis and necrosis in its path.
#26 Pathogenesis â Primary Care Notebook
https://primarycarenotebook.com/pages/dermatology/abscess/pathogenesis
An abscess starts around a bacterial focus. The origin of the infective agent is extremely varied e.g. puncture wounds of the skin, haematogenous spread from a primary infection, perforation of the gastrointestinal tract. […] The inflammatory response is initiated. Neutrophils are attracted to the area by chemotactic products. They are overwhelmed by infection, die, and release proteolytic enzyme products. […] Within the abscess cavity, destruction of cells and proteolysis of the products leads to the production of more chemotactic factors. Consequently, more neutrophils and macrophages ingress into the centre of the abscess where liquefactive necrosis is occurring. […] If the abscess does not drain by surgical intervention or tracking along tissue planes, macrophages begin to replace neutrophils as the dominant population of cells within the pyogenic membrane. […] An increasingly large abscess can press on external blood vessels causing thrombosis and necrosis in its path.
#27 Pathogenesis of Staphylococcus aureus Abscesses
https://pmc.ncbi.nlm.nih.gov/articles/PMC4450319/
The pyogenic abscess begins as a localized host acute inflammatory response to bacterial infection. […] As an abscess forms, it acquires several characteristic features. The center of the abscess contains an acute inflammatory exudate composed of many viable and necrotic PMNs, tissue debris, fibrin, and live bacteria. […] Abscess formation is a mechanism used by the host to contain and ultimately eliminate the pathogen. […] Indeed, some SSTIs resolve spontaneously in the absence of treatment. Notably, PMNs play a prominent role in the formation and resolution of abscesses. […] The accumulation and persistence of PMNs, followed by necrotic cell lysis, contribute to the overall pathology of S. aureus SSTIs. […] Staphylococcus aureus produces an array of potential virulence factors that play an important role on every level of host-pathogen interactions, including immune evasion molecules that allow bacteria to circumvent host innate and adaptive immunity.
#28 Pathogenesis of Staphylococcus aureus Abscesses
https://pmc.ncbi.nlm.nih.gov/articles/PMC4450319/
These molecules can be categorized according to their functions, and include those that do the following: i) affect PMN recruitment, ii) moderate the effects of phagocyte microbicides, iii) alter phagocytosis, and iv) cause host cell lysis (cytolytic toxins). […] The ability of Hla to cause host cell cytolysis (and thus destabilize the dermis) and elicit neutrophil recruitment likely plays a central role in the pathogenesis of SSTIs. […] The importance of Coa and vWbp in the formation of S. aureus abscesses is best illustrated by recent vaccine studies, in which active and passive immunization with antibodies against Coa and vWbp significantly reduced number of lesions in a murine kidney abscess model.
#29 The role of Staphylococcus aureus quorum sensing in cutaneous and systemic infections | Inflammation and Regeneration | Full Text
https://inflammregen.biomedcentral.com/articles/10.1186/s41232-024-00323-8
The pathophysiology of S. aureus infection is substantially influenced by phenotypic changes resulting from factors beyond Agr. […] Understanding the fundamental bacterial property that enables MRSA to adapt to various environments and eventually gain resistance is an urgent need to fight against this bacterium. […] The quorum sensing (QS) system is the ability of bacteria to adjust gene expressions in response to their population density. […] Agr functions as a central quorum sensing (QS) system in S. aureus, allowing bacteria to adjust gene expression in response to population density. […] Depending on Agr expression, S. aureus secretes various toxins, contributing to virulence in infectious diseases. […] The predominant factors of enhanced virulence in CA-MRSA was initially believed to rely on the bacterial ability to evade phagocytes killing by Panton-Valentine leukocidin (PVL), a pore-forming toxin to kill immune cells.
#30 Skin Infections Caused by Staphylococcus aureus | HTML | Acta Dermato-Venereologica
https://www.medicaljournals.se/acta/content/html/10.2340/00015555-3466
S. aureus is by far the main infectious bacteria isolated from abscesses. The majority of primary or spontaneous abscesses are caused by S. aureus producing PVL. […] The emergence of suppurative skin infection due to community-acquired methicillin-resistant S. aureus. Methicillin has been available since 1961, it was the first semi-synthetic penicillin resistant to penicillinase produced by most of S. aureus at that time. Its introduction was quickly followed by the appearance of MRSA. This resistance is linked to the synthesis of a modified penicillin-binding protein with less affinity to betalactams, PLP2a, leading to resistance to all beta-lactams. […] Almost all of CA-MRSA, including the major clones, produce the PVL toxin, which explains the predominance of suppurative skin infections as clinical presentations of CA-MRSA infections.
#31 Rapid, Non-Classical Mechanism of Leukocyte Recruitment to Staphylococcus Aureus Skin Infection | DG
https://repository.digital.georgetown.edu/handle/10822/1059508
Swift recruitment of phagocytic leukocytes is critical to prevent infections when bacteria breach through the protective layers of the skin. […] In a mouse model of S. aureus cutaneous infection, we found that as early as 4 hours post infection, neutrophil influx was entirely dependent on a family of S. aureus secreted toxins called phenol-soluble modulins (PSMs). […] Accordingly, EGR1-/- mice had significantly larger skin abscesses compared to wild-type (WT) mice. […] Taken together, this thesis reveals a mechanism that is critical for the early leukocyte response to invading S. aureus on the skin and attributes a previously unknown key role to secreted bacterial toxins and the transcription factor EGR1 in that process, providing a paradigmatic example of an innate host defense mechanism that is pathogen-specific in mode and extent.
#32 Contribution of Staphylococcus aureus Coagulases and Clumping Factor A to Abscess Formation in a Rabbit Model of Skin and Soft Tissue Infection | PLOS One
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0158293
Staphylococcus aureus produces numerous factors that facilitate survival in the human host. S. aureus coagulase (Coa) and von Willebrand factor-binding protein (vWbp) are known to clot plasma through activation of prothrombin and conversion of fibrinogen to fibrin. […] Here, we evaluated the contribution of Coa, vWbp and ClfA to S. aureus pathogenesis in a rabbit model of skin and soft tissue infection. […] Unexpectedly, we found that fibrin deposition and abscess capsule formation appear to be independent of S. aureus coagulase activity in the rabbit infection model. […] Although a specific mechanism remains to be determined, we conclude that S. aureus Coa, vWbp and ClfA contribute to abscess formation in rabbits. […] Fibrin deposition is a process critical to abscess formation and thereby contributes to host defense against invading S. aureus.
#33 Pathogenesis of Staphylococcus aureus Abscesses
https://pmc.ncbi.nlm.nih.gov/articles/PMC4450319/
These molecules can be categorized according to their functions, and include those that do the following: i) affect PMN recruitment, ii) moderate the effects of phagocyte microbicides, iii) alter phagocytosis, and iv) cause host cell lysis (cytolytic toxins). […] The ability of Hla to cause host cell cytolysis (and thus destabilize the dermis) and elicit neutrophil recruitment likely plays a central role in the pathogenesis of SSTIs. […] The importance of Coa and vWbp in the formation of S. aureus abscesses is best illustrated by recent vaccine studies, in which active and passive immunization with antibodies against Coa and vWbp significantly reduced number of lesions in a murine kidney abscess model.
#34 Contribution of Staphylococcus aureus Coagulases and Clumping Factor A to Abscess Formation in a Rabbit Model of Skin and Soft Tissue Infection | PLOS One
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0158293
Staphylococcus aureus produces numerous factors that facilitate survival in the human host. S. aureus coagulase (Coa) and von Willebrand factor-binding protein (vWbp) are known to clot plasma through activation of prothrombin and conversion of fibrinogen to fibrin. […] Here, we evaluated the contribution of Coa, vWbp and ClfA to S. aureus pathogenesis in a rabbit model of skin and soft tissue infection. […] Unexpectedly, we found that fibrin deposition and abscess capsule formation appear to be independent of S. aureus coagulase activity in the rabbit infection model. […] Although a specific mechanism remains to be determined, we conclude that S. aureus Coa, vWbp and ClfA contribute to abscess formation in rabbits. […] Fibrin deposition is a process critical to abscess formation and thereby contributes to host defense against invading S. aureus.
#35 Contribution of Staphylococcus aureus Coagulases and Clumping Factor A to Abscess Formation in a Rabbit Model of Skin and Soft Tissue Infection | PLOS One
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0158293
The S. aureus coagulases have been linked previously to abscess development in murine systemic and subcutaneous models of infection. […] A role for coagulases and ClfA has not been reported in a rabbit model of S. aureus SSTI. […] Our data indicate that all three of these molecules contribute to the formation of S. aureus abscesses in the experimental rabbit infection model. […] However, we found that the direct contribution of S. aureus Coa and vWbp to capsule formation and fibrin deposition was limited compared to that reported for the S. aureus murine kidney model. […] Collectively, the data obtained from our rabbit infection model confirm previous findings that Coa, vWbp and ClfA are involved in the pathogenesis of S. aureus SSTI and contribute to the host proinflammatory response to infection.
#36 Contribution of Staphylococcus aureus Coagulases and Clumping Factor A to Abscess Formation in a Rabbit Model of Skin and Soft Tissue Infection | PLOS One
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0158293
The S. aureus coagulases have been linked previously to abscess development in murine systemic and subcutaneous models of infection. […] A role for coagulases and ClfA has not been reported in a rabbit model of S. aureus SSTI. […] Our data indicate that all three of these molecules contribute to the formation of S. aureus abscesses in the experimental rabbit infection model. […] However, we found that the direct contribution of S. aureus Coa and vWbp to capsule formation and fibrin deposition was limited compared to that reported for the S. aureus murine kidney model. […] Collectively, the data obtained from our rabbit infection model confirm previous findings that Coa, vWbp and ClfA are involved in the pathogenesis of S. aureus SSTI and contribute to the host proinflammatory response to infection.
#37 Contribution of Staphylococcus aureus Coagulases and Clumping Factor A to Abscess Formation in a Rabbit Model of Skin and Soft Tissue Infection | PLOS One
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0158293
Staphylococcus aureus produces numerous factors that facilitate survival in the human host. S. aureus coagulase (Coa) and von Willebrand factor-binding protein (vWbp) are known to clot plasma through activation of prothrombin and conversion of fibrinogen to fibrin. […] Here, we evaluated the contribution of Coa, vWbp and ClfA to S. aureus pathogenesis in a rabbit model of skin and soft tissue infection. […] Unexpectedly, we found that fibrin deposition and abscess capsule formation appear to be independent of S. aureus coagulase activity in the rabbit infection model. […] Although a specific mechanism remains to be determined, we conclude that S. aureus Coa, vWbp and ClfA contribute to abscess formation in rabbits. […] Fibrin deposition is a process critical to abscess formation and thereby contributes to host defense against invading S. aureus.
#38 Staphylococcus aureus lipoproteins promote abscess formation in mice, shielding bacteria from immune killing | Communications Biology
https://www.nature.com/articles/s42003-021-01947-z
Despite being a major bacterial factor in alerting the human immune system, the role of Staphylococcus aureus (S. aureus) lipoproteins (Lpp) in skin infections remains largely unknown. […] Our data suggest that S. aureus Lpp induce skin inflammation and promote abscess formation that protects bacteria from innate immune killing. This suggests an intriguing bacterial immune evasion mechanism. […] During staphylococcal skin infection, microbe-associated molecular patterns (MAMPs) of S. aureus are recognized by pattern recognition receptors (PRRs), leading to activation of the host defense system. As a result, a local immune reaction with the production of proinflammatory cytokines is initiated and recruitment of phagocytes to the local infection site is induced, thus giving rise to the local formation of skin abscesses or skin necrosis.
#39 Staphylococcus aureus lipoproteins promote abscess formation in mice, shielding bacteria from immune killing | Communications Biology
https://www.nature.com/articles/s42003-021-01947-z
S. aureus itself also contributes to the abscess formation by producing specific virulence factors, which also play a role in structuring fibrin capsule that surround the abscess. […] The long-chain N-acylated Lpp, recognized by TLR2-TLR1 receptors, silence both innate and adaptive immune responses. […] Our results in a murine model demonstrate that subcutaneous injection of purified S. aureus Lpp induced skin inflammation via TLR2 with rapid infiltration of leukocytes to skin tissue, which led to an imbalance of local hemostasis toward a procoagulant state. […] Expression of Lpp in S. aureus increased the severity of skin infections and bacterial load in local tissues. […] The SA113 lgt mutant strain led to significantly reduced skin lesions than those of the parental strain from day 3 up to day 10 postinfection.
#40 Staphylococcus aureus lipoproteins promote abscess formation in mice, shielding bacteria from immune killing | Communications Biology
https://www.nature.com/articles/s42003-021-01947-z
S. aureus itself also contributes to the abscess formation by producing specific virulence factors, which also play a role in structuring fibrin capsule that surround the abscess. […] The long-chain N-acylated Lpp, recognized by TLR2-TLR1 receptors, silence both innate and adaptive immune responses. […] Our results in a murine model demonstrate that subcutaneous injection of purified S. aureus Lpp induced skin inflammation via TLR2 with rapid infiltration of leukocytes to skin tissue, which led to an imbalance of local hemostasis toward a procoagulant state. […] Expression of Lpp in S. aureus increased the severity of skin infections and bacterial load in local tissues. […] The SA113 lgt mutant strain led to significantly reduced skin lesions than those of the parental strain from day 3 up to day 10 postinfection.
#41 The Zwitterionic Cell Wall Teichoic Acid of Staphylococcus aureus Provokes Skin Abscesses in Mice by a Novel CD4+ T-Cell-Dependent Mechanism | PLOS One
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0013227
Zwitterionic polysaccharide (ZPS) components of the bacterial cell envelope have been shown to exert a major histocompatibility complex (MHC) II-dependent activation of CD4+ T cells, which in turn can modulate the outcome and progression of infections in animal models. […] We demonstrate here that WTA activates T cells in a MHC II dependent manner, and that T cells activated in vitro by WTA induce skin abscesses in mice. […] Our results demonstrate that the zwitterionic WTA of S. aureus induces CD4+ T-cell proliferation in an MHCII-dependent manner, which in turn modulates abscess formation in a mouse skin infection model. […] We identified a novel role for zwitterionic WTA, together with CP, in the induction of subcutaneous abscess formation through a mechanism dependant upon T-cell activation. […] We present a novel function of WTA as a ZPS that can modulate CD4 T cell-dependent development of skin abscesses in mice.
#42 Scientists decipher a mechanism in serious skin infections | German Center for Infection Research
https://www.dzif.de/en/scientists-decipher-mechanism-serious-skin-infections
Weve now also been able to prove that the increased insertion of the sugar polymer into the cell envelope creates a change in the immune reaction in the case of skin infections. This, he added, increased the ability of these aggressive bacteria to cause particularly serious skin infections in animal experiments. […] The authors were in a position to decipher the molecular mechanisms more precisely, which underlie the modification in the cell envelope. This will open up the possibility of deliberately preventing the modification process in serious skin infections caused by CA-MRSA strains in the future. […] This kind of therapeutic approach would give the human immune system the chance to combat the infection more efficiently itself, Weidenmaier said. These so-called anti-virulence strategies have been increasingly explored in recent times; in this case, the pathogen itself is not attacked, but its pathogenic effect. In contrast to classic antibiotic treatment, an anti-virulence strategy should lead to lower resistance rates, the scientist explained. Because the bacterial cell is not killed off or inhibited in its growth, it is subject to less evolutionary pressure.
#43 Molecular Pathogenesis of Staphylococcus aureus Infection | Pediatric Research
https://www.nature.com/articles/pr2009125
S. aureus has been generally recognized to survive well both inside and outside of host cells. In the extracellular milieu, S. aureus must overcome opsonization by complement and antibodies, which directly or indirectly leads to killing of S. aureus or uptake by phagocytes through Fc or complement receptors. S. aureus avoids opsonophagocytosis by expressing on its surface a capsule, clumping factor A, protein A, and a number of complement inhibitors, all of which inactivate or prevent host opsonins from binding or targeting the bacterium for destruction. […] Upon arriving at the infection site, neutrophils unleash a battery of antimicrobial substances, including antimicrobial peptides, reactive oxygen species (ROS), reactive nitrogen species, proteases, and lysozyme. Defense against ROS is mediated in S. aureus by deployment of a large number of antioxidant enzymes that neutralize ROS and reactive nitrogen species.
#44 Molecular Pathogenesis of Staphylococcus aureus Infection | Pediatric Research
https://www.nature.com/articles/pr2009125
S. aureus has been generally recognized to survive well both inside and outside of host cells. In the extracellular milieu, S. aureus must overcome opsonization by complement and antibodies, which directly or indirectly leads to killing of S. aureus or uptake by phagocytes through Fc or complement receptors. S. aureus avoids opsonophagocytosis by expressing on its surface a capsule, clumping factor A, protein A, and a number of complement inhibitors, all of which inactivate or prevent host opsonins from binding or targeting the bacterium for destruction. […] Upon arriving at the infection site, neutrophils unleash a battery of antimicrobial substances, including antimicrobial peptides, reactive oxygen species (ROS), reactive nitrogen species, proteases, and lysozyme. Defense against ROS is mediated in S. aureus by deployment of a large number of antioxidant enzymes that neutralize ROS and reactive nitrogen species.
#45 Molecular Pathogenesis of Staphylococcus aureus Infection | Pediatric Research
https://www.nature.com/articles/pr2009125
As a preemptive measure, S. aureus counters by secreting specific toxins, which lyse neutrophils. S. aureus expresses a large number of two-component toxins many of which have specificity for human but not mouse cells; therefore, many of their functions have not been characterized. […] A severe bacterial infection normally induces the host to mount an adaptive immune response within 7-10 days to limit the ongoing infection and prevent future reinfections. However, one of the hallmarks of S. aureus biology is the ability of the pathogen to infect the human host repeatedly throughout life. The mechanism underlying evasion of adaptive immune response is poorly understood; however, studies have shown that staphylococcal enterotoxins, TSST, and Eap (a MHC class II analog) could all alter T cell functions by targeting the T cell receptor activation pathway. […] Other virulence mechanisms of clinical significance include biofilm formation which allows S. aureus to persist on plastics and resist host defenses or antibiotics, and small colony variants which help S. aureus survive in a metabolically inactive state under harsh conditions.
#46 Molecular Pathogenesis of Staphylococcus aureus Infection | Pediatric Research
https://www.nature.com/articles/pr2009125
As a preemptive measure, S. aureus counters by secreting specific toxins, which lyse neutrophils. S. aureus expresses a large number of two-component toxins many of which have specificity for human but not mouse cells; therefore, many of their functions have not been characterized. […] A severe bacterial infection normally induces the host to mount an adaptive immune response within 7-10 days to limit the ongoing infection and prevent future reinfections. However, one of the hallmarks of S. aureus biology is the ability of the pathogen to infect the human host repeatedly throughout life. The mechanism underlying evasion of adaptive immune response is poorly understood; however, studies have shown that staphylococcal enterotoxins, TSST, and Eap (a MHC class II analog) could all alter T cell functions by targeting the T cell receptor activation pathway. […] Other virulence mechanisms of clinical significance include biofilm formation which allows S. aureus to persist on plastics and resist host defenses or antibiotics, and small colony variants which help S. aureus survive in a metabolically inactive state under harsh conditions.
#47 Molecular Pathogenesis of Staphylococcus aureus Infection | Pediatric Research
https://www.nature.com/articles/pr2009125
As a preemptive measure, S. aureus counters by secreting specific toxins, which lyse neutrophils. S. aureus expresses a large number of two-component toxins many of which have specificity for human but not mouse cells; therefore, many of their functions have not been characterized. […] A severe bacterial infection normally induces the host to mount an adaptive immune response within 7-10 days to limit the ongoing infection and prevent future reinfections. However, one of the hallmarks of S. aureus biology is the ability of the pathogen to infect the human host repeatedly throughout life. The mechanism underlying evasion of adaptive immune response is poorly understood; however, studies have shown that staphylococcal enterotoxins, TSST, and Eap (a MHC class II analog) could all alter T cell functions by targeting the T cell receptor activation pathway. […] Other virulence mechanisms of clinical significance include biofilm formation which allows S. aureus to persist on plastics and resist host defenses or antibiotics, and small colony variants which help S. aureus survive in a metabolically inactive state under harsh conditions.
#48 The role of Staphylococcus aureus quorum sensing in cutaneous and systemic infections | Inflammation and Regeneration | Full Text
https://inflammregen.biomedcentral.com/articles/10.1186/s41232-024-00323-8
Agr has been described to generally downregulate adhesion factors, collectively referred to as microbial surface components recognizing adhesive matrix molecules (MSCRAMMs). […] The contamination of indwelling medical devices is another route of infection that occurs frequently in the hospital setting. […] Biofilm formation starts from bacterial attachment to a surface, production of the extracellular matrix, and the disassembly of the biofilm to disseminate to other sites. […] Agr reportedly affects biofilm formation either negatively or positively depending on the formation step. […] Agr activation suppresses some toxin expression. […] Thus, expressing protein A instead of Agr-regulated toxins may contribute to virulence in various settings. […] The pathophysiology of S. aureus infection is substantially influenced by phenotypic changes resulting from factors beyond Agr.
#49 Skin Infection: Pictures, Types, Causes, and Treatments
https://www.healthline.com/health/skin-infection
Bacterial skin infections occur when bacteria enter the skin, either from an outside source or because they are present on the skin. They can enter the skin through a hair follicle or after a wound. […] The cause of a skin infection depends on the pathogen involved. […] These infections occur when bacteria enter the body through a break in the skin, such as a cut or a scratch. […] A break or cut in the skin may allow pathogens to get into the deeper layers of the skin. […] Skin infections can spread beyond the skin and into tissues under the skin or the bloodstream, especially in people with a compromised immune system. […] When this happens it can lead to sepsis, a potentially life-threatening condition. […] Some infections will go away on their own or respond to over-the-counter creams.
#50 Cellulitis: Practice Essentials, Background, Pathophysiology
https://emedicine.medscape.com/article/214222-overview
Cellulitis usually follows a breach in the skin, such as a fissure, cut, laceration, insect bite, or puncture wound. In some cases, there is no obvious portal of entry and the breach may be due to microscopic changes in the skin or invasive qualities of certain bacteria. Organisms on the skin and its appendages gain entrance to the dermis and multiply to cause cellulitis. Patients with toe-web intertrigo and/or tinea pedis as well as those with lymphatic obstruction, venous insufficiency, pressure ulcers, and obesity are particularly vulnerable to recurrent episodes of cellulitis. […] The vast majority of cases of cellulitis are likely caused by Streptococcus pyogenes and, to a lesser degree, by Staphylococcus aureus. In rare cases, cellulitis results from the metastatic seeding of an organism from a distant focus of infection, especially in immunocompromised individuals. Distant seeding is particularly common in cellulitis due to S pneumoniae (pneumococcus) and marine Vibrio species. Neisseria meningitidis, Pseudomonas aeruginosa, Brucella species, and Legionella species have also been reported as rare causes of cellulitis resulting from hematogenous spread.
#51 Superficial Pyoderma in Dogs: Etiology & Pathogenesis of the Infection
https://insights.nextmune.com/superficial-pyoderma-in-dogs-etiology-pathogenesis-of-the-infection
Allergy patients in particular are predisposed to secondary pyoderma due to the intrinsic deficiency of long-chain ceramides in the intercellular lipids of the stratum corneum, resulting in a defect of the protective surface barrier. […] Inflammation due to allergy or self-induced lesions can further disrupt the skin barrier due to the passage of exudate via the transepidermal route. […] The bacterial population on the skin surface of atopic subjects appears to be more numerous than that of normal subjects, and mainly consisting of staphylococci, as the corneocytes of allergic dogs allow better adhesion to the bacteria. […] High humidity and temperature favour an increase in the bacterial load in the skin. […] On the other hand, excessive dryness of the skin can also lead to an imbalance in the surface ecosystem and encourage infections. […] In general, all states of immunodepression, whether congenital, acquired or iatrogenic, favour skin infections.
#52 Superficial Pyoderma in Dogs: Etiology & Pathogenesis of the Infection
https://insights.nextmune.com/superficial-pyoderma-in-dogs-etiology-pathogenesis-of-the-infection
Allergy patients in particular are predisposed to secondary pyoderma due to the intrinsic deficiency of long-chain ceramides in the intercellular lipids of the stratum corneum, resulting in a defect of the protective surface barrier. […] Inflammation due to allergy or self-induced lesions can further disrupt the skin barrier due to the passage of exudate via the transepidermal route. […] The bacterial population on the skin surface of atopic subjects appears to be more numerous than that of normal subjects, and mainly consisting of staphylococci, as the corneocytes of allergic dogs allow better adhesion to the bacteria. […] High humidity and temperature favour an increase in the bacterial load in the skin. […] On the other hand, excessive dryness of the skin can also lead to an imbalance in the surface ecosystem and encourage infections. […] In general, all states of immunodepression, whether congenital, acquired or iatrogenic, favour skin infections.
#53 Superficial Pyoderma in Dogs: Etiology & Pathogenesis of the Infection
https://insights.nextmune.com/superficial-pyoderma-in-dogs-etiology-pathogenesis-of-the-infection
Allergy patients in particular are predisposed to secondary pyoderma due to the intrinsic deficiency of long-chain ceramides in the intercellular lipids of the stratum corneum, resulting in a defect of the protective surface barrier. […] Inflammation due to allergy or self-induced lesions can further disrupt the skin barrier due to the passage of exudate via the transepidermal route. […] The bacterial population on the skin surface of atopic subjects appears to be more numerous than that of normal subjects, and mainly consisting of staphylococci, as the corneocytes of allergic dogs allow better adhesion to the bacteria. […] High humidity and temperature favour an increase in the bacterial load in the skin. […] On the other hand, excessive dryness of the skin can also lead to an imbalance in the surface ecosystem and encourage infections. […] In general, all states of immunodepression, whether congenital, acquired or iatrogenic, favour skin infections.
#54 Bacterial Skin Abscess | IntechOpen
https://www.intechopen.com/chapters/71743
Patients with skin and soft tissue infections may appear with the abscess. […] Risk for developing skin abscess factors includes disruption of the skin barrier, edema, venous insufficiency, and immune suppression. […] The most common microbiologic cause of abscess, a commonly group Streptococcus or Streptococcus pyogenes; Staphylococcus aureus (including methicillin-resistant strains) is a notable but less common cause. […] The most common cause of abscess skin is Staphylococcus aureus (either methicillin or midwife to methicillin. Staphylococcus aureus aureus), occurring in up to 75% of cases; many patients infected with MRSA do not have risk factors. […] The abscess can also be fatal in rare cases, such as when it is in an area where pressure on vital organs such as the trachea in the case of abscess in the neck area.
#55 Bacterial Skin Abscess | IntechOpen
https://www.intechopen.com/chapters/71743
Patients with skin and soft tissue infections may appear with the abscess. […] Risk for developing skin abscess factors includes disruption of the skin barrier, edema, venous insufficiency, and immune suppression. […] The most common microbiologic cause of abscess, a commonly group Streptococcus or Streptococcus pyogenes; Staphylococcus aureus (including methicillin-resistant strains) is a notable but less common cause. […] The most common cause of abscess skin is Staphylococcus aureus (either methicillin or midwife to methicillin. Staphylococcus aureus aureus), occurring in up to 75% of cases; many patients infected with MRSA do not have risk factors. […] The abscess can also be fatal in rare cases, such as when it is in an area where pressure on vital organs such as the trachea in the case of abscess in the neck area.
#56 Bacterial Skin Abscess | IntechOpen
https://www.intechopen.com/chapters/71743
Patients with skin and soft tissue infections may appear with the abscess. […] Risk for developing skin abscess factors includes disruption of the skin barrier, edema, venous insufficiency, and immune suppression. […] The most common microbiologic cause of abscess, a commonly group Streptococcus or Streptococcus pyogenes; Staphylococcus aureus (including methicillin-resistant strains) is a notable but less common cause. […] The most common cause of abscess skin is Staphylococcus aureus (either methicillin or midwife to methicillin. Staphylococcus aureus aureus), occurring in up to 75% of cases; many patients infected with MRSA do not have risk factors. […] The abscess can also be fatal in rare cases, such as when it is in an area where pressure on vital organs such as the trachea in the case of abscess in the neck area.
#57 Superficial Pyoderma in Dogs: Etiology & Pathogenesis of the Infection
https://insights.nextmune.com/superficial-pyoderma-in-dogs-etiology-pathogenesis-of-the-infection
Allergy patients in particular are predisposed to secondary pyoderma due to the intrinsic deficiency of long-chain ceramides in the intercellular lipids of the stratum corneum, resulting in a defect of the protective surface barrier. […] Inflammation due to allergy or self-induced lesions can further disrupt the skin barrier due to the passage of exudate via the transepidermal route. […] The bacterial population on the skin surface of atopic subjects appears to be more numerous than that of normal subjects, and mainly consisting of staphylococci, as the corneocytes of allergic dogs allow better adhesion to the bacteria. […] High humidity and temperature favour an increase in the bacterial load in the skin. […] On the other hand, excessive dryness of the skin can also lead to an imbalance in the surface ecosystem and encourage infections. […] In general, all states of immunodepression, whether congenital, acquired or iatrogenic, favour skin infections.
#58 Cellulitis: Practice Essentials, Background, Pathophysiology
https://emedicine.medscape.com/article/214222-overview
Cellulitis usually follows a breach in the skin, such as a fissure, cut, laceration, insect bite, or puncture wound. In some cases, there is no obvious portal of entry and the breach may be due to microscopic changes in the skin or invasive qualities of certain bacteria. Organisms on the skin and its appendages gain entrance to the dermis and multiply to cause cellulitis. Patients with toe-web intertrigo and/or tinea pedis as well as those with lymphatic obstruction, venous insufficiency, pressure ulcers, and obesity are particularly vulnerable to recurrent episodes of cellulitis. […] The vast majority of cases of cellulitis are likely caused by Streptococcus pyogenes and, to a lesser degree, by Staphylococcus aureus. In rare cases, cellulitis results from the metastatic seeding of an organism from a distant focus of infection, especially in immunocompromised individuals. Distant seeding is particularly common in cellulitis due to S pneumoniae (pneumococcus) and marine Vibrio species. Neisseria meningitidis, Pseudomonas aeruginosa, Brucella species, and Legionella species have also been reported as rare causes of cellulitis resulting from hematogenous spread.
#59 Furuncles and Carbuncles – Dermatologic Disorders – MSD Manual Professional Edition
https://www.msdmanuals.com/professional/dermatologic-disorders/bacterial-skin-infections/furuncles-and-carbuncles
Furuncles (boils) are skin abscesses caused by staphylococcal infection, which involve a hair follicle and surrounding tissue. […] Methicillin-resistant Staphylococcus aureus (MRSA) is a common cause. […] Abscesses are incised and drained. Intermittent hot compresses are used to facilitate drainage. […] Antibiotics, when used, should be effective against MRSA, pending culture and sensitivity test results. […] Furuncles frequently recur and can be prevented by applying liquid soap containing either chlorhexidine gluconate with isopropyl alcohol or 2 to 3% chloroxylenol. […] Patients with recurrent furunculosis should be treated for predisposing factors such as obesity, diabetes, occupational or industrial exposure to inciting factors, and nasal carriage of S. aureus or MRSA colonization.
#60 Furuncles and Carbuncles – Dermatologic Disorders – MSD Manual Professional Edition
https://www.msdmanuals.com/professional/dermatologic-disorders/bacterial-skin-infections/furuncles-and-carbuncles
Furuncles (boils) are skin abscesses caused by staphylococcal infection, which involve a hair follicle and surrounding tissue. […] Methicillin-resistant Staphylococcus aureus (MRSA) is a common cause. […] Abscesses are incised and drained. Intermittent hot compresses are used to facilitate drainage. […] Antibiotics, when used, should be effective against MRSA, pending culture and sensitivity test results. […] Furuncles frequently recur and can be prevented by applying liquid soap containing either chlorhexidine gluconate with isopropyl alcohol or 2 to 3% chloroxylenol. […] Patients with recurrent furunculosis should be treated for predisposing factors such as obesity, diabetes, occupational or industrial exposure to inciting factors, and nasal carriage of S. aureus or MRSA colonization.
#61 Furuncles and Carbuncles – Dermatologic Disorders – MSD Manual Professional Edition
https://www.msdmanuals.com/professional/dermatologic-disorders/bacterial-skin-infections/furuncles-and-carbuncles
Furuncles (boils) are skin abscesses caused by staphylococcal infection, which involve a hair follicle and surrounding tissue. […] Methicillin-resistant Staphylococcus aureus (MRSA) is a common cause. […] Abscesses are incised and drained. Intermittent hot compresses are used to facilitate drainage. […] Antibiotics, when used, should be effective against MRSA, pending culture and sensitivity test results. […] Furuncles frequently recur and can be prevented by applying liquid soap containing either chlorhexidine gluconate with isopropyl alcohol or 2 to 3% chloroxylenol. […] Patients with recurrent furunculosis should be treated for predisposing factors such as obesity, diabetes, occupational or industrial exposure to inciting factors, and nasal carriage of S. aureus or MRSA colonization.
#62 Purulent Skin and Soft Tissue Infections: Furuncles, Carbuncles, and Cutaneous Abscesses – Skin and Soft Tissue Infections – Bacterial Diseases – Infectious Diseases – Diseases – McMaster Textbook of Internal Medicine
https://empendium.com/mcmtextbook/chapter/B31.II.18.73.2.
Furuncles and carbuncles are typically caused by Staphylococcus aureus (both methicillin-susceptible Staphylococcus aureus [MSSA] and methicillin-resistant Staphylococcus aureus [MRSA]). Infections secondary to a penetrating trauma or involving the perioral or perineal area increase the likelihood of a polymicrobial infection, including S aureus, Streptococcus pyogenes, gram-negative bacilli, and anaerobes. Depending on host factors and exposures, other causes can include blastomycosis, cryptococcosis, nontuberculous mycobacterial infection, and nocardiosis. […] Purulent SSTIs often affect healthy, immunocompetent adults. Risk factors are similar to those for nonpurulent SSTIs (see Table. Risk factors for nonpurulent skin and soft tissue infections). Additional risk factors include immunocompromised state (particularly neutrophil defects), suboptimal hygiene (eg, sharing contaminated hygiene items like shaving razors), hot and humid climates, MRSA carriage, and additional MRSA risk factors (see Nonpurulent Skin and Soft Tissue Infections: Erysipelas and Cellulitis).
#63 Purulent Skin and Soft Tissue Infections: Furuncles, Carbuncles, and Cutaneous Abscesses – Skin and Soft Tissue Infections – Bacterial Diseases – Infectious Diseases – Diseases – McMaster Textbook of Internal Medicine
https://empendium.com/mcmtextbook/chapter/B31.II.18.73.2.
Furuncles and carbuncles are typically caused by Staphylococcus aureus (both methicillin-susceptible Staphylococcus aureus [MSSA] and methicillin-resistant Staphylococcus aureus [MRSA]). Infections secondary to a penetrating trauma or involving the perioral or perineal area increase the likelihood of a polymicrobial infection, including S aureus, Streptococcus pyogenes, gram-negative bacilli, and anaerobes. Depending on host factors and exposures, other causes can include blastomycosis, cryptococcosis, nontuberculous mycobacterial infection, and nocardiosis. […] Purulent SSTIs often affect healthy, immunocompetent adults. Risk factors are similar to those for nonpurulent SSTIs (see Table. Risk factors for nonpurulent skin and soft tissue infections). Additional risk factors include immunocompromised state (particularly neutrophil defects), suboptimal hygiene (eg, sharing contaminated hygiene items like shaving razors), hot and humid climates, MRSA carriage, and additional MRSA risk factors (see Nonpurulent Skin and Soft Tissue Infections: Erysipelas and Cellulitis).
#64 Overview of Bacterial Skin Infections – Skin Disorders – MSD Manual Consumer Version
https://www.msdmanuals.com/home/skin-disorders/bacterial-skin-infections/overview-of-bacterial-skin-infections
Bacterial skin infections develop when bacteria enter through hair follicles or through small breaks in the skin that result from scrapes, punctures, surgery, burns, sunburn, animal or insect bites, wounds, and pre-existing skin disorders. […] Skin that is inflamed or damaged is more likely to become infected. In fact, any break in the skin predisposes a person to infection. […] Abscesses should be cut open by a doctor and allowed to drain, and any dead tissue must be surgically removed.
#65 Abscesses – Infectious Diseases – Merck Manual Professional Edition
https://www.merckmanuals.com/professional/infectious-diseases/biology-of-infectious-disease/abscesses
Predisposing factors to abscess formation include impaired host defense mechanisms (eg, impaired leukocyte defenses), the presence of foreign bodies, obstruction to normal drainage (eg, in the urinary, biliary, or respiratory tracts), tissue ischemia or necrosis, hematoma or excessive fluid accumulation in tissue, and trauma, including surgery. […] Systemic antimicrobials are not routinely given but are indicated as adjunctive therapy if the abscess is deep (eg, intra-abdominal), if abscesses are multiple, if there is significant surrounding cellulitis, or perhaps if size is 2 cm. […] Antibiotics directed against S. aureus, in addition to incision and drainage, should be given if there is evidence of a systemic inflammatory syndrome.
#66 Abscesses – Infectious Diseases – Merck Manual Professional Edition
https://www.merckmanuals.com/professional/infectious-diseases/biology-of-infectious-disease/abscesses
Predisposing factors to abscess formation include impaired host defense mechanisms (eg, impaired leukocyte defenses), the presence of foreign bodies, obstruction to normal drainage (eg, in the urinary, biliary, or respiratory tracts), tissue ischemia or necrosis, hematoma or excessive fluid accumulation in tissue, and trauma, including surgery. […] Systemic antimicrobials are not routinely given but are indicated as adjunctive therapy if the abscess is deep (eg, intra-abdominal), if abscesses are multiple, if there is significant surrounding cellulitis, or perhaps if size is 2 cm. […] Antibiotics directed against S. aureus, in addition to incision and drainage, should be given if there is evidence of a systemic inflammatory syndrome.
#67 Furuncles and Carbuncles – Dermatologic Disorders – MSD Manual Professional Edition
https://www.msdmanuals.com/professional/dermatologic-disorders/bacterial-skin-infections/furuncles-and-carbuncles
Furuncles (boils) are skin abscesses caused by staphylococcal infection, which involve a hair follicle and surrounding tissue. […] Methicillin-resistant Staphylococcus aureus (MRSA) is a common cause. […] Abscesses are incised and drained. Intermittent hot compresses are used to facilitate drainage. […] Antibiotics, when used, should be effective against MRSA, pending culture and sensitivity test results. […] Furuncles frequently recur and can be prevented by applying liquid soap containing either chlorhexidine gluconate with isopropyl alcohol or 2 to 3% chloroxylenol. […] Patients with recurrent furunculosis should be treated for predisposing factors such as obesity, diabetes, occupational or industrial exposure to inciting factors, and nasal carriage of S. aureus or MRSA colonization.
#68 The Role of Staphylococcus aureus Virulence Factors in Skin Infection and Their Potential as Vaccine Antigens
https://www.mdpi.com/2076-0817/5/1/22
Staphylococcus aureus (S. aureus) causes the vast majority of skin and soft tissue infections (SSTIs) in humans. […] S. aureus has become increasingly resistant to antibiotics and there is an urgent need for new strategies to tackle S. aureus infections. […] Recent discoveries have highlighted that interleukin-17-producing T cells play a particularly important role in the immune response to S. aureus skin infection and suggest that vaccine strategies to specifically target these types of T cells may be beneficial in the treatment of S. aureus SSTIs. […] The virulence potential of many CWA proteins has been demonstrated in infection models; however, there is a paucity of information regarding their roles during SSTIs. […] It is estimated that 90% of CA-MRSA infections present as SSTIs.
#69 Scientists decipher a mechanism in serious skin infections | German Center for Infection Research
https://www.dzif.de/en/scientists-decipher-mechanism-serious-skin-infections
Weve now also been able to prove that the increased insertion of the sugar polymer into the cell envelope creates a change in the immune reaction in the case of skin infections. This, he added, increased the ability of these aggressive bacteria to cause particularly serious skin infections in animal experiments. […] The authors were in a position to decipher the molecular mechanisms more precisely, which underlie the modification in the cell envelope. This will open up the possibility of deliberately preventing the modification process in serious skin infections caused by CA-MRSA strains in the future. […] This kind of therapeutic approach would give the human immune system the chance to combat the infection more efficiently itself, Weidenmaier said. These so-called anti-virulence strategies have been increasingly explored in recent times; in this case, the pathogen itself is not attacked, but its pathogenic effect. In contrast to classic antibiotic treatment, an anti-virulence strategy should lead to lower resistance rates, the scientist explained. Because the bacterial cell is not killed off or inhibited in its growth, it is subject to less evolutionary pressure.
#70 Scientists decipher a mechanism in serious skin infections | German Center for Infection Research
https://www.dzif.de/en/scientists-decipher-mechanism-serious-skin-infections
Weve now also been able to prove that the increased insertion of the sugar polymer into the cell envelope creates a change in the immune reaction in the case of skin infections. This, he added, increased the ability of these aggressive bacteria to cause particularly serious skin infections in animal experiments. […] The authors were in a position to decipher the molecular mechanisms more precisely, which underlie the modification in the cell envelope. This will open up the possibility of deliberately preventing the modification process in serious skin infections caused by CA-MRSA strains in the future. […] This kind of therapeutic approach would give the human immune system the chance to combat the infection more efficiently itself, Weidenmaier said. These so-called anti-virulence strategies have been increasingly explored in recent times; in this case, the pathogen itself is not attacked, but its pathogenic effect. In contrast to classic antibiotic treatment, an anti-virulence strategy should lead to lower resistance rates, the scientist explained. Because the bacterial cell is not killed off or inhibited in its growth, it is subject to less evolutionary pressure.
#71 The Role of Staphylococcus aureus Virulence Factors in Skin Infection and Their Potential as Vaccine Antigens
https://www.mdpi.com/2076-0817/5/1/22
These studies highlight the concept that specific immune responses may be of greater importance at distinct sites of infection. […] Consequently the requirements for a vaccine may need to be tailored to the type of infection that it is aimed at preventing. […] If prophylactic vaccines or other forms of immunotherapy to treat S. aureus SSTIs are to be developed as an alternative to antibiotics, we need a greater understanding of the specific roles of individual virulence factors during infection at this site, as they may be important targets in future therapies. […] SSTIs are caused by microbial invasion of the layers of skin and underlying soft tissues. […] Abscesses can form in the dermis, epidermis and subcutaneous tissue and function primarily to contain the pathogen, preventing the spread of infection to adjacent healthy tissue.