Hubbry Logo
PusPusMain
Open search
Pus
Community hub
Pus
logo
8 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Pus
Pus
Pus
View on Wikipedia
from Wikipedia

Pus
Pus with blood coming out of ring finger
SpecialtyInfectious disease

Pus is an exudate, typically white-yellow, yellow, or yellow-brown, formed at the site of inflammation during infections, regardless of cause.[1][2] An accumulation of pus in an enclosed tissue space is known as an abscess, whereas a visible collection of pus within or beneath the epidermis is known as a pustule, pimple or spot.

Description

[edit]

Pus consists of a thin, protein-rich fluid (historically known as liquor puris[3][4]) and dead leukocytes (white blood cells) from the body's immune response (mostly neutrophils).[5] During infection, T helper cells release cytokines, which trigger neutrophils to seek the site of infection by chemotaxis. There, the neutrophils release granules, which destroy the bacteria. The bacteria resist the immune response by releasing toxins called leukocidins.[6] As the neutrophils die off from toxins and old age, they are destroyed by macrophages, forming the viscous pus. Bacteria that cause pus are called pyogenic.[6][7]

Although pus is normally of a whitish-yellow hue, changes in the color can be observed under certain circumstances. Pus is sometimes green because of the presence of myeloperoxidase, an intensely green antibacterial protein produced by some types of white blood cells. Green, foul-smelling pus is found in certain infections of Pseudomonas aeruginosa. The greenish color is a result of the bacterial pigment pyocyanin that it produces. Amoebic abscesses of the liver produce brownish pus, which is described as looking like "anchovy paste". Pus from anaerobic infections can more often have a foul odor.[8]

In almost all cases when there is a collection of pus in the body, a clinician will try to create an opening to drain it. This principle has been distilled into the famous Latin aphorism "Ubi pus, ibi evacua" ("Where there is pus, evacuate it").

Some disease processes caused by pyogenic infections are impetigo,[9] osteomyelitis, septic arthritis and necrotizing fasciitis.

An abscess is an enclosed collection of pus.
Duodenoscopy image of hepatopancreatic ampulla with pus exuding from it, indicative of cholangitis

Pyogenic bacteria

[edit]

Many species of bacteria may be involved in the production of pus. The most commonly found include:[10]

Staphylococcus aureus bacteria is the most common cause of boils.

Historical terminology

[edit]

In the pre-asepsis era, surgeon Frederick Treves (1853–1923) wrote, "Practically all major wounds suppurated. Pus was the most common subject of converse [among surgeons], because it was the most prominent feature in the surgeon's work. It was classified according to degrees of vileness." [11]: 347  But pus of the right kind was considered desirable.[12]: 80  "If a patient was lucky ... a thick cream-colored odorless fluid would appear within five or six days"; such "laudable" pus was considered "a sure sign that the wound would heal" [11]: 344  because it meant "Nature has put up a bold fight against the invader".[13] "On the other hand, if the pus gradually became watery, blood tinged and foul smelling, it was designated 'sanious' [14] [or 'ill-conditioned' ] [15] and the wound condition was considered unfavorable".[14] It later came to be understood that "laudable" pus generally implied an invasion of relatively benign staphylococcus, while "ill-conditioned" pus usually meant the more dangerous streptococcus was present.[11]: 345 [14]: 247 

See also

[edit]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Pus

View on Grokipedia
from Grokipedia
Pus is a viscous, opaque produced by the body during acute , particularly in response to bacterial , consisting primarily of dead and living (leukocytes), liquefied tissue debris, proteins, and microorganisms. It typically appears as a thick, whitish-yellow or greenish fluid that accumulates in tissues or cavities, such as abscesses, where it serves as a localized collection to contain and isolate pathogens from surrounding healthy tissue. The formation of pus, known medically as suppuration, results from the influx of neutrophils and other immune cells to the site of , where they engulf and destroy invaders through , leading to cellular death and the release of enzymes that break down surrounding tissues. Clinically, pus is a hallmark of pyogenic infections caused by like Staphylococcus aureus or Streptococcus species, and its presence often indicates the need for drainage, antibiotics, or surgical intervention to prevent spread. While pus formation is a protective mechanism, excessive or chronic suppuration can lead to complications such as tissue damage, , or the development of fistulas if not properly managed.

Definition and Characteristics

Definition

Pus is a viscous produced by the body as part of the inflammatory response to , serving as a of the immune system's efforts to combat pathogens and damaged tissue. It consists primarily of leukocytes, necrotic tissue debris, and microorganisms, forming a thick, protein-rich known as liquor puris. This material accumulates at sites of inflammation, such as wounds or abscesses, where it helps isolate and eliminate harmful agents. Unlike other types of exudates, pus is distinctly purulent, meaning it embodies a pus-like quality due to its high content of dead inflammatory cells and liquefied tissue, setting it apart from clearer, thinner serous fluid or blood-containing sanguineous exudate. Serous exudate, for instance, resembles watery plasma and lacks the opaque, cellular density of pus, while blood-tinged drainage indicates vascular involvement rather than purulent inflammation. This purulent character underscores pus's role as a marker of active immune engagement rather than simple transudation or hemorrhage. In clinical observation, pus typically presents as a creamy, opaque fluid with a viscous consistency, commonly appearing , , or white depending on the underlying infection's characteristics and microbial involvement. The yellowish hue often reflects neutrophil-derived enzymes and debris, while greenish tones may arise from specific bacterial pigments, though the exact shade provides diagnostic clues without altering its fundamental purulent identity.

Physical and Chemical Properties

Pus typically appears as a thick, opaque with color variations that reflect the underlying infectious process. The most common coloration is yellow or whitish-yellow, resulting from the accumulation of dead neutrophils. Green pus is characteristic of infections caused by , due to the production of the pigment . In terms of consistency, pus is viscous and creamy, distinguishing it from thinner serous or sanguineous fluids, owing to its elevated content of proteins and cellular debris. The of pus is generally acidic, with a mean value of approximately 6.68 and a range of 6.0 to 7.3 in periapical abscesses, influenced by produced through bacterial . Pus often exhibits a foul , attributable to the metabolic byproducts of anaerobic bacteria breaking down proteins into volatile compounds.

Physiology of Formation

Inflammatory Process

The inflammatory process culminating in pus production is initiated by tissue damage or microbial invasion, which stimulates resident immune cells such as macrophages and dendritic cells to recognize damage-associated molecular patterns (DAMPs) or pathogen-associated molecular patterns (PAMPs) via receptors. This recognition triggers the rapid release of pro-inflammatory cytokines, including interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α), which orchestrate the acute inflammatory response by activating endothelial cells and further immune recruitment. These cytokines promote of arterioles and venules in the affected area, increasing blood flow and causing the classic signs of warmth and redness, while simultaneously enhancing through endothelial contraction and gap formation. The resulting leakage of plasma fluid, proteins, and solutes into the interstitial space forms a protein-rich , which provides the fluid matrix essential for subsequent cellular accumulation and the development of purulent material. Activation of the , often via the alternative or pathways in response to microbial components or tissue injury, generates anaphylatoxins like C3a and C5a that amplify inflammation by further promoting permeability and . Concurrently, such as interleukin-8 (IL-8) are secreted by activated cells, directing the directed migration of leukocytes, primarily neutrophils, from the bloodstream to the site via selectin-mediated rolling, adhesion, and diapedesis. If the inciting stimulus persists or the acute response fails to resolve , the transitions to a chronic state, marked by sustained signaling, mononuclear cell dominance, and potential organization of the into encapsulated collections of pus surrounded by and .

Stages of Abscess Development

The development of an represents a localized progression of the inflammatory response, culminating in the accumulation of pus within a walled-off cavity. This process typically unfolds in three sequential stages, driven by the interplay between invading pathogens and the host's immune defenses. In the initial stage, pathogens infiltrate the tissue through mechanisms such as direct implantation, contiguous spread from adjacent infections, or hematogenous dissemination, triggering an acute inflammatory response. rapidly accumulate at the site, drawn by chemotactic signals, where they attempt to phagocytose and kill the invaders, often in response to pyogenic bacteria like . This neutrophil infiltration marks the onset of cellulitis-like , with early bacterial replication occurring amid the influx of immune cells. As the infection intensifies, the second stage involves liquefactive necrosis, where proteases and reactive oxygen species released by activated neutrophils degrade surrounding viable and necrotic tissue, creating a central cavity. This enzymatic digestion transforms the necrotic debris, dead leukocytes, and liquefied tissue into pus, which accumulates under pressure within the expanding space, further isolating the pathogens from systemic circulation. The process is exacerbated in hypoxic environments, promoting anaerobic bacterial growth and pus consolidation. The third stage features the formation of a , or pseudocapsule, around the abscess cavity, composed of deposits and derived from surrounding fibroblasts and vascular elements. This barrier, reinforced by over time, effectively contains the pus and limits dissemination, although it may also shield persistent from antibiotics and immune clearance. In mature abscesses, this encapsulation stabilizes the , potentially leading to chronicity if not drained. Several factors influence the progression through these stages, including host immunity, bacterial load, and anatomical location. Compromised host immunity, such as in or , impairs function and delays wall formation, accelerating abscess expansion and recurrence. Higher bacterial loads overwhelm initial defenses, hastening and cavity development, while lower inocula may resolve without abscessation. Anatomical site plays a critical role; superficial abscesses often progress more rapidly to fluctuance due to limited , whereas internal organ abscesses, like those in the , may form larger collections influenced by compartmental barriers but face challenges in drainage.

Composition

Cellular Elements

Pus is characterized by a high concentration of leukocytes, predominantly polymorphonuclear leukocytes (PMNs) such as neutrophils. These neutrophils migrate to the site of , phagocytose pathogens, and undergo , forming the bulk of the viscous material observed. In parasitic infections, may increase in proportion within the pus, reflecting their role in combating larger extracellular parasites through and toxicity. In chronic pus formations, such as those in persistent abscesses, the cellular profile shifts to include a greater presence of macrophages derived from monocytes and lymphocytes involved in adaptive immunity, aiding in prolonged containment and remodeling. These mononuclear cells facilitate tissue repair but can contribute to granuloma-like structures if the infection persists. The non-viable components include necrotic epithelial cells from surrounding tissues, strands from the cascade, and remnants of or other pathogens engulfed during . This debris arises from tissue breakdown and failed clearance, adding to the opaque, semisolid consistency of pus. The recruitment of these cellular elements occurs via chemotactic signals during the inflammatory process.

Molecular and Fluid Components

Pus consists of a matrix derived from an ultrafiltrate of plasma, characterized by elevated protein concentrations exceeding 3 g/dL, which arises from increased during acute . This high-protein content differentiates pus from transudates like serum, enabling it to form a viscous medium that encapsulates inflammatory debris and microbial elements. The base includes water, electrolytes, and low-molecular-weight solutes that mirror plasma composition, supporting the migration and function of immune cells at the infection site. Key plasma-derived proteins in pus include immunoglobulins such as IgG and IgA, which promote opsonization of pathogens and neutralize microbial toxins through antigen-antibody interactions. Complement proteins, including components like C3 and C4, are abundantly present and facilitate , opsonization, and direct of via the membrane attack complex. Acute-phase reactants, notably (CRP), are upregulated in pus and bind to on bacterial surfaces to enhance and complement activation, serving as a critical marker of the inflammatory response. Enzymatic components, primarily released from granules, include , a muramidase that hydrolyzes in bacterial cell walls to aid microbial killing. elastase, a , degrades , , and other extracellular matrix proteins, contributing to tissue breakdown and the characteristic observed in pus formation. These enzymes not only combat but also perpetuate by damaging host tissues. Other molecular elements encompass from disintegrated cell membranes, which add to the viscous texture, and bacterial toxins that amplify within the . Bacterial contributions, such as exotoxins from pyogenic organisms, further modulate the biochemical environment of pus by promoting additional leukocyte recruitment.

Etiology and Pathogens

Pyogenic Bacteria

Pyogenic bacteria are defined as pathogens capable of inducing suppurative inflammation, characterized by the accumulation of pus in infected tissues due to intense infiltration and . These bacteria primarily include gram-positive cocci such as and (group A Streptococcus), as well as certain gram-negative bacilli like . They are distinguished from other pathogens by their ability to trigger localized abscesses and systemic responses through targeted strategies. The mechanisms by which pyogenic promote pus formation involve multiple factors that disrupt host defenses and amplify inflammatory responses. Production of exotoxins, such as those secreted by S. pyogenes, directly damages host cells and recruits neutrophils to the infection site, leading to and pus accumulation. capsules, present in like S. aureus and K. pneumoniae, enable evasion of by masking bacterial surface antigens and inhibiting complement activation. Additionally, formation allows these to adhere to host tissues or medical devices, creating a protective matrix that shields them from immune clearance and antimicrobial agents while sustaining chronic inflammation. These processes collectively contribute to the development of abscesses during acute infections. Common infections associated with pyogenic bacteria highlight their clinical significance in various body sites. S. aureus is a leading cause of skin abscesses, where it invades hair follicles or wounds, resulting in localized pus-filled collections that often require drainage. S. pyogenes frequently underlies suppurative pharyngitis, manifesting as exudative tonsillitis with pus on the tonsillar surface, and can extend to and infections like or . K. pneumoniae, particularly hypervirulent strains, is implicated in pyogenic , where it causes necrotizing lung infections with purulent exudates, as well as liver abscesses filled with thick pus. Antibiotic resistance trends among pyogenic pose significant challenges to treatment, particularly in community settings. Methicillin-resistant S. (MRSA) has emerged as a dominant in community-acquired pus infections, with studies reporting prevalence rates of 50-60% among and abscesses in departments across the . This resistance, mediated by the gene encoding altered , complicates empirical therapy and increases reliance on alternatives like or clindamycin. Similar patterns are observed in S. pyogenes with resistance and in K. pneumoniae with extended-spectrum production, underscoring the need for culture-guided management.

Non-Bacterial Causes

Pus formation, characterized by the accumulation of necrotic tissue, inflammatory cells, and fluid, can arise from non-bacterial etiologies, including fungal and parasitic infections as well as sterile inflammatory processes. These causes often occur in specific clinical contexts, such as or tissue trauma, and result in that mimic bacterial ones but require distinct diagnostic approaches. Fungal infections, particularly by , are a significant non-bacterial cause of pus in immunocompromised hosts, where the invades mucosal surfaces or deep tissues, leading to abscess formation. In such patients, C. albicans can disseminate hematogenously, forming subcutaneous or visceral filled with pus-like material composed of neutrophils, fungal elements, and debris, as seen in cases of multiple lower limb without evident primary breach. These infections are opportunistic, thriving in or post-transplant states, and pus from candidal abscesses may appear creamy white due to yeast pseudohyphae and inflammatory . Parasitic infections, exemplified by , induce pus through protozoal invasion of tissues, most notably in amoebic liver abscesses. This parasite, transmitted via fecal-oral route, breaches the intestinal mucosa and migrates to the liver via portal circulation, causing and a sterile or anchovy-paste-like pus consisting of acellular debris, trophozoites, and minimal inflammatory cells. The pus in these abscesses is typically thick, chocolate-brown, and odorless, distinguishing it from bacterial pyogenic collections, and represents the host's response to parasitic rather than direct microbial proliferation. Sterile causes of pus-like exudates stem from non-infectious inflammation, such as reactions or autoimmune disorders. In reactions, implanted materials like dermal fillers or surgical hardware trigger chronic granulomatous inflammation, potentially leading to sterile es with pus formed by aggregates and without viable pathogens. For instance, poly-D,L-lactic implants have been associated with late-onset sterile pus collections due to persistent macrophage activation. In autoimmune conditions like , aseptic abscess syndrome manifests as deep, -rich abscesses with pus-like material, often in muscles or subcutaneous tissues, driven by dysregulated innate immunity rather than infection; these may accompany rheumatoid nodules that occasionally suppurate into pus-filled cavities. Viral involvement in pus formation is rare and typically indirect, occurring through secondary bacterial that complicates viral tissue damage. Respiratory viruses like impair and epithelial barriers, facilitating bacterial overgrowth and subsequent development with classic purulent ; similarly, viruses such as can induce reactive sterile es around lesions, though true pus requires superimposed . These cases highlight pus as a downstream consequence of viral-induced immunosuppression or , rather than direct cytopathology.

Clinical Aspects

Role in Infections

Pus serves as a key clinical marker of acute bacterial infections, indicating the accumulation of inflammatory exudate in response to microbial invasion. In systemic infections, such as empyema, pus collects in the pleural space as a complication of pneumonia, where bacteria from the lung parenchyma extend into the pleural cavity, leading to purulent effusion that impairs lung expansion and oxygenation. Similarly, in abdominal infections, peritonitis often arises from pus formation in intra-abdominal abscesses, where localized collections of purulent material result from perforation of viscera or postoperative contamination, triggering widespread peritoneal inflammation. In localized infections, pus manifests as a prominent feature in common presentations like furuncles and carbuncles, which are deep-seated infections involving hair follicles and subcutaneous tissues, forming painful, fluctuant nodules filled with purulent material due to staphylococcal invasion. Dental abscesses similarly present with pus accumulation at the root apex or in periodontal spaces, often stemming from untreated caries or trauma, resulting in swelling, pain, and potential drainage through gingival fistulas. The volume and persistence of pus provide important prognostic indicators in infections; large volumes suggest extensive tissue involvement and uncontrolled bacterial proliferation, while prolonged presence despite initial interventions signals ongoing and heightened risk of . If left untreated, pus accumulation can lead to serious complications, including fistula formation where chronic drainage tracts develop between abscess cavities and adjacent structures, and spread of to neighboring tissues, exacerbating local damage and potentially causing systemic dissemination.

Diagnosis and Management

Diagnosis of pus-related conditions typically begins with clinical evaluation, followed by laboratory and imaging studies to confirm the presence of infection and identify the underlying . Gram staining of pus samples provides rapid preliminary identification of bacterial morphology and Gram characteristics, aiding in initial pathogen differentiation such as Gram-positive cocci suggestive of staphylococci or streptococci. Culture and sensitivity testing of pus is the gold standard for definitive identification and antimicrobial susceptibility determination, guiding and typically taking 24-48 hours for results. Imaging modalities like and computed tomography (CT) are essential for localizing abscesses, with offering high sensitivity for superficial collections due to its ability to detect hypoechoic fluid pockets, while CT provides superior specificity for deeper or complex abscesses by delineating extent and involvement of adjacent structures. Management of pus-forming infections prioritizes source control through drainage, combined with antimicrobial therapy when indicated. () remains the cornerstone for superficial abscesses, effectively evacuating purulent material and promoting healing without routine antibiotics for uncomplicated cases in immunocompetent patients. For infections involving (MRSA), a common pyogenic bacterium, empiric antibiotics such as intravenous are recommended, particularly in severe cases or after failed drainage, with dosing adjusted based on culture results and patient factors. In deep-seated infections, surgical is crucial to remove necrotic tissue and pus, reducing the bacterial load and preventing systemic spread, often performed under imaging guidance for precise localization. For sterile pus, as seen in aseptic abscess syndrome associated with autoinflammatory disorders, management focuses on anti-inflammatory agents rather than antimicrobials, with high-dose corticosteroids providing dramatic improvement by suppressing the neutrophilic response. The Infectious Diseases Society of America (IDSA) guidelines for skin and soft tissue infections emphasize as first-line for purulent lesions, adjunctive antibiotics for systemic signs or comorbidities, and broad-spectrum coverage initially for severe cases pending culture results.

Historical Context

Early Recognition

The concept of "laudable pus"—a creamy, non-fetid discharge seen as beneficial in —is traditionally attributed to , where (c. 460–370 BCE) described observations of pus in suppurating wounds, distinguishing between white, non-offensive types indicating a better and sanious, muddy varieties signaling poorer outcomes, though modern scholarship clarifies he did not view pus as inherently necessary for recovery. This perspective, drawn from clinical examinations, influenced the belief that suppuration was a natural stage in resolving injuries, though recent analyses suggest the full idea of "laudable pus" developed later. Galen (129–200 CE), building on Hippocratic foundations, integrated suppuration into his humoral theory, viewing pus as a product of imbalance among the four humors—, , , and black bile—particularly associating it with excess hot and dry altering bodily fluids. Traditionally, is credited with promoting "laudable pus" in treatment to restore equilibrium, but contemporary indicates he advocated reducing suppuration through methods and saw pus primarily in abscesses as aiding drainage rather than encouraging it as essential for healing; he emphasized observing pus quality, favoring thick, odorless varieties as less harmful. These ideas shaped Roman and later medical doctrines, prioritizing the body's restorative capacities. During the medieval period, pus played a central role in wound care, especially amid frequent battle injuries from swords, arrows, and s, where surgeons routinely monitored suppuration as a prognostic indicator. Practitioners, influenced by Galenic texts translated into Latin, applied poultices, wine irrigations, and dressings to stimulate what was believed to be "laudable pus" formation, thinking it cleansed s of toxins and prevented humoral corruption; for instance, in treating suppurating gashes from combat, they would abscesses to promote drainage while avoiding "malignant pus" characterized by foul and thin consistency. This approach persisted in monastic infirmaries and camps, with empirical observations from medieval conflicts reinforcing the view that controlled suppuration aided , though some innovators like Hugh of began questioning its necessity by the 13th century. In the 18th and early 19th centuries, before the advent of germ theory, surgeons such as John Hunter (1728–1793) advanced understandings of pus through detailed anatomical studies and battlefield observations, describing it as a uniform product of without attributing it to external agents. In his treatise on inflammation and wounds, Hunter noted that pus formed consistently in response to tissue injury, classifying it as part of the body's reparative process—arising from altered vascular and cellular activity—rather than a separate pathological entity, based on dissections and experiments on animals and cadavers. He distinguished healthy suppuration in resolving abscesses from excessive or putrid forms that signaled poor outcomes, advocating conservative management to support natural drainage, which laid groundwork for viewing , and its pus byproduct, as adaptive rather than inherently destructive.

Evolution of Terminology

The term "pus" derives from the Latin pūs, which itself stems from the puon (πυόν), denoting a associated with decay or , reflecting early understandings of suppuration as a process of rotting tissue. This entered medical during Roman times, as evidenced in texts by authors like , who described purulent discharges in surgical contexts without distinguishing microbial origins. In medieval and early modern English medical literature, pus was often referred to obliquely through terms like "" for the purulent discharge from wounds or "" for a thinner, serous variant, evoking humoral theories where such fluids balanced bodily excesses. These descriptors persisted alongside the concept of "laudable pus," traditionally rooted in ancient traditions but now recognized as a later interpretive development, viewed as a positive sign of healing by expelling corrupt humors. The marked a pivotal shift in terminology, driven by Louis Pasteur's germ theory demonstrations in the 1860s, which linked putrid infections and pus formation to microbial activity, and Robert Koch's subsequent isolation of pus-producing like in the 1880s. This bacteriological framework discredited "laudable pus" as a indicator, reframing suppuration instead as a pathological response to invasion, with "pus" standardized to denote the inflammatory comprising dead leukocytes, , and debris. By the , obsolete terms such as "matter" and "" largely vanished from clinical usage, supplanted by precise bacteriological descriptors, while international standards like the World Health Organization's (ICD-11, effective 2022) formalized distinctions between pyogenic (pus-forming) bacterial infections, typically from sources like staphylococci, and non-pyogenic infections from other etiologies, such as viral or fungal processes. This evolution underscores how advancing refined pus-related nomenclature from metaphorical to etiologically grounded terminology.

References

  1. https://medlineplus.gov/ency/article/001353.htm
  2. https://www.ncbi.nlm.nih.gov/books/NBK593218/
  3. https://pmc.ncbi.nlm.nih.gov/articles/PMC4450319/
  4. https://my.clevelandclinic.org/health/diseases/14466-anal-fistula
  5. https://my.clevelandclinic.org/health/symptoms/pus
  6. https://www.medicalnewstoday.com/articles/249182
  7. https://www.healthline.com/health/pus
  8. https://www.woundsource.com/blog/identifying-different-types-wound-drainage
  9. https://my.clevelandclinic.org/health/symptoms/25033-serous-drainage
  10. https://www.verywellhealth.com/what-to-do-about-pus-from-a-wound-or-incision-3157314
  11. https://emedicine.medscape.com/article/226748-overview
  12. https://www.nethealth.com/blog/pus-proficiency-understanding-purulent-drainage/
  13. https://pubmed.ncbi.nlm.nih.gov/19460003/
  14. https://www.ncbi.nlm.nih.gov/books/NBK482349/
  15. https://www.merckmanuals.com/en-ca/professional/infectious-diseases/anaerobic-bacteria/overview-of-anaerobic-bacteria
  16. https://pmc.ncbi.nlm.nih.gov/articles/PMC7122703/
  17. https://pmc.ncbi.nlm.nih.gov/articles/PMC7123337/
  18. https://www.merckmanuals.com/professional/infectious-diseases/biology-of-infectious-disease/abscesses
  19. https://pmc.ncbi.nlm.nih.gov/articles/PMC3087859/
  20. https://medicine.osu.edu/-/media/files/medicine/departments/otolaryngology/atlas-of-head-and-neck-pathology/a/abscess-and-phlegmon.pdf
  21. https://www.ncbi.nlm.nih.gov/books/NBK519573/
  22. https://pmc.ncbi.nlm.nih.gov/articles/PMC97762/
  23. https://www.ncbi.nlm.nih.gov/books/NBK26846/
  24. https://www.ncbi.nlm.nih.gov/books/NBK585043/
  25. https://www.ncbi.nlm.nih.gov/books/NBK556038/
  26. https://pocketdentistry.com/7-chronic-inflammatory-processes/
  27. https://www.aafp.org/pubs/afp/issues/2006/0401/p1211.html
  28. https://pmc.ncbi.nlm.nih.gov/articles/PMC7825503/
  29. https://pmc.ncbi.nlm.nih.gov/articles/PMC4562417/
  30. https://pmc.ncbi.nlm.nih.gov/articles/PMC3432757/
  31. https://pmc.ncbi.nlm.nih.gov/articles/PMC7951234/
  32. https://www.sciencedirect.com/topics/medicine-and-dentistry/neutrophil-granule
  33. https://pmc.ncbi.nlm.nih.gov/articles/PMC3888517/
  34. https://pmc.ncbi.nlm.nih.gov/articles/PMC10464199/
  35. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/pyogenic-bacterium
  36. https://pmc.ncbi.nlm.nih.gov/articles/PMC5592399/
  37. https://www.clinicalmicrobiologyandinfection.com/article/S1198-743X%2822%2900281-6/fulltext
  38. https://www.pearson.com/channels/microbiology/asset/ffd89569/explain-the-different-actions-of-pyogenic-and-pyrogenic-toxins
  39. https://www.intechopen.com/chapters/82701
  40. https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2015.00015/full
  41. https://pmc.ncbi.nlm.nih.gov/articles/PMC4451395/
  42. https://www.ncbi.nlm.nih.gov/books/NBK587098/
  43. https://journals.asm.org/doi/10.1128/spectrum.00640-23
  44. https://pmc.ncbi.nlm.nih.gov/articles/PMC12230386/
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC8325443/
  46. https://stm.cairn.info/revue-european-journal-of-dermatology-2022-4-page-540?lang=en
  47. https://www.idsociety.org/practice-guideline/candidiasis/
  48. https://medlineplus.gov/ency/article/000211.htm
  49. https://www.pathologyoutlines.com/topic/liveramebicabscess.html
  50. https://www.ncbi.nlm.nih.gov/books/NBK430832/
  51. https://dermnetnz.org/topics/foreign-body-granuloma
  52. https://bnrc.springeropen.com/articles/10.1186/s42269-022-00970-2
  53. https://www.iasp-pain.org/aseptic-abscess-syndrome-in-rheumatoid-arthritis-patient/
  54. https://www.the-rheumatologist.org/article/case-report-abscess-as-a-manifestation-of-autoinflammatory-disease/
  55. https://pmc.ncbi.nlm.nih.gov/articles/PMC7358648/
  56. https://www.nature.com/articles/s41598-023-45320-y
  57. https://www.ncbi.nlm.nih.gov/books/NBK544279/
  58. https://www.merckmanuals.com/professional/dermatologic-disorders/bacterial-skin-infections/furuncles-and-carbuncles
  59. https://pmc.ncbi.nlm.nih.gov/articles/PMC3858730/
  60. https://medlineplus.gov/lab-tests/bacteria-culture-test/
  61. https://pmc.ncbi.nlm.nih.gov/articles/PMC3395037/
  62. https://academic.oup.com/cid/article/59/2/e10/2895845
  63. https://www.ncbi.nlm.nih.gov/books/NBK507882/
  64. https://pmc.ncbi.nlm.nih.gov/articles/PMC9267245/
  65. https://pmc.ncbi.nlm.nih.gov/articles/PMC5538214/
  66. https://onlinelibrary.wiley.com/doi/10.1111/j.1445-2197.2005.03338.x
  67. https://www.longdom.org/open-access/the-conquest-of-pus-a-history-of-bitumen-creosote-and-carbolic-acid-17748.html
  68. https://pmc.ncbi.nlm.nih.gov/articles/PMC2706344/
  69. https://www.cambridge.org/core/services/aop-cambridge-core/content/view/963852897C157B6BF07F43E42D98E22A/S0025727300023711a.pdf/treatment_of_wounds_through_the_ages.pdf
  70. https://pmc.ncbi.nlm.nih.gov/articles/PMC2001919/
  71. https://www.jameslindlibrary.org/articles/john-hunter-learning-from-natural-experiments-placebos-and-the-state-of-mind-of-a-patient-in-the-18th-century/
  72. https://www.etymonline.com/word/pus
  73. https://www.oed.com/dictionary/pus_n
  74. https://www.biologyonline.com/dictionary/pus
  75. https://www.herbalhistory.org/home/wp-content/uploads/2024/05/Rudys-List-of-Archaic-Medical-Terms-1.pdf
  76. https://2001translation.org/concordance/%25CE%25B9%25CC%2593%25CF%2587%25CF%2589%25CF%2581
  77. https://uknowledge.uky.edu/cgi/viewcontent.cgi?article=1107&context=microbio_facpub
  78. https://icd.who.int/browse11/l-m/en
  79. https://www.findacode.com/icd-11/code-698540116.html
  80. https://www.findacode.com/icd-11/code-1324834502.html
Add your contribution
Related Hubs
User Avatar
No comments yet.