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Bubo

A bubo (from the Greek βουβών boubṓn, meaning "groin")^[1] is an inflammatory swelling of one or more lymph nodes, typically painful and tender, representing reactive infectious lymphadenopathy.^[2] Buboes most commonly occur in the groin (inguinal), armpit (axillary), or neck (cervical) regions and are a hallmark symptom of certain bacterial infections, particularly bubonic plague caused by the bacterium Yersinia pestis, where they develop 2–7 days after exposure via flea bites.^[3]^[4] They can vary in size from pea-like to as large as an egg and may suppurate (form pus), though they also appear in other conditions such as chancroid, lymphogranuloma venereum, and tuberculosis.^[5] Historically, buboes were prominently described during outbreaks of the Black Death in the 14th century, contributing to the term "bubonic" plague.^[6]

Definition and Characteristics

Definition

A bubo is defined as an acute or chronic inflammatory enlargement of one or more lymph nodes, typically exceeding 1 cm in diameter and often presenting as painful and tender swellings.^[7]^[5]^[8] These enlargements occur in lymph nodes, which function as key components of the immune system by filtering lymph fluid and mounting responses to infections.^[9] In distinction from general lymphadenopathy, which encompasses any abnormal enlargement of lymph nodes due to a broad range of reactive, neoplastic, or other processes, a bubo specifically refers to suppurative lymphadenitis characterized by pus-forming inflammation that results in fluctuant, soft swellings.^[10]^[11]^[12] The term "bubo" originates from the Ancient Greek word boubōn, meaning "groin" or "swelling," and entered medical literature around the 14th century to describe such glandular inflammations.^[13]^[2]

Physical Characteristics

Buboes are most commonly located in the inguinal (groin) and femoral regions, followed by the axillary (armpit) and cervical (neck) regions; they are often unilateral and correspond to the site of primary infection drainage.^[14] Initially, a bubo presents as an erythematous, warm, and extremely tender swelling of one or more lymph nodes, with the overlying skin elevated and possibly tense.^[4] As the condition progresses, the node enlarges to a typical size of 1-5 cm in diameter, though it can reach up to 10 cm, developing fluctuance indicative of pus accumulation within.^[4] The skin may show discoloration ranging from red to purple, and in severe cases such as bubonic plague, it can progress to necrosis with blackening of the affected tissue.^[15] Palpation often reveals matting of adjacent nodes, creating a firm, adhered mass.^[16] In advanced stages, buboes may spontaneously rupture, draining foul-smelling pus and potentially forming fistulas or leading to scarring upon healing.^[17] This evolution is particularly noted in infections like lymphogranuloma venereum and chancroid, where suppurative complications are common.^[18]

Causes and Pathophysiology

Primary Infectious Causes

Buboes, as inflamed and often suppurative lymph nodes, primarily arise from bacterial infections that invade the lymphatic system following initial entry through the skin or mucous membranes, triggering an acute immune response characterized by rapid bacterial multiplication and regional lymphadenitis.^[19] The most notorious primary infectious cause is Yersinia pestis, the bacterium responsible for bubonic plague, which is transmitted to humans via the bites of infected fleas, particularly Xenopsylla cheopis, the Oriental rat flea that vectors the pathogen from rodent reservoirs.^[20] Following inoculation, Y. pestis evades initial phagocytosis, proliferates locally, and disseminates through bacteremia to seed draining lymph nodes, where it induces massive inflammation and necrosis within an incubation period of 2-6 days.^[21]^[22] Another key pathogen is Haemophilus ducreyi, which causes chancroid, a sexually transmitted infection acquired through direct contact with genital ulcers during sexual activity.^[23] The bacteria penetrate the skin or mucosa, leading to painful ulcers, and in 25-50% of untreated cases, progress to suppurative inguinal buboes via lymphatic spread and an intense neutrophilic response.^[23]^[24] Lymphogranuloma venereum (LGV), caused by invasive serovars L1-L3 of Chlamydia trachomatis, represents a systemic chlamydial infection typically transmitted sexually and more prevalent in tropical and subtropical regions between 20° north and south latitudes.^[12]^[25] After initial mucosal inoculation, the obligate intracellular bacteria disseminate hematogenously or lymphatically, provoking a granulomatous inflammatory response that culminates in fluctuant or suppurative buboes, often accompanied by proctitis in advanced cases.^[12] Francisella tularensis, the etiologic agent of tularemia, is a highly virulent zoonotic bacterium transmitted primarily through tick or deer fly bites or by handling infected animals such as rabbits and rodents.^[26] In its ulceroglandular form—the most common presentation—the pathogen enters via cutaneous abrasions or arthropod bites, replicates intracellularly in macrophages, and traffics to regional lymph nodes, eliciting a pyogenic response that forms tender, sometimes suppurative buboes alongside a primary ulcer.^[27] Historically, bubonic plague caused by Y. pestis was the predominant form during the Black Death pandemic of 1347-1351, accounting for the majority of cases that resulted in widespread mortality across Europe.^[28] In modern times, global incidence of plague remains low, with fewer than 5,000 human cases reported annually, primarily in endemic foci in Africa, Asia, and the Americas.^[15]

Secondary and Non-Infectious Causes

Secondary infectious causes of bubo-like swellings often arise from contiguous spread of bacteria from skin wounds or soft tissue infections, leading to acute suppurative lymphadenitis. Staphylococcus aureus and Streptococcus pyogenes are the most common pathogens responsible for these cases, particularly in children and following minor trauma or abscesses in the extremities.^[29] These infections result in painful, erythematous lymph node enlargement that may progress to fluctuance if untreated, distinguishing them from primary systemic infections like plague.^[30] Rare viral etiologies can also produce secondary lymphadenitis mimicking bubo. Herpes simplex virus occasionally causes focal necrotic lymphadenitis with paracortical hyperplasia, though this is uncommon and typically associated with disseminated herpetic infection in immunocompromised individuals.^[31] Another notable rare cause is cat-scratch disease due to Bartonella henselae, acquired via scratches or bites from infected cats; it presents with regional lymphadenopathy resembling buboes in approximately 90% of cases, often 1-3 weeks post-inoculation, accompanied by a primary cutaneous papule.^[32] Non-infectious etiologies encompass malignancies, autoimmune disorders, and drug reactions that produce firm, non-suppurative nodal enlargements frequently misdiagnosed as infectious buboes. Lymphomas, such as non-Hodgkin's lymphoma, can manifest as painless, firm inguinal or axillary nodes mistaken for buboes, as seen in cases where biopsy reveals diffuse large B-cell histology rather than infection.^[33] Autoimmune conditions like Kikuchi-Fujimoto disease involve histiocytic necrotizing lymphadenitis, presenting with tender, mobile cervical nodes (1-7 cm) in 60-90% of cases, often unilateral but without suppuration or positive cultures.^[34] Drug-induced pseudolymphomas, exemplified by phenytoin, trigger systemic reactions including generalized lymphadenopathy, fever, rash, and hepatosplenomegaly, resolving upon drug withdrawal.^[35] Differentiation from primary infectious buboes relies on clinical features: non-infectious swellings are typically painless, rubbery, and bilateral without systemic fever or fluctuance, whereas infectious forms are tender, unilateral, and associated with warmth and leukocytosis.^[36] Biopsy and imaging are essential for confirmation, as non-infectious causes lack neutrophilic infiltrates and show polyclonal lymphoid expansions.^[10]

Clinical Presentation and Associated Conditions

Symptoms in Key Diseases

In bubonic plague, patients typically present with sudden onset of high fever ranging from 38°C to 41°C, accompanied by chills, severe headache, and malaise, alongside the development of painful, swollen inguinal lymph nodes known as buboes.^[37]^[15] If untreated, the infection can progress rapidly to septicemia, with a mortality rate of 30% to 60%.^[15] In chancroid, buboes emerge following the appearance of one or more painful, ragged genital ulcers, often with associated dysuria, purulent urethral discharge, and regional tenderness; these lymphadenopathic swellings are suppurative and occur in up to 50% of untreated cases.^[38]^[23] The condition tends to be more severe and less responsive to treatment in uncircumcised males due to the pathogen's preference for the foreskin environment.^[38]^[23] Lymphogranuloma venereum (LGV) often begins with a transient, painless primary chancre at the site of inoculation, which may go unnoticed, followed by constitutional symptoms such as fever, malaise, and myalgias, leading to the formation of matted, tender inguinal buboes that can suppurate or fistulize.^[12]^[39] Anorectal involvement, manifesting as proctocolitis with rectal pain, discharge, and tenesmus, is a prominent feature, particularly in cases among men who have sex with men.^[12] In tularemia, particularly the ulceroglandular form, an ulcer develops at the site of bacterial entry, such as a skin wound or tick bite, accompanied by low-grade fever, regional lymphadenopathy with tender epitrochlear, axillary, or cervical buboes, and systemic symptoms like headache and fatigue.^[40]^[41]

Complications

Untreated or severe buboes can rupture, releasing pus that leads to secondary infections such as cellulitis, abscess formation, or chronic fistulas.^[38] In chancroid, suppurative buboes may result in genital scarring or urogenital fistulas even after effective therapy, while inguinal lymphadenitis occurs in less than 50% of cases and heals slowly if fluctuant.^[38] Similarly, in bubonic plague, bubo enlargement can cause rupture with discharge of malodorous pus, facilitating local tissue damage and secondary bacterial invasion.^[42] Systemic dissemination from ruptured buboes heightens mortality risk, particularly in plague where bacteremia can seed secondary pneumonic plague, enabling airborne transmission.^[36] Untreated pneumonic plague has a near-100% fatality rate if not addressed within 24 hours, compared to 30–60% for bubonic plague alone.^[36] This progression underscores the bubo's role as a nidus for hematogenous spread, exacerbating outcomes in endemic settings.^[36] Hemorrhagic transformation of buboes in Yersinia pestis infections can lead to necrosis and gangrene, contributing to the "Black Death" moniker through tissue sloughing and acral involvement from disseminated intravascular coagulation.^[43] In severe cases, this results in blackened, necrotic extremities and lymph nodes, amplifying disfigurement and sepsis risk.^[43] Chronic sequelae from lymphatic obstruction include post-lymphogranuloma venereum (LGV) elephantiasis, characterized by genital swelling and fibrosis due to persistent inflammation.^[39] This tertiary manifestation arises from untreated infection, causing strictures, fistulas, and lymphedema in the genitalia or rectum.^[39] During the 14th-century Black Death pandemics, complications like secondary pneumonic spread and septicemia from bubonic plague contributed to an estimated 25 million deaths across Europe, representing about one-third of the population.^[28]

Diagnosis

Diagnostic Methods

Diagnosis of buboes begins with a thorough physical examination, where clinicians palpate the affected lymph nodes to assess for tenderness, size, and fluctuance, which can indicate suppuration or abscess formation.^[44] In cases of suspected bubonic plague, fine-needle aspiration of the bubo is performed under sterile conditions to obtain material for immediate microscopic evaluation via Gram stain, revealing characteristic bipolar staining (safety-pin appearance) of Yersinia pestis, and for culture confirmation.^[44] This procedure requires enhanced biosafety precautions due to the risk of aerosol generation and potential transmission.^[45] Laboratory testing is essential for pathogen identification. Polymerase chain reaction (PCR) assays targeting Y. pestis genes, such as pla or caf1, offer high sensitivity and rapid results from bubo aspirates, blood, or sputum, making them a cornerstone for confirming plague. For lymphogranuloma venereum (LGV), definitive diagnosis relies on LGV-specific PCR genotyping of Chlamydia trachomatis serovars L1-L3 from bubo aspirates, rectal swabs, or urethral specimens.^[12] Serologic tests, including IgM detection for LGV (titers >1:64) or complement fixation titers, support diagnosis when molecular tests are unavailable, though they are less specific.^[46] Blood cultures are recommended to detect bacteremia, particularly in systemic infections like plague, where Y. pestis can be isolated from blood.^[15] Imaging modalities aid in characterizing buboes and ruling out complications. Ultrasound is commonly used as a first-line tool to differentiate abscess from solid lymphadenopathy, with pus appearing as a hypoechoic collection with internal debris and posterior enhancement.^[47] Computed tomography (CT) or magnetic resonance imaging (MRI) provides detailed evaluation of deep-seated nodes, assessing for necrosis, fistula formation, or extension into surrounding tissues.^[48] Biopsy via fine-needle aspiration cytology can reveal granulomatous inflammation or suppurative changes in buboes associated with infections like LGV or tuberculosis, guiding further management.^[39] However, excisional biopsy is generally avoided in suspected plague due to the aerosolization risk during tissue manipulation.^[45] According to CDC guidelines, suspected plague cases warrant immediate bubo aspiration for Gram stain, culture, and PCR, alongside blood cultures, with treatment initiated empirically without awaiting results.^[44] The World Health Organization emphasizes laboratory confirmation through culture or PCR from bubo pus, combined with epidemiological criteria such as exposure to infected rodents or fleas.^[15]

Differential Diagnosis

The differential diagnosis of bubo encompasses a range of infectious, malignant, and non-infectious conditions that mimic the presentation of acutely enlarged, tender lymph nodes, particularly in inguinal, axillary, or cervical regions, requiring careful clinical evaluation to exclude alternatives.^[4] Infectious mimics include acute lymphadenitis from various pathogens. Viral causes, such as Epstein-Barr virus (EBV) in infectious mononucleosis, typically produce bilateral, generalized cervical lymphadenopathy accompanied by fatigue, sore throat, and hepatosplenomegaly, differing from the unilateral, suppurative, and highly painful buboes associated with bacterial infections like Yersinia pestis.^[10] Fungal infections, including histoplasmosis, can lead to mediastinal or hilar lymphadenopathy with systemic symptoms like fever and cough, though inguinal involvement is rarer; differentiation relies on exposure to endemic areas (e.g., bird droppings) and confirmatory antigen testing or biopsy revealing intracellular yeasts.^[49] Bacterial etiologies such as streptococcal or staphylococcal lymphadenitis often stem from contiguous skin infections with visible cellulitis or lymphangitis, unlike the hematogenous spread in plague-related buboes.^[4] Additional infectious differentials include tularemia (linked to rabbit or tick exposure) and cat-scratch disease (history of feline contact with regional adenopathy), both featuring less fulminant inflammation than plague buboes.^[50] Malignancies must be considered, particularly Hodgkin lymphoma, which manifests as painless, rubbery, and mobile lymph nodes—often cervical or mediastinal—with possible B symptoms (fever, night sweats, weight loss), in stark contrast to the acute tenderness, fluctuance, and suppuration of infectious buboes. Lymphomas progress chronically with systemic involvement detectable via imaging or biopsy showing Reed-Sternberg cells, helping to exclude acute infectious processes.^[10] Other non-infectious conditions include inguinal hernia, presenting as a reducible, non-tender mass exacerbated by Valsalva maneuver, without fever or overlying erythema, readily distinguished by clinical reduction or ultrasound.^[51] Hidradenitis suppurativa involves recurrent, painful groin abscesses from apocrine gland inflammation, forming sinus tracts over time but lacking the isolated nodal focus and acute febrile illness of buboes.^[52] In endemic tropical areas, lymphatic filariasis causes chronic, progressive inguinal swelling due to parasitic obstruction, often with lymphedema rather than discrete acute nodes, confirmed by peripheral blood smears for microfilariae.^[53] Key differentiators for buboes include their typical unilateral distribution, rapid onset (within days), exquisite tenderness, and association with fever and relevant exposures (e.g., fleas or rodents), whereas malignancies exhibit indolent, painless enlargement with constitutional symptoms, and non-infectious masses show mechanical or chronic features without inflammation.^[4] A diagnostic algorithm commences with a thorough history emphasizing travel to endemic regions, animal or vector exposure, and sexual contacts, followed by laboratory evaluation (e.g., complete blood count, inflammatory markers) and imaging (e.g., ultrasound for node architecture); negative bacterial cultures or serologies can effectively exclude infectious causes like plague or LGV.

Management and Treatment

Historical Approaches

In the 14th century, medieval treatments for plague-related buboes focused on empirical surgical and humoral interventions. Physicians, including the French surgeon Guy de Chauliac, advocated lancing or bursting the painful swellings in the groin or armpits to drain pus and relieve pressure, believing this released toxic "poisons" accumulated in the body according to prevailing Galenic theory. This procedure often involved heated rods or irons to cauterize and open the buboes, though it carried risks of further tissue damage and spread of infection. Chauliac, who survived a mild case while treating patients in Avignon during the 1348 outbreak, documented these methods in his Chirurgia Magna, emphasizing rest and supportive care alongside surgery.^[54]^[55] Folk and herbal remedies supplemented these practices, reflecting widespread desperation amid high mortality. Applications of sliced onions or vinegar-soaked cloths to the buboes aimed to draw out infection through supposed antiseptic properties, while leeches facilitated bloodletting to restore humoral balance by reducing excess blood. Quarantine measures implemented in Florence in 1348, such as isolating the afflicted in designated areas and restricting movement, contributed to curbing transmission, with city ordinances enforcing separation of healthy from sick households. Giovanni Boccaccio's Decameron (1353) vividly captured these horrors, describing buboes varying from apple-sized to egg-like and noting their spontaneous bursting as a potentially favorable prognostic sign, indicating survival beyond the acute phase when many perished beforehand.^[54]^[56]^[57] By the 19th century, bacteriological insights transformed understanding of buboes as symptoms of Yersinia pestis infection. In 1894, Alexandre Yersin isolated and cultured the plague bacillus during an outbreak in Hong Kong, confirming its role in causing the characteristic lymphadenopathy. Early 20th-century serum therapies, derived from immunized animals, offered initial promise but yielded limited efficacy; for instance, one series of 92 cases reported 42% mortality, comparable to the roughly 50% fatality in untreated bubonic plague. Incision and drainage persisted as a standard surgical approach into the 1940s, but without antibiotics, these interventions frequently led to secondary bacterial infections, complicating recovery and contributing to overall poor outcomes.^[58]^[59]

Modern Interventions

Modern interventions for buboes primarily involve prompt antibiotic therapy tailored to the underlying infectious cause, alongside supportive measures and selective surgical procedures to alleviate symptoms and prevent complications. For bubonic plague caused by Yersinia pestis, first-line antibiotics include gentamicin (5 mg/kg IV/IM daily for adults) or streptomycin, administered for 10-14 days, which reduces mortality to less than 5% when initiated early.^[60] Fluoroquinolones such as ciprofloxacin (400 mg IV every 8 hours or 750 mg PO every 12 hours for adults) are also recommended as first-line options, with a recent randomized trial demonstrating that 10 days of oral ciprofloxacin monotherapy achieves a treatment failure rate of 9.0%, noninferior to combination aminoglycoside-ciprofloxacin regimens.^[60]^[61]^[62] In cases of chancroid due to Haemophilus ducreyi, single-dose azithromycin (1 g orally) or ceftriaxone (250 mg IM) is effective, resolving symptoms within 7 days in most patients.^[38] For lymphogranuloma venereum (LGV) caused by Chlamydia trachomatis, doxycycline (100 mg orally twice daily for 21 days) is the preferred regimen, with alternatives including azithromycin (1 g orally weekly for 3 weeks).^[12] Supportive care focuses on symptom relief and infection control. Analgesics such as ibuprofen are used to manage pain from inflamed buboes, while elevation of the affected limb and warm compresses promote comfort and reduce swelling.^[60] For contagious cases like plague, patients require isolation with droplet precautions to prevent airborne transmission, particularly during the first 48 hours of antibiotic therapy.^[60] Surgical interventions are reserved for symptomatic relief and are performed under antibiotic cover to minimize dissemination risk. Needle aspiration through intact skin is preferred over incision and drainage for fluctuant buboes in LGV and chancroid, as it reduces the chance of secondary ulceration or fistula formation; incision is considered only if aspiration fails or for abscesses larger than 5 cm.^[12]^[38] In plague, buboes typically resolve without intervention, but aspiration may be used cautiously for large, suppurative nodes to avoid aerosolization, while full incision is discouraged due to the risk of spreading infection.^[63] Guidelines emphasize empiric therapy pending confirmation. The CDC recommends presumptive doxycycline for suspected LGV with severe lymphadenopathy or proctocolitis, achieving cure rates over 98%.^[12] WHO protocols for plague include doxycycline (100 mg PO twice daily for 7 days) as post-exposure prophylaxis for close contacts to prevent secondary cases.^[64] Outcomes with early intervention are favorable, with buboes resolving in 80-90% of cases across etiologies; for plague, most patients show reduced bubo size or complete resolution within 7 days of starting antibiotics.^[65] As of 2023, ongoing surveillance by CDC and WHO monitors Y. pestis resistance, which remains rare but includes isolated strains with multidrug profiles, underscoring the need for susceptibility testing in endemic areas.^[63]^[66]

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Differential Diagnosis Acute pulmonary histoplasmosis: causes of atypical pneumonia. Chronic pulmonary histoplasmosis: tuberculosis, mycobacterial, ...Missing: bubo | Show results with:bubo
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Based upon morphological features and immunochromatography based antigen-assay, a diagnosis of filarial lymphadenitis caused by Wuchereria bancrofti was made.Missing: hernia hidradenitis
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