Bubonic plague is caused by Yersinia pestis. Spread to people through bites from infected fleas, it forms flea-borne biofilms that promote bacterial transmission during feeding. After 2–6 days, it often brings fever and painful, swollen lymph nodes (buboes) in areas like the groin, armpit, or neck. This page walks through the bacterium’s biology, how it circulates as a zoonosis in rodent reservoirs, and how testing and early antibiotics affect outcomes.
Key Takeaways
- Bubonic plague bacterium Yersinia pestis is a Gram-negative, non-motile, coccobacillus-shaped, facultative anaerobic rod
- Yersinia pestis genome consists of a 4.65 Mb main chromosome and three plasmids: pPCP1 (9.6 kb), pMT1 (96 kb), and pFra (100 kb)
- The pathogen forms biofilms in the flea proventriculus, leading to blockage and regurgitation during feeding
- Classic symptom of bubonic plague is painful swelling of lymph nodes called buboes, typically in groin, armpit, or neck
- Incubation period for bubonic plague ranges from 2-6 days, average 4 days
- Fever in bubonic plague patients often exceeds 101°F (38.3°C), accompanied by chills and headache
- Untreated bubonic plague mortality rate is 50-90%, dropping to 10-20% with antibiotics if treated early
- Streptomycin is the first-line treatment for plague, with 85-100% efficacy if given within 18 hours of symptoms
- Gentamicin is an alternative, with success rates over 90% in bubonic plague cases
- Primary transmission of bubonic plague occurs via bites from infected fleas, mainly Xenopsylla cheopis
- Fleas become blocked by Y. pestis biofilm, regurgitating bacteria into host during blood meal
- Plague is a zoonosis maintained in rodent populations worldwide, with over 200 rodent species as reservoirs
- The Black Death pandemic of 1347-1351 is estimated to have caused the death of 75 to 200 million people across Eurasia and North Africa
- In the 14th century, the bubonic plague wiped out approximately 30-60% of Europe's population, equating to 25-50 million deaths
- Justinian Plague (541-549 AD) killed an estimated 25-50 million people in the Eastern Roman Empire
Bubonic plague is caused by Yersinia pestis, spreads via infected flea bites, and is often fatal without early antibiotics.
Related reading
01 · Category
Bacteriology And Pathogen20 stats
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Bubonic plague bacterium Yersinia pestis is a Gram-negative, non-motile, coccobacillus-shaped, facultative anaerobic rod
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Yersinia pestis genome consists of a 4.65 Mb main chromosome and three plasmids: pPCP1 (9.6 kb), pMT1 (96 kb), and pFra (100 kb)
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The pathogen forms biofilms in the flea proventriculus, leading to blockage and regurgitation during feeding
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Y. pestis has a type III secretion system encoded by the plasmid pCD1, injecting Yop proteins to inhibit phagocytosis
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The F1 capsule antigen of Y. pestis is a key virulence factor encoded by caf operon on pFra plasmid, antiphagocytic
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Y. pestis lipopolysaccharide (LPS) lacks the O-antigen, making it less endotoxic compared to other Enterobacteriaceae
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The Pla plasminogen activator on pPCP1 plasmid promotes dissemination by fibrinolysis and bacterial spread
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Y. pestis temperature-regulated virulence; expresses F1 capsule at 37°C but not at flea temperature of 25°C
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The pathogen has two chromosomes in some strains, but primarily one with megaplasmids
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Y. pestis evolved from Y. pseudotuberculosis about 1,500-20,000 years ago via plasmid acquisition and pseudogene accumulation
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Y. pestis has 149 pseudogenes reducing metabolic capabilities compared to Y. pseudotuberculosis
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pMT1 plasmid encodes murine toxin (Ymt) essential for flea survival and transmission
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Yops (Yersinia outer proteins) like YopH phosphatase and YopE disrupt actin cytoskeleton in host cells
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Capsular antigen F1 is 98% sensitive for serological diagnosis in convalescent phase
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Y. pestis siderophores like yersiniabactin scavenge iron from host transferrin
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The pathogen inhibits dendritic cell migration via Pla protease activity
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Genomic island HPI (high-pathogenicity island) confers siderophore production
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Y. pestis grows optimally at 28°C in fleas, shifting to 37°C virulence genes in mammals
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Over 7,000 genes in Y. pestis CO92 strain, with 10% insertion sequences causing rearrangements
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LcrV protein modulates host immune response, inducing IL-10 anti-inflammatory cytokine
Interpretation
Bacteriology And Pathogen Interpretation
Within Bacteriology And Pathogen, Yersinia pestis stands out as a Gram negative, facultative anaerobe whose genome is only 4.65 Mb on a main chromosome plus three plasmids and whose major virulence tools are tightly plasmid linked, including a type III secretion system on pCD1 and the antiphagocytic F1 capsule encoded on pFra, while its O antigen absent LPS makes it less endotoxic than many other Enterobacteriaceae.
02 · Category
Clinical Manifestations20 stats
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Classic symptom of bubonic plague is painful swelling of lymph nodes called buboes, typically in groin, armpit, or neck
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Incubation period for bubonic plague ranges from 2-6 days, average 4 days
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Fever in bubonic plague patients often exceeds 101°F (38.3°C), accompanied by chills and headache
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Buboes are extremely painful, tense, tender, and warm, measuring 1-10 cm in diameter
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About 1-15% of bubonic plague cases progress to septicemic plague without buboes
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Pneumonic plague features cough with bloody or watery sputum, chest pain, and difficulty breathing
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Septicemic plague presents with high fever, chills, extreme weakness, abdominal pain, shock, and purple skin blotches
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Untreated bubonic plague has a case-fatality rate of 30-60%
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Recovery from bubonic plague takes about 1 week, but suppuration of buboes may require incision and drainage
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In pharyngeal plague, sore throat, pain on swallowing, and cervical lymphadenopathy are common
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Gastrointestinal symptoms like nausea, vomiting, diarrhea occur in 10-50% of bubonic cases
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Delirium and hypotension develop in 20-50% of untreated cases progressing to sepsis
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Buboes most common in femoral (groin) nodes (50-70%), followed by axillary (20-30%)
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Skin lesions like petechiae and purpura appear in septicemic plague due to DIC
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Pneumonic form has incubation of 1-3 days, rapidly fatal within 24 hours without treatment
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Meningitis rare (1%), with CSF showing pleocytosis and gram-negative rods
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Post-plague syndrome includes fatigue, headache lasting months in 20% survivors
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Leukocytosis with left shift (10,000-20,000 WBC/mm³) typical in blood work
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Thrombocytopenia (<100,000/µL) in 50% of septicemic cases due to consumption
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Elevated liver enzymes (ALT/AST 2-5x normal) in 30-40% of cases
Interpretation
Clinical Manifestations Interpretation
In the clinical manifestations of bubonic plague, patients typically develop intensely painful buboes within a short 2 to 6 day incubation period with fever often above 101°F, while about 1 to 15% progress to septicemic plague without buboes, and pneumonic cases show respiratory symptoms like cough with bloody or watery sputum.
03 · Category
Diagnosis, Treatment, And Prevention19 stats
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Untreated bubonic plague mortality rate is 50-90%, dropping to 10-20% with antibiotics if treated early
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Streptomycin is the first-line treatment for plague, with 85-100% efficacy if given within 18 hours of symptoms
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Gentamicin is an alternative, with success rates over 90% in bubonic plague cases
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Diagnosis confirmed by PCR detecting ypo2088 or F1 gene, or culture from bubo aspirate/blood
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Serology (passive hemagglutination) shows IgG titers ≥1:16 post-infection
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Plague vaccine (HVO) no longer available; live attenuated EV76 used in some countries with 70-90% efficacy against bubonic
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Rodent control via zinc phosphide bait reduces plague risk by 80% in endemic areas
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Flea control with insecticides like deltamethrin reduces transmission by 95% in treated areas
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Post-exposure prophylaxis with doxycycline (100 mg BID x 7 days) prevents plague in 90% of cases
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Doxycycline 100 mg BID x 10 days is second-line treatment, 95% survival if early
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Ciprofloxacin 400 mg IV BID effective alternative, used in mass prophylaxis
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F1 antigen rapid dipstick test 90-100% sensitive/specific in field
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Gram stain of bubo aspirate shows bipolar staining "safety pin" bacilli in 60% cases
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Chest X-ray in pneumonic plague shows bilateral patchy infiltrates
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rF1V vaccine candidate induces 100% protection in mice against bubonic
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Insecticide-treated clothing reduces flea bites by 85% in endemic zones
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Avoiding sick/dead animals prevents 90% human exposures in US
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Quarantine for pneumonic contacts 7 days or until sputum negative
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Levofloxacin 750 mg daily x 10 days prophylaxis efficacy >95%
Interpretation
Diagnosis, Treatment, And Prevention Interpretation
For diagnosis, treatment, and prevention, the key trend is that rapid medical action dramatically improves outcomes, with untreated bubonic plague mortality of 50 to 90% falling to 10 to 20% when antibiotics are started early and treatments like streptomycin reaching 85 to 100% efficacy if given within 18 hours.
04 · Category
Epidemiology And Transmission20 stats
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Primary transmission of bubonic plague occurs via bites from infected fleas, mainly Xenopsylla cheopis
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Fleas become blocked by Y. pestis biofilm, regurgitating bacteria into host during blood meal
03
Plague is a zoonosis maintained in rodent populations worldwide, with over 200 rodent species as reservoirs
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Human cases often follow die-offs in rodent populations due to high flea infestation
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Pneumonic plague transmits person-to-person via respiratory droplets, with R0 estimated at 1.3-2.0
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In the US, 80% of plague cases since 1970 occurred in rural New Mexico, Arizona, or California
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Globally, 1,000-2,000 human cases reported annually to WHO, with 100-200 deaths
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Madagascar accounts for 90% of global plague cases, with endemic foci in central highlands
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Plague bacilli multiply in flea gut, forming proventricular blockage within 1-2 days post-infection
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Rodent fleas prefer rats (Rattus spp.), transmitting plague with efficiency up to 30% per bite
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Secondary pneumonic plague develops in 10-15% of untreated bubonic cases via bacteremia
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In Madagascar, 95% cases are bubonic, 4% pneumonic, 1% septicemic
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US average 7 cases/year (range 1-17), 80% in Western states since 1970
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Fleas transmit at 1-28 bacteria per bite, but blockage increases to thousands
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Sylvatic cycle in prairie dogs (Cynomys spp.) main US reservoir, epizootics precede human cases
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Person-to-person spread rare except pneumonic, last US cluster 1924-1925
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Climate factors like El Niño increase rodent fleas, boosting cases by 200%
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Congo rats (Rattus losea) key amplifier in Asian cycles
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DNA from Black Death victims confirms Y. pestis as cause, branch 2.MED
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Global seroprevalence in endemic areas 1-20%, indicating exposure
Interpretation
Epidemiology And Transmission Interpretation
Bubonic plague transmission is largely driven by flea and rodent ecology, with fleas infected by Y. pestis biofilms causing most human outbreaks after rodent die offs, while pneumonic plague can spread person to person with an R0 estimated at 1.3 to 2.0 and in the US 80% of cases since 1970 have clustered in rural New Mexico, Arizona, or California.
05 · Category
Historical Epidemics20 stats
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The Black Death pandemic of 1347-1351 is estimated to have caused the death of 75 to 200 million people across Eurasia and North Africa
02
In the 14th century, the bubonic plague wiped out approximately 30-60% of Europe's population, equating to 25-50 million deaths
03
Justinian Plague (541-549 AD) killed an estimated 25-50 million people in the Eastern Roman Empire
04
The Third Pandemic began in Yunnan, China in 1855 and spread globally, causing over 12 million deaths by 1960
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In 1665-1666, the Great Plague of London killed about 100,000 people, roughly 20% of the city's population
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Plague outbreaks in India between 1896-1918 resulted in over 12 million deaths
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The 1720-1722 Marseille plague killed approximately 40% of the city's population, around 100,000 people
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In the 14th century China, the plague is believed to have killed up to 25 million people before spreading to Europe
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Hong Kong plague outbreak of 1894 saw 2,535 deaths in a population of 300,000
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The 1900 Sydney plague killed 38 out of 40 cases identified
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The Black Death reached Sicily in October 1347 via ships from the Black Sea
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Plague in Avignon 1348 killed 50-60% of population, including Pope Clement VI's court
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The 1527-1531 Italian plague killed 20-50% in affected cities like Florence
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Bombay plague of 1896-1898 had 11,000 deaths in first year alone
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The 1710-1711 Moscow plague killed about 100,000-150,000 people
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Vienna plague 1679 killed 76,000, nearly a quarter of the population
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14th century Florence lost 60% of its population to plague in 1348
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Plague in Cairo 1348-1349 killed 40% of the population
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1894 Hong Kong outbreak led to discovery of Y. pestis by Yersin and Kitasato
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US plague introduction in 1900 via rats on ships from Hong Kong to San Francisco
Interpretation
Historical Epidemics Interpretation
Across historical epidemics, plague repeatedly drove catastrophic population losses, including Europe’s 14th century decline of about 25 to 50 million deaths and even larger tolls like the Black Death’s estimated 75 to 200 million deaths, showing how these outbreaks were capable of reshaping whole regions rather than staying local.
report visual · Breakdown
How bubonic plague spreads (and what drives it)
Bubonic plague transmission is tightly linked to flea/rodent cycles and to the bacterial changes that occur across environments.
10%
Over 7,000 genes in Y. pestis CO92 strain, with 10% insertion sequences causing rearrangements
90%
Gentamicin is an alternative, with success rates over 90% in bubonic plague cases
Reference
Cite This Report
This report is designed to be cited. We maintain stable URLs and versioned verification dates. Copy the format appropriate for your publication below.
APA
Felix Zimmermann. (2026, February 13). Bubonic Plague Statistics. Gitnux. https://gitnux.org/bubonic-plague-statistics
MLA
Felix Zimmermann. "Bubonic Plague Statistics." Gitnux, 13 Feb 2026, https://gitnux.org/bubonic-plague-statistics.
Chicago
Felix Zimmermann. 2026. "Bubonic Plague Statistics." Gitnux. https://gitnux.org/bubonic-plague-statistics.
Sources & references
18 datasets cited across this report · attribution is report-level