Course Title: Microbiology and Immunology 2500
Lecture: The Black Death
Instructor: Dr. Idowu Olawoye (iolawoye@uwo.ca)
Institution: Western University Canada
Recognize the impact of microbes on societies
Understand the historical context of plague
Comprehend the pathogenic mechanisms of Yersinia pestis and its various forms of plague
Type of Bacteria: Gram-negative, rod-shaped
Pathogenic Species:
Y. enterocolitica: Causes yersiniosis (rare diarrhea and abdominal pain)
Y. pseudotuberculosis: Primarily an animal pathogen; can cause tuberculosis-like symptoms in animals and enteritis in humans
Y. pestis: Causative agent of the plague
Discovery: Identified by Alexandre Yersin and Kitasato Shibasaburo in the late 1800s
Virulence: Highly virulent; can lead to death in 2-4 days due to sepsis or pneumonia
Colonization: Not an efficient colonizer of humans
Incubation Period: 3-7 days
Acute Symptoms:
Sudden onset of fever, chills, headaches, muscle pain, and weakness
Painful lymph node swellings (buboes) in armpits, legs, neck, or groin
Severe health issues: high fever, delirium, mental dete
How we know Y. pestis caused black death?
took teeth of people infected by the plague and were able to sequence the genome from the bodies
strain that caused black death and plague of Justinian are different. However, both strains share a common ancestor, which provides insight into the evolution of Yersinia pestis and its various pathogenic forms.
Timeframe: 6th century (541-542 AD)
Impact: Spread throughout Europe, resulting in ~50% population death rate
Duration: Cycled for ~200 years until 750 AD, killing an estimated 100 million people
Origin: Linked to Yersinia pestis, spread from Asia to Europe in late 1340s
Impact: Global population reduced from ~450 million to ~350 million; ~25 million Europeans (1/3) died
Response: Widespread panic, beliefs in divine retribution, persecution of minorities, collapse of social structures
Origin: Started in China (1850s), spread worldwide until 1959
Casualties: Over 12 million deaths in China and India; reached San Francisco in 1900
Current Status: Y. pestis remains established in Southwestern U.S.
Transmission: Primarily from rodents via fleas; classified as a zoonotic pathogen
blocks hunger of flea which causes flea to infect more people trying to satisfy hunger
Mechanism: Causes blocking in fleas, biofilm formation leads to regurgitation of bacteria during feeding
Infective Dose: As few as 10 cells can cause infection; Y. pestis grows in innate immune cells and lymphoid organs
Consequences: Swelling lymph nodes (buboes); can multiply in the bloodstream, elevating mortality risk
Immune Evasion: Can evade the innate immune response allowing for unchecked proliferation
Key Factors:
Type III secretion system for injecting virulence factors
Phospholipase to aid survival in fleas
Plasminogen activator (clot buster for dissemination)
Yersiniabactin (iron-binding siderophore)
Mutated LPS structure for immune evasion
Description: Most common form; transmitted via flea bites
Symptoms: Painfully swollen lymph nodes (