lecture 10: the black death continued.

the fate of the flea: (4)

• after x. cheopis feeds on an infected rat, the ingested plague bacteria multiply rapidly in the fleas midgut and spine-filled proventriculus and form noticeable colonies in just a few days

• as colonies grow/coalesce they eventually are larger enough to occlude the proventriculus - blocking the midgut, causing the flea to starve

• blocked/starving fleas repeatedly attempt to feed by using their pharyngeal muscles to draw blood into the foregut which causes distension of the esophagus but no movement of blood past the proventricular back

• eventually the flea is forced to relax its pharyngeal muscles which results in yersinia pestis contaminated blood being pushed from the distended esophagus back into the feeding site (causing infection of the vertebrate host)

2 characteristic bubonic plague symptoms:

• hemorrhaging under the skin (skin darkens with blood - ‘black plague’ - darkened skin)

• swollen, tender, painful lymph nodes (known as bubo - bubonic plague)

lymph node sites in the body: (3)

throughout the body; neck, armpit, groin

lymph vessels and nodes: (4)

• critical part of the immune system - moving lymph throughout the body

• lymph vessels carry foreign or unhealthy matter back to node for ‘processing’

• lymph nodes enlarge attempting to learn & destroy this matter - the enlarged/enflamed nodes are a sign the immune system is engaged with something (where bubos are enflamed lymph nodes learning about the bubonic plague)

• site of ‘learning’ for the immune system

plague etiology: 3 different kinds

• bubonic plague

• septicemic plague

• pneumonic plague

bubonic plague: etiology

• affects lymph nodes (bubos)

• if left untreated, can enter the bloodstream, then travel to lungs

septicemic plague: etiology

• affects blood stream (organs)

• after lymph nodes, or breaks in skin and direct CONTACT with plague infected animal (eg. animal skinning/hunting)

pneumonic plague: etiology

• cough, difficulty breathing, bloody sputum (presents with different symptoms because it is affecting a different bodily system)

• can be considered a tertiary event or can be got through direct INHALATION of plague bacterium

what commensal is particularly plague susceptible?

kitties - including respiratory droplets from cats suffering from pneumonic plague

cats increase the risk of… WHEN?

peridomestic transmission to humans - WHEN permitted to roam freely in areas where plague has been identified

• ex: actively hunting rodents - 1 of the key sources of plague bacterium

sample of yersinia pestis used in a 1990s DNA sequencing project came from a…

vet in colorado who died in 1992 after a plague infested cat sneezed on him while he was trying to rescue it from beneath a house

the plague through history:

while the plague certainly remains an important public health issue today, its impact in historical times is believed to have been devastating

1st plague pandemic:

plague of justinian (541-544CE to 750CE)

2nd plague pandemic:

medieval black death (1347-1351 CE; 17th century, 1665 = Great Plague of London)

3rd plague pandemic:

1850s emergence in China, epidemic by 1894, then across world (including: india, north america: 1850s-mid 20th century)

who (both) identified the plague bacterium:

1894 Alexandre Yersin & Dr. Kitasato Shibasaburo (also identified the bacterium - Japanese physician/bacteriologist)

• 1898 Paul-Louis Simond identifies the black rat, rat flea, human connection

plague pandemics total death count:

overall to date, killed some 200 million persons

black death pandemic (medieval): (5)

• epidemic began 1200-1300s in asia

• moved via trade routes (silk route) to southern europe (sicily) in 1347

• infected rats & fleas (ex: thru furs)

• bounced back and forth from asia, europe and africa

• killed: 30% of european population - 44-55 million

how was the medieval black death explained (at the time):

miracles of st Francis Xavier (example) - religious faith/belief promoted as there was no germ theory of disease way back when

miracles of st francis xavier: painting (4)

painting and analysis by boeckle 1996

• peter paul rubens commissioned (by catholic church) in 1617; xavier (1506-1552) not yet canonized (1622) (celebration and promotion)

• commissioned because xavier was considered for sainthood

• canonization - when someone (after death) is promoted to sainthood

• meant to depict events that had taken place in his missionary work: india, japan, china

analysis of possible plague victim in miracles of st francis xavier: (5)

• possible victim cured of bubonic plague - symbolizing claim that xavier has stayed the plague in japan (caused the epidemic to go away)

• used the popular reclining posture given to plague victims in art in this era

• make shift bed of straw (associated with plague)

• close to death - since grave diggers are already at work in the painting

• armpit is examined by 3 women (repetition of this imagery - lymph association/bubos)

rubens knowledge of plague while painting miracles of st francis xavier:

knowledge came secondhand (he himself never experienced plague) he emulated artists who did live through plague epidemics BUT was restricted because of changes in permitted imagery (censorship) (hinting at bubo through armpit association)

miracles of st francis xavier at a symbolic level:

plays on the link drawn by the catholic church between between the bubonic plague and the sin of heresy - where the top of the painting has different gods in the sky, i.e. these people are dying due to the sin of heresy (believing in any religion other than the catholic church)

black death in the context of the medieval times:

heresy caused pestilence (widespread plague pandemic), to be conquered by faith in the church - over time these ideas would be challenged by medical observations (plague = bacterial disease)

• characterized by high mortality, no germ theory of diseases and no effective treatments

how was plague depicted in art before the catholic churches censorship:

depicted people dying in streets, mass graves/trenches for plague victims - the chaos of death

medieval times practices:

• bleeding

• water casting

bleeding: (4) - medieval practice

blood letting - balancing the 4 humours

• not effective against plague

• possibly some benefit to plague victims - just feeling cared for

• also used more often as a diagnostic tool

watercasting: (2) - medieval practice

original urinalysis: sampled patients urine, how cloudy or clear; presence of anomalies; smell; even taste

• where tasting pee was an early diagnostic tool for diabetes because it would be sweeter (note that this wasn’t during medieval times obviously)

plague investigations: how do we know it was truly bubonic plague that killed so many during medieval times? (3)

• bio archaeology: problem of physical evidence of plague in past populations…

• plague is an acute & fatal disease therefore it does not leave osteological signs (osteological paradox)

• so we study ancient dna

osteological paradox:

we cannot say plague didn’t affect this population because there is no osteological evidence - there just isn’t evidence for it under this exact study/analysis form

gilbert et al (2004) aDNA:

method: extract pathogen DNA (plague bacteria) from dental pulp cavities

enamel: teeth provide a lasting contamination free refuge where pathogen aDNA may survive

teeth: living tissues, with connection to the blood supply - anything going through blood circulation can potentially meet up with blood vessels in the teeth

Gilbert set up: 2 independent teams, sampled from 5 specific sites (plague pits), 108 samples (2000 standardization - protocol for aDNA to avoid contamination)

results: no evidence of yersinia pestis DNA

conclusion: aetiology of one of the manor pandemics of the last millenium remains unproven by molecular techniques - we cannot confirm the middle ages pandemic was attributable to plague

what is the issue with gilbert et al (2004) findings?

bos et al (2011) found opposing evidence as did wagner et al (2014)

compare findings with the work of chris duncan, susan scott and robert duncan:

they investigated archives; written records at the time, performing historical epidemiology: pathogenicity, virulence, infectivity, etc.

duncan and scott (2005) questioned what?

the significance placed on swollen lymph nodes - for the whole 20th century the view that the black death was caused by bubonic plague, was based solely on the appearance of one symptom and it was universally accepted without question

• yersin & simmonds work was in 1894 & 1898 respectively - we made assumptions about previous pandemics

duncan and scott note (transmission the spread of disease):

• it originally touched down in europe at a port in sicily (1347); by 1350s it was scattered throughout europe

• continued to resurface; rise in frequency after 1550 (improved transportation, larger population)

what did work: preventing the spread of disease

northern italy adopted a 40 day quarantine period (quarantine - root word quart)

• england did not adopt quarantine until 1500s, and then only 30-days

what did not work: preventing the spread of disease

removal of those with symptoms pest houses, isolation of sick in their homes:

• likely because they were more infectious prior to appearance of symptoms

• pest houses - not hospitals; places of doom and gloom where people were taken to die (cause sickness and additional lack of care there)

duncan & scott (2005) argued what? (7)

black death was not due to bubonic plague because of the following reasons:

• no rigorous aDNA evidence (tooth studies)

• case mortality 100% (bubonic plague mortality more variable) & contact transmission

• unexpected symptoms (ex: bleeding from nose, vomiting blood, insatiable thirst) - not typically associated with bubonic plague

• iceland had plague epidemics (15th ce.) - persisted throughout winter; argued freeze should have hindered the flea plague vector (generally in northern europe) - lull in case mortality (that we did not see)

• no black rat in rural england or nordic countries

• bubonic plague typically spreads slowly (black rat homebody)

bubonic plague typically spreads slow… what did duncan and scott find?

black death covered the expanse from sicily (initial touch down) to arctic circle in under 3 years - should have been much slower if it were bubonic…

hufthammer & walloe (2013) explain the absence of rattus rattus: (3)

• confirmed archaeologically in norway/denmark/sweden/finland - not sustainable environment/“patchily distributed” (ended up here through ships but were not very successful at surviving in nordic territories - ideal for black rats is tropic/subtropical)

• if not rats/rat fleas, other vectors needed:

• human flea (pulex irritans) & human body louse (pediculus humanus corporis) (aka body lice) - proposed vector

duncan & scott offer an alternative: (2)

argue a disease with a long infectious period (particularly when asymptomatic - 20 days) was effective in moving the disease in days of slow travel

• hemorrhagic plague - possibly viral, symptoms similar to ebola and marbug virus

hufthammer and walloe alternative:

ex: pulex irritans - perhaps less efficient, dont get blocked but vector over longer time period, numerous & travel with people, survive long feeding intervals

monecke et al (2009): modelling the black death (3)

• refers to long incubation - need rat population collapse (x. cheopis then seek humans)

• refers to the unexpected symptoms - high levels of plague bacteremia

• which leads to the natural question - could the black death’s high mortality be the result of uniquely virulent plague bacteria

bos et al (2011): findings (2)

• ruled out the possibility that black death yersinia pestis possessed genetic mutations leading yo its increased virulence instead…

• molecular changes in pathogens are but one component of a constellation of factors contributing to changing infectious disease prevalence and severity, where genetics of the host population, climate, vector dynamics, social conditions, and synergistic interactions with concurrent diseases should be foremost in discussions of population susceptibility