The second subunit focuses on providing students with a historical prospective on epidemics and how these epidemic events shaped the way humans respond to pathogen outbreaks. This subunit focuses on the events of the black plague, otherwise known as the bubonic plague, outbreaks during the 6
th
century, the late middle ages, and more recently in the 2013 outbreak in Mandritsara, Madagascar. The events of these outbreaks are briefly outlined below.
Bubonic plague is a disease associated with the bacteria
Yersinia pestis
, a Gram negative coccobacillus often found in single cells, but occasionally seen in strepto- (chain like) formations.
Yersinia pestis
is a zoonotic pathogen, like many other emerging infectious diseases. This means its natural host species is not humans but it has developed the ability to operate within a human host, often with devastating effects. Other examples of zoonotic diseases include the HIV virus and Ebola,
Yersinia pestis
is transmitted through the natural reservoir of wild rats by flea bites. As the flea bites the host, the bacteria are transmitted through the regurgitated liquid infecting rodents. Non-infected fleas pick up the bacteria by biting infected rats and vice versa. This disease is introduced into human populations when an infected flea bites a human host.
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The bacteria will enter the host through the skin and cause sudden onset of high fevers and buboe, from which the disease receives its name. These bubuoe often occur in the groin but may also appear in any lymphatic vessel. In early outbreaks,
Y. pestis
caused death in 30-50% of Europe's population.
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It is important to note that the census of this time is unreliable and these numbers are the best prediction of historians. There are three varieties of plague caused by
Y. pestis
, each with varying symptoms and mortality rates.
The first type of plague is the common bubonic plague (30-75% mortality rate) characterized by aches, high fever, and the characteristic swellings of lymph nodes. It was likely that patients suffering from the bubonic form of the plague died within the first week. Pneumonic plague had a significantly higher (90-95%) mortality rate than the bubonic form and was characterized by bloody sputum and respiratory distress. The final form of the plague, septicemic plague, was the least common and the most deadly with a 100% chance of mortality.
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Suffers of septicemic plague were often spotted with dark purple patches as their bodies underwent consumptive coagulation, providing the alternative name of "Black Death". The high mortality rate was assisted by a second aerosol mode of transmission where healthy individuals in contact with those infected were able to breathe in the exhaled bacterium and develop the disease.
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The response to the first pandemic outbreak of plague in the 6
th
century, or the Justinianic plague, caused wide spread pneumonic and septic forms in addition to the buboe. While there is no consensus of the plague's origin, it swept through the Mediterranean and is reported to have caused as many as 10,000 deaths per day as it decimated Constantinople, although these numbers are thought to be highly exaggerated due to the hysteria and lack of accurate census.
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Bodies were buried in mass graves and left in the streets and in homes to rot. Because the plague ran so quickly through the population, it burned itself out—lacking hosts to continue the transmission cycle—and fell into a stage of hibernation. There were several small outcroppings of the plague after the Justinianic plague, as there were small outcroppings before but it wasn't until the Middle Ages that another large pandemic arose.
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These same events were mirrored in the 1330s as plague once again reared in the East along the ship trade routes from China through India, Syria, and Egypt into Eastern Europe. Much like the Justinianic plague, the disease was transmitted from flea to person and eventually through aerosol between infected hosts and healthy humans. The plague caused mass hysteria as it seemingly jumped through the air to infect whole families and whole blocks of cities. Doctors lanced buboe and practiced bloodletting, or bathed patients in rosewater to cleanse them of what was assumed to be 'foul vapors' or evil spirits.
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The affected thought the plague was a punishment from God and prompted many to engage in flagellation and join the monasteries in order to seek salvation. Those left to cart out the dead wore the long beaked plague masks stuffed with flowers and herbs as a way to stifle the bad vapors and prevent them from coming into contact with the disease. By the mid 1350s, the plague burned through Europe, leaving an estimated 25 million—one third of Europe's population—buried in its wake.
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As improvements in sanitation were made, the threat of contacting these diseases decreased. Advances in modern medicine and a better understanding of the causative factors behind these diseases reduce the impact of plague outbreaks when they do occur. While most students look at the bubonic plague through the lens of history, there are in fact still outbreaks occurring in modern times. For example, in December 2013, a re-emergence of the pneumonic plague was reported in the upper part of the island infecting 84 and killing 32. In the year before, there were 60 reported deaths from the plague—attributed mostly to a decline of sanitation and treatment options as a result of the region's increased political turmoil.
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One teaching strategy that is highly encouraged for this experiment is an infectious pathogen lab. The lab exposes students to transmission and R
0
(pronounced R naught), or the reproduction rate of a virus. This is usually measured by the number of people an infected individual transmits the virus or bacterium of interest. For example, R
0
for the measles (rebeola)—a highly contagious, viral outbreak that can be spread through aerosol—can range between 12 to 18 people depending on the particular infectious strand in that outbreak.
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That means for every person who develops measles, they are likely to spread that pathogen to over a dozen people before it is no longer virulent. To provide some prospective, most flu viruses have an R
0
slightly over 1. In this lab, students model an outbreak system using an R
0
of 2. For laboratory instructions, please visit the lesson plan and resource sections at the end of this document.
Teaching strategies for this unit also include the creation of a word wall featuring key vocabulary. As seen in the previous unit, microbiology and pathology is terminologically dense and may require many exposures to frequently encountered words in order to garner a more complete understanding. It is highly recommended that students are introduced to common epidemiology and pathology terminology. Students should be encouraged to define the words using context clues presented by the textual readings that they are using for the unit.
Students should also discuss the relevance of the terminology to the plague unit to both the currently studied plague and other emerging infectious diseases. For example, students should be able to identify the host, pathogen, symptoms, and reservoir of any bacterial or parasitic infection and extrapolate information to decide whether a disease is emerging or re-emerging or whether it should be considered a local outbreak, epidemic, or pandemic.
Students also have a unique opportunity to compare a relatively well known historical outbreak pattern with an emerging outbreak. Students can identify key factors that have altered the impact of this outbreak in Mandrisita, including how the change in infrastructure, the breakdown of medical and sanitation practices, and how political turmoil can impact the spread of infectious agents.
