I can start off by stating that “the Extraordinary disease” that struck Nantucket in 1763, and referred to by the writer of this article, was not yellow fever, or at least not just yellow fever.  We usually think about yellow fever as an epidemic that struck North American from about 1790 onwards.  There were probably other importations of this disease prior to 1790, with some diagnosed as a fever different from the typical malaria passing through the various ports and harbors.  But the differentiation of yellow fever from other fevers  like malaria was not a readily achieved process.  In fact, even the term malaria was not used for the diagnosis of fever.  In general we see diagnoses that refer to a fever’s cyclicity, the waxes and wanes in the rises and falls of body temperature and the initiation or reinitiation of the cold sweat that develops during certain periods in these cycles.  Even the use of the term yellow fever was not appropriately managed during these first years of its possible presence.  Biliary fever was a well known term and often used, and the bile versus yellow fever terminology did manage to be confusing at times, since bile can be usually yellow in color, but sometimes black (going back to the older 4 humours theory).

Yellow fever and biliary fever were terms used synonymously for quite a while, at least into the first decade of the 1800s.  This caused some confusion between the classic biliary fevers existing since the four humours philosophy was developed, versus the new form of disease being propagated in the Western Hemisphere by a local vector no one knew anything about.  This disease managed to impact mostly or only the three Americas throughout most of its first 50 years of history.  Yellow fever was not a European disease, but rather a disease unique to the Americas, that by following the traditional geographic interpretation of disease for this time, passed from the tropical part of the world into the cooler tropcial regions and then into the temperate zones, and finally the cooler temperate regions by summer’s end.  It was this fever that gave birth to the United State’s own unique take on diseases and where one was raised or grew up.

In general, it was believed that one adapted to the new environment he/she moved to, over a generation or two, and had children usually better adapted to living in a given area than the parents.  This Lamarckian philosophy rising from Erasmus Darwin’s views of life on the planet helped to make the study of medical geography an essential part fo the American medical schooling and apprenticeship discipline.  The first true American United States doctors were experts in medical topography and medical climatology for the Americas first, the rest of the world second.  For the first decade or two of the nineteenth century, Europe believed it was exempt from having to deal with this disease, but had its own epidemics to contend with coming from the other parts of Europe and Asia, as well as the continent of Africa.

Heinrich Berghaus’s Yellow Fever map, from my page on this same 1848 Medical geography book.

Yellow fever struck the New England region of the colonies about the same time of year as was expected for other fevers, like the agtue.  It came to the islands of martha’s Vineyard and Nantucket from the tropics during the warmest months of the year, in late summer and early fall.  But in the case of a latecomer to this annually repetitive history, yellow fever (not yet called that at the time) arrived in this region for the first time, following the traditional disease migration patterns, infecting the most heavily travelled port towns and cities before infecting more rural settings.  The problem is, the disease that arrived on Nantucket came after the typical fever period of late summer, and extended well into the cold autumn and immediately pre-winter months.  The realiztion of this difference in behavior of this recurring disease pattern made religious leaders ponder its reasons.  The most common religious philosophy for the time equated this epidemic, like nearly all others, to natural pheomena indicative of God’s messages like comets, meteors, earthquakes and terrible storms complete with deadly lightning events.  But such was not necessarily the case for the Nantucket event.  No storm drove the Nantuckians off their precious living quarters located within a very scantily settled island community devoted to whaling, fishing, and boat-buidling.

Yellow fever was just the first of two epidemics that struck the island that year.  The second epidemic, considered a continuation of the summer disease cycle, was actually typhoid, which back then could have been either the flea-related typhus or the Rickettsia related typhoid fever.  Its causes were very different.

Typhus came to shore on Nantucket due to rodents traveling the ropes that were used to tie the ships to the piers.  They could even come to shore by way of swimming and the transfer of shipped goods to mainland.  All of this could have taken place in the summer as well, along with the transfer of mosquito-carried yellow fever on board.  But equally likely was the transfer of these rodents to the mainland during the colder months of the year, with their subsequent movement into the warmer building settings once the coldest months of winter began approaching in November and December.

This “Extraordinary disease” therefore is a combination of yellow fever, introduced a couple of decades before it became diagnosed for the first time as a separate entity, and from that point on as a well known disease either of local origin, of ship origin, or carried in from the tropics, followed by what was then just known as another fever.  Typhus came to be its own entity quite soon after these years in American medical history; typhoid due to Rickettsia still had another decade or two before it became its own unique entity.

The article reviewed on this page is an excellent example of how the application of Sequent Occupancy theory to changes in landuse and living patterns over time can be used to provide us with insights into a given region’s medical and disease history. Through this analysis of a isolated island community, colonial setting, the changes in disease patterns over time can be clearly illustrated.

The reason I decided to review this article pertains to a historical questions that appear to be unresolved

  1. what disease struck Nantucket but not Martha’s Vineyard in 1763?
  2. how and why did it strike one island and not the other?
  3. what made this disease so different from the expectations for the time that led the writer to call it an “extraordinary disease”?

Before even reviewing this disease and the islands’ histories in details, we can come up with some possible guesses as to what this disease was.

We could simply claim it to be a disease of an ecological nature, with all of the ecological, natural or manmade requirements found only or mostly on Nantucket Island.

We could also decide that this disease is a run of the mill infectious disease that came in either from the other island, or by ship, and that the reason the main island (Martha’s Vineyard) was not ravaged by it has to do with the ethnicity of its residents, their living practices, and their medical history background. We could base this argument on the fact that Nantucket was inhabited mostly by indigenous and poor people and families, and in some ways its population was less dense, more diffuse, but also “less experienced” when it comes to previous exposure to other human-borne diseases like mumps, measles, rubella, diphtheria, etc. This could also meant that more than likely poor sanitation was also an issue, resulting in more dysentery in the form of occupational diseases (bad food stores, rotting seafood, carcasses, unhealthy latrine settings), salmonella poisoning, or some sort of animal-born disease that infects humans as well such as ticks, lice, fleas or intestinal worms.

The third possibility is that this is a disease that struck just one island, a disease that for various biological and ecological reasons has the ability to form disease-rich and disease-poor regions, often in close proximity with each other. Examples of ecologically dependent diseases that are bacterial or fungal in nature also fit this scenario. These organisms exist in the region regardless of human absence or presence. Most recently, a fungal disease was suggested as a cause for this epidemic.

William Aitken’s 1872 map of this region.  We can tell this is a much later interpretation; notice yellow fever normally never reaches New England on this map.  This suggests its early migrations so far north were a consequence of the economics, “commodities”, and trade routes for the time.  My section on African, Caribbean and African-American disease and slavery will review this more.  [Link to Aitken’s map]

Making The Right Diagnosis. One thing that is common to strange diseases from the past is the tendency for very different, radical theories to develop in order to explain the phenomenon. These historians often don’t take in the full picture of this scenario. This is typically the case for MD’s who would like to be historians as well. They often pull together some of the worst facts and try to come up with an explanation for something that they lack much historical knowledge and wisdom about about. MDs for example are the worst historians when it comes to herbal medicine and alternative medicine history, often seeming brainwashed by the attitude they develop about professions with philosophies counter to their own. When it comes to history, these writers fail to realize that the diagnostic terms of today weren’t around in the past, and the same for vcertain diseases. Pneumonia for example didn’t exist in 1800, just Catarrh, for which influenza and one’s common reaction to the “cold” were about to be so named. Contemporary MD historians make some of the worst diagnoses for the past when they fail to pay heed and understand the terminology and meaning of prior diagnoses being made for diseases. A most embarassing example of this is seen by the consistent errors that pop up with Oregon trail history, with even MDs citing Asiatic cholera events during the years they simply could not be happening–cases of dysentery that should have been diagnosed as accurately for back then as is theoretically possible for today, even without the aid of the microscope, just a knowledge or the symptomatology and some common sense.

Such is the case for this “Extraordinary” event that struck the islands off Rhode Island, and apparently failed to make it to the mainland or across the waters to Long Island. Some writers like to profess this as being a disease that has erupted randomly out of nowhere, as if it did not not engagie in the typical rules of nature like most or all organisms. These sensationalistic diagnoses are good food for the publisher but bad meat for the true historian. Once inaccurate history, for example an error, gets published, it is there for good for other students and teachers to read, and typically believe in. By doing so, these writers do accomplish this feat of nature that is usually not possible, making their case that 1 in a million example capable of eliciting of disease patterns that are normally unlikely. In the end it comes down to looking for common truths first, uncommon and incredible truths later.

When I was arguing my diagnosis for the trail cholera west of Fort Laramie back in 2000, I came upon this sort of wisdom out there in the medical history field as it was managed by non-historians. Some epidemiologists and microbiologists were in fact looking for new strains that could be used to explain past epidemics, claiming they were due to a unique series of mutations resulting in a higher virulence and symptomatology, very deadly in nature but also very extinct soon after. Such a theory is possible, but when it also assumes that reverse technology is the case genetically, meaning that genes are capable of evolving very fast, very early, to very complex genotypes, and then die back off due to over-selection (too many) or hyperselection (too fast) events, de-evolving back to their original state, the story loses some of its credibility (not all).

With my theory, there was a possible persistence of Vibrio cholera off the Mississippi Delta between the first two epidemic periods (ca. 1830 and 1849-52), and the likelihood that vibrio remained in this region ever since as a part of the local ecology but in very small amounts. Repeated tests in fact confirm this theory, with evidence that a refusal to accept this hypothesis has persisted from 1855 to the late 1900s, indicated by recurring positive tests for this particular vibrio along with random outbreaks of human diseases induced by this vibrio, in a region where the pathogen is theoretically no longer there.

Disease ecology fits into the sequent occupancy model in that a pathogenic organism can become introduced to an ecosystem, cause human disease, and then seemingly die off, reasserting itself in the local ecological setting without requiring any human involvement. This means that from stage 1 in sequent occupancy onward, a disease can be introduced that once it becomes ecologically stable, can remain there are express itself in different ways according to the various stages of development the infected area is in. The initial onset that occurs in earlier stages (1 and 2), may in turn result in little to no activity in stage 3 of sequent occupance, followed by a sudden re-eruption of the epidemic due to increases in population density and changes in occupancy, land use and ecological patterns. Now, a full fledged epidemic is ready to happen. The parallel in history to this in the United States pertains to the behavior of yellow fever, which caused isolated incidents in the mid to late colonial years, many unidentified as such at the time but later noted as such by epidemiologists, but which suddenly took on epidemic behavior patterns demonstrating various forms of diffusion once urban settings became more developed and population densities increased, for example in New York and Philadelphia, this country’s first two major yellow fever epidemic cities. This stepwise evolution of the disease from occasional to epidemic in nature can in turn be related to the Martha’s Vineyard-Nantucket epidemics, to see how the Rhode Island disease history compares with the New York-Philadelphia history.

The Role of Sequent Occupancy. My approach to this situation is to first look at the stages of development the island community was in, then looks at its history to see how certain epidemics or diseases may have related to these stages of development, and then define how the disease somehow fits into this scenario. As usual, I will refer to this as my sequent occupancy based theory for the Nantucket Epidemic.


Part I – Fevers in General

Martyn Wyndgard’s Place

During the very early 1600s, a settler by the name of Martin Wyndgard settled on an island just south of the shores of what would later be Massachusetts and Rhode Island. Known as Martin Wyndgard’s land, it had some very unique features reminiscent of the famous Isle of Wight setting located at the southern end of England.

Martin Wyndgard’s land was a small island floating just a few feet above the surface of a large body of ocean water–this ocean water would later be known as the Long Island Sound. Soon, the Long Island Sound became the site for a number of very important, highly prosperous industries for the New York-New England region. Ship building, fishing and whaling were the most important of these industries. By establishing such industries, its first settlers had reasons to set up hamlets to provider workers with daily living supplies, which increased in size and number as these businesses continued to be naturally self-sustaining and successful.

Over time, the name ‘Wyndgard’s’ was converted to its homophonic equivalent “Vineyard’ and the first name Martin to ‘Martha’. In this way, the contemporary name of this island was born, a name that perhaps also produced a much greater attraction for this property, which established some of its more permanent settlements by the early 1700s.

Like many early North American and United States coastal homestead settings, there was a mixed cultural history of this region. The islands were comprised of Native American and European populations. The two major island settings sitauted next to each other–Martha’s Vineyard and Nantucket–had different settlement styles and histories. Martha’s Vinyard was predominantly settled by Europeans and Euroamericans by the mid 1700s. Nantucket still had a very large area occupied primarily by Native Americans. In time, the habitability of both of these islands made them attractive to incoming future colonists by the late 1700s, when the Island of Nantucket was settled by missionaries with the goal of converting the indigenous people into Christianity. From this point on, Martha’s Vinyard continued to increase in size with non-indigenous groups.

Assigning Hierarchies

From this history of settlement of these islands we see evidence for the following three states of traditional sequent occupancy provided by past researchers:

  • Wilderness
  • Pioneer
  • Early Farming/Missionary.

Each of these stages has a particular set of disease patterns that can be used to better understand the living environment. In terms of economic development, these two island settings were in some sort of relationship between Stages I and II in the following figure.

The lesser developed of the two islands was Nantucket. So one possible way of interpreting these two island settings is to view Nantucket as a Stage I community, and Martha’s Vineyard as Stage II. In turn, for the above Stage II depiction, the larger, more progressive communities cited are the mainland port cities of Providence and , extending as far away as Boston. In this scenario of the above case history, Stage II economic development exists, inferring some fairly regular economically driven transportation behaviors, and an early form of economic geographer Gordon Pyle’s hierarchical diffusion pattern.

Most economically based events took place between the more colonized port settings, hamlets and villages of Martha’s Vineyard, in turn forwarding many of these goods to the more indigenous settled, less colonized island of Nantucket. In terms of disease spread patterns, this suggests that regardless of whether or not a hierarchical diffusion pattern prevailed, that it was more likely for a disease to strike Martha’s Vineyard before reaching Nantucket, or impacting the two at about the same time, in a non-hierarchical fashion.

Reviewing the history of each of these islands however, we see that the worser form of the epidemic in question struck Nantucket and avoided or missed Martha’s Vineyard. This means that either the cause for the illness is endemic and natural to the Nantucket setting, or is a consequence of the persistence of the epidemic cause that struck both island settings earlier in the year.

We can also interpret these disease diffusion patterns in terms of sequent occupancy defined environments, as follows:

Wilderness settings, for example, have that classical combination of diseases consisting primarily of accidents and injuries, relating to periods of famine, and numerous occupational habits. The farming-livestock raising setting is fairly small in size, uncrowded for the most part, and the proximity of both people and domestic animals to the wilderness is such that certain vector related disease patterns endemic to the region might occasionally surface, like tick and mosquito-related biting patterns, but lacking the fever types normally associated with more advanced social settings.

Pioneer settings retain some of the injury and accident related medical needs, but add to this the need for care related to uses of fairly primitive farming and food preparation equipment. Gardens have been established so garden-related problems can ensue, such as food contamination or disease development.

Early Farming establishments, with missionary settings nearby, add a large amount of domestic lifestyle patterns to otherwise fairly primitive lifestyles. Livestock are now living in more cramped quarters, and now have an ability to transfer diseases not only to each other but also to potential human victims. Whereas in the Pioneer setting, certain livestock diseases might be occasionally present, in these more developed settings this problem become a serious health issue.

Associated with larger farming establishments are mercantile businesses and operations, meaning that transportation is now more active to and from these regions. Whereas during the pioneer stage, an infectious disease may be brought in by ship, and then allowed to diffuse throughout the region, on occasion taking a few victims, in this more dynamic population setting where aggregates of homesteads are found serving as stores, hotels, and even restaurants, it is more possible for direct human-to-human contact to occur, and for in-migrated disease causing substances or agents, such as vermin, germs or poisons, to be passed from one person to the next, one object to the next, or by way of shared drinking water facilities.

This means that whereas in the farming setting, diarrhea may be a problem due to contamination and poor food storage and processing, in the hamlet like setting of a young agricultural business area we can see problems with a severe form of diarrhea known as opportunistic dysentery developing, brought about by water sources contaminated by piles of waste and plant or animal remains, toilet closets improperly managed, and/or poor placement of a source of contagion to sources for spread and diffusion of the pathogens. In these settings, the people carrying infectious diseases like small pox and measles now have opportunities to pass the disease onto one or more families, assuming travel between communities is common and involves personal home visits.

Likewise, proximity of potential disease bearing animals to each other is new to this setting, enabling certain diseases to spread more effectively. The crowding conditions of livestock raising barns make for poor sanitation, and provide zoonotic diseases with the opportunities needed to spread and impact other animals. If effectively spread, they could result in numerous deaths, followed by the possibility of human infection in some cases. In the case of the initiation of a diarrhea or dysentery epidemic due to poor sanitation following an animal slaughter or the infection of a total herd, the decaying carcasses and insects landing on them are capable of spreading germs to the local soil, waterways, and the surface of wild animals, making for an increasing number of potentially pathogenic events involving people. This development of new diseases due to new industries takes an even greater step when these slaughterhouses, metal working facilities, tanners and the like facilitate the onset of new occupational lung disorders and the development of certain forms of fungal and bacterial disorders, asthma and fevers.

This way of interpreting the earliest years of the Martha’s Vineyard and Nantucket setting is very important to understanding its medical history. Throughout its history, the settlers on these islands experienced several epidemics. The kinds of epidemics that prevailed have never been completely identified. By applying sequent occupany philosophy to the study of the medical history of these settlements, we have yet another way to argue for and against certain epidemics from prevailing on the island during specific periods in its occupation history. This way of interpreting the evolving community settings on this island should help to answer the following, malingering question that persist about the history of this fairly unique island community . . .

What forms of diseases led to the near extinction of mostly its indigenous settlers, the first time through around 1617, followed by an even more substantially impacting and fatal epidemic from 1763 to 1764?

To better understand Rev. Oliver’s 1763 experience, it helps to extend our review of this settlement to a century earlier. The diseases striking then represent some of the earlier stages in this settlement’s medical geography history. The epidemics that took place during this time demonstrate the stage of development these islands were in and from this information we can deduce the kinds of diseases most likely to infect the islands during this time as well as much later. As the details about how this first epidemic was spread, including the fact that its second time through only one of the two islands was struck, we are provide us with one of the most important details about the possible disease to strike Nantucket, but stay clear of Martha’s Vineyard. This allows us to more appropriately identify the most likely disease responsible for the 1763/4, and to confirm the likelihood that it was due to a distinctly different cause that the late summer events.

Prior to 1850, there were three distinct epidemic periods and three distinct epidemics that took place at Martha’s Vinyard and Nantucket. Each of these individual epidemics depict and characterize the nature of new diseases for three distinct periods of time in the islands’ history.

  1. The first disease [17th C] may well have been the basic consequence of European diseases striking an otherwise virgin community setting which up until that time served only or mostly indigenous cultural needs. By adding to this scenario the in-migration of a few fairly basic farming families, the most infectious of those contagious diseases for the time, namely small pox and measles, may have well been the cause for the first epidemical deaths for this setting. Such is the case for most other indigenous cultural settings in early North American European migration history. More than likely such is also the case for this period of time in Martha’s Vinyard history.
  2. The second disease [18th C] came as a result of “civilization” according to the earliest European writers, philosophizing political writers, and righteous religious writers supporting the goal of converting the entire world to Christianity. This epidemic actually consisted of two epidemic diseases, each with its own characteristic month-defined diffusion patterns. These two diseases is the main topic of this review, and will be discussed in detail later.
  3. The third disease [19th C], or should I say disease type, is that of an industrialized culture, and impacted the sailors at sea more than the farmers on land. It is a collection of different kinds of maladies that ensue in a given region once settlement and early industrialization have taken place. The consequences of these “improvements” or changes in lifestyle include the increase prevalence of chronic diseases like diabetes and consumption, and the development of very specific, often infection related diseases like pleurisy.

Important to note as well is the fact that a number of epidemic periods existed in the island communities during their colonial and early post-colonial history. Aside from these three epidemics there were dozens of other epidemic disease patterns which for the most part bypassed the island communities but remained quite common to the shoreline settings. In some reviews of epidemiological history for this time, many to most of the years of settlement had an epidemic or endemic disease pattern taking place in some town or hamlet in any of the settlements established, European/Euroamerican or not.

[Insert links to sources for these lists?]

The Primary Diseases

The primary diseases focused upon for the epidemics are measles, small pox, yellow fever, typhus and typhoid fever (linked together back then, with typhus/typhoid not really differentiated from the other fevers however until the 1790s).

Stages 1 and 2 — Measles and Small Pox? or Purely environmental?

Soon after the Puritans arrived to north of this area, communities were established nearby and to the south and some were stricken by a substantially fatal epidemic disease never truly identified.

Traditionally, modern history writers and readers are very familiar with most of the severe epidemic disease patterns to develop and become fatal to indigenous peoples. Typically small pox and measles are the first diseases that come to mind whenever this particular inter-cultural, political controversy is discussed (see my Cree page on this as an example). Still, there are other diseases important to part of North American history, with the fever so fatal to indigenous people residing in Martha’s Vineyard and Nantucket Island to be one of the more important examples of a non-human contagious epidemic patterns to impact this part of American history and culture.

About 1617, these islands were struck by their first major epidemic. Over the years several diagnoses have been proposed for this epidemic. The traditional diagnosis over the years would have been measles or small pox due to such an early onset of the cases in settlement history.

These two highly infectious diseases have not been linked to the Martha’s Vinyard and Nantucket Epidemics. These problems did occur, however, and their diagnosis was fairly easy. During the 17th century, even differentiating these diseases and the common cold from each other was a task for some doctors. The terms applied to such common diseases often focused on more widely used words, like distemper. Even as late as the 1730s, physician like Cadwallader Colden of New York referred to the very different diagnoses as sore throat, croup, and the worst, diphtheria, as various stages of “throat distemper”, which in turn could be the consequence of a measles or small pox case taking a turn in how it affected the body.

It is important to note that measles and small pox were often interpreted as different stages of the same disease induced by the environment. More serious forms of this same disease could be such conditions as the bullae associated with Plague, diphtheria, certain presentations of the consumption (i.e. with hemoptysis and spitting up black rotten lung tissue), or even certain tumors and cancers. Such beliefs came as a result of the belief that the cause for disease could be some entity (humour or energy) traveling about the body, creating havoc with the functionality of the stomach, followed by the liver and then lungs, only to become fatal once the heart was afflicted.

Both measles and small pox have Stage I and Stage II related requirements. They require direct human contact, which usually took place in a well established living setting, or communal place. The related scarlet fever and mumps epidemics develop due to similar reasons, but tend to be more likely to form and infect victims in a well-established, non-solitary community like setting. Likewise for certain other diseases like diphtheria and dysentery, the latter not being amoebic dysentery but rather the forms of dysentery induced by various opportunistic species of bacteria, such as shigella and listeria. This ensues usually a result of poor sanitation related to crowding, or numerous animal (livestock) deaths and the results of their remaining carcasses. Another important livestock disease potentially introduced during the Stage II period is the tularemia of sheep and hogs, several salmonella species like S. intermedia (a species common to animals, and only effective as a pathogen on a weakened old, disabled, undernourished people).

In a later writing about this disease pattern, a Stage II Sequent Occupance disease pattern is identified as the possible cause. Were the livestock and farming setting developed enough, this might have been possible. The problem with this theory is that although it entails naturally-born soil organisms as the cause, the ability of the disease to spread the way it did is somewhat questionable. At such an early period of time, it is possible that Stage II exists, but Stage I remained very likely. This means there are other epidemic like events that could have led to the 1617 deaths.

Alexander Keith Johnston’s map of Yellow Fever in North America, with Asiatic Cholera migration routes, ca. 1856-1862 [Link]

Stage 3 – Yellow Fever

The most traditional Stage II disease to strike the New World was yellow fever. This disease made its way into this country fairly early, during the mid to late 1700s. But until the very late 1700s, it wasn’t yet an epidemical disease that repeatedly intruded upon all of the New World communities. The yellow fever began to appear in some repeated fashion between 1790 and 1793. But even then, it impacted cities in different ways in terms of timing and diffusion behaviors. In some parts of the United States, large cities could be impacted with neighboring towns never made to suffer. Other parts of this country demonstrates signs of isolated epidemic patterns developing, these areas positioned so deep into the interior of the country that other more local features would be defined as causes, and the disease even provided a name indicating its place of unique origin and cause, such as Genessee River or Lake fever.

This conflicted with beliefs at the time about the causes for yellow fever. The major dilemma epidemiologist were facing was trying to determine if this fever was of local origin, due to miasma generated by nature or effluvium generated by people, or of foreign origin, transported from tropical settings abroad into temperate zone region during the weeks and months these ports most closely resembled the tropical climate settings, the period between late August and late October.

The impacts that older theories had upon only yellow fever investigation and treatment lasted just a few years. Quite soon, the possible routes of migration for yellow fever into this country were better defined, and many of the cities with the most risk for these epidemics identified based on the nature of their commercial development.

By 1800, the yellow fever was a well-known and better understood cause for deaths that tended to prevail first in the larger cities. Places in the outskirts still lacked much of a link to yellow fever epidemics, leading many writers to speculate other versions and causes for fever that existed whenever and whereever the yellow fever hit the countryside, well distanced from urban settings. In western New York, one medical topographer and land developer gave this epidemic the name Lake Fever. In foreign countries, certain small countries refused to assign a link between their fever, and the more deadly and more feared yellow fever. When this fever caused numerous deaths at a missionary establishment near the Ivory Coast of Africa, the mission was to blame for the disease, which in turn also was given its name Bumela. This was an attempt made to reduce the success of the anti-slavery missions then going on in this setting, to further enable the ongoing slave trade on the islands nearby to continue to be prosperous.

Likewise, Martha’s Vineyard and Nantucket were island communities not close enough to the major populations to have any associations with their terrible epidemic and endemic disease histories. This enabled later doctors and historians to keep the identification of the second major epidemic striking these islands either diagnosed in retrospect as yellow fever brought in by slave ships, or a type of fever unique to these islands, and thus deserving of their name, their fame, their claim to being an important part of American medical history.

Sequent Occupancy tells us this disease is possible due to the ongoing shipping that was going on. It was a very early period in the Islands’ stage 2 history for Martha’s Vineyard, Stage I for Nantucket, a place settled mostly by indigenous people and their missionary service providers. The story of Bumela comes back to haunt this tale about Nantucket as well. When this island was hit, only the indigenous people died. The old-timers might liken it to the old-time scorn that took place whenever measles or small pox came into a region with indigenous people. But we know that the sanitation and living conditions could also be to blame for part of why one group of settlers were struck by the “Extraordinary Disease” and another spared of fatalities.

But even more so, the place where the people were living tells us why they became fatally infected. The indigenous missions places were situated in the more lower parts of the island setting, with brackish marshes and wetlands located throughout their local setting. Far west of the shipping ports on this island was the only community to be spared the fatality of this fever that struck. It was far enough away from the place where the boats carrying this disease docked, and had some offshore winds from the south, north and west to assist in keeping it disease-free.

Usually the ships carried this disease into the mainland first during the 18th and early 19th century, but may have begun taking direct routes to this place at times, or may have even held onto the disease long enough while docked in the mainland, to revive it and bring it over to Martha’s Vineyard and Nantucket in 1763. This year of introduction of yellow fever is very early for this island’s and region’s history. But it is possible that the mosquito carrying this disease was brought in with the infection and then disharged as ballast or allowed to hatch from once potable water carriers, or there were infected human carriers on board capable of infecting the local swarms of mosquitoes developing. Most cases carried into the colonies during this time came by way of ships heading up from the Carribean to bring wares and people.

What makes this yellow fever epidemic so unbelievable as the cause for the November-December cases for the “Extraordinary disease” is the time of the year it took place. Some writers say that it started in the late summer, by August and September, struck hard in October, and maybe even into November, but then managed to go away for a short while, only to re-emerge in December. For this to be yellow fever, it would have had to be a very warm winter, for the cold nights would in theory kill all the mosquitoes off, by November at the latest. It is therefore also possible that yellow fever did strike by way of a ship coming in, but then went away for the rest of the year, allowing another epidemic to arise once the months got cold and the people were forced to remain inside.

By mosquito ecology alone, this suggests that the yellow-fever like epidemic known as an “Extraordinary disease” may not have even been yellow fever at all, but instead another infectious disease or murine origins, like a plague, dysentery, or the like. This rodent could have come in during the warmer months, and then set up a nest for the winter inside the homes of these settlers. This possible outcome is detailed more in the next section.

The Worldwide Distribution of Typhoid or Dengue according to Rudolph Matas, 1889 [Link]

Stage 3 – Typhoid or Typhus.   This disease that appeared in the immediately pre-winter weeks was a disease with an animal vector that could survive during this period of the year, at the latitude we are talking about.  This rules out mosquito-bred diseases for the most part, and increases the likelihood that this disease had to be animal born by a mammal, in particular some form of rodent.  The classic scenario for this scene during this time of the year is the rodent leaving ships late in the day and at night, once activities at the port quite down, by way of water, plank or rigging rope, and especially during the darker hours when the air on board become colder thereby driving it off the ship.  This is more than likely the cause for the final events that made this disease extraordinary.

I find it safe to say that based simply upon the disease calendar we are given for these events. the “Extraordinary” disease was confused with the late summer-autumn fever or yellow fever.  Since neither were differentiated into their own distinct diseases at the time of Oliver’s experience, It wasn’t until the late 1790s that typhus could be separated out from the standard four fever types (continuous, remittent, itnermittent, ague), followed soon after by biliary fever, a term made popular by Benjamin Rush, and yellow fever, a term sometimes used to refer to a particularly deadly form of biliary fever.  The identification and differentiation of these latter two disease types wasn’t perfected until the 1810s, and even then it was still more often referred to as simply a more malignant form of Benjamin Rush’s biliary fever.

Sequent Occupancy and Nantucket

Applying sequent occupancy directly to Nantucket’s history, we find that for the island communities on Martha’s Vineyard and Nantucket island there are three distinct periods of development that can be identified for the communities formed between 1600 and 1800.  The changes in living patterns these two island experienced also results in distinct changes in their disease patterns.  These diseases are

  1. 17th C.: any common fever, measles or small pox, or even locally restricted fungal or bacterial disease
  2. 18th C, esp. post-1790: Yellow Fever, along with the easily diagnosed continuous, remittent, intermittent and ague fevers, mostly the different forms of malaria, and perhaps east coast (not Rocky Mountain) spotted fever.
  3. late 18th C, esp. 1763 in this case: typhoid fever, and event which actually tended to precede the yellow fever in terms of introduction to new territories.


A portion of Robert Felkin’s 1889 world map of Yellow fever distribution, depicting the involvement of Africa that ensued during the 19th century.  It also suggests a strong link to the Slave Trade insutry, although Africans themselves were fairly immune to this problem, whereas “poorly adapted” Europeans were not. [Link to my page with Felkin’s maps]

Part II – A New Disease

According to Rev. Oliver, the Extraordinary disease that struck the islands of Martha’s Vinyard and Nantucket in 1763, had probably arrived for the first time in this more deadly state.  The rapid and fairly persistent waves of fatality he observed over the next several months is what led him to refer to it as “the extraordinary disease” in the article he wrote about it published in the Philosophical Transactions (see below).   Without the highly trained physicians needed to be able to differentiate the various forms of intermittent, remittent, continuous and ague fevers then known to exist, we are left having to rely mostly upon Oliver’s interpretation of these epidemics, and his conclusion that the Summer and early Autumn diseases were the same, which may not be the case.

According to Oliver, this epidemic struck from the months of August to late November, with its first wave occuring briefly in August.  The August cases were then followed by a lull, followed by a second wave of the disease this time resulting in a much larger number of deadly cases throughout the months of September and October.  These deaths were again followed by a lull in cases, leading up to the re-eruption of a disease in the months of November and December which Rev. Oliver and others considered to be a recurrance of the September-October epidemic.

There are very few records detailing the weather in the region during this period in the history of these island settings.  So, it is very possible that some incredibly unique warm spell took place in this region during these months of 1763.  The reason a warm spell has to be considered for this areas history pertains to the disease behavior and types proposed by subsequent historians reviewing this unique tale of local history.

Most historians view the 1763 epidemic as one that pretty much persisted through the late summer to late fall months, forming two peaks in their activity.  The formation of two peaks due to a single disease introduction is not unusual, and has been shown to happen in the more recent studies engaged in by spatial epidemiologists focused on the measles epidemics behaviors in the well isolated populations setting of Iceland.


The more likely reason for these two sequential epidemic eruptions may in fact be simply the fact that two very different epidemics impacted the region.  The first was the traditional late summer epidemic, probably brought in by ships, and the second a more typical late fall, early winter epidemic fairly common to the coldest months of the year.  This theory allows for the two seasonal weather conditions to be normal in terms of temperature, and does not require a fairly hard to believe fall warm spell, accompanied by an ability of the disease causing factor (the infected ships) to manage to carry this disease long past their expected periods of disease migration.


Since the last epidemic for the year took place during some of the colder months of the year, this is the reason it is termed “extraordinary” by Oliver. For many such diseases, these lengthy periods of lulls in cases and deaths between waves was very unusual he states. Adding to the uniqueness of this resurgence so close to the winter months were its unique symptoms and its ability to take the lives of all members for a family, features not seen for prior fever epidemics. This also tells us it is an event distinct from the late summer yellow fever.

At first, the “Extraordinary” disease Oliver described appears to be an early introduction of yellow fever into a New England colonial setting, before it was even called yellow fever, by a ship arriving from a southern state or an island in the Carribean.  This was followed by the second resurgence of the epidemic in late summer, early fall.  However, the late fall, early winter epidemic appears to be a second, distinct ship-born illness, one that could be spread without the need for mosquitoes, such as typhus or the “plague” (Rickettsia). (The requirement of the mosquito for the spread of yellow fever was never known by physicians around this time.) This lack of understanding, and the strong associations drawn by Oliver between all three disease periods, are what led to him to apply the ‘Extraordinary’ label its recurrence.

Two features made the yellow fever epidemic difficult to identify by physicians around 1800. The first was its symptoms, the second, it manner of spread to an isolated island community setting. The Colonies of North America had a very limited experience with yellow fever during the mid 1700s. This made it difficult for even the most experienced physicians to distinguish it based upon traditional teachings and writings. This was even more difficult for Oliver, who probably lacked a formal education on the presence and appearances of fevers in the world. Since yellow fever was for the most part a New World disease linked to the tropics and slave trade, the teachings on this topic were somewhat limited.

The typical training in fever diagnosis for this time focused on malaria, known back then as intermittent fever with ague. Much of the focus on diagnosing fevers concentrated on the numbers of days that passed between recurring cycles of fever, chills and then sweats–all signs of malaria (‘mal aria’ was not a term used much then). This periodicity was used to differentiate these somewhat predictable and diagnosable patterns from the other fever of the area, such as continual fever, a fever due to influenza and the approaching cold snaps and seasonal related fevers.

By the mid-1700s, the geography of fevers appeared to be related very closely to certain climatic and wind patterns, and short, seasonal meteorological patterns. Features such as latitude, proximity to a lake or mountain, rates of recurrance in relation to local wind patterns, all seemed to play important roles in when, how and where the epidemic might commence. Certain features common to the landscape like marshes and putrid ocean or estuary bays were considered most indicative of such disease ridden regions, not only for fever, but also consumption and rheumatism. On occasion, we even find mention of the impacts of the torrid zone on disease patterns, writings which at times seemed to be written mostly by people judged to different thinkers, outsiders in a field well under the control of a certain well defined political and scientific leaders.

Geographic names assigned to new diseases was not yet the standard.  If it were, we might even expect the Reverend to call such as epidemic the Nantucket Fever oir the like, but such  was not the case.

Another interpretation of the local disease history of this long-lived disease is that for two diseases possible, one was endemic and the other epidemic, with the epidemic cause being the first, and the endemic cause being the latter of the two epidemic periods.   The first is the yellow fever, striking the area during the late summer. The second disease, striking in November and December, was probably a form of the plague, either brought in by rodents on board ships arriving from down south, or due to their already ecological presence on the island. Or it may be the disease posted in other writings of some sort of natural ecological cause.

The worldwide distribution of typhoid or dengue according to Felkins, 1889.

Indian Sickness

Because it was neither a true intermittent, remittent, constant or ague type of fever, Oliver needed a different term for it. The name for this disease that was assigned by the locals was simply “Indian Sickness”, because it impacted mostly the Indians.

There is one writing that eludes to the confusion that occurred between Indian Sickness and the other fevers that naturally developed. Again, keep in mind that yellow fever is not yet distinguished from the other fevers so succinctly as it was in the early 1800s. It took the 1790s epidemics to provide the cases needed for doctors to see that this fever was very different in terms of symptoms, fatality and even possible causes.

The common natural resource we linked to fevers during this time was the climate and weather patterns, and it was the documentation of a particular weather pattern that added to the confusion that may have developed when early doctors were trying to understand Indian Sickness.

The most common story and disease name assigned to it during the 1800s very much resembled the creation of the “Indian Summer” period by by New York’s Quaker physician Shadrach Ricketson. It was during this particular time of the year, generally speaking during the months of October and November, that the season-related behaviors of this disease would have allowed the warmer weeks of summer to re-express themselves just a little while longer. This could have happened right up to the day when the December case of the fever erupted spoken about by Oliver. But such an event is very unlikely, and more sensationalist in nature if we want to use it to believe that the December fevers were due to the normally summer-bound yellow fever causes. Normally, all it takes is an overnight frost with freezing temperatures to stop this fever from recurring, if they are do to mosquitoes. Such is not the case for rodents however, and may even be why the rodents become a major part of this story in December, with nighttime temperatures now reaching below freezing temperatures.

Rodents made their way on and off of ships by way of ropes, walkways and sometimes muck and water. As pests they brought with them numerous causes for disease, ranging from bacteria and fleas to chiggers and other arthropods as a part of their dander. For a rodent to disembark from a ship at dock in the winter seems very unlikely due to wind and cold. But it is possible for this animal to engage in this process during the warmer weeks of the year as well as Indian Summer. This time of the year gives then the time they need to settle down in local fields, barns, and homes, before reassembling in homesteads and farm houses for the winter.

The fact that Martha’s Vineyard was not impact, just Nantucket, also helps to eliminate the airborn mosquito as a possible cause. It was the land travel habits of rodents that restricted them and their disease to just the Nantucket Island. Therefore it seems more likely that this history had at least two diseases to blame for all of these “Extraordinary” cases of illness and deaths. The similarity of their symptoms only suggest the Summer and Falls diseases were somehow related, but not necessarily due to a shared cause. For this period in medical history, the theoretical causes then considered for this epidemic may have appears to be ever-present whenever this disease pattern struck. To some it could have been the local sources effluvium or miasma emanating from the swamps and then migrating from one home to the next.

This Indian Sickness has the following to note about its exact identification. The identity of this disease has changed significantly over the years. Even the most recent medical historians remain unable to define an exact cause of either of these two diseases so fatal to mostly the local Native American culture.

The most important and most prevalent epidemic diseases on the North American continent during this time included:

  • yellow fever (mosquito-vectored, viral)
  • malaria
  • cholera (not asiatic cholera, just cholera, opportunistic bacteria like Salmonella intermedia)
  • spotted fever (several causes, mammal and insect vectors included, esp. ticks)
  • typhus (mouse-born, fleas)
  • typhoid (Rickettsia)

Early references to these diseases defined them differently over time, and as time and the memory of this epidemic passed the once well-defined boundaries that were set between disease occuring closely together were also lost.

We see evidence for this in the recapitulations of this disease published and republished beteen 1765 and 1860. It took just several decades, several generations or retelling this story for some of its details to be lost. By the tome fifty years had passed, the kind of epidemic to strike the region aqlso changed slightly, as the way that we characterized the numerous kinds of diseases also underwent significant philosophical change. This interweaving of tradition and philosophy with new clinical discoveries and scientific observations made it even harder for medical writers and medical history writers to demonstrate any sort of congruency in their theories about the Martha’s Vineyard-Nantucket epidemic.

Another half century later, the emergence of yet another new theory and series of theories about disease, due to the rise of the bacterial theory, carried the tales about the history of the 1763/4 epidemic even further from its original claims and “truths”. What was originally referred to as Indian Fever” and referred to as Intermittent Fever” partially made its way into the realms of possibilities about it relationship with yellow fever, and then the 20th century virus discovered to be responsible for yellow fever. By the end of the 20th century, those remaining unlinked clues to it identification, brought about by changes in the stories being retold, led more recent epidemiologist to bring yet another class of diseases into the list of possible identifications for “Indian Fever.”

Helping this process along was the identification of “Indian Summer” some time in 1806 or 1807. “Indian Summer” was a name given to that warm spell that occured well into the autumn and immediately pre-winter months. This term was first put down in writing in a note by Shadrach Ricketson, at a time when climate was strongly related to disease behaviors especially when it came to periodic endemic and epidemic disease patterns. Had the “Indian Fever” erupted at a time, under the climate conditions of an “Indian Summer”, this use of the popular name could have remained fairly popular, if not made even more popular.

Also during this period of time in American medical history there developed this belief that certain racially or ethnically define “temperaments” made certain groups of people more susceptible to certain illnesses brought on by specific climates, weather patterns, winds and natural electricity exposures than other groups of people. The broad support for this belief that developed between the 1790s and 1820s due to a new interpretation of Erasmus Darwinism and zoonoses enabled even more of an argument to development resulting in a much stronger following of this new belief system.

When Indian fever struck Martha’s Vineyard and Nantucket, its unique behavior of infected and becoming fatal to only the Native Americans residing on this island made the disease look very much to be following this notion of race, evolution and survival. Evidence for this in turn appears in some comments included in the writings on this epidemic during the early 1800s. Those people most familiar with the ‘Indian Summer’ concept would have realized that the summer-autum nature of yellow fever, an epidemic that presented itself most strongly between the months of August and October, could have very easily erupted during the Indian Summer periods that occurred every now and then in local climate history. Individuals familiar with the Indian Summer theory and Indian Fever epidemic, in 1815-1820, would have rightfully proposed or concluded that ‘perhaps the 1763-4 epidemic took place in December as well due to that year’s Indian Summer.

Was a meteorologic record kept supporting this?

The intrusion of yellow fever into a colony setting is typical for late summer/early fall. Since it is transmitted via mosquitoes, yellow fever is a rarity to the same location by November and December. The events Rev. Oliver refers to that mimic the fall events were probably brought in by a vessel, but due to the season were more likely a result of rodents on the ships than mosquitoes. This method of disease diffusion is fairly common, and involved the rodents taking harbor on the ships and tehn exiting them once a new port is reached by way of following the ropes to the piers at night. The fact that this “Extraordinary disease” struck at least twice during the colder months, and demosntrated a significant period of time between cases, suggests that whatever its cause was had to be capable of residing for days to weeks before finding new victims. Thus the reason for this distinction between yellow fever during the late summer warm months and the second type of epidemic that took place during the much colder pre-winter months.

Taking this logic one step further, one needs to ask how is it that one of the two islands got hit but not the other?

In addition, one of the primary differences between the Martha’s Vinyard and Nantucket events is the uniqueness of the Extraordinary disease on Nantucket. If the disease that struck both islands were airborn (considered miasmatic back then, mosquito-related today), it could have travelled between islands. To accomplish this, three climatic requirements exist.

  1. First, the temperatures would have have to be particularly warm that year enabling the source or actual substance of the miasma–mosquitoes–to remain present between the October cases and engage in later travel in November and December.
  2. Second, there had to be a source for these mosquitoes in November. A local source is possible but highly improbable due to climate behaviors. This the other source has to be an incoming ship from down south or a place where the mosquitoes can lay their eggs and avoid the first killing frost.
  3. Third, there had to be an association of this epidemic between Martha’s Vinyard and the island of Nantucket. Mosquito-bred disease patterns have the added capability of dispersing by air to other locations. A mosquito-bred disease on one island could possibly spread to the other island.

So if the disease which struck mostly Nantucket later in the year were not at all mosquito or yellow fever related, but instead rodent related, this would explain the limited patterns of distribution this disease presented and its ability to attack just specific communities and households, thereby not infecting the far western end of the mostly indigenous inhabited island of Nantucket.








Did Derwent Whittlesey know about Benjmin Rush’s theory?  More on Sequent Occupancy and Rush’s “Species” Stages

An early version of the Sequent Occupancy philosophy was first penned in 1786 by Benjamin Rush. Rush referred to the different types of people associated with these different stages in life as species. The word species was a very common term applied to the growing taxonomy field, but also had some philosophical associations with other aspects of science. Studies related to the economy of man and mankind’s growth and development was one such area where this term species had some relationships made in the common press.

An online version of the Oxford Dictionary has the following entry for the word species (link)

Species – noun (plural )

    • 1 (abbreviation: sp., spp.) Biology a group of living organisms consisting of similar individuals capable of exchanging genes or interbreeding. The species is the principal natural taxonomic unit, ranking below a genus and denoted by a Latin binomial, e.g. Homo sapiens.

      • Logic a group subordinate to a genus and containing individuals agreeing in some common attributes and called by a common name.

      • 2a kind or sort: a species of invective at once tough and suave
        • used humorously to refer to people who share a characteristic or occupation: a political species that is becoming more common, the environmental statesman
      • 2b Chemistry & Physics a particular kind of atom, molecule, ion, or particle: a new molecular species

    • 3 Christian Church the visible form of each of the elements of consecrated bread and wine in the Eucharist.

The philosophy of changes in land use made use of the term species according to definition 2a in the above note. This way of thinking in the social sciences developed largely as a result of the work of naturalists like Erasmus Darwin, the grandfather of the very famous Charles Darwin whose evolution theory became popular in the 1850s.

Rush’s presentation on the Species of the New World settlers was penned a few years after the Revolutionary War was over and just a year before the Treaty of Paris was signed officially ending this war. In spite of its timing during this period of United States development and growth, it never really developed much of a following by United States physicians, much less physicians abroad.

Benjamin Rush’s version of this philosophy was based on the assumption that everything pertaining to land use prior to colonial settlement was unimportant. He barely touched upon any details of the events of colonial settlement history pertaining to the indigenous lifestyles. Nor was any mentioned made in his essay about the semi-Christianized, post-heathen lifestyle that some of these indigenous groups had developed. Rush interpreted these times in history as periods in need of change and development. This new way of interpreting the world and its resources was part of the much larger stewardship movement then developing worldwide.

If we ignore for a moment Rush’s exclusion of indigena from his ‘species theory’, the other parallels that exist between his theory and the more contemporary or recent sequent occupancy theory become noticeable. These can then be used to better understand the “extraordinary disease” pattern that had developed on the newly settled (resettled) lands of Martha’s Vinyard and Nantucket. This disease history can be better defined through the use of sequent occupancy theory.

There is an intersting logic behind Rush’s philosophy of Species of Man.  Evolution and creation were all but solidified as popular beliefs during the last decades of the eigtheenth century and the first for the nineteenth century. Especiation, the formation of two distinct types of the same organism, was not yet clearly defined as a given for nature. Nevertheless, the door to this possibility was now opened for science. Religion was less a part of the scientist’s life, in exchange for practicing alternative religious philosophy practices related to Masonry and the Odd Fellows, mysticism and the Quaker notion of Universal energy. So, nature was considered to be evolving, and soon, man would become a part of this evolutionary process, making it possible for the principal by-product of man–culture–to also become a part of the evolutionary process. For this reason, Rush’s sense about the man as a Genus and the different types of people as Species is understandable, although never mentioned as such in his writings, just symbolized by his descriptions.

When we review Rush’s theory wit hregard to the current Sequent Occupancy theory and contemporary medical geography philosophy, we find that the stages Rush defined in this essay are remarkably similar to those produced nearly a century later by Derwent Whittlesey and associates. These include the early pioneer setting, followed by a small family farming setting, followed by the peak in anticipated development for this region–the development of large farm and agriculture settings the purpose of which was to supply the more heavily populated town and city settings with much needed lumber and food supplies, various fabric producing materials like wool and cotton, and the necessities of life such as dyes produced by dye plants and medicines shipped over from Europe and grown on highly productive soil.

Whether or not Whittlesey was ever at all influenced by Rush’s philosophy is uncertain.  Rush’s manner of interpreting these stewardship roles never really developed much of a following over the next 75 years. By the end of the 1800s, a century after Rush published his essay, American geographers developed much the same philosophy in the midwest when the term “sequent occupancy” was introduced to the geography profession. It was introduced primarily by Derwent Whittlesey, although no real documentation of who first coined this term could be found. Unlike Rush’s model, this new manner of interpreting land use changes over time included the indigenous cultural settings as its earliest stage. The four stages that then made up the sequent occupancy theory were: wilderness (indigenous), pioneer, early farming, and agriculture.

This way of interpreting land use later became a standard for many economic geography researchers, but wasn’t really that popular until after World War II. By the mid-1950s, this way of viewing places and people was very popular, taught in most geography programs, and applied to many regional studies techniques. Due to the value of mapping during World War II, Medical Geography and Disease Ecology became a knowledge base and skillset uniquely required during the previous war. Geographer Jaques May took the lead role in assisting the government in developing their medical cartography field, leading the way to a new generation of medical geographers.

By the 1960s, these medical geography applications led to more detailed documentation and review of land use and settlement patterns. The knowledge of where diseases can develop was also important to documenting the changes in land use over time. Well utilized land wasn’t always healthy land. Overutilized land wasn’t always extremely unhealthy land. For the first time, the United States was reaching that point of being able to control some highly contagious and often fatal diseases like polio, diphtheria, tuberculosis, and perhaps even measles. All of these changes began changing our perspectives on epidemic and endemic diseaqse patterns, was saw just the pathogen and the people, the microcosm rather than the macrocosm, the germ, bacteria, virus and prion, instead of its natural living settings.

By the late 1970s and early 1980s, this topic of geography and disease was no longer popular in academic geography literature. Disease ecology and environmental science were now the popular terms to use. Geography received little to no support by those in United States medicine, although there were always thos few who managed to keep this geography specialty alive, not a specialty for your thesis or dissertation, just a sub-specialty in something yet to be recognized as spatial epidemiology.


My own revival of the use of the concept of sequent occupancy for studying changes in places over time for my work came about due to its unique applications. Old-timers in the field were arguing about the past meanings and applications of this term. Determinism was often a main term used in the arguments I was often up against at first. My applications of sequent occupancy to modeling social and physical diseases over time in a given place however was very different than claiming one was assigned a fate in life due to the older lines of reasoning. In terms of better understanding disease ecology and disease changes over time and space, sequent occupany had very valuable applications for use as a way to model disease patterns in order to better understand them, not necessarily predict them. With this better understanding comes the better predictions, a method of analysis not in any way like that of determinism.

It is safe to say that diseases have a number of causes, some individual and psychological, some social and cultural in nature, some physiological and anatomical in origin, some behavioral related and linked to such human behaviors as eating patterns, exercise and outdoor recreational activities, and still others linked to the most basic elements of life such as genetics, the nature of our interaction with the environment, the kinds of occupations we pick given the current living situation in terms of time, place and available manmade and natural resources. Sequent occupancy theory has a valuable application to studying both historical and modern day medical geography. In this case, I am using these same modeling techniques to understand the changes in disease patterns from the past. As I already illustrated elsewhere, understanding the geography of the diseases of the past provides us with important insights into the re-eruption of older, once nearly extinguished diseases in the future.

Three of the most influential writers during the 18th century period in young medical geography history were Riverius, Frederick Hoffman, and Christoph Homann. Riverius composed an essay on epidemic and endemic disease patterns, noting their behaviors to be mostly within certain climatic settings. Hoffman was mostly a chemist and pharmacist, but had developed some of his own conclusions about the behavior of endemic and epidemic disease patterns relative to the phlogiston theory for disease he strongly promoted, which in turn had been re-defined and adapted in a new form by New York physician Samuel Mitchell during the mid to late 1790s. Based on this new version of the phlogiston theory, diseases could in turn be discussed in terms of how and why the physiographic and climatic characters of places can often be used to define or better understand their healthiness versus unhealthiness, and their likelihood of providing the medical needs for those who chose to reside in and try to adapt to these new places. Christoph Homann, a follower of these two early medical geographers (or geosophers as he termed them) was a geographer and cartographer whose occupational goal was focused on the development of new world mapping techniques. In 1797, in the forward to the new medical journal he was chief editor for, Medical Repository, Mitchell termed this study of the possible fusion of place and medical science as geognosy.)

In his dissertation written sometime around 1720, and published in 1729 as , Homann defined the Geosophem or geosophy study of the world in relation to health and disease. His Dissertation focused on the need to merge medical knowledge and lessons with the teachings of geography.

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