In 1852, one particular death on the Oregon Trail stood out.  It was the death of a fairly young girl, Susannah, the first born of John K. and Josephine (nee Massie) Bristow.  On the day of her death in late April/early May in the western part of Nebraska, little Susannah was between 9 and 15 months of age.  Her exact birthdate is not known.  

Susannah died about 4 to 5 weeks following her mother Josephine’s death.  Josephine died on April 6th due to the common epidemic occuring along this part of the trail, Asiatic cholera.  She died just three days after her team passed the most likely source for this disease–the contaminated waters around Fort Kearney built adjacent to the Platte River flood plain.  

No record of Susannah’s death is found in any of the writings or documents produced on the trail.  In fact, were it not for a letter sent back the following winter from Oregon to members of the Bristow family residing back east in Illinois, we might have never learned about Susannah’s very early death, much less her existence.   In this letter, John and Josephine’s daughter Susannah is noted for the first and last time by anyone in his family.  This is probably because the women who mentioned her name was not immediately related to John Bristow.  Most relatives would have never mentioned Susannah’s existence out of respect for John’s tragic losses during the overland journey.   

The lady who mentioned Susannah’s existence was a member of a nearby wagon train team.  They grew up in the same part of Illinois, but at most were distant relatives of the Bristows.   Most of the members of this team were more like a once-removed cousin of John, his wife and their daughter.   Following the death of Josephine in the Plains along the Platte River, John passed his young daughter Susannah to the other train, possibly because one of the members there had one of her own babies to breast feed.  John’s hope was that this would improve Susannah’s chance of surviving till the end of this journey.  Her best chances for survival were to continue to be breastfed since she was such a young age.   For the remaining part of this journey, John’s oldest son, Elijah, Jr., a child from his first wife, remained with him on the wagon.   In the end, only John and Elijah, Jr. made it successfully to Oregon.

John’s daughter died several weeks while travelling on the other train.  This could have been due to any of several types of medical problems common to the trail then.  The most common cause for young children, especially newborns, was often referred to as Infant’s Cholera or cholera infantile.  Adults dying from “cholera” or cholera-like conditions typically died due to the fairly common cholera morbus, a severe diarrhea which results in dark colored stools and a considerable loss of fluids and nutrients.  Infant’s cholera, like cholera morbus, has numerous possible causes.  These causes exclude those for Asiatic cholera, the disease that had just killed Susannah’s mother Josephine Bristow.  But typically the non-Asiatic cholera deaths usually occurred due to dehydration and an increased weakness of the body in general due to stress and limited food and water intake.  Generally speaking, the cholera that kills infants is a simple case of prolonged diarrhea or on occasion an infection induced by poor sanitation.

While trying to link the daughter’s death to one of these generic forms of cholera during the course of these studies, it appeared more and more unlikely that this was the case.  Why did only John’s child die, and not the other children who were very young and some of them breast-feeding on the other train?   If Susannah had contracted some infectious form of infant’s cholera, or even Asiatic cholera, wouldn’t she have passed this on to adults and children in the other train as well?   Those on the other train may have feared this, but due to the needs of a distant family member agreed to take care of little Susannah.

We know from the rest of the story of this train, as told by the lady writing the original letter, that it was not the case that Susannah carried any sort of infection to the other train.     Were Susannah’s death due to an infectious disease common to young children, by passing his daughter to another train, she would have infected others on that train.  This means that more than likely, because the children on the other train did not die as soon as expected with the passage of an infectious and highly contagious disease, it was more likely that Susannah did not die from an infectious disease at all.

So what did little Susannah die from?


Insight into this endemic disease on the Overland trail and Great Plains appears in an 1856 natural history of disease map by Alexander Keith Johnston — Milk Sickness!

If we try to imagine this situation, we come to an even better understanding of the question as to whether the daughter died of some form of cholera or diarrhea condition or not.  After passing his daughter over to the next wagon train, one has to ask –what was the mother with a breast feeding child thinking? did it occur to her that this child could carry some disease that might infect her own children?  Will breast feeding the Bristow girl in turn make it more likely that her kids, or perhaps her own self, become infected with the same deadly disease?

It is possible that these types of fears could have left the new breast-feeding mother concerned about John’s daughter with only one option–to choose a method of feeding the young girl that would reduce any opportunities of passing along the Bristow family disease to other family members by way of such intimate contact.   This meant the new mother probably limited her most personal interactions with the young girl.  Since she and her family probably had a strong biblical background, she must have been overly cautious about making a decision that could become a threat to the very young Bristow’s life.  For the preservation of her own family, and as a part of her family’s heritage, she may have felt the need to look for other options to take for attending to the needs of Bristow’s daughter.  Due to these fears the breast-feeding mother had, the possible replacement of personal breastfeeding with cattle milk was not at all unexpected.  According to the matrons of this other family, the contagion on Bristow’s daughter was by no means going to infect their daughters as well.   This meant that daughter Susannah would have to survive on oxen or cattle milk.

The History of Milk Sickness

On October 15, 1818, the mother of Abraham Lincoln, Nancy Hanks Lincoln, died from an epidemic making its way through Dubois County, Indiana.  It ended up this epidemic was due to the common weed for this dairy farm country—Eupatorium rugosum or white snakeroot.  Nancy Hanks was just 34 years of age.  Her surviving son, Abraham Lincoln, was only nine.

The cause for this local epidemic would later be determined to be a linked to the local cattle grazing upon the local flora and the effects of this misgrazing on milk products.   This illness was first known as the alkali sickness due to the nature of the soil on which it was most frequently found.  This illness would ultimately become  known as “milk sickness.”  

Since its distribution  appears limited to the Midwestern states, and portions of the mid-Atlantic states around North Carolina, the early years of North American settlement tended to lack this problem in their medical history.  North Carolina colonists experienced milksickness about 1776.  In 1797 it was noted by Irwin F. Mather in his book The Making of Illinois.  During the early 1800s, Milksickness was experienced by Kentuckians, and was written about by Herndon in his Life of Abraham Lincoln.  In Herndon’s book, the  story of the milk sickness epidemic in 1818 in Pigeon Creek, Kentucky, described.  This provides an early example of how some physicians and scientists were trying to link disease to peculiar features of the local environment.  Most of the time these features were related to water, geological and soil conditions.  The following observations made by a Kentuckian farmer named Herndon, for example, stated: [From Abraham Lincoln: the true story of a great life. Volume 1 (New York, 1892) by William Henry Herndon, Jesse William Weik, pp. 22-25.  See more complete review of this selection of text below]: 

“In the fall of 1818, the scantily settled region in the vicinity of Pigeon Creek–where the Lincolns were then living–suffered a visitation of the dread disease common in the West in early sick days, and known in the vernacular of the frontier as the milksick!  It hovered like a spectre over the Pigeon Creek settlement for over 10 years and its fatal visitations and inroads among the Lincolns, Hanks, and Sparrows finally drove that contingent into Illinois…It not only took off the people but it made safe havoc among the cattle.  One man testifies that he lost four milk cows and 11 calves in one week.  This in addition to risking his own life, was enough, he declared, to ruin him, and prompted him to leave for points further west!…Early in October of the year 1818, Thomas and Betsy Sparrow fell ill of the disease and died within a few days of each other….Meanwhile Abe’s mother had fallen a victim of the insidious disease.  Her sufferings, however, were destined to be of brief duration.  Within a week she, too, rested from her labors.”

What Herndon tells us with this writing is that the growing behavior of Eupatorium had something to do with its tendency to suddenly result in rampant local cattle deaths and human sickness.   With the early settlement of the Old Southwest came the increased incidence of Eupatorium poisoning for horse and cattle, especially near Texas and New Mexico in Pecos Valley and within later settlements along the Mississippi River.  Due to this unexpected case of intoxication, Pioneers themselves also experienced the effects of Eupatorium by ingesting the milk produced by cattle which fed on this plant. 

A midwestern interpretation of “alkali disease”  was that it was due to the geographical relationship of abundant white snakeroot field settings with certain parts of the prairie lands containing alkaline enriched aquifers, creekbeds and riverways.  In Oregon Trail history, this placed some of the most in sections of middle and western Nebraska where the alkaline waters lie and cattle deaths became frequent due to drinking this water.  The Flora of the Great Plains book demonstrates a distribution of this plant, on a per county basis, that pretty much defines the most at risk portions of the overland trail for milk sicknessm which relates directly to where and when daughter Bristow died just four weeks after her mother.

It would be until the 1860s that the exact cause for this condition became known, due in part to some faulty theories out there.  In 1852, one of the more famous physicians from a Northwest medical college in the Midwest (back then “the Great Northwest” was only as far west as Minnesota), Daniel Drake took on the role of heading the research of milk sickness for the newly formed American Medical Association, his committee “The Committee on Milk Sickness, So Called.”  at the time, several much older theories for milk sickness existed, many of which reflected past theories for disease related to miasma, contagion, and effluvium.  In 1858, Drake  presented a paper theorizing that this illness was due to a poisoning brought on by cattle eating poison ivy (Rhus toxicodendron), the toxin he theorized was passed into their milk following ingestion.   The recognition that a species of Eupatorium rather than Rhus was causing milk sickness would not occur until three years later in 1861.  

Toxicology of White Snakeroot

So what is the nature of snakeroot poison?  Due to its volatile oil and resins, this plant is capable of producing a bitter milk due to cattle secreting these chemicals as a part of the milk production process.  Its main toxin, Tremetol, and perhaps two other toxic components in this plant–a resinous acid and volatile oil–were responsible for its most detrimental effects. 

These chemicals are capable of making the milk potentially toxic to the liver during its first pass through following digestion.  The result is potential exacerbation of prior liver problems in adults and onset of liver problems in younger children.  An adult with a long history of drinking for example would more than likely succumb to this form of sickness than individuals without such a history. In addition, the build up of other compounds with the solid organ systems (i.e. Pancreas and Kidney) are capable of leading to organ failure and perhaps cancer formation.  During the early to mid-19th century, only a few chemical industries existed that could result in people at risk for such conditions.  These industries would include tanning perhaps and some of the early farm chemicals trades, such as those related to lime or oxalate production.  Once the applications of chemicals to certain industries became more widely distributed, more people were at risk for this problem.  The early photographic industry of the 1840s is a prime example of this, as well as the hatmaker business.     

Contemporary livestock health specialist James F. Couch of the United States Department of Agriculture coined the term Tremetol for the toxin in Eupatorium.  It is a complex alcohol contained within all parts of the plant.  Its solubility in meat is slight, but not out of the question regarding meat production by steer and other farm animals.  Cases of human Tremetol poisoning due to meat consumption are not noted upon brief inspection of the literature.  The most common problem associated with this plant for humans is milk-induced intoxication; to livestock tremetol is a neuromuscular toxin.


Oxen, Cattle and other Farm Animals and Livestock

According to Thomas G. Hull, horses, cattle and sheep are potential victims of this malady.  The causative factor, be it Eupatorium or Haplopappus, produces similar symptoms. The tremetol first causes: “drooping of head and ears, dull appearance, loss in weight, abnormal thirst, obstinate constipation, and general inactivity.” [p. 411]  The term trembling sickness comes from the “characteristic trembling of the voluntary muscles.”  During its advanced stages, this trembling sickness turns into a muscular debility, making the animal unable to rise from a lying position on the ground.  The breath is pungent upon expiration.  During the worst stages of this intoxication, pulse and respiration are irregular and a coma may ensue; the next stage is death. According to Hull, different animals and even different breeds have different likelihoods for recovery.

Cattle bearing milk may carry the toxins and not yet produce symptomatology of their intoxication.  This increases the likelihood of causing human intoxication in the form of milk sickness.  A cow lactating is less likely to show the disease due to riddance of the toxin through the milk that is produced.  A non-lactating therefore is more likely to show symptoms and therefore become a fatality.

In horses, the symptoms are very much the same.  Hull gives excessive drooling and slobbering due to paralysis of throat muscles as an added symptom.  Hull claims the horse’s expected longevity following intoxication is around three days.   

Sheep intoxication mimics that of cattle.  Other domesticated and farm animals are susceptible to this as well, ranging from aves to pets, though the incidence of this is considerably less and appear less related to much of Oregon Trail history. 


With pioneer families, the primary scenario that stands out regarding intoxication pertains to a drought-induced lack of grass feed, along with a matching increase in the amount of potentially palatable and highly visible  Eupatorium species along certain parts of the trail.  Along dry areas, where water was low,  Eupatorium poses a major threat for emigrants and their oxen, horse and cow due to its retention of greenness.   This increased availability of Eupatorium and reduced grazability of graminae are also possibly related to the deaths of grazing animals.  The breast feeding mother may very well take action against claims of abandonment or improper mothering of a newborn.   This is diminished by using the local cattle to feed this child instead.


       1. Eupatorium spp. (ca. 40 spp.) [White Snakeroots]

            in particular:   

  •  E. ageratoides, serotinum, and urticaefolium, found on the East Coast inland to the Great Plains, stopping at Missouri; also known as Richweed, Squaw Weed, Polewort.
  •  E. altissimum, and rugosum tall thoroughwort, distribution continues westward into mid-Nebraska.
  •  E. purpureum (Joe Pye weed) and E. perforatum (Boneset) are also prevalent in Nebraska, but not toxic in this fashion.

      2. Haplopappus spp., [Rayless goldenrods] (formerly Aplopappus spp.)

            in particular:   

                  a. H. heterophyllus (Rayless Goldenrod) [displayed]

                  b. A. fruticosus

Source of independent images:

Growth Habits

Eupatorium tends to grow in regions along the edges of fields, near shade trees, and in dense clusters or colonies that cover partly lit forest floors.  To be sure you got  rid of it, the farmers felt you had to simply remove the shade trees.

Causative factor(s)

Phytochemistry: Tremetol, with a resinous acid and aromatic, each of the latter two possibly a sesquiterpene or sesquiterpene lactone.  Other less likely possibilities: a quinone and phytosterol.


According to distribution maps in the Atlas of the Flora of the Great Plains, the most likely species of White Snakeroot involved with this medical problem in western Nebraska on the Oregon Trail is Eupatorium rugosum Houtt..  It is concentrated mostly at the eastern end of Nebraska along the Missouri River and immediate tributary flood plain, but hugs the trail along the Mormon routes and the routes from St. Joseph and St. Louis, all the way to Fort Kearney.  It then ceases to continue along the trail once Fort Kearney is passed, only to pop up again in Lincoln County.  This is about one or two day’s travel following one’s departure from Fort Kearney.  This suggests the possibility that this plant was somehow carried along the trail from the eastern state counties to its last deposit on the Oregon Trail, a route which other trail-bound floral tended to take during the 1840s and 1850s, in particular Polygonum persicaria

This distribution of Eupatorium rugosum comes into play in OregonTrail medical history during the peak years of cholera deaths. Most of the cholera deaths occur following the departure from the jump-off sites heading into in Eastern Nebraska as well as following the departure from Fort Kearney, where pioneers stop to replenish their stores.  The most heavily concentrated deaths along the Oregon Trail are just across the river from Fort Kearney, a little west of the crossing.  These pioneers usually dies from cholera and most of them were adults; the children were spared.   But this sets the stage for the next series of deaths than can ensue for families with newborn children whose mothers are now deceased.  The young children and newborns once subsisting on mother’s milk, due to the mother’s death, may have to be transferred to another wagon train bearing a nursing mother.  In cases where there was no wet nurse available, the child in turn is fed cattle milk.  In western Nebraska, especially during drought-stricken years, this cow milk was the threat to the youngest pioneers.  A newborn child with an immature liver would most likely suffer more than an adult drinking Eupatorium-infested milk, which typically has a fairly unpalatable taste.   In such cases, the time before this change in dietary patterns becomes deadly is perhaps a week to a month.  In John Kennedy Bristow’s case, his newborn Susannah became the next victim of the mother’s death, due to lack of a safer, more appropriate milk produced by a nursing mother.   

Approximate Center of Alkali Country and Milk Sickness Territory  


Relation to Oregon Trail Natural History

Why were livestock on the Oregon Trail poisoned by these weeds? 

The focus of deaths in October 1818 suggests that Eupatorium had to grow to maturity and be very common in the fields of it to be eaten.   But this also implies that either the normal grass feed available for cattle in the grazing lands was not as prevalent as it once was, or that the proximity of livestock to shade-bearing regions made this plant more available to them for foraging.  During rainy seasons, it would appear more prevalent due to its rich color, which would remain a rich color during the drought seasons as well. 

These changes in the environment are due to very specific changes, especially in regions where cohabitation between man, farm animals and local fauna have not changed.  Either they represent a change in farming behaviors, graziers, grazing populations, local environmental stability, and/or climate, or they are due to drought.  The increased consumption of flora with weed-like growth behaviors like Eupatorium and Haplopappus increases the likelihood of animal deaths due to intoxication.  Some past meteorological evidence shows that 1818 was a drought-ridden year, thus reducing graminae, at the expense of making these weeds more noticeable and more available for grazing.


Abraham Lincoln: the true story of a great life. Volume 1 (New York, 1892) by William Henry Herndon, Jesse William Weik.  Accessed at Google Books.

See the Whole Story below.

William I. Christensen.  Milk Sickness: A Review of the Literature.  Economic Botany 19(3) (July – Sept., 1965). pp. 295-300.


One Response to “Epidemics blooming on the Trail”

  1. […] Brian Altonen, a medical science and public health expert, took a look at the diseases running rampant through wagon trains and found the heartbreaking case of Susannah, a little girl who died just a month after her mother. Her disease wasn’t contagious — no one else caught it from her — but the pioneers didn’t know this at the time. […]

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