It was the mass grave that got their attention. Four bodies crammed into one casket, with one child outside but with the casket. Multiple graves are not common in Yakutia, Siberia. Examination of the late 17th to early 18th century mummies indicates that burial came quickly after death. The casket contains one adult male over age 30, an adult female, an adult female under age 23, a male child about 5 years old, and outside the casket a child about 4 years old.
The French and Russian team led by Philippe Biagini undertook pathological and genetic analysis of all five mummies. They were able to confirm that the older woman is the mother of the young adult woman and the adult male. They took lung and tooth specimens from each mummy at the site (in situ). Finding iron inclusions in the lungs of the young female (mummy 2), suggested to the team that she suffered a pulmonary hemorrhage shortly before death. They don’t say how they jumped from there to screening for smallpox or what other pathogens were considered. Oddly, they make no mention of any smallpox lesions on the mummy. (Without other bioarchaeological data, is it possible that this team only received the tooth and lung specimens, but not the remainder of the mummy?)
The DNA was divided among three labs. Three short sections of Variola (smallpox) genome were amplified by at least two labs each. They failed to amplify long stretches of the virus, suggesting that there are no intact virons left in the mummy. Their phylogenetic analysis grouped this virus, PoxSib, with Variola but distinct from both clade 1 and clade 2. They suggest that PoxSib could be an ancestral strain to both clade 1 and clade 2 or a strain that has not been previously sampled. Biagini et al. suggest this virus may have come to Siberia with the Russian conquest in early 18th century, possibly connected with a documented outbreak in 1714. This grave comes from the same culture as previously analyzed graves that isolated the first ancient whooping cough.
Biagini, P., Thèves, C., Balaresque, P., Géraut, A., Cannet, C., Keyser, C., Nikolaeva, D., Gérard, P., Duchesne, S., Orlando, L., Willerslev, E., Alekseev, A., de Micco, P., Ludes, B., & Crubézy, E. (2012). Variola Virus in a 300-Year-Old Siberian Mummy New England Journal of Medicine, 367 (21), 2057-2059 DOI: 10.1056/NEJMc1208124 See supplemental appendix for most of the detail.
I love looking at infection maps. Hat-tip to Michael Walsh at Germscape for finding this map. There is a lot of information on this map and unfortunately any text that might have come with it at Lapham’s Quarterly is not readily available. So we have the map to figure out without any explanation. The red arteries represent the origin of Leprosy in central Africa and the blue veins represent the origin of smallpox in northern Africa and its spread. Transmission lines for malaria are not shown; the yellow areas seem to represent modern endemic malaria. The geographic highlights either document transmission events or major steps in the study of malaria, smallpox and leprosy.
At the height of its expansion, there are few places on earth that malaria did not penetrate. Today malaria is found primarily in tropical regions but that wasn’t always so. The map to the right illustrates the malarial deaths listed in the 1870 US federal census. Malaria once was endemic, at one time or another, in most of the United States east of the Mississippi River and around the Gulf of Mexico. Likewise it was endemic in parts of 19th century Britain. In temperate regions of the world it is the humans who carry the parasite through the winter and infect the spring mosquitoes. Contrary to general knowledge, most malaria in the United States dwindled long before the arrival of DDT. Improving the standard of living and eliminating unnecessary standing water are the most important ways to decrease malaria. Early American physician Benjamin Rush knew this over two centuries ago.
The Gettysburg address is one of the best known speeches ever delivered by an American president. Few Americans know how close Lincoln came to not delivering it, or that its brevity may owe something to how poorly Lincoln was feeling as he wrote and delivered the address.
The battle of Gettysburg was fought in July of 1863 but the cemetery wasn’t dedicated until November. Lincoln was a late addition to the program, asked only 17 days before the event. In the days between agreeing to give the address and leaving for Gettysburg, Lincoln’s young son Tad lay ill with a high fever and rash. Details of Tad’s illness are vague and are really based on his father’s diagnosis. Lincoln was understandably distracted, two of sons had previously died from what is believed to have been typhoid fever. When the president left for Gettysburg, Mary Todd Lincoln stayed behind with Tad. The president took his valet William H Johnson, a free black man who came to Washington from Illinois with the Lincoln family, with him to Gettysburg. What follows is based on a case study compiled by Goldman and Schmalsteig (2007).
On the train to Gettysburg Lincoln began to tell his staff that he was feeling weak, but he finished editing his address and continued on to Gettysburg. When the arrived Lincoln rode to the cemetery on horseback and viewed the area and plans. When the program began Lincoln sat on the platform for over two hours while classical scholar Edward Everett spoke and during a short musical piece. Lincoln was feeling weaker all the while and observers called his color ‘ghastly’. When the President finally got up, he stunned the crowd with his short address; most were caught so unawares that they missed it. Lincoln judged the crowds silence as disappointment and left Gettysburg himself disappointed. On the train back to Washington Lincoln grew feverish and weaker still. His valet William Johnson sat up with the President wiping his face with a wet cloth to cool him.
By the time Lincoln returned to Washington, his weakness had progressed and he had become feverish with severe headaches and back pain. By the fourth day of symptoms, a red rash appeared that developed into scattered blisters by the next day. A good description of the rash and its development are lacking. The president’s personal physician Dr Robert King Stone first diagnosed him with a cold, then ‘bilious fever’ (an early name for malaria), and then scarletina (scarlet fever). Both scarlet fever and malaria were common in early 19th century America including in Lincoln’s home state of Illinois. Goldman and Schmalsteig reviewed Dr Stone’s records; oddly, he apparently never mentions this illness though he attended the president through the entire period. As the rash progressed, Dr Washington Chew Van Bibber was called in for a consultation. After examining the President, he diagnosed a mild case of smallpox (varioloid). Much later Dr Van Bibber’s version of a conversation with the President was recorded in the autobiography of another surgeon:
‘Mr President, if I were to give a name to your malady, I should say that you have a touch of varioloid.’ [the old fashioned name for smallpox]. ‘Then am I to understand that I have the smallpox?’ Lincoln asked, to which the doctor assented. ‘How interesting’, said Mr Lincoln. ‘I find that every now and then unpleasant situations in life may have certain compensation. As you came in just now, did you pass through the waiting room?’ He replied, ‘I passed through a room full of people’. ‘Yes, that’s the waiting room, and its always full of people. Do you have any idea what they are there for?’ ‘Well’, said the Doctor, ‘perhaps I could guess.’ ‘Yes,’ said Mr Lincoln, ‘they are there, every mother’s son of them, for one purpose only; namely to, to get something from me. For once in my life as President, I find myself in a position to give everybody something!’ (Goldman & Schmalsteig, 2007, p. 106).
By day 10 of symptoms, the fever was decreasing and the rash was beginning to itch and peel. The weakness persists the longest, preventing him from returning to work for official business for 25 days. Visitors report that he was beginning to walk briefly by December 7 (day 19 of symptoms) and that marks of the rash were visible but few if any remained as facial scars. On Dec 15 he was able to work for a few hours and went to a play at Ford’s theater. A month later on January 12 he was reported as having regained most of his old vigor, though still underweight.
The diagnosis is primarily based on three factors: the appearance of a rash, a three week illness, and contemporary physicians diagnosis of smallpox. In Goldman and Schmalsteig’s analysis, the diagnosis appears correct from the available information and they note that a three week illness is too long for most other possibilities. Additionally, we know that his son Tad had been ill with a fever for two weeks before Gettysburg, though his disease less well recorded than his fathers and no photos of father or son ever showed visible pox scars. Given that two of Lincoln’s sons had previously died of what is believed to have been typhoid fever it must be considered. However, as his physicians never diagnosed him with typhoid and they should have been very familiar with that disease, so we can rule it out. Typhoid can produce a rash but not blisters.
The last clue comes from Lincoln’s valet William H Johnson, who did develop smallpox and died of it before January 12. In an interview with the Chicago Tribune on that day, Lincoln told the reporter than he didn’t believe that he gave smallpox to Johnson. Goldman and Schmalsteig believe that a mid-January death for the valet Johnson is the right timing for a disease contracted while caring for Lincoln in late November given the incubation period of about two weeks and then Johnson’s own illness to run its fatal course. Further, when Johnson died Lincoln secured a place for him in Arlington National Cemetery under a grave stone marked “citizen”, all paid for by President Lincoln. However, from 1863 there was also a Freedman’s Village where former slaves lived on the Arlington estate and many were buried there. Lincoln’s choice of the Arlington cemetery may not have been unusual for the times and need not imply that the President felt any guilt over Johnson’s smallpox. Although they imply that Lincoln’s actions suggest he contracted it from the President, Goldman and Schmalsteig point out themselves, that we don’t know how much smallpox was circulating in Washington at the time. If it was circulating around residents and staff at the White House, it is possible that Johnson contracted it from someone else.
Goldman and Schmalsteig’s recent analysis was not only to determine if Lincoln really had smallpox, but also to determine whether he had a full blown case or a mild case due to previous vaccination (or variolization). Modern vaccinations following Jenner’s original protocol use the related vaccinia virus (cowpox) to illicit immunity that will protect against smallpox. Variolization takes material from an active smallpox lesion and inoculates a healthy person through a cut in the skin. Variolization is riskier than vaccination because it can produce a full blown case of smallpox. Yet, smallpox was so devestating, with such a high mortality rate (about 30%), that people were willing to undergo variolization and the mild case of smallpox it usually created, to increase their chances of surviving smallpox. Jenner’s method grew in popularity after its introduction because it was so much safer but its unclear how completely Jenner’s process was accepted during Lincoln’s youth. Regardless, Goldman and Schmalsteig could not find any evidence that Lincoln had been immunized against smallpox by either method.
There was great concern among the public over the President’s illness. At one point rumors circulated around Washington that the President was dying (Goldman and Schmalsteig, 2007). Despite his contagious condition causal references from his visitors seem to suggest that the President had frequent visitors during his illness including an old ally Rep. Owen Lovejoy of Illinois. He went to the Ford theater on December 15, perhaps to show himself to the public. We can only imagine the effect that these rumors could have had on the war effort in the winter of 1863-4 if they had spread widely. Two photos on were taken one and two months after his recovery respectively (shown here). We have several photographic portraits of Lincoln but for two of them to have come so closely after his illness is remarkable. It has often been said that the weight of the Presidency aged Lincoln, and no doubt it did, as it does every President, but smallpox may have taken its toll too.
Goldman and Schmalsteig assert that Lincoln’s physicians tried to pass off his disease as the mild (immune-modified) form of smallpox but they really don’t outline any evidence of anything more than respecting the President’s privacy. They seem to be placing a lot of emphasis on the physicians use of the term varioloid, that in the 20th century meant a mild case in a vaccinated person, but as they admit was a common term for all smallpox in the 19th century. They conclude that the President did have a full immune-unmodified case of smallpox based on the length of his illness. With a 30% fatality rate, the public had a right to be concerned over the President’s health. Approximately 1 out of 3 cases didn’t make it: the President and Tad survived, his valet William Johnson didn’t. We can only imagine the effect of the President’s death in December 1863 could have had on the war.
Goldman AS, & Schmalstieg FC Jr (2007). Abraham Lincoln’s Gettysburg illness. Journal of medical biography, 15 (2), 104-10 PMID: 17551612