What Typhoid Mary tells us about the spread of Covid-19
Typhoid Mary was the first rock-star human disease super-spreader. Even if you don’t know who she was, you’ve probably heard her name. She’s the embodiment of a disease spread by a human or animal vector who herself has become immune to it.
Typhoid Mary’s tale has a lot to tell us about how the Sars-CoV-2 virus, or Covid-19 proliferates. Because of her, we now know that people who have recovered from a mild bout of a deadly infectious disease can go on to infect those around them.
When it comes to transmissability, the two diseases are not really dissimilar. A person infected with Typhoid is likely to infect 1.2 people. A person infected with Covid-19 is likely to infect 2 people.* One percent of people who develop Typhoid will likely die of the disease. Covid-19 is fatal in 3.2 percent of cases.
These numbers tell us a few things: Covid-19 is three times deadlier than Typhoid, for instance.
But what they don’t show is how the actual death rates are entirely determined by national, state, and local management — or mismanagement — of a catastrophic disease outbreak.
In 1906, Typhoid killed 600 New Yorkers. At that time, Typhoid fever was about three-fold more deadly than it is now: 10% of patients who contracted it succumbed. By contrast, from the beginning of the Covid-19 outbreak — from March 1 of this year until October, 5, 2020 — Covid-19 has killed 23,852 people in New York city alone.
That’s 40 times as many people killed by Covid-19 than by Typhoid 114 years ago.
A bit about Typhoid Mary. She was born Mary Mallon in Ireland in 1869 and immigrated to New York in 1883. In 1906, she started working as a cook for the family of Charles Henry Warren, a wealthy New York banker, at a home on the north coast of Long Island. Mr. Warren liked to entertain. From 27 August to 3 September, six of the eleven who people visited or lived in the house developed Typhoid fever, a disease caused by the bacterial pathogen Salmonella typhi. Mary Mallon herself developed a mild infection and recovered.
Typhoid is transmitted primarily through contact with feces or water contaminated by the bacteria. It doesn’t take a lot of Salmonella typhi to infect someone. A few bacilli shed from the hands of the person preparing the salad or the peaches-and-cream are all it takes. Cooking food kills the bacteria; raw food is an excellent harbor for it. Most types of Salmonella can live on dry surfaces for many months, even longer in humid or low temperature conditions. Typhoid spreads exclusively by ingestion of the Salmonella bacillus.
The Sars-CoV-2 virus spreads primarily through direct contact with a carrier or respiratory droplets from coughs and sneezes, or through airborne transmission in poorly-ventilated indoor areas. It can survive without breaking down for about 72 hours on stray surfaces such as doorknobs, subway seats or bare skin. Because it’s a virus, unlike the Salmonella bacillus, it cannot replicate without the machinery and metabolism of a human or animal host cell.
A sanitary engineer, George Sober, was retained by Mr. Baker as a microbial sleuth to figure out where the repeated Typhoid infections originated. The disease was not, he discovered, hiding in the local oysters, as he’d originally theorized. The source was human. The cook, Mary Mallon, was herself the fount of the infection. When she learned of Sober’s plan to hand her over to the New York state health authorities who would put her in quarantine, Mary Mallon fled back to the city.
At that point, Typhoid Mary’s life became game of cat and mouse.
In March 1907, Sober started stalking her. With the New York health commissioner’s assistance, Sober was able to bring her in. A stool sample tested positive for Salmonella typhi. She was transferred to Riverside Hospital on North Brother Island Island, where she was quarantined in a cottage. She sued the New York health department, unsuccessfully, for her release. A few years later, she got lucky. Sort of. In 1911, Typhoid Mary was sprung from captivity by a new health commissioner. Her release was contingent on her honouring a promise that she’d never work as a cook again. Soon, however, she was again chopping vegetables and whipping cream for clients throughout New York and New Jersey. She didn’t know any other work. Cooking was her livelihood.
In 1915, a cluster of Typhoid cases broke out at at the Sloane Maternity Hospital, in Manhattan. A new cook who called herself “Mary Brown” had started work in the hospital’s kitchen just before the outbreak. Soper was again brought in. He confirmed the cook was indeed Typhoid Mary. In the space of three months, she’d infected at least 25 people — doctors, nurses and staff. Two of them died.
Typhoid Mary was returned to North Brother Island where she remained until her death in 1939.
The way public officials managed Mary’s Typhoid infection in 1915 compared with the handling of Covid-19 makes me wonder what year we’re actually living in. The public servants of 2020 entrusted with preventing the progression of the deadliest infectious disease ever seen are an abysmal failure.
If recent events are any indication, things will only get worse.
In the days before he announced he was sick with Covid-19 on October 2, Donald Trump met with a numerous officials in a series of meetings. No one wore masks. People hugged. No one socially distanced.
Numerous people who attended the White House Rose Garden Ceremony on September 26 where Trump introduced Judge Amy Coney Barrett as his next Supreme Court nominee have come down with the disease. As of this writing around twenty people close to Trump, including advisors, assistants and assorted hangers-on have had positive Covid-19 tests. A New York Times journalist who travelled on Air Force One tested positive, as did another journalist. It’s a well-known fact that asymptomatic people can be infected with the virus and be active carriers. They can infect other people. It’s unknown how many people in the audience at the Rose Garden event have tested positive. The White House will also not divulge when Trump’s last negative Covid-19 test was; or what day, exactly he tested positive. He could have been spreading the disease for a week before he had symptoms.
Judge Barrett herself contracted the disease last summer. She is said to have “displayed mild symptoms“ and had “a positive test result.”
That was in July. Early July? The end of July? Now it’s early October. Judge Amy Coney Barret could still be shedding the virus.Trump himself could have infected everyone present at any one of the White House gatherings the last week in September.
According to the White House, Barrett is tested daily for Covid-19. Her test was negative on October 2. No one will say a word about her diagnosis: the White House declined to comment. A member of Barrett’s family did not respond to a request for comment.
A paper published in the journal Infection, Disease and Health had a great deal to say on this topic. Here is their table of highlights:
- Viral shedding has been demonstrated up to 63 days after symptom onset.
- The distinction between viral shedding and infectivity is important for the development of quarantine guidelines and policy.
- There is an earlier peak in viral load in SARS-CoV-2 than seen in SARS.
- Quantitative viral loads are higher in the nose than the throat.
- It is likely that asymptomatic and presymptomatic transmission is occurring.**
Circling the wagons around Judge Barrett and Trump, and refusing to answer questions about their health status only creates suspicion and panic. We knew, even before Trump was admitted to hospital, that he spreads disease every time he opens his mouth. But is Judge Barrett still shedding the virus? Is it possible she’s a carrier?
Only time will tell, I guess, but in the meantime, I’ll place my bet on the pathogens. Sars-CoV-2 and Salmonella typhi are extremists extrodinaire: amoral, impervious to argument, and sheathed in an unhaltable will to survive regardless of who or what gets slaughtered along the way.
**Widders, A et al (2020). SARS-CoV-2: The viral shedding vs infectivity dilemma. Infection, Disease & Health, 25, 210–215.