Polio and COVID-19

David Shurtleff, MD, FAAP
Retired Pediatrician

I have been asked by several friends and my daughter, Hillary, to recount my memories of the Polio epidemic of 1955 as compared to the SARS CoV2 virus. Since there have been multiple requests, I am subjecting my memories to a document that I can share not only with current requests but for those in the future. Let me begin by stating these memories date back 75 years and cannot be trusted as true because the author suffers from being a fabulist. I recommend anyone reading this document who wants more accurate information to seek other sources. Remember that the author was involved in the care of patients on an hourly basis 24/7.

Next, let me state these two viruses and the environments in which they attacked us are very different but do retain some similarities. I will list the differences, similarities, anecdotes, followed by generalities at which I have arrived due to experience.

First, Polio was a virus spread primarily (we think?) via water and stool contamination. COVID 19 by droplets and personal contact. More recent scientific and communication advances compared to 1955 lead us to minute-by-minute information of what COVID 19 is and how it is spread. In 1955 we had only relatively little epidemiologic data and nowhere near as immediate transfer of information. Next, Polio affected the muscle and midbrain nerves that controlled vital functions and COVID 19 affects primarily respiratory organs. Next, an attenuated vaccine had recently been developed for Polio and both single and double immunization administrations had been administered to some patients in the area of the 1955 epidemic. There is no vaccine for COVID 19.  President Franklin D. Roosevelt, himself a paralyzed survivor of Polio, was forcefully supportive as was his government. Next, the training structure in which I was involved was in the early stages of transferring from one in which there were general internships followed by “General Practice” or application to “Residencies” in specialties. During this time we also were expected to remain in residence in the hospital until all our patients were completely cared for and we could then exit the hospital signed out to our partner “intern” or “resident” until our presence was next needed. Finally, and most important, the Polio epidemic in which I was involved as a new intern straight out of medical school was in New England with Boston was the center of the epidemic, Polio was endemic in the southern U.S. and episodic in the northern U.S., whereas COVID 19 is a pandemic.

What, then, are the similarities? Both viruses are, essentially, invisible and unknown to the public, generating fear and suspicion amongst some who in 1955 blamed the epidemic on science, the introduction of the new Polio vaccine and currently some believe in incorrect statements  which repeatedly contradict known science. Both viruses kill, with Polio showing a propensity to attack the young and pregnant women whereas COVID 19 targets the elderly, but both have deadly effects amongst all ages. National resources mobilized to send nurses from the endemic areas of the southern U.S. to Boston in 1955 and volunteers are contributing to the care of COVID 19 by coming into affected areas such as New York. Both viruses killed by interfering with respiration, polio by paralyzing either the regulation of breathing (Bulbar Polio) or paralyzing the muscles of the lungs. Both received respirators from out of the hospitals overloaded with patients. In 1955, we at the Massachusetts Hospital (MGH), received ours from the Massachusetts Institute of Technology (MIT) across the Charles River when they invented, for the first time machine driven respirators (Note: that the recently reported “new” mechanical respirators were designed at MIT a decade ago refers only to the details of the type {The type referred to as a decade-old concept involves two mechanical arms pressing together to squeeze the bag now called an Ambu Bag –for the original designed by Bird in 1955 see below.}). Respirators are now being shared between epidemic centers from across the country. Spread of the Polio viruses (there were three) were thought to be spread by fecal contamination of water and I am unaware of whether that is now thought to be the only method of spread. We did not have DNA and RNA to track the spread of Polio whereas today we believed for a while that COVID 19 was spread by direct contact and now suspect it is being spread by droplets, although the size and distance the infectious particles travel are still unknown. These changing scientific beliefs have further exacerbated the public’s fear of COVID 19. By far the most important similarity between the viruses is that Polio affected only certain persons and was most likely spread by asymptomatic carries just as we have suspected asymptomatic carriers can spread SARS CoV2. Both epidemics have been controlled by sequestration but of two wholly different types as will be illustrated below.

Remembering Polio
This next paragraph will now change to a description of how I remember the epidemic illustrating some of the generalities stated above. I remember the first day of my reporting for my internship as July 1, 1955 in the emergency room at MGH with my Assistant resident, Kazuo K. Kimura, PhD, MD, also known as Kaz, and a senior resident named Peabody. We were responsible for new cases entering the emergency room in an area separated from the other emergency room. We were also the inpatient team on the “Polio Ward.” We examined an acutely ill man in his 50’s, did a Lumbar puncture and identified him as having non-paralytic poliomyelitis or another enterovirus.  He was amongst a number of acutely ill polio patients we either sent home or, if paralyzed, admitted to the hospital. This male patient returned a few hours later after developing paralysis in the tunnel leading north out of Boston. Upon his return, he was admitted to our “ward.”

The number of patients soon increased to the point where the hospital created a separate area for care of respiratory-impaired patients by entirely gutting a floor of the hospital’s private building. This area had cement flooring and reinforced cement support columns, windows, doors and respirators including iron lungs, rocking beds and “turtle” respirators. The iron lungs were 8-foot-long tanks closed except for one end where the patient’s head protruded. They operated by producing a negative pressure in the tank expanding the chest and pulling the diaphragm done by pulling out the abdomen. The rocking beds moved the patient from the head down to foot down on a 45-degree slant each to allow the abdomen to slide up and down expanding the lungs. The “turtle” respirators were added to our tools later. They were plastic devices that fit from the collarbone to the pubic bone and fit snugly along the margins. Negative pressure pulled the abdomen out, the diaphragm down and expanded the lungs. The final piece of apparatus was an anesthesia respirator with an Ambu bag that we were required to pump by hand. Oxygen mixed with room air inflated the bag and we hand compressed the bag that led to a one-way valve that allowed the mixture to inflate the patient’s lungs. This fourth type of respirator was required for bulbar polio patients that we recognized as developing shock when we attempted to place them in an iron lung or “turtle.” We alternated squeezing the bag because our forearms cramped painfully after prolonged squeezing.  Seeing this problem led Mr. Bird, an MIT engineer, to develop a mechanical system consisting of a plastic cylinder around the bag. To this cylinder there was a nipple that allowed it to be attached to the positive pressure tubing carrying CO2. The bag was still attached to the oxygen and room aid at a lower pressure. As the CO2 pressure in the cylinder rose and fell the bag first emptied into the patient’s lungs and subsequently refilled as the pressure in the cylinder lowered. Before the invention of Bird’s respirator, we required a larger staff of nurses. Our local Boston nurses were only those who were quarantined with the medical staff providing only a skeleton 8-hour shift leading to another necessity for more nurses that was supplied by the volunteer nurses from the southern U.S. Both physicians and nurses were quarantined for sleeping and eating separated from the other hospital staff for 2 ½ months.

Following stabilization of the 1955 crisis the medical and nursing team remained caring for the “Polio Ward” patients and the MGH ward was closed. They then transferred the sequestered nurses and doctors with the patients to the Boston Infectious Disease Hospital, The Haynes Memorial Hospital, where they were separately caring for other Polio patients. By the time of our transfer in August the respirator patients were in a much larger room that allowed considerably more space for each patient. We were, however, still required to care for the Polio patients on the ward but also to treat newly arriving patients in the emergency room.

Having covered the generalities and a few specifics, this next section will recount instances known to the author that illustrate my experiences. The emergency room experience I remember at the Haynes was a college-age young woman who arrived late in the epidemic with fever of several days and paralyzed legs. The student performing the lumbar puncture, under my guidance, was amazed, as was I, when the first drops of spinal fluid were thick with white cells. I grabbed the vial and fled to the laboratory where I stained and viewed under the microscope white cells and pairs of bean shaped cocci – meningococci! Although a rare presentation, it is well described in textbooks of the disease presentation before antibiotics. I raced back to the emergency room and had the patient on penicillin and sulfur drip within the 20-minute timeline set by the Professor of Infectious Disease, Louis Weinstein, with whom I had studied on several electives as a medical student.

My earliest memory of the epidemic was being fired. A private orthopedic surgeon had admitted an entirely healthy child to the private ward over the July 4th weekend since the parents could not obtain a sitter. He requested that I, as an intern, (only interns were allowed to write orders) order the patient to participate in the Hubbard tanks in which our Polio patients were being treated to relieve their painful muscle spasms secondary to their paralysis from the Polio. (This was our adaptation of the Kenny Treatment of hot packs.) It is reported that I refused  in a less than polite manner and in a disreputable state with a crumpled and soiled white uniform with several day’s beard reminding the surgeon that Polio was spread by contact with contaminated water and our Polio patients were using those tanks. He reported me to the Chair of the Pediatric Department in what words I do not know but I was fired. Protests by the other house staff reversed that decision.

Another case early in the epidemic involved a young teenage girl for whom I provided cross coverage. She was in pain with an enlarged abdomen thought by her attending physician and family to be a pregnancy expressed as a lower abdomen round mass. Careful history and examination suggested urinary bladder from a paralyzed urinary sphincter. Since I had never catheterized a female, I sought assistance from a nurse and after a difficult time bypassing the spastic sphincter, we drained the first 200 cc. I then stopped the flow and waited for several minutes to resume periodic draining the several 1,000 cc content. I had learned of fatal shock from young women who due to cultural fear of admitting they needed to urinate had suffered an accident, completely emptied an extremely enlarged bladder and died of shock. Needless to say, the young woman and her parents were immensely appreciative of the diagnosis, particularly since she recovered without further symptoms.

Another case was an unconscious, young, teenage boy with Bulbar Polio who was having his trachea opened as I was holding his head describing what the surgeons were doing. When he  breathed, he regained the ability to talk and related to me appreciation for what was going on since he was conscious and thought we believed him dead. He had recently been in an alcohol use prevention class and remembered that the autopsy began with an incision at the top of the chest. He remained with us as a Bulbar Polio patient until stabilization and was allowed home on a visit in early August with the admonition to avoid solid foods. He remained on a tracheostomy. Unfortunately, he disregarded the instructions, ate fresh garden peas (one of his favorite foods), aspirated one into the bronchi, had a vagal response with cardiac arrest and died.

There were two instances of fatigue that occurred in the midst of the epidemic that are sharp in my memory. First, I leaned against a rocking bed and fell asleep during rounds. They turned the bed on. I did not awake so they took a picture and continued the rounds. The second was watching our senior resident, Dr. Peabody, slip gradually into a circular framed metal structure on wheels holding a bag used for a soiled clinical clothing container. He was tall and extremely thin. He slid into the container until only his head, arms and legs from the knees down were visible. We left him sleeping and continued the rounds.

Two sad cases remain. The first was a middle-aged businessman in an iron lung next to a window. His children climbed the fire escape outside the window and communicated with him through the glass. He died at the end of August after many months. The other was in the past a Catholic Mother of the Year, a businesswoman with 12 children. Despite being in an iron lung she collected Scotch whisky from friends and nurses and kept  a jug beside her iron lung. One night she somehow sipped through a long straw the entire contents of the jug and died of acute alcohol poisoning.

These two cases and the family of my friend since the 4th grade in school have led me to believe there were asymptomatic cases of Polio. None of those two iron lung patients just mentioned were affected by Polio. My oldest friend, Jim’s, brother was paralyzed by Polio but not the remainder of his family. Also none of our Polio Team came down with paralytic Polio.

These last observations have led me to believe that SARS CoV2 will also be proven to have many more cases of asymptomatic disease than currently are thought to exist. These will be discovered and cause two important changes. First, a lowered death rate by increasing the denominator and, secondly, explain the vast, rapid spread of the COVID 19 illness. Hopefully IgA and IgG will identify these silent cases and help guide the opening of our economy by identifying people who are immune to COVID 19.