Poliomyelitis: Newark 1916: "The Grip of Terror"

By Sandra W. Moss, MA;MD

POLIOMYELITIS: NEWARK 1916 THE GRIP OF FEAR is a study of the devastating "scourge" that struck the city of Newark a century ago. Most victims were infants and toddlers for whom there were no effective treatments, no vaccines, and no iron lungs. Per capita, Newark was the hardest hit of any American city, with 1,360 cases and 363 deaths. The book draws heavily on newspaper accounts, public health documents, and the accounts of physicians who faced the epidemic with uncertain knowledge and no effective treatment. Public health officials, as in all epidemics, desperately sought to limit the spread of disease and, in the process, risked creating a medical police state. Hundreds of survivors faced a lifetime of disability, giving poliomyelitis its particular power to terrify.

• Language: English
• Publisher: Xlibris US
• Release date: Jun 17, 2016
• ISBN: 9781514469163

Sandra W. Moss, MA;MD

Dr. Sandra Moss practiced and taught general internal medicine in central New Jersey for many years. In 2005, she completed a master's degree in the history of technology, medicine, and the environment from the federated history program of the New Jersey Institute of Technology and Rutgers University. Dr. Moss has published numerous articles, chapters, and reviews in the field of medical history, and regularly addresses diverse audiences on a variety of topics in the history of medicine. She is past president of the Medical History Society of New Jersey and of the American Osler Society. Her previous books, The Country Practitioner: Ellis P. Townsend and His Brave Little Medical Journal (2011) and Edgar Holden, M.D., of Newark, New Jersey: Provincial Physician on a National Stage (2014) were published by Xlibris.

Book preview

POLIOMYELITIS:

NEWARK, 1916

THE GRIP OF TERROR

SANDRA W. MOSS, M.D., M.A.

Copyright © 2016 by Sandra W. Moss, M.D.

All rights reserved. No part of this book may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the copyright owner.

Rev. date: 06/17/2016

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CONTENTS

List Of Illustrations

Dedication

Acknowledgments

Introduction

Reflections On The Polio Summer Of 1916

Chapter 1

Beginnings, July 1916

Chapter 2

The Newark Trajectory

Chapter 3

Public Health

Chapter 4

Diagnosis And Treatment

Chapter 5

Other Remedies—False Promises

Chapter 6

Restricting Children’s Activities: Shutting Down Summer

Chapter 7

Travel Restrictions

Chapter 8

Negotiating School Closings And Openings

Chapter 9

Public Health And The Public

Chapter 10

Hospitals And Baby Clinics

Chapter 11

After-Care: Henry Coit And The Sub-Committee On Relief

Chapter 12

Looking Back—Looking Forward

Selected Bibliography

LIST OF ILLUSTRATIONS

Frontispiece: Charles V. Craster, M.D., Newark Health Officer

1. Charles S. Caverly, M.D., Rutland, Vermont

2. William S. Disbrow, M.D., President Newark Board of Health

3. Newark Department of Health case reports

and deaths for July, 1916

4. Daily Newark case reports and deaths, July–September, 1916

5. Summary of Newark and Essex County statistics by date and age

6. Distribution of Newark cases by ward

7. Editorial cartoon: Newark pioneer pitches in to aid clean-up

8. Dr. Eugene Witte of Trenton, promoter of a secret polio cure

9. Advertisement for Lysol disinfectant,

A Necessity in Epidemic

10. Letter from a child to the poliomyelitis relief fund

11. Henry Leber Coit, M.D., founder of Babies’ Hospital, Newark

12. Typical newspaper coverage at the height of the epidemic

13. List of children’s deaths for a single day in August

14. Essex County Isolation Hospital, Belleville, ca. 1930s

15. Newark City Hospital, ca. 1910s

16. Parents of polio victims gathered outside

Newark City Hospital

17. Editorial cartoon: Public and private fight against poliomyelitis

18. Editorial cartoon: Appeal for donations to fund braces

19. Home for Crippled Children, Newark

20. Rehabilitation ward at Home for Crippled Children

21. Electrical stimulation apparatus at Home

for Crippled Children

22. Annual polio statistics for New Jersey: 1910–1952

23. Salk vaccine trials announcement, April 12, 1955

COVER

When Anxious Parents Are Permitted a Glimpse of Their Afflicted Babes at City Hospital

Newark Evening News headline, August 14, 1916

On August 14, 1916, families were allowed a brief glimpse of their quarantined babies and toddlers from the grounds of Newark City Hospital. Parents whose children who were too sick to be brought to the windows by the nursing staff were simply sent home—not knowing if they would ever see their afflicted babes again.

Source: Newark Evening News, August 14, 1916

Courtesy: Photographic collection, Newark Public Library

DEDICATION

FOR MY PARENTS

RALPH AND CELIA WOLMAN

WHO FEARED FOR THEIR THREE YOUNG CHILDREN

DURING TORONTO’S POLIO SUMMERS

Like many of my contemporaries, I remember the polio summers of the 1950s. When I broke my arm in 1952 or 1953, I was treated at Sick Children’s Hospital (familiarly Sick Kids) in Toronto. The pediatric orthopedist who set my arm was Dr. William Mustard, who, in 1952, developed an innovative muscle transfer operation to stabilize polio-weakened hips—the Mustard procedure. I vaguely remember walking with my father toward the clinic, perhaps for a cast check, and passing the iron lungs in the hallway. Though I do not remember the faces of the children imprisoned within, I recall that my father said they were out in the hallway to get some fresh air. Perhaps so—or perhaps overwhelmed polio wards were spilling out into the hallways. Those of us with memories of those years never really forgot about the mid-century polio epidemics—or about the seemingly miraculous vaccines of Salk and Sabin that gave back the summers. Today, younger generations encounter polio through newspaper articles about post-polio syndrome, reports of terrorist murders of vaccinators in Pakistan and Nigeria, the almost successful global initiative to eradicate polio from the face of the Earth, and the potentially dangerous hubbub created by parents who refuse to vaccinate their children against polio and other devastating contagious diseases of childhood.

ACKNOWLEDGMENTS

It is a pleasure to acknowledge the assistance and expertise of librarians and archivists at Special Collections and University Archives at Rutgers University, Newark Public Library, the National Library of Medicine, and Rutgers Medical School Special Collections in the History of Medicine.

Stuart Galishoff, historian of Newark public health, published the first major study of the Newark polio epidemic in 1976 (Stuart Galishoff, Newark and the Great Polio Epidemic of 1916, New Jersey History 94 (1976): 101–11). This book builds on the foundation laid in Galishoff’s study of forty years ago.

Laura Walshin kindly provided expert proofreading assistance.

CHARLES%20V.%20CRASTER.jpg

Frontispiece: Charles V. Craster, M.D., Newark Health Officer

Source: New Jersey and Its Builders, ca. 1925

Courtesy: Rutgers University Special Collections and University Archives

INTRODUCTION

REFLECTIONS ON THE POLIO SUMMER OF 1916

NO NATIONALITY OR CONDITION OF SOCIAL LIFE WAS EXEMPT FROM INFECTION

A century has passed since the Newark poliomyelitis epidemic of 1916, but the lessons of the epidemic are worth revisiting through contemporary reports and documents. Poliomyelitis—infantile paralysis—is but a hazy memory to many New Jerseyans. Older citizens will recall the epidemics of the 1940s and 1950s, which terrorized American parents summer after summer. Philip Roth’s recent novel, Nemesis, tells the story of one young Newark man, a physical education instructor, who witnesses the havoc in the city as a (fictional) 1944 epidemic sought out its victims. In fact and in fiction, for many survivors poliomyelitis sabotaged futures and reverberated through wounded lives.

Current concerns over the threat posed by incomplete vaccination rates in the United States, terrorist attacks on vaccinators in Pakistan and Nigeria, and the disabling late complications of post-polio syndrome in older survivors, as well as the World Health Organization’s initiative for global eradication of the virus, keep polio in the news. Newark’s visceral and public health responses to the 1916 polio epidemic also provide insight into our remarkably similar (if technologically more sophisticated) responses to threats such as SARS and Ebola.

The word epidemic brings to mind medieval scenes of bubonic plague—victims dying in the streets, social chaos, and frantic efforts to comprehend and control the visitation. In this sense, an epidemic is self-evident to all observers. However, epidemiologists and public health officers offer a much more precise definition that begins with an understanding of endemic disease: the seasonal or perennial baseline of a particular infectious disease in a population. If the incidence of an infectious disease such as diphtheria or scarlet fever or cholera peaks in a community at a level higher than baseline, then epidemiologists refer to an outbreak or an epidemic.¹ If the epidemic is widespread or is particularly virulent, then the general public becomes aware of an epidemic in the conventional sense.

Medical historian Charles E. Rosenberg frames epidemics as dramas moving through a series of acts: Epidemics start at a moment in time, proceed on a stage limited in space and duration, following a plot line of increasing and revelatory tension, move to a crisis of individual and collective character, then drift toward closure.² In the summer of 1916, as war raged in Europe, the curtain rose in Newark, dramatis personae assumed their roles, and the tragedy unfolded.

Epidemic diseases were frequent visitors to New Jersey in the centuries and decades before the 1916 polio epidemic. Malaria and smallpox stalked the colonies and the young nation. A terrifying epidemic of throat distemper (most likely diphtheria but possibly a highly virulent streptococcal infection) claimed children—sometimes all the children in a family within the span of a few days—in the northern colonies in 1735 and 1736. Diphtheria, with its rubbery membrane occluding the upper air passages, continued to strangle New Jersey children throughout the nineteenth century. In the 1790s, epidemics of yellow fever spread to New Jersey from Philadelphia, killing many New Jerseyans as well as fleeing Philadelphians seeking refuge from their besieged port city.³ A series of worldwide cholera epidemics passed through New Jersey in the mid-nineteenth century; in 1832, scores of Irish laborers died of cholera along the Delaware and Raritan Canal worksites and were buried in unmarked graves.⁴

Infectious diseases spread like wildfire through the Newark almshouse, an institution plagued by crowding, inadequate nutrition, filth, and primitive sanitary facilities. In effect, the almshouse was the default infectious disease hospital for Newark’s poor. During the cholera epidemic of 1832, a sick woman was removed to the almshouse, where cholera had not yet appeared among the inmates. Within four days, the disease tore through the almshouse, killing many residents. During the 1849 epidemic, a traveler who collapsed on the road from New York was taken to the almshouse. The result, wrote the almshouse physician, was the same as if a match had been thrown into a powder mill… . The infection took, and thirty-eight deaths followed, including the worthy superintendent.⁵

At the almshouse, seepage from the privy vault leaked into the well supplying the drinking water for the almshouse, thus explaining the rapid spread of infections such as typhoid and cholera. The city erected a small wooden cabin nearby for temporary use as a pesthouse, a facility marked by neglect and profound human misery.⁶ Despite the availability of smallpox vaccine in the United States for over a century, physicians in Newark and elsewhere perennially lamented the low vaccination rates in the population. Their fears were realized in 1901 and 1902, when smallpox struck a total of 1,288 residents of Newark with 258 deaths.⁷

One year before the 1916 polio epidemic, infections now preventable by municipal sanitation and vaccines (or treatable by antibiotics) took their predictable annual toll in Essex County: typhoid (21), measles (19), scarlet fever (21), diphtheria and croup (64), whooping cough (54), tetanus (10), and syphilis (40). Infantile diarrhea, a perennial killer of babies, was caused by an array of viral and bacterial infections. The grimmest reaper in Essex County, especially among young adults, was tuberculosis (962 deaths).⁸

Poliomyelitis deaths in the entire state between 1910 (when the disease first became reportable) and 1915 numbered in the double digits. In the four years following the 1916 epidemic, annual reports of polio ranged from forty-two to ninety-one statewide.⁹ Such illnesses, striking annually (often seasonally) at a fairly steady and predictable rate, are by epidemiological definition endemic.

Long before poliomyelitis became a feared epidemic and a household word, small outbreaks and sporadic cases, often in rural communities, were reported in Europe. In 1789, British physician Michael Underwood described debility of the lower extremities in children. In 1840 Jacob von Heine in Germany defined infantile spinal paralysis as a distinct disease. The first clearly documented outbreak in the United States occurred in 1894 in Rutland, Vermont. Dr. Charles S. Caverly of Rutland, president of the Vermont State Board of Health, systematically investigated 123 cases, with 10 deaths and 50 permanently disabled survivors. He astutely recognized that the disease showed no partiality to that class of the population whose habits and surroundings are the most unsanitary. In other words, polio did not seem to be what was then referred to as a filth disease. Well aware of the germ theory and the progress of European research, Caverly mentioned the possibility of a specific poison. He also observed a high fatality rate in adults and a predominance of male victims.¹⁰

fig%201%20CHARLES%20S.%20CAVERLY.jpg

Fig. 1. Charles S. Caverly, M.D., Rutland, Vermont.

Source: The Vermonter, v. 4(2), September 1918

Courtesy: Leahy Library, Vermont Historical Society

The infectious nature of poliomyelitis was conclusively demonstrated by Swedish physician Ivar Wickman during an epidemic in 1905. Wickman also realized that many cases were abortive (i.e., did not progress to paralysis). A few years later poliovirus was successfully transmitted to monkeys in the laboratory, thus providing a costly and complex research model. By 1908, it was known that the disease was transmitted by a virus, an agent small enough to pass through a porcelain filter that trapped bacteria but too small to be seen by the most powerful microscopes of the day.¹¹

At the time of the 1916 epidemic, the disease was known as poliomyelitis (from the Greek for grey and marrow, referring to the gray matter of the spinal cord), acute anterior poliomyelitis (referring to the location of damage within the spinal cord), or infantile paralysis (a misleading term because many older children and adults were also attacked, often with greater severity). The shortened term polio was not used until the mid-twentieth-century epidemic years.¹² In the Newark Evening News and the Newark Sunday Call, terms such as scourge and plague dominated the headlines—unambiguous code words that spoke to the hearts of a terrified public.

The uptick in infantile paralysis first observed in Brooklyn in the early summer of 1916 alarmed public health officials, who quickly recognized an epidemic. The disease spread to New Jersey with the report of a single fatal case in Newark in the first week of July. With new cases reported daily, the health officer officially declared on July 14th that an epidemic of poliomyelitis existed in Newark. It would last for three brutal months.

A century after the 1916 epidemic, the scientific understanding of polio has expanded exponentially. The virus, an RNA picornavirus, exists in three serotypes. Infection with one strain leads to the production of long-lasting (possibly lifetime) strain-specific immunity, but leaves the individual susceptible to the other two strains in future epidemics. At the time of the 1916 polio epidemic, physicians believed that poliovirus was transmitted primarily through respiratory secretions. However, it is now known that poliovirus is transmitted mainly by the fecal-oral route (contaminated water, food, or fingers). The virus replicates in the pharynx (throat) and gastrointestinal tract (viral shedding in the stool lasts for several weeks, whether or not the individual—now a carrier—is clinically ill). The incubation period for non-paralytic disease is three to six days (range four to thirty-five days) and seven to twenty-one days for paralytic cases. About one quarter of infected individuals develop a minor viral illness, often indistinguishable from a typical flu-like illness.

Less than 5 percent of victims progress to a transient non-paralytic meningitis-like illness with drowsiness, irritability, and muscle pain and stiffness. Improvement in hours or days might herald a return to perfect health—this abortive or non-paralytic form of poliomyelitis also confers strain-specific lifelong immunity. However, for weeks after apparent recovery, these children become carriers and sources of infection for non-immune contacts. In less than 1 percent of those infected, the virus enters the blood stream and attacks the spinal cord or brain. There is a sudden onset of muscle weakness and pain, with progressive paralysis of one or more limbs. This spinal type of paralytic poliomyelitis was referred to as anterior poliomyelitis because the anterior [front] horn cells of the spinal cord, which control nerve impulses to the muscles, are primarily affected.

Without proper nerve stimuli, affected muscles suffer flaccid paralysis (limp inactive muscle tone—as opposed to spastic paralysis characterized by increased and often uncoordinated muscle tone). In 1916, physicians recognized that while the paralysis sometimes improved spontaneously over time, in many cases there was permanent muscle atrophy (wasting) with persistent paralysis. The muscles and limbs targeted in the acute stage varied with each case, but the lower extremities were involved more often. For reasons still not understood, the incidence in boys was greater than that in girls. The disease tended to be more severe in older children and adults. In the most critical cases, invasion of the base of the brain (bulbar poliomyelitis) led to meningitis- or encephalitis-like symptoms with paralysis of swallowing and breathing muscles (including the diaphragm), leading to a difficult and distressing death from respiratory failure within hours or days of onset.¹³ A quarter of Newark children who contracted clinical polio died of bulbar poliomyelitis. The physicians at Newark City Hospital witnessed many of these deaths. One physician referred to bulbar with its ghastly respirations.¹⁴ The iron lung, introduced in the late 1920s and 1930s, helped tide some children over this crisis, but in 1916 there was no technology for respiratory support.

Paralyzed children (and some adults) infected by the poliovirus constituted the public face of polio; asymptomatic carriers were unidentifiable and were not seen as threats. It is now known that 90 to 100 percent of susceptible household contacts of an active case seroconvert (develop antibodies to polio indicating invasion of the virus). Thus, it is likely that the overwhelming majority of Newarkers were at some point active, but asymptomatic, carriers of the disease.¹⁵

The known facts going into the 1916 epidemic were not encouraging. Health officials at the time were aware of the role of asymptomatic carriers, but had no way of identifying or controlling the movements of these major vectors of disease transmission. Victims with clinical evidence of paralysis were thought to be infectious to others for about six to eight weeks. In June 1916, Public Health News, a monthly publication of the New Jersey State Department of Health, reviewed the current medical knowledge and uncertainties about polio. Earlier epidemics had been marked by a fatality rate of 11 to 12 percent, with 50 percent residual incapacitation in survivors. (The fatality rate in the Newark epidemic would prove to be much higher at 26.7 percent). The author, a state health official, stressed the epidemiological evidence for the carrier state and cautioned against promiscuous intermingling with others. In the absence of any protective immunization through the use of immune serum from recovered donors, the best treatment to prevent deformity is rest, more rest, and still more rest (the three rests were in boldface). Epidemics invariably ended: There is some evidence to indicate that there are natural limitations to an outbreak of poliomyelitis, because the susceptible material of a population is soon exhausted.¹⁶

Wade H. Frost of the United States Public Health Service summed up the pattern of transmission as it was understood in 1917. Since contact with another polio victim could be traced in less than 20 percent of cases, there must be numerous sources of infection other than the recognized cases. Frost also stressed the role of the asymptomatic carrier.

Because polio was confined to humans (except for laboratory acquired polio in primates), Frost favored the view that the disease was transmitted by person-to-person contact. Infection of water supplies, milk supplies and general food supplies has usually been eliminated as an important agency in the spread of this disease. Alternative theories invoked contaminated milk, transmission from lower animals including cats and dogs, and carriage from person to person by insect vectors (omnipresent flies, buzzing around garbage cans and invading unscreened windows were obvious suspects).¹⁷

A novel theory was proposed by Dr. Charles Braddock, a New Jersey native who had spent his career fighting tropical diseases as chief medical inspector of the royal Siamese government. Braddock detected similarities between the behavior of yellow fever epidemics (known to be carried by a species of mosquito) and the polio epidemic. Both diseases flourished in hot moist weather and ended with the cooler weather (when mosquitoes die). Braddock, working in New York at the end of his career, believed the mosquito infestation to be unusually severe and the absence of screens most obvious in the poorer, harder-hit districts of the city. The mosquito vector theory also seemed to explain the puzzling incidence of polio cases among the well-to-do. The New York Times quoted Braddock’s letter in the New York Medical Journal; the theory seemed sensible on the surface, but lacked any scientific foundation.¹⁸ Braddock’s mosquito theory never gained traction.

Although there was no diagnostic laboratory test in 1916, the presence of inflammatory cells in the spinal fluid supported the diagnosis made at the bedside by the physician. Improvement, if it was to occur at all, often became evident at two to three weeks after onset and continued for several months. Survivors of paralytic polio were believed correctly at the time to carry strain-specific antibodies to the virus in their blood serum. Experimental treatment with such convalescent serum from recovered donors was attempted in New York and in a few instances in Newark during the 1916 epidemic.

A critical step in making sense of an epidemic for both the public and health officials is the assignment of responsibility, often framed as blame.¹⁹ In past centuries, divine wrath aimed at a sinful citizenry often seemed like the most plausible explanation. Marginalized ethnic and religious groups were convenient scapegoats; for example, European Jews were frequent victims of homicidal mobs and vicious civil administrations when epidemics struck. It was well known by 1916 that most epidemic diseases such as typhoid preyed on the crowded urban poor and other victims of inadequate municipal sanitation. It was the poor and presumably unhygienic immigrant families in