Why Nine Camden Children Died from Smallpox Vaccines in 1901

A Glenolden physician blamed his patients' parents.



The H.K. Mulford ladies’ baseball team, circa 1901

Blame the parents. It’s a time-honored strategy that usually works—especially if said parents are poor or foreign-born.

That was the excuse used in 1901 by a physician representing a Glenolden pharmaceutical manufacturer. Nine Camden children died from smallpox vaccines administered at their schools. Apparently, they were tainted with tetanus. At the time, no one saw it as a conflict of interest for the school district to ask a company employee to pinpoint the problem.

Tetanus, said famed art collector Albert C. Barnes, was simply “in the air,” waiting for “any cut or scratch … to give it a lodging place.” In actuality, tetanus is caused by a bacterium commonly found in soil, dust and manure. The real problem, he said, was “the lower class of people who, by their own carelessness, poisoned the wounds with tetanus, or lockjaw, bacteria.”

The vaccine began with pharmacist Henry K. Mulford, who decided that he was no longer content to simply sell pills. Born in Bridgeton, N.J., Mulford graduated from the Philadelphia College of Pharmacy in 1887 and immediately bought out the venerable “Old Simes” drugstore where he had worked as a student.

Shortly after, Mulford launched his own line of pharmaceuticals. By 1891, he and a partner had incorporated as the H.K. Mulford Co. They were operating two laboratories, selling more than 800 different medical products, and had a branch office in Chicago.

The Pure Food and Drug Act was still 25 years in the future, so pharmacists—or anyone—could make and sell any potion. According to historian Louis Galambos, Philadelphia in the 1880s had more than 140 pharmaceutical entrepreneurs, most selling retail and wholesale.

Still, Mulford wanted more—and he found it in New York. As the nation’s major destination for immigrants, New York also had the greatest concentration of tenement housing­—and the problems that came with it. Tuberculosis, pneumonia and diphtheria were the leading causes of death. For that reason, New York City had become a leader in public health. The city’s Metropolitan Board of Health was established in 1866. Later, its division of pathology, bacteriology and disinfection would conduct scientific research on infectious diseases.

By 1894, New York’s scientists had imported the work of German and French microbiologists and were experimenting with an antitoxin that was effective against diphtheria. (Unlike a vaccine, which protects against contracting a disease, an anti-toxin counteracts an already-present infection.) The news caused great excitement, but the New York pharmacists were not quite ready—and certainly not prepared to supply the whole country. “Neither [Mulford nor his partner] was trained in the new medical science,” wrote Galambos. “But they recognized the opportunities embodied in the ‘clamor’ for a diphtheria antitoxin and moved decisively to position H.K. Mulford Co. to become a leader in the new field.”

Mulford raided the University of Pennsylvania staff, which had recently established a hygiene lab. Joseph McFarland, a lecturer on bacteriology and pathological histology, had studied in Heidelberg, Germany, and Vienna. He knew the scientific literature and was familiar with the accomplishments in New York. Mulford offered a part-time job to McFarland, who’d been supporting himself with part-time teaching jobs.

McFarland understood the principle: Horses were inoculated with gradually increasing doses of diphtheria toxin, isolated from cultures of the bacillus grown in vitro. Eventually, the animals became “hyperimmune,” meaning their blood contained massive quantities of diphtheria antibodies. They were then bled from the jugular vein, and the serum was separated by straining. However, Mulford needed a source of diphtheria toxin and a step-by-step understanding of the process.

Fortunately, he had contacts in New York, who agreed to turn over—for free—both toxin cultures and detailed instructions. “Personal relationships and this kind of cooperative behavior were important elements in the complex process of innovation taking place in the 1890s,” wrote Galambos. “In later years, when institutional settings became more bureaucratic and relationships more formal, communication would no longer be as simple.”

Setting up took time. Mulford needed equipment, a medium to grow the toxin, and to be near the horses. In West Philadelphia, company employees prepared a lab located on the second floor of a large stable, an atmosphere “not conducive to bacteriological work.”

The race was on. New Yorkers treated their first two cases successfully in January 1895. In Detroit, the Parke-Davis pharmaceutical company was pursuing commercial production. “Staff members with good professional credentials strengthened the company’s claim that it was a scientifically advanced organization,” wrote Galambos. “Though the techniques for producing antitoxin—it was, for instance, strained through cheesecloth—seem to us unbelievably crude, Mulford’s laboratory was, by the standards of that day, an unusually meticulous commercial organization.” 

In the summer of 1895, after months of intense work, H.K. Mulford offered the first commercial diphtheria antitoxin for sale. By 1902, Mulford’s annual sales were more than $1 million. By 1910, the company had 950 employees and was grossing $3 million a year.

Success brought expansion. In 1896, Mulford moved production to rural Glenolden, separating its biological lab from the stables. A 200-acre site along South Avenue would boast 52 buildings, including a large stable and a cow barn. A state board of health report stated that the facility was of “exceedingly high standing … the stables being scrupulously clean, the animals sound and vigorous, the laboratory arrangements good, the technique careful and thorough, and the product of somewhat greater strength than advertised.” 

As a major player in the pharmaceutical industry, Mulford naturally stayed in touch with fast-moving developments in immunology. Its second big thing was a tetanus antitoxin. That was followed, in 1898, by a decision to create a smallpox vaccine.

Making a smallpox vaccine was different, though. The process was based on observations of similarities between smallpox and the much milder cowpox. English physician Edward Jenner had studied these in the 1700s, noticing that cowpox causes lesions on the udders of infected cows and could be transferred to humans who handle the udders. The exciting discovery: Those who’d had cowpox were immune to smallpox.

The production of a smallpox vaccine began by gathering the fluid seeping from lesions on the udders of infected cows. Smallpox vaccination spread widely, but was equally opposed, with some critics believing it caused syphilis. Mulford’s reputation for excellent sanitation overcame distaste for what was essentially pus scraped from the undersides of cows.

By 1901, Mulford had a product, and Camden had a need. In early October, an 8-year-old girl died of smallpox, followed by her father and seven of her siblings. In the ensuing panic, the Camden school board announced that it would enforce an 1887 law requiring all students be vaccinated. Mulford bid for the contract and won. By the end of October, the arms of about 5,000 children had been scraped and rubbed with Mulford pus.

The first tetanus case appeared on Nov. 1, when William Brower, 16, fell ill and died. He’d been vaccinated 19 days earlier, and his mother drew a link. Eight others soon followed. With one exception, all had been vaccinated at school with the Mulford vaccine. Those vaccinated by a free clinic in downtown Camden or by their own physicians were unaffected.

Soon after, there was a smallpox outbreak at Pennsylvania Hospital, where physicians responded by vaccinating 4,500 people in the facility. They ran out of vaccine, before using a batch from Mulford for the remaining individuals, of which five patients died.

Local physicians were mostly united in defense of vaccination and Mulford. “Vaccination does not produce tetanus,” said Dr. William Kensinger, who had inoculated the Brower boy.

For an explanation, the Camden school board called in an expert. Barnes was only 29 and had not yet developed Argyrol, the antiseptic that would make his fortune. The founder of the Barnes Foundation had made his way through University of Pennsylvania Medical School by boxing, then studied abroad and came home to work as a consulting chemist for Mulford. He quickly rose to advertising and sales manager. The choice of Barnes to investigate can only be explained by the innocence of the times.

Barnes’ report emphasized that more than a million people in the Philadelphia area had been vaccinated without incident, Camden and the hospital being the only exceptions. “In the Camden cases,” he wrote in the New York Times, “the patients’ arms after vaccination were neglected by the parents of the children. In not one of the cases had the vaccination received proper care, but had been exposed to infection from every possible source.”

Newspapers soon adopted Barnes’ argument. Tetanus—common in soil, dust and manure found in barnyards—was just “in the air.” It was “highly unfortunate,” concluded the Philadelphia Sun, “that a period of prevalence of tetanus germs should have coincided with a period of vaccination.”

Nothing against Mulford was ever proven, and the case was considered nothing more than an anomaly.

It did prove, though, that blaming the parents works.  

Edit ModuleShow Tags