By Brandon Holler
Diphtheria is a highly contagious bacterial infection that was discovered in the 1880s by F. Loeffler a German bacteriologist at the University of Greifswald. The name of the bacterium responsible for Diphtheria is Corynebacterium diphtheriae. The bacterium that causes diphtheria is is unique, because it is itself infected by a bacteriophage. The disease presented itself in the most virulent manner during the autumn of 1918 in London when about a third of those who passed did so from diphtheria. Diphtheria visibly effects the nose and throat of its victims. It resides in the lungs and affects the lungs and in special cases it can spread to the liver, spleen and other organs.
Diphtheria was much more common in younger patients than in older, more mature patients. In one area tested there was 141 confirmed cases for children and only 5 for adults. Results like this were a common place in the late 1800s and early 1900s. The biggest problems were in schools and hospitals; when one child would get it, it was only a matter of time before the whole school or hospital shared their fate. This got so bad that cities would create “Quarantine Schools” and “Isolation Hospitals” or other ways to do everything they could to prevent further spread of diphtheria. The hospitals were modified versions of overflow hospitals from World War II. They were exclusively used for diphtheria patients due to the numerous other virulent bacterial infections circulating around. The main infectious agents included Scarlet Fever, Diphtheria and Measles. Some patients would come down with more than one infection due to the close contact they had with other patients as it was more important to maintain the healthy status of those unaffected. The average stay for a patient was 28 days and the mortality rate was around 10%.
Diphtheria presents as a thick white membrane in the back of patient’s throats. The normal symptoms of diphtheria are sore throat, fever, swollen glands and weakness. Patients were immediately quarantined in the 1930s when showing any abnormal condition of the skin, eyes, ears, throat or nose. In the late stages of the infection the neck and upper trunk area swell up and is often followed with redness. The diphtheria toxin fills the membrane with fluid, and this often partially or completely blocks of the larynx and suffocates the patient. Extra precautions were taken with children regarding any of the symptoms. Conditions worsened over a period of days and were instructed to see doctor at the earliest possible time in order to minimize its effects and hopefully prevent as much as they could. Left untreated the patient would develop a slew of various other medical problems, assuming they remained alive. Cases reported long term breathing difficulties, nerve damage, and heart damage. Once the toxins fill the lungs it begins to move on to other parts of the body. In some cases, it can even manifest itself onto the patient’s skin in the form of ulcers covered with the hallmark white membrane along with redness and swelling around the affected area.
Once in the hospital doctors erred on the side of caution, often mislabeling colds and other illness as diphtheria. The early onset of the infection was very similar to these infections and it wasn’t until later in the infection that the hallmark signs of diphtheria presented themselves. One could pick up the infection through many routes. The most common routes of infection are airborne droplets, direct contact with an afflicted item, or touch of an open wound. The droplets were spread most commonly from coughs, wheezes, and sneezes of victims which was then inhaled by uninfected person. Direct contact with afflicted items such as tissues or drinking after someone who has diphtheria, in addition to things like towels and clothes. When a healthy person encountered these things their risk of infection increased dramatically. Almost certainly one would contract diphtheria after touching the wound of an afflicted patient. The white film over the outer wounds and in the throat were covered in the bacteria.
Treatment options for diphtheria were very limited. The main medicine used was “Diphtheria Toxoid Anti-Toxin”. It was used as both an immunization to prevent the disease(anti-toxin) and as a treatment for the disease(toxoid). It was made from antitoxins in goats’ blood. Before the medicine was released in 1913 the mortality rate of those affected was approximately 20%. Intriguingly, after the medication was released in 1913, the number of cases of diphtheria increased and the mortality rates decreased. For the cases which progressed to laryngeal blockage the only real option was a tracheotomy. The survival rate of the procedure was quite low, but it would considerably relive pressure and resistance of air flow in the patient.
Bibliography: MOH Reports
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