Bone saws from the 17th and 18th centuries

Bone saws were some of the most commonly-used medical instruments during the Renaissance, as amputation was one of the most common surgical procedures performed.

Unfortunately for the patients, just like so much else during the 17th and 18th centuries, style and status was a huge thing for the surgeons, like so many other elites in society. Since the surgeries were often performed in surgical theaters, a great way for surgeons to show off their status was with ornately decorated surgical instruments - and the bone saws were often the most ornate of all.

Aside from being uncomfortable to hold, the gilt or carved cedar or ebony handles, and the ornately-embellished frames, were perfect places for bacteria to fester, and to transfer from patient-to-patient. The more elite the surgeon, the fancier the saw - and the deadlier the consequences.

Models located at Science Museum London, originally created ca. 1650-1780.

Ways To Die: Amoebic Dysentery and Amoebiasis

First off, let’s get this out of the way - dysentery is not always amoebic, and the term “dysentery” refers only to the condition of having bloody diarrhea (bloody flux), caused by an infectious pathogen in the large intestine.

There are viral, protozoan, and bacillary dysenteries, in addition to the amoebic dysentery that shows up so often in tropical medicine. As a side-note, the dysentery that reared its ugly head in Oregon Trail (and on the real Oregon trail) would have been either bacillary (Shigellosis) or amoebic, depending upon the season and the location.

Amoebic dysentery and amoebiasis are caused by the amoebic pathogen Entamoeba histolytica. This single-celled organism is hardy, and able to spread easily, especially in environments where proper sanitation is not practiced.

Infection occurs by fecal-oral transmission, and begins when an encysted parasite is ingested by an individual, due to improper handling of food, water, fecal matter, or poor hand-washing practices. When the organism reaches the stomach, the acid dissolves the tough cyst surrounding the amoeba, and the now-active trophozoite (bottom) moves into the small intestine.

There are several paths that E. histolytica is known to take from here; for 90% of those infected, they’ll experience no symptoms, but will still spread encysted amoebas in their feces, possibly infecting others. Of course, acute amoebic dysentery (center left) is a possibility, and occurs in approximately 10% of infected patients. Many times, the amoebas will lie dormant in the mucosal wall of the small intestine, and not cause dysenteric symptoms until months or years later. Sometimes, chronic, long-term infection can occur (center right), especially when there is no or inadequate treatment. However, that is much more common in bacillary dysentery than amoebic dysentery. Of the 10% who become symptomatic, only 16% will experience severe ulceration and long-term damage of the intestine, and that number is much lower with proper anti-amoebic treatment.

In some people, the amoeba makes its way through the intestinal wall, and into the bloodstream. From there, it can cause amoebic liver abscesses (top), compromising liver function, and sometimes mistaken for cancers. With some Latin American strains of E. histolytica, the semi-dormant amoebae will burrow into the lining of the ascending colon or rectum, and cause a long-lasting cellular response, which eventually can end up forming a large granulomatous mass. Other strains of this amoeba can cause severe swelling and flask-shaped ulcers in the lining of the large intestine.

The most important part of treating amoebic dysentery is continuous rehydration therapy - the rapid loss of fluids severely hinders the activity of the immune system and the body at large. Amoebicides (anti-amoebic medications) are also used these days, to speed recovery. In a typical amoebic dysentery case, the patient will recover within one week, assuming a basic standard of care.

Images:
Top: Large amoebic liver abscess protruding from the epigastrum.
Center left: Intestines affected by acute amoebic dysentery.
Bottom: Entamoeba histolytica in the mucosa of the small intestine.
Center right: Intestines affected by chronic amoebic dysentery. 
Source: Dysenteries; their differentiation and treatment. Leonard Rogers, 1913.

Read more:
Diseases of the Oregon Trail at APHL, by Michelle Forman
Dysentery in the Bad Bug Book, United States FDA

Bubonic Plague - Yersinia pestis

Yersinia pestis is always a fun little organism to see under the microscope. It’s a Gram-negative, rod-shaped bacteria, but it looks more like a safety-pin than a “rod” because of the natural bi-polar staining pattern of the organism. The species was found to be the causative agent of bubonic plague during an 1894 epidemic in Hong Kong, by Alexandre Yersin. Until 1967, however, it was categorized with the Pasteurella genus, and was known as Pasteurella pestis.

There are several strains of Y. pestis, and three different manifestations of the plague:

• Bubonic plague - Incubation period of 2-6 days with few symptoms, while bacteria multiply within lymph nodes. Sudden fever and headache at end of incubation period, with complete loss of energy. The characteristic buboes (lymph swellings) appear at this point, as the lymph nodes swell to enormous proportions thanks to the bacteria within them. The inguinal (groin) nodes generally are the first to show signs of infection.
  
  
• Septicemic plague - Same bacteria, different strain of Y. pestis, and way worse. From what we know, primary septicemic plague is generally caused by one unique strain, or by any strain in immuno-compromised patients. When the other manifestations of the disease cause overwhelming sepsis prior to death, this is known as secondary septicemic plague. Primary septicemic plague is characterized by hypotension, shock, hepatosplenomegaly (swollen spleen and liver), and death. Sometimes very few or even no outward symptoms develop before the patient is killed by the bacteria’s internal effects.
  
  
• Pneumonic plague - Caused by direct inhalation of bacteria (often person-to-person), with initial site of infection being the lungs. Different strains have different degrees of ability to transfer in this manner, but it generally requires prolonged contact with infected persons or animals. Causes tracheal and bronchial hemorrhaging, large amounts of alveolar exudate, congestion of the lungs, and pleural edema. Often quickly spreads to other organs, much like bubonic plague.

While all three manifestations of the disease can be deadly, the incidence of death is greatly reduced by IV antibiotics, and thanks to modern sanitation standards, outbreaks in developed countries are unheard of.

Still, Yersinia pestis isn’t, and probably never will be, completely exterminated. Wild animals such as rodents, prairie dogs, and some marsupials and primates are known to both be affected by and serve as reservoirs for the bacteria. This means that even if humans somehow stopped acquiring the plague for a while, the bacteria itself would still be around, and we would still be able to contract it.

Interestingly, a 2011 study in the journal Nature showed that the strain of Y. pestis which caused the Black Death in both the 1st century C.E. and the early Middle Ages may no longer be extant. The genome of the bacteria analyzed from victims of those plagues showed a more ancient form of Y. pestis that lacked a number of the mutations that exist in current-day strains, which are known to have caused all epidemics beyond the Renaissance.

Have I gone on about the plague enough? If not, check out way more information than you’ll ever use about the pathogen at CIDRAP Bioterrorism and PLoS Pathogens!

Images:

• Bacillus of Bubonic Plague - Elementary Bacteriology and Protozoology, for the use of Nurses. Herbert Fox, 1919.
• Swelling of inguinal bubo in U.S. soldier - From the U.S. Centers for Disease Control and Prevention, ca. 1970.
• Plague victims being blessed by priest - Omne Bonum. James le Palmer, 1360.
• Mass grave of plague victims- From Martiques, France, dated to the last pandemic of plague in Europe, between 1720 and 1722.
• Plague Riot of Moscow - Depicts the rioting during and after the 1770s Moscow epidemic.

Treponema pallidum manifestations

Top Right: Treponema pallidum pallidum - Venereal Syphilis
Top Left: Treponema pallidum pertenue - Gangosa (Yaws)
Bottom: Treponema pallidum pertenue - Frambosia (Yaws)

The spirochete Trepanoma pallidum has several subspecies that affect man, though only T. p. pallidum (syphilis) is transmitted via sexual contact. The other common disease caused by the spirochete is yaws. This tropical disease was largely ignored for most of the 20th century, as it rarely affects affluent countries.

Its course of infection can sometimes resemble syphilis, with the ulcerating gummas, multiple stages of infection, and destruction of tissues, but it is transmitted via skin-to-skin contact, and is not known to cross the placental membrane (meaning that, unlike syphilis, babies cannot be born with it). The tissue destruction within the muscles, skin, and bones, is a feature of tertiary yaws, which arises years after the initial infection. When the facial tissues are destroyed, the disease is commonly called gangosa.

[A Treatise on the Diseases of the Skin. Henry W. Stelwagon, 1923]

[Human Parasitology. Damaso Rivas, 1920.]