Posts tagged infectious diseases

pitchforking: biomedicalephemera: Top: Cow-milker infected from the teats of a cow with natural cow-pox. Large depressed vesicle with a small central crust, tumid (swollen) margin, surrounded by well-marked areola and considerable surrounding induration (hardness associated with swelling) Bottom: Same case, one week later. Reddish brown crust typical of recovering cow-pox cases, on a reddened elevated and indurated base. Many mammalian species have members of the Orthopoxviridae that are specialized to exist within their systems - humans have smallpox, cows have cowpox, monkeys have monkeypox, and so on (note: chicken pox is NOT a member of this group - its name comes from an old English word meaning “Itchy”, and is completely unrelated). However, sometimes, the similar viruses can cross species barriers, as in the case of cowpox. Though the viruses are specialized to their host species enough that they don’t easily spread between atypical hosts, they’re related enough that once an individual is infected with one pox virus, their immune system is able to to recognize and fend off the whole lot of them. This is why, with the assistance of cowpox (Vaccinia) cultures in administered vaccines (rather than all of humanity having to be in direct contact with cows…), smallpox was able to be eradicated in the wild. A Text-Book of Bacteriology, including the Etiology and Prevention of Infectious Diseases. Edgar M. Crookshank, 1897. Ahh, what a perfectly timely post. This answers the question that had been bothering me in the back of my mind about chickenpox and smallpox immunity. I should probably clarify that chickens DO have an Orthopoxvirus that affects them and is called “chickenpox”, but it’s not transmissible to humans (that we know of), and isn’t the Varicellovirus that causes the “chicken pox” we’re all so familiar with. The “pox” part of “chicken pox” comes from the bumps that it causes, similar to the pox viruses. Samuel Johnson and Dr. Barnhart (1740s) explained its name as meaning “of no great danger” compared to smallpox, but some current etymologists lean towards its origin being a corruption of the Old English “giccan” - “to itch”. The term is thought to have been used colloquially for over 1500 years, but not defined in a “modern” medical sense until the 17th century.

pitchforking:

biomedicalephemera:

Top: Cow-milker infected from the teats of a cow with natural cow-pox. Large depressed vesicle with a small central crust, tumid (swollen) margin, surrounded by well-marked areola and considerable surrounding induration (hardness associated with swelling)

Bottom: Same case, one week later. Reddish brown crust typical of recovering cow-pox cases, on a reddened elevated and indurated base.

Many mammalian species have members of the Orthopoxviridae that are specialized to exist within their systems - humans have smallpox, cows have cowpox, monkeys have monkeypox, and so on (note: chicken pox is NOT a member of this group - its name comes from an old English word meaning “Itchy”, and is completely unrelated).

However, sometimes, the similar viruses can cross species barriers, as in the case of cowpox. Though the viruses are specialized to their host species enough that they don’t easily spread between atypical hosts, they’re related enough that once an individual is infected with one pox virus, their immune system is able to to recognize and fend off the whole lot of them. This is why, with the assistance of cowpox (Vaccinia) cultures in administered vaccines (rather than all of humanity having to be in direct contact with cows…), smallpox was able to be eradicated in the wild.

A Text-Book of Bacteriology, including the Etiology and Prevention of Infectious Diseases. Edgar M. Crookshank, 1897.

Ahh, what a perfectly timely post. This answers the question that had been bothering me in the back of my mind about chickenpox and smallpox immunity.

I should probably clarify that chickens DO have an Orthopoxvirus that affects them and is called “chickenpox”, but it’s not transmissible to humans (that we know of), and isn’t the Varicellovirus that causes the “chicken pox” we’re all so familiar with.

The “pox” part of “chicken pox” comes from the bumps that it causes, similar to the pox viruses. Samuel Johnson and Dr. Barnhart (1740s) explained its name as meaning “of no great danger” compared to smallpox, but some current etymologists lean towards its origin being a corruption of the Old English “giccan” - “to itch”. The term is thought to have been used colloquially for over 1500 years, but not defined in a “modern” medical sense until the 17th century.

biomedicalephemera

Top: Cow-milker infected from the teats of a cow with natural cow-pox. Large depressed vesicle with a small central crust, tumid (swollen) margin, surrounded by well-marked areola and considerable surrounding induration (hardness associated with swelling) Bottom: Same case, one week later. Reddish brown crust typical of recovering cow-pox cases, on a reddened elevated and indurated base. Many mammalian species have members of the Orthopoxviridae that are specialized to exist within their systems - humans have smallpox, cows have cowpox, monkeys have monkeypox, and so on (note: chicken pox is NOT a member of this group - its name comes from an old English word meaning “Itchy”, and is completely unrelated). However, sometimes, the similar viruses can cross species barriers, as in the case of cowpox. Though the viruses are specialized to their host species enough that they don’t easily spread between atypical hosts, they’re related enough that once an individual is infected with one pox virus, their immune system is able to to recognize and fend off the whole lot of them. This is why, with the assistance of cowpox (Vaccinia) cultures in administered vaccines (rather than all of humanity having to be in direct contact with cows…), smallpox was able to be eradicated in the wild. A Text-Book of Bacteriology, including the Etiology and Prevention of Infectious Diseases. Edgar M. Crookshank, 1897.

Top: Cow-milker infected from the teats of a cow with natural cow-pox. Large depressed vesicle with a small central crust, tumid (swollen) margin, surrounded by well-marked areola and considerable surrounding induration (hardness associated with swelling)

Bottom: Same case, one week later. Reddish brown crust typical of recovering cow-pox cases, on a reddened elevated and indurated base.

Many mammalian species have members of the Orthopoxviridae that are specialized to exist within their systems - humans have smallpox, cows have cowpox, monkeys have monkeypox, and so on (note: chicken pox is NOT a member of this group - its name comes from an old English word meaning “Itchy”, and is completely unrelated).

However, sometimes, the similar viruses can cross species barriers, as in the case of cowpox. Though the viruses are specialized to their host species enough that they don’t easily spread between atypical hosts, they’re related enough that once an individual is infected with one pox virus, their immune system is able to to recognize and fend off the whole lot of them. This is why, with the assistance of cowpox (Vaccinia) cultures in administered vaccines (rather than all of humanity having to be in direct contact with cows…), smallpox was able to be eradicated in the wild.

A Text-Book of Bacteriology, including the Etiology and Prevention of Infectious Diseases. Edgar M. Crookshank, 1897.

Oral manifestations of childhood illnesses 1. Oral thrush - Caused by the Candida fungus overgrowing on the mucous membranes of the mouth. Also known as candidiasis when it occurs elsewhere on the body (such as vaginal candidiasis).2. Varicella - Chicken pox. Have you ever had chicken pox in your mouth? It’s awful.3. Stomatitis herpetica or Aphthosa [Herpetic stomatitis] - Caused by the same herpes infection of the mouth that causes cold sores, but blisters and mild ulceration can occur. This condition usually occurs when the child first contracts Herpes simplex I.4. Stomatitis ulcerosa or Scorbutus - The oral manifestation of scurvy in children. The bone weakness, dry mouth, and immune dysfunction in scurvy often causes tooth weakening, loosening, and extreme gingivitis.5. Follicular tonsillitis - The “standard” childhood tonsillitis, with infection of the palatine tonsils. If the infection doesn’t subside, removal of the tonsils is still the most common treatment.6. Diphtheria - There are many oral manifestations of diphtheria, including “pseudo-membranes” covering the trachea, severely impairing breathing. The exotoxins exuded by Corynebacterium diphtherium can also cause thick, thrush-like patches in the pharyngotrachea. Pediatrics: The Hygienic and and Medical Treatment of Children. Thomas Morgan Rotch, 1901.

Oral manifestations of childhood illnesses

1. Oral thrush - Caused by the Candida fungus overgrowing on the mucous membranes of the mouth. Also known as candidiasis when it occurs elsewhere on the body (such as vaginal candidiasis).
2. Varicella - Chicken pox. Have you ever had chicken pox in your mouth? It’s awful.
3. Stomatitis herpetica or Aphthosa [Herpetic stomatitis] - Caused by the same herpes infection of the mouth that causes cold sores, but blisters and mild ulceration can occur. This condition usually occurs when the child first contracts Herpes simplex I.
4. Stomatitis ulcerosa or Scorbutus - The oral manifestation of scurvy in children. The bone weakness, dry mouth, and immune dysfunction in scurvy often causes tooth weakening, loosening, and extreme gingivitis.
5. Follicular tonsillitis - The “standard” childhood tonsillitis, with infection of the palatine tonsils. If the infection doesn’t subside, removal of the tonsils is still the most common treatment.
6. Diphtheria - There are many oral manifestations of diphtheria, including “pseudo-membranes” covering the trachea, severely impairing breathing. The exotoxins exuded by Corynebacterium diphtherium can also cause thick, thrush-like patches in the pharyngotrachea.

Pediatrics: The Hygienic and and Medical Treatment of Children. Thomas Morgan Rotch, 1901.

Examining Rats for Bubonic Plague - New Orleans, 1914 A group of rats on a ship at the Port of New Orleans died en masse in 1914, and were found to be infected with the bubonic plague. At the same time, a stowaway was killed in a card game, and brought to the morgue in a strange condition, discovered to be pneumonic plague - highly contagious from person-to-person. A campaign of sulfonamide treatment, hospitalization, quarantine, and massive rat eradication was undertaken by city officials as soon as the news arrived. For the next six years, the plague cropped up in small pockets of the city where rats were not well-controlled, and in the poorest slums where public officials didn’t care to venture. However, despite the continued infections cropping up, the management of the outbreaks was far more well-executed than the political and public relations catastrophe that was the San Francisco outbreak in 1900. The 1950 movie Panic in the Streets was based off of this outbreak. Read more about the plague in America at Puff the Mutant Dragon. [image]

Examining Rats for Bubonic Plague - New Orleans, 1914

A group of rats on a ship at the Port of New Orleans died en masse in 1914, and were found to be infected with the bubonic plague. At the same time, a stowaway was killed in a card game, and brought to the morgue in a strange condition, discovered to be pneumonic plague - highly contagious from person-to-person.

A campaign of sulfonamide treatment, hospitalization, quarantine, and massive rat eradication was undertaken by city officials as soon as the news arrived.

For the next six years, the plague cropped up in small pockets of the city where rats were not well-controlled, and in the poorest slums where public officials didn’t care to venture. However, despite the continued infections cropping up, the management of the outbreaks was far more well-executed than the political and public relations catastrophe that was the San Francisco outbreak in 1900.

The 1950 movie Panic in the Streets was based off of this outbreak.

Read more about the plague in America at Puff the Mutant Dragon.

[image]

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.]

The Life-Cycle of Spirochaeta duttoni, as elucidated by William Boog Leishman Fig 1-6. General character of organismFig 6-8. Transverse divisionFig 9. Longitudinal divisionFig 10-11. Unknown method reproduction, thought to be conjugationFig 12. Coiled form in peripheral bloodFig 13. Swollen form in liverFig 14-15. Skein-like forms in the spleenFig 16. Encysted form Spirochetes such as Spirochaeta duttoni and Trepanoma pallidum pallidum (syphilis) were originally grouped with other eukaryotic parasitic organisms such as protozoa, because their methods of reproduction (both longitudinal and transverse division) made discerning their true nature confusing at first. All spirochetes are now known to be Gram-negative helically-coiled bacteria. The species “Spirochaeta duttoni” (now Borrelia duttoni) causes African tick fever, which causes general muscle pain, fever, chills, nausea, and a generalized rash. The bacteria has the ability to change its surface proteins to evade the immune system for some time, and as such often relapses after initial treatment.  [Human Parasitology. Damaso Rivas, 1920.]

The Life-Cycle of Spirochaeta duttoni, as elucidated by William Boog Leishman

Fig 1-6. General character of organism
Fig 6-8. Transverse division
Fig 9. Longitudinal division
Fig 10-11. Unknown method reproduction, thought to be conjugation
Fig 12. Coiled form in peripheral blood
Fig 13. Swollen form in liver
Fig 14-15. Skein-like forms in the spleen
Fig 16. Encysted form

Spirochetes such as Spirochaeta duttoni and Trepanoma pallidum pallidum (syphilis) were originally grouped with other eukaryotic parasitic organisms such as protozoa, because their methods of reproduction (both longitudinal and transverse division) made discerning their true nature confusing at first.

All spirochetes are now known to be Gram-negative helically-coiled bacteria. The species “Spirochaeta duttoni” (now Borrelia duttoni) causes African tick fever, which causes general muscle pain, fever, chills, nausea, and a generalized rash. The bacteria has the ability to change its surface proteins to evade the immune system for some time, and as such often relapses after initial treatment. 

[Human Parasitology. Damaso Rivas, 1920.]

Diphtheria Antitoxin - 1895 Diphtheria is a killer by the toxins it excretes, which can cause necrosis, myocarditis, and, most dangerously, the putrid-smelling pseudo-membrane that can line the pharynx and trachea, preventing breathing. Antitoxins were the first solution to these toxins. Antibodies against the toxin were taken from the serum of large animals (horses) who were inoculated with the toxin produced by the C. diphtheriae bacteria. The amount of toxin was small enough that it only produced an immune reaction in the animal, and did not poison them. When someone contracted diphtheria, the antitoxin could be injected, and this inactivated the circulating toxin created by the bacteria. While it did not kill the bacteria itself, the immune system was capable of doing that on its own when it wasn’t busy being dissolved and ripped apart by the toxins. Unfortunately, the antitoxin could not inactivate toxins created by bacteria that were already bound to tissues, so the earlier it was administered, the better. Combined with the refinement of the tracheotomy (so that patients could breathe, even with a pseudo-membrane covering their airway), the antitoxin dropped the mortality rate of diphtheria from 40-45% down to around 12-15%.  Image: Production of antitoxin by inoculation of horses. One of the first bottles of antitoxin produced at the Hygienic Lab, later known as the National Institutes of Health.

Diphtheria Antitoxin - 1895

Diphtheria is a killer by the toxins it excretes, which can cause necrosis, myocarditis, and, most dangerously, the putrid-smelling pseudo-membrane that can line the pharynx and trachea, preventing breathing.

Antitoxins were the first solution to these toxins. Antibodies against the toxin were taken from the serum of large animals (horses) who were inoculated with the toxin produced by the C. diphtheriae bacteria. The amount of toxin was small enough that it only produced an immune reaction in the animal, and did not poison them.

When someone contracted diphtheria, the antitoxin could be injected, and this inactivated the circulating toxin created by the bacteria. While it did not kill the bacteria itself, the immune system was capable of doing that on its own when it wasn’t busy being dissolved and ripped apart by the toxins. Unfortunately, the antitoxin could not inactivate toxins created by bacteria that were already bound to tissues, so the earlier it was administered, the better.

Combined with the refinement of the tracheotomy (so that patients could breathe, even with a pseudo-membrane covering their airway), the antitoxin dropped the mortality rate of diphtheria from 40-45% down to around 12-15%. 

Image: Production of antitoxin by inoculation of horses. One of the first bottles of antitoxin produced at the Hygienic Lab, later known as the National Institutes of Health.

With all of the news hubbub about the brain-eating amoeba from Louisiana (Naegleria fowleri), I was wondering if there's any historical information about it? Apologies if this has been asked before! — Asked by bittergrapes

In fairness to Louisiana, Naegleria fowleri is all over the place ;P Actually, its prevalence in LA is lower than in many other water-logged states, since their coastal marshes are bracken water, and N. fowleri doesn’t like the ocean (though clearly it’s fine with salt, given the neti pot incidents).

As for its history, N. fowleri is a relative newcomer to the stage of Things That Can Kill You, at least in terms of our knowledge of it. R.F. Carter and M. Fowler discovered it in 1965, down in Australia. It was actually used as the example to prove the hypothesis that there were highly adaptive amoebo-flagellates out there that could live both 100% freely in the environment, as well as establish themselves within the human body, when given the opportunity and loss of original environment. You know, like when one introduces a liquid into the sinuses and the amoeba gets caught on something, and it doesn’t get washed out. It’s lost its initial environment (which it would prefer to stay in, since adaptation to a new environment is physically demanding), but it can still survive just fine.

Meningitis from amoebas (Primary Amoebic Meningitis - PAM) like what N. fowleri causes hasn’t been known for too long, either. Though the pathogenicity of Entamoeba histolyca (the source of amoebic dysentery) was established back in 1875, the fact that it could establish itself in the central nervous system and cause such rapid death wasn’t known until I believe the Korean war, though I’m not positive on that fact. Either way, we didn’t know amoebas were such nasty bugs (even if they DID already kill us with dysentery) until the mid-20th century or so.

Herpes zoster gangrenosum Outbreak of herpes zoster (shingles) along the trigeminus cranial nerve (first branch), causing at first intense pain, then eruption of dermatological symptoms. Initially presents on upper eyelid, then progresses upward to the hairline and down nose, shaply limited by median line of face. Vesicles often appear on the eye itself, which can lead to iritis, keratitis, scleritis, or paralysis of the muscles that move the eye. Though considerable disfigurement is not uncommon (especially in gangrenous outbreaks), fatal results from this disease are rare. When vesicles involve the cornea, vision impairment is common, but not always permanent. Atlas of External Diseases of the Eye. Richard Greeff, 1914.

Herpes zoster gangrenosum

Outbreak of herpes zoster (shingles) along the trigeminus cranial nerve (first branch), causing at first intense pain, then eruption of dermatological symptoms. Initially presents on upper eyelid, then progresses upward to the hairline and down nose, shaply limited by median line of face. Vesicles often appear on the eye itself, which can lead to iritis, keratitis, scleritis, or paralysis of the muscles that move the eye.

Though considerable disfigurement is not uncommon (especially in gangrenous outbreaks), fatal results from this disease are rare. When vesicles involve the cornea, vision impairment is common, but not always permanent.

Atlas of External Diseases of the Eye. Richard Greeff, 1914.

Advanced Tuberculosis of the Testicle You can clearly see the bulging outgrowths (tubercules - hence the name tuberculosis) of the testicle pushing into the epididymis, and the cavitation within the testicle body. If a testicle like this were not removed, it is not unlikely that tubercules would interrupt the fairly delicate blood supply, and necrosis of the tissue would follow. A Textbook of the Genito-Urinary Diseases.  Charles W. Bonney, 1912.

Advanced Tuberculosis of the Testicle

You can clearly see the bulging outgrowths (tubercules - hence the name tuberculosis) of the testicle pushing into the epididymis, and the cavitation within the testicle body. If a testicle like this were not removed, it is not unlikely that tubercules would interrupt the fairly delicate blood supply, and necrosis of the tissue would follow.

A Textbook of the Genito-Urinary Diseases.  Charles W. Bonney, 1912.

Those afflicted with “king’s evil” gather ‘round the king to receive the Royal Touch in hopes of a cure.

Those afflicted with “king’s evil” gather ‘round the king to receive the Royal Touch in hopes of a cure.

Quite frankly, I find the concept of “infectious dandruff” terrifying.

Quite frankly, I find the concept of “infectious dandruff” terrifying.

A case of cancrum oris following whooping cough. While whooping cough was resolving, a black sore was noted on the cheek. The sore remained there for 5 days, and on the fifth day spread to the gums and all the nearby teeth fell out. Cheek sloughed away soon after. Standard treatment for noma (gangrenous stomatitis) was given, but to no avail. Child died within 72 hours. Though noma was and is a serious disease, it was rarely so quickly fatal, especially when treated. On autopsy, the bronchi were inflamed and filled with mucous as happens with children who die of broncho-pneumonia. The author of the book noted that noma and cancrum oris were two separate conditions. From what I can find in the modern literature, cancrum oris is now considered an antiquated term for noma, and noma is a disease of varying degrees.  Somewhat frighteningly, the only successful method of arresting the advance of what was known as “cancrum oris” was noted to be destroying all gangrenous tissue with nitric acid. These days, very strong antibiotics and greatly improved nutrition are the typical cures, though gangrenous tissue does still have to be excised in the end. At least we don’t have to burn it off with acid. From The Surgical Diseases of Children. By J. Cooper Forster, 1860.

A case of cancrum oris following whooping cough. While whooping cough was resolving, a black sore was noted on the cheek. The sore remained there for 5 days, and on the fifth day spread to the gums and all the nearby teeth fell out. Cheek sloughed away soon after. Standard treatment for noma (gangrenous stomatitis) was given, but to no avail. Child died within 72 hours. Though noma was and is a serious disease, it was rarely so quickly fatal, especially when treated. On autopsy, the bronchi were inflamed and filled with mucous as happens with children who die of broncho-pneumonia.

The author of the book noted that noma and cancrum oris were two separate conditions. From what I can find in the modern literature, cancrum oris is now considered an antiquated term for noma, and noma is a disease of varying degrees. 

Somewhat frighteningly, the only successful method of arresting the advance of what was known as “cancrum oris” was noted to be destroying all gangrenous tissue with nitric acid. These days, very strong antibiotics and greatly improved nutrition are the typical cures, though gangrenous tissue does still have to be excised in the end. At least we don’t have to burn it off with acid.

From The Surgical Diseases of Children. By J. Cooper Forster, 1860.

Syphilis and its Treatments. Wilfrid S. Fox, 1920.

Syphilis and its Treatments. Wilfrid S. Fox, 1920.