Category Archives: Plague

Contagion and Pestilence in Isidore of Seville’s Etymologies

Saint Isidore of Seville (c. 560–636). Bishop, confessor and Doctor of the Church. Altarpiece of Saint Isidore. 15th century. Diocesan Museum of Calatayud. Spain.

Before Isidore of Seville became the patron saint of the internet, he was known for over a thousand years as a font of knowledge.  Isidore was not an innovator; he was a master of synthesis. It is through Isidore that we have an orderly account of the learned knowledge of the Late Roman world.  He was conscious of the fact that he was saving information at risk of being lost.  His Etymologies, written in twenty sections between 621 and 636, was both the Latin dictionary and encyclopedia of the entire medieval period. Isidore is not always correct — there is a lot of sounds-like etymology– but his explanations were accepted throughout the medieval period. So, Isidore is an ideal source to gain an understanding of how modern terms like contagion and pestilence were defined from the early seventh century in the midst of the first plague pandemic.

From Book IV: On Acute Illnesses:

17. Pestilence is a contagion that as soon as it seizes on one person quickly spreads to many. It arises from corrupt air and maintains itself by penetrating the internal organs. Although this is generally caused by powers in air, it never occurs without the consent of God. 18. It is called pestilence (pestilentia) as if it were pastulentia, because it consumes (depascere, ppl. depastus) like fire, as Vergil, Aen. 5.683): The pestilence descends on the whole body*. Likewise contagion (contagium) is from ‘touching’ (contingere), because it contaminates anyone it touches. 19. The swellings (inguen) (ie. bubonic plague) are so called from their striking the groin (inguen). Pestilence is also called plague (lues), so called from destruction (labes) and distress (luctus), and is so violent that there is no time to anticipate life or death, but weakness comes suddenly together with death. (p. 110-111).

The general definition of both pestilence and contagion, along with their spellings in Latin, are recognizable to us today. The modern editors note that Vergil is using pestilence as a metaphor for the burning of a Trojan ship. It is on the origin or mechanism of pestilence where we differ. Isidore’s world understood medicine as a function of airs and humors, a topic for another time. He also writes of plague again in his On the Nature of Things, which was less influential than the Etymologies. In a later post I will look at what the Venerable Bede does with both the works of Isidore and Pliny in his own On the Nature of Things.

Inguen as the term for a swelling in the groin is the what draws my attention. Inguen is the root for the modern word inguinal; as in inguinal bubo.  Two of the most important European historians of the first pandemic, Gregory of Tours and Paul the Deacon, used the term inguinaria for the pandemic. Unfortunately, inguinaria is usually literally lost in translation. Rather than leaving inguinaria as the early medieval term for bubonic plague, it is usually translated as the less specific ‘plague’ or a little better ‘inguinal plague’. Even in the translation above, it is translated as swelling with the original word in parenthesis.

Bubo is likewise said to come from the Greek word for groin, boubon (βουβών), but I have not found a source to discuss its earliest use. Isidore does not discuss the term bubo or the Greek term boubon, presumably using inguen instead. Greek boubon translates into Latin as inguen, both meaning groin or swelling the groin. Ironically “inguinal bubo” then duplicates the same meaning. It would be interesting to know if boubon or bubonic is a word used for the first pandemic (541-c. 750) in the Eastern Roman empire.

One of the important inferences from the derivation of inguen/boubon is that it supports the groin as the primary site of early infection. So while buboes can be found in the axilla and neck, and there are other transmission routes, it was recognized from the beginning as a disease of the groin. This in turn supports fleas as the primary transmission vector, since as insects found on the floor most of the time, they usually bite on the legs resulting in an inguinal bubo.

Reference: Barney, SA, Lewis, WI, Beach, JA, and Berghof, O. (trans and ed). The Etymologies of Isidore of Seville. Cambridge, 2006.

Plague in Surat: 20 Years Later

I can’t let 2014 pass in a few weeks without mentioning that this fall was the twentieth anniversary of the plague outbreak in Surat, India — a major turning point in modern plague history and in the development of the (re)emerging infectious disease paradigm.

In the final accounting, 53 people died of plague, mostly pneumonic, but there are over 5000 cases classified as suspected and at least half a million people fled across India. Compared to other pneumonic plague outbreaks in Africa within the last twenty years, the number of deaths was small and the mortality rate tiny (1% of suspected cases). The government response was not only woefully inadequate but also exacerbated the damage within India and scared the rest of the world.

The lessons learned from Surat are really what is important.

  • The need for a national database to keep track of seemingly isolated cases and the need for surveillance of rodents, even when there haven’t been any human cases in many years. Better surveillance established since 1994 has identified several more plague outbreaks in India and enough evidence of enduring plague foci in the country.
  • The need for transparency, willingness to accept foreign help and the futility of trying to hide the epidemic from the press.
  • The costs of unsupported allegations of biological warfare or terrorism are too high to make unless there is certainty. It ultimately does not deflect responsibility away from the government for the response. The political costs for governments who make official erroneous allegations are greater than accepting responsibility for the outbreak.

In this month’s issue of the Indian Journal of Microbiology, the full genomic sequence of Yersinia pestis collected at Surat in 1994 and at a 2002 outbreak in India was released. Four samples were sequenced and they are all four different strains. Unfortunately, they did not do a phylogenetic analysis to indicate where they fit on the Y. pestis tree.

Twenty years ago it was the double hit of plague in Surat in 1994 and the discovery of antibiotic resistant plague in Madagascar in 1995 that raised concern about re-emerging infection diseases. Antibiotic resistant strains of Yersinia pestis have continued to appear in Madagascar and now insecticide resistant fleas are a problem as well. While public health processes and surveillance are better than in 1994, there has been no improvement plague incidence or concerning resistant strains.

Ebola is currently extracting the toll that was feared of plague in Surat two decades ago. If Surat was the warning that acute pandemics are still possible, Ebola is showing how far we still have to go 20 years later. Both plague in Surat and Ebola in 2014 are also reminding us that knowing what to do to stop an epidemic is not enough, execution is everything.

Further reading on Surat:

Barrett, Ron. (2008) “The 1994 Plague in Western India: Human Ecology and the Risks of Misattribution” p. 49-71 in Terrorism, War, or Disease? Unraveling the Use of Biological Weapons. Edited by A.L. Clunan, P.B. Lavoy, and S. B. Martin. Stanford Security Studies. Stanford University Press. This is the best analysis of the Surat outbreak that I have found.

Ziegler, Michelle (2014) The Black Death and the Future of the Plague. The Medieval Globe, 1: 183-199 for an overview of plague since 1994.

Mahale, K. N., Paranjape, P. S., Marathe, N. P., Dhotre, D. P., Chowdhury, S., Shetty, S. A., et al. (2014). Draft Genome Sequences of Yersinia pestis Strains from the 1994 Plague Epidemic of Surat and 2002 Shimla Outbreak in India. Indian Journal of Microbiology, 54(4), 480–482. doi:10.1007/s12088-014-0475-7

For more on antibiotic resistant plague, see this past post and on the most recent reported pneumonic plague outbreak in Madagascar.

A Synopsis of an Unusual Pneumonic Plague Outbreak in Madagascar, 2011

Plague appears in Madagascar every year, but it can still come as a surprise. It did in the January of 2011 when it appeared in an area of northern Madagascar that had never had an outbreak before. Not only was it a new area, but all of the cases were pneumonic. Not one case of bubonic plague. Eleven people were dead before antibiotics were given to the first patients on January 28. Vincent Richard and colleagues describe the outbreak in the forthcoming January issue of Emerging Infectious Diseases.

The index case was a thirteen year old boy who worked in a copper mine and developed a headache, fever and chills on a trip to his home village on January 6. He progressed to a fever, headache, a cough, severe chest pain and bloody sputum before dying at home on January 14. By January 22, his mother, her husband, daughter and granddaughter had died. Three other family members were showing symptoms of pneumonic plague when a neighboring family began to care for them beginning the second round of infections in twelve other people.  Visitors to the second household transmitted it to three more households. The last two fatal cases (19 & 20) were the brother who carried his sister to a traditional healer who was the last fatal case dying on February 9.

Plague transmission (Richard et al, 2015)
Plague transmission (Richard et al, 2015)

The epidemiological investigation identified 41 contacts: 17 from infected households and 25 who had more fleeting contact with a fatal case. None of these contacts had plague specific symptoms. All contacts were serum tested for plague with the Rapid Diagnostic Test (RDT, ‘the dipstick’) and all, but two who refused, were given prophylactic antibiotics. Details of how the contacts are connected are shown in the graphic above and narrated in the report by Richards et al in Emerging Infectious Diseases. Only two of these carriers were seropositive; one had a cough and refused antibiotics (c25) but did not progress. He is not considered a symptomatic case in the report. Three other contacts had mild pulmonary symptoms but were seronegative. They are not considered plague cases.  The wife of a fatal case cared for her husband and shared his bed until his death; she never turned seropositive.

Public health response followed the WHO protocols but was hampered by the outbreak being spread over seven villages 30 km from the index household in an area where plague had not been previously reported. This slowed the identification of contacts and dispensing antibiotics. Unfortunately postmortem specimens were not collected so there were only five specimens from symptomatic cases  to analyze. Initial sputum samples for three cases were positive for the Yersinia pestis F1 antigen by the RDT dipstick and all five specimens were transported about 900 km to the Institut Pasteur de Madagascar in Antananarivo to be analyzed. All attempts to culture Yersinia pestis from the specimens in bacterial media and mice failed.  Diagnoses were confirmed and titers quantitated by an ELISA based immunological detection for three cases. Cases were classified as suspected (17), presumptive (2) and confirmed (3) based on the WHO diagnostic criteria. The two presumptive cases were the seropositive non-symptomatic contacts. This highlights a problem with the WHO criteria since one seropositive case refused antibiotics and never developed plague specific symptoms. Presumptive should be a higher standard than suspected, which is based on clinical symptoms alone.

All cases that developed symptomatic pneumonic plague had the same symptoms: fever, chest pain, a cough, and bloody sputum. They were infectious for 48-72 hours after a 4-6 day latency period. This relatively long latency period allowed antibiotics to prevent the development of symptomatic plague in contacts. The effect of antibiotics on symptomatic patients was stark; five treated patients survived while all fifteen untreated patients died. With such a drastic difference between treated and untreated, the overall 75% case fatality rate is not really reflective of the virulence of the pathogen. Antibiotics alone determined the survival of symptomatic cases. Of the 36 people living in infected households, 20 developed symptomatic plague for an attack rate of 55% within the households; non-household contacts are excluded from the attack rate calculation.

Investigation of the presumptive focus is not begin until two months after the beginning of the plague response. Trapping of rodents in the area around the initial two villages,  Ambakirano and Ankatakata, produced 64 rodents and five dogs were sampled. Only one greater hedgehog (1 of 6) and two dogs were seropositive for Yersinia pestis by ELISA.  As wide ranging carnivores who are fairly resistant to plague, seroconversion in dogs is considered to be a good sentinel indicator. No fleas were collected; no dead rats were observed. All 51 black rats collected were seronegative, but Yersinia pestis DNA was isolated from the spleens of five rats. All strains fit the Malagasy specific 1.ORI3-k SNP pattern. There was enough minor variation in CRISPRs (a type of genetic fingerprinting information) to suggest a pre-existing enzootic focus is present. With such benign animal evidence, there is no reason to think that there was an epizootic that spilled over to humans. This is not surprising considering there were no bubonic cases. All of the human cases appear to be connected to the index case and to have passed human to human. Unfortunately, there is no mention of investigating a potential plague focus near the copper mine where the index case was working before symptoms appeared on his way to his home village.

While the survivors of the 2011 outbreak responded well to streptomycin, resistant strains were reported in the 2011 outbreak to Richards et al (2015) as personal communication. It is unclear if this means in an animal isolate from the region or another outbreak in 2011. Resistant strains have been reported in Madagascar since 1995 and are now apparently persistent.

This outbreak highlights how difficult it is to initially identify a pneumonic only outbreak. Spread by droplets, transmission can be broken by simple masks or, the Malagasy team suggests, even hygiene like turning away from others while coughing or covering the mouth and nose. People were able to care for and bury their dead without contracting disease.  On the other hand, antibiotics alone stopped the outbreak. Whether or not it would have ended on its own, we will never know. Although only two contacts were seropositive, prophylactic antibiotics likely prevented more infections.

References:

Richard V, Riehm JM, Herindrainy P, Soanandrasana R, Ratsitoharina M, Rakotomanana F, et al. Pneumonic plague outbreak, northern Madagascar, 2011. Emerg Infect Dis [Internet]. 2015 Jan [ahead of print publication 5 Dec 2014]. http://dx.doi.org/10.3201/eid2101.131828.

See my previous post for more information on antibiotic resistant Yersinia pestis in Madagascar.