Category Archives: ecology

The Promiscuous Human Flea

Female Pulex irritans, the human flea, from the Katja ZSM collection (CC3.0)
Female Pulex irritans, the human flea, from the Katja ZSM collection (CC3.0)

by Michelle Ziegler

The human flea seems like a misnomer today. We are not its current primary host, but that doesn’t mean that it once wasn’t our primary flea.  Pulex irritans  was first described by Carl Linnaeus as the “house flea” in 1758 (Krasnov 2012:4) and it is still found in homes in many parts of the world.

For the most part, the human flea is a nuisance, an irritant as its name implies. Except when it isn’t, when it occasionally transmits Yersinia pestis, the plague, to people. Pulex irritans has been  in homes with human plague cases from Arizona to Madagascar (Archibald & Kunitz, 1971; Ratovonjato et al, 2014). In 2006, Drancourt, Houhamdi, and Raoult argued that either the human flea or louse played a major role in human plague epidemics.

Human fleas have been found in the homes in several areas where plague occurs. P. irritans infected with Y. pestis were found on a dog in a home of a plague victim on Navajo land in Arizona in 1968. They also report knowledge  Y. pestis being isolated from  P. irritans fleas on dogs in the home of an infected child in Kayneta in 1968 (Archibald & Kunitz, 1971).   A recent survey of plague regions in Tanzania found 50% of the fleas in homes were P. irritans (Haule et al, 2013). A recent survey of fleas in Madagascar found that 98% of the fleas found inside control homes  in the control region of the study were Pulex irritans (Miarinjara et al, 2016). The fact that they did not find them in the homes within the area of the plague outbreak a month earlier may be due to extensive spraying of insecticide to end the epidemic. Human fleas are suspected of being the vectors for a variety of zoonotic diseases in Iran today (Rahbari, Nabian, & Nourolahi, 2008).

The human flea, Pulex irritans, has had a very interesting and convoluted history. All of the Pulex fleas are thought to have evolved in South America, perhaps on guinea pigs or piccary . P. irritans is the only member of its genus  that has left the Americas.  It made it to Eurasia long before the “Columbian Exchange”.  So it crossed a land bridge at some point to begin spreading in Eurasia, and it need not have crossed on a human.  Ötzi the 5000 year old ice mummy from the Italian Alps yielded two human fleas from his  artifacts (Schedl, 2000). P. irritans has also been found Egypt from 3500 BC  (Bain 2004) and 1350-1323 BC (Panagiotakopulu, 2001) showing that it does well in warm, dry climates also. So not only where they present for the entire known period of plague but they have been specifically found in warm and cold regions. Pulex irritans has been found in floor debris of uncovered sites from Roman Britain (Kenward, 1998). They were common inhabitants of early medieval Irish homes (O’Sullivan, 2008).  They are fairly common finds in Norse Greenland settlements. Unfortunately flea surveys have not been done on most continental archaeological sites (or at least I haven’t found them).

So why is P. irritans called a promiscuous flea? It has nothing to do with sex! In this case promiscuous means that it will feed off of a wide variety of host species. It has a truly impressive host range beyond humans including pigs, dogs, cats, goats and sheep, cattle, chickens, porcupines, multiple species of foxes, wolves, coyotes,  golden jackel of Iran,  badgers, prairie dogs,  rabbits, wild cats,  and mice. There are undoubtably more species that could be added. It seems to be very common on foxes in North America and Europe. These are, of course, primarily predators of rodents.  Given its wide range of hosts, its distribution and frequency among hosts has probably fluctuated wildly due to environmental and biodiversity changes over the last millennia.

Such a wide host range also makes it a potential bridging vector, one that can move disease between a wild reservoir to a domestic space transmitting it to domestic rodents, pets, and humans. Importantly, bridging vectors work in both directions, meaning that it could be instrumental in developing a wildlife reservoir after a human epidemic in a new region.

General flea life cycle (CDC). Adults are only 5% of flea biomass.

flea-pyramid-1P. irritans has a life cycle that is well suited to thriving in buildings like houses, barns, sheds, and animal nests or dens. Most of their biomass is in the egg stage. Small white eggs are often laid on the host but almost always fall off on to the floor. They do particularly well on the floor of stables and animal sheds where fermenting manure and debris keeps the eggs warm and moist.  They also do well in human homes where it is usually warmer and more humid than outdoors. They breed all year around. The eggs will hatch into larvae that resemble maggots within 4-6 days. The very active larvae will feed on organic debris including feces of the adult flea and other animals. After three molts it will develop a cocooned pupae where it will undergo a metamorphosis to the adult flea. It can remain in the pupa for several months if necessary until the conditions are suitable. So although human fleas are usually not present in stables or sheds during the coldest months the pupa can easily span the winter to emerge as adults in the early spring. This may explain why they are often the most abundant in the spring when all of the pupae from the late fall and winter emerge. It is unclear if the lifecycle pauses inside a heated human home. A well fed adult can live up to 513 days and even starved can last 135 days (Krasnov, 2012: 54). It is unclear how long they live after being infected by Yersinia pestis (or other pathogens). Fleas only feed on blood as adults so this is their only phase that can be infected by Yersinia pestis.

Modern infestations of P. irritans in Greece and Iran can give a few insights into its disease ecology. Sheep and goats are consistently the most heavily infested animals with P. irritans in modern Iran and Greece. In parts of Iran, P. irritans is the most common flea captured from humans or domestic livestock: goats, sheep, cattle and chickens (Moemenbellah-Fard et al, 2014; Rahbari,  Nabian, & Nourolahi, 2008;  Rafinejad et al, 2013). In some modern surveys, P. irritans is over 90% of the fleas collected in rural areas, found on sheep, goats, cattle, humans and chickens — “wherever the animal infestation was high the fleas easily transmitted to humans” (Rahbari et al, 2008:44). In Greece, Christodoulopoulos et al. (2006) made a very important observation:

“fleas accumulated in the goat environment with each successive generation leading to an increase in their number. This conclusion could be corroborated by the observation that the most successful flea control measure was the change of barn location with movement of the goats to another far away new-constructed barn.” (p. 142-143)

So even with modern insecticides, sheep dips, and building techniques available, the infestation of the building could not be controlled. This has implications for human housing. Observations of flea ecology in Iran back this up, albeit without addressing methods of eliminating infestations.

The Iranian reports discuss human flea bites more. Noting that men who worked with animals had a higher bite rate. Bites are primarily around the ankles and lower legs, often multiple bites in a row.  In Iran they noted that human reactions to the flea bites varied from highly allergic to no sensitivity at all (Rahbari, Nabian, & Nourolahi, 2008). This is a difference in human immunology to the fleas and sensitivity is likely to alter the immune response to not only the bite but also bacteria in the bite. There is also likely to be heterogeneity in which humans and animals are bitten.

As we begin to take Pulex irritans more seriously as a plague vector, there is a lot of basic biology that needs to be done yet. How long can they survive infected? How does it effect their feeding behavior? Some studies showed that a small percentage of P. irritans can block, so what effect does that have on transmission in that small percent of fleas?


Archibald, W. S., & Kunitz, S. J. (1971). Detection of plague by testing serums of dogs on the Navajo Reservation. HSMHA Health Reports, 86(4), 377–380.

Bain, A. (2004). Irritating intimates: the archaeoentomology of lice, fleas, and bedbugs. Northeast Historical Archaeology, 33(1), 81–90.

Barnes, Jefferey. (22 April 2014)  Human flea, Arthropod Museum Notes, Number 108. University of Arkansas.

Buckland, P. C., & Sadler, J. P. (1989). A biogeography of the human flea, Pulex irritans L.(Siphonaptera: Pulicidae). Journal of Biogeography (UK).

Christodoulopoulos, G., Theodoropoulos, G., Kominakis, A., & Theis, J. H. (2006). Biological, seasonal and environmental factors associated with Pulex irritans infestation of dairy goats in Greece. Veterinary Parasitology, 137(1-2), 137–143.

Dobler, G., & Pfeffer, M. (2011). Fleas as parasites of the family Canidae. Parasites & Vectors, 4, 139–139.

Drancourt, M., Houhamdi, L., & Raoult, D. (2006). Yersinia pestis as a telluric, human ectoparasite-borne organism. The Lancet Infectious Diseases, 6(4), 234–241.

Eisen, Rebecca J., David T. Dennis, and Kenneth L. Gage. “The Role of Early-Phase Transmission in the Spread of Yersinia pestis.” Journal of medical entomology 52.6 (2015): 1183-1192.

Haule, M., Lyamuya, E. E., Kilonzo, B. S., Matee, M. I., & Hangombe, B. M. (2013). Investigation of fleas as vectors in the transmission of plague during a quiescent period in North-Eastern, Tanzania. Journal of Entomology and Nematology, 5(7).

Hufthammer, Anne Karin, and Lars Walløe. “Rats cannot have been intermediate hosts for Yersinia pestis during medieval plague epidemics in Northern Europe.” Journal of Archaeological Science 40.4 (2013): 1752-1759.

Kenward, H. (1999). Insect remains as indicators of zonation of land use and activity in Roman Carlisle, England. Reports from the Environmental Archaeology Unit (Vol. 99, pp. 1–30).

Kotti, B. K. (2015). Fleas (Siphonaptera) of mammals and birds in the Great Caucasus. Entomological Review, 95(6), 728–738.

Krasnov, Boris (2012) Functional and Ecological Ecology of Fleas: A Model for Ecological Parasitology. Cambridge University Press.

Laudisoit, A., Leirs, H., Makundi, R. H., Van Dongen, S., Davis, S., Neerinckx, S., et al. (2007). Plague and the human flea, Tanzania. Emerging Infectious Diseases, 13(5), 687–693.

Miarinjara A, Rogier C, Harimalala M, Ramihangihajason TR, Boyer S. Xenopsylla brasiliensis fleas in plague focus areas, Madagascar. Emerg Infect Dis. 2016 Dec [3 Sept 2016].

Moemenbellah-Fard, M. D., Shahriari, B., Azizi, K., Fakoorziba, M. R., Mohammadi, J., & Amin, M. (2014). Faunal distribution of fleas and their blood-feeding preferences using enzyme-linked immunosorbent assays from farm animals and human shelters in a new rural region of southern Iran. Journal of Parasitic Diseases, 40(1), 169–175.

O’Sullivan, A. (2008). Early medieval houses in Ireland: social identity and dwelling spaces. Peritia, 20, 225–256.

Panagiotakopulu, E. (2001). Fleas from pharaonic Amarna. Antiquity, 75, 499–500.

Pulex irritans, Animal Diversity Web, accessed 18 June 2016.

Rahbari, S., Nabian, S., & Nourolahi, F. (2008). Flea infestation in farm animals and its health implication. Iranian Journal of Parasitology, 3(2), 43–47.

Rafinejad, J., Piazak, N., Dehghan, A., Shemshad, K., & Basseri, H. R. (2013). Affect of some environmental parameters on fleas density in human and animal shelters. American Journal of Research Communication.

Ratovonjato, J., Rajerison, M., Rahelinirina, S., & Boyer, S. (2014). Yersinia pestis in Pulex irritans Fleas during Plague Outbreak, Madagascar. Emerging Infectious Disease, 20(8), 1414–1415.

Reilly, E. (2003). The contribution of insect remains to an understanding of the environment of Viking-age and medieval Dublin.  pp. 40-61 In: Medieval Dublin IV. Four Courts Press.

Schedl, W. (2000). “Contribution to insect remains from the accompanying equipment of the Iceman”. pp. 151-155 In S. Bortenschlager & K. Oeggl (Eds.), The Iceman and his Natural Environment. Springer.

Yakhchali, M., & Bahramnejad, K. (2015). A survey of Pulex irritans (Linnaeus 1758, Siphonaptera: Pulicidae) infestation in sheep and residential areas in Kurdistan Province, Iran. The Iranian Journal of Veterinary Science and Technology, 7(1), 40–47.


Dogs as Plague Sentinels and Vectors

Marmot fighting a wild dog in northern Tibet (Source: China Tibet Online/ Xinhua)

I’ve been a little obsessed with thinking about dogs and the plague lately. Dogs are often overlooked in historic plague discussions because they usually survive plague and dog-specific fleas are not associated with transmitting plague. Yet, dogs can host many of the fleas common among rodents and others that do transmit the plague including the cat flea (Ctenocephalidis felis) and the human flea (Pulex irritans) (Gage, Montenieri, & Thomas 1994). In a case controlled study of nine US cases of bubonic and septicemic plague in 2006, having dogs in the home and particularly sleeping with a dog was a significant risk factor, probably by flea transfer (Gould et al, 2008).  There is also a growing awareness that dogs can also transmit pneumonic plague directly to humans. Like other aspects of plague biology, there is a lot going on under a veneer of normalcy.

Dogs do readily contract the plague; it’s just not apparent to casual observation. In the American state of New Mexico, 62 domestic dogs were diagnosed with plague just between the years 2003 and 2011 — 97% survived (Nichols et al, 2014).  The dogs were diagnosed by an increase of Yersinia pestis F1 antibody greater than four times greater than the recovered level, by isolation of Yersinia pestis from a body fluid or by direct flourescent antibody assay of a tissue specimen. All of them had some physical sign of infection with fever and lethargy being found in 100% of cases, but buboes or lymphadenopathy (enlarged lymph nodes) were found in only 23% and these were all in the jaw and neck region. The mean time for recovery was two days, although all but one did receive at least one dose of antibiotics. Potential sources of plague exposure are from prairie dogs, ground squirrels, chipmunks, and rabbits. Only three of the dogs had any fleas at all, but as these dogs were pets, most had received anti-flea treatment.

Monitoring plague in working dogs and other carnivores is the most efficient method of doing plague surveillance in the vast semi-arid grasslands that harbor some of the most enduring plague reservoirs. Dogs are especially useful because their immunity only lasts about six months, so a detectable level (titre) of plague antibody indicates recent contact with an infected animal. Gage, Montenieri, and Thomas (1994:6) estimated that  “sampling even a few rodent consuming carnivores, such as coyotes, can be roughly equivalent to sampling hundreds of rodents for evidence of plague infection”. The earliest serologic survey that I have found was done in Navajo lands in 1966-1968. In this same survey  in 1968, “the plague organism was isolated from a pool of fleas (Pulex irritans) taken from the household dogs of a person with plague” (Archibald & Kunitz 1971). Carnivores are now routinely monitored in the US.  Surveying herding dogs in Iran was able to show that the long unmonitored plague foci is still active (Esamaeili et al., 2013). Recent Chinese F1 antibody surveys in the Gansu province are more ominous: in 2012 4.55% of dogs were positive, but it had jumped to 10% of dogs by 2014 (Ge et al, 2014). Another  2014 survey of multiple Yersinia species in dogs found 25% of dogs in Gansu province and 18% of dogs in Qinghai province to be positive for Yersinia pestis F1 antibody, while no plague-free provinces had a single dog that had a positive antibody titre (Wang et al, 2014).

Consumption is the likely primary route of infection for dogs.  The 62 dogs from New Mexico are believed to have been primarily infected by consumption of a plague infected rodent or rabbit (Nichols et al, 2014). In a 2014 case study from China, an infected marmot was taken from a dog, butchered and divided among five dogs. All five dogs developed positive antibody titers for  plague and the shepherd who took the marmot from the dog developed pneumonic plague (but not his brother who butchered the marmot). Aerosol transmission was supported by  the isolation of Y. pestis from sputum and throat samples (Ge et al, 2014). One dog not fed the marmot was negative for the F1 antigen. Three of the 151 human contacts given prophylactic antibiotics developed an antibody titre but did not manifest disease. According to Chinese policy, the five positive dogs were euthanized and the local marmots were depopulated (Ge et al., 2014).

Dogs can transmit plague to humans through fleas that feed on the dog, fleas carried by the dog from the rodent source of the infection,  through bites or scratches, or by aerosols from dogs that develop a systemic infection. While dogs are usually thought of transmitting infected fleas to people, the  number of pneumonic cases linked to dogs is increasing. The first confirmed transmission of pneumonic plague from a dog to a person occurred in China in 2009 (Wang et al, 2015). The index case in turn transmitted pneumonic plague to eleven people. Three of these twelve cases died with the other nine cases confirmed by Y. pestis F1 antibody titres. All of the Y. pestis isolates were later typed to “biovar antiqua” — a reminder that older strains are still very virulent (Wang et al, 2009). In June 2104, in Colorado, a dog transmitted pneumonic plague to three caregivers, one of whom transmitted it to another person. All of four of these cases survived and 88 additional people were given prophylactic antibiotics (Runfola et al, 2015). Three of China’s 2014 plague cases in Gansu province within the Qinghai-Tibet plague focus area  were pneumonic plague in herders.  All three arrived at the medical center too late for effective antibiotic treatment and died (Li et al, 2016). Chinese authorities believe that two of these men may have contracted plague from infected dogs and the third directly from a marmot (Lie et al, 2016).

Dog transmitted plague seems to usually result in family or small settlement size outbreaks. I do wonder about the potential role of dogs in the Bronze Age cases of plague (Rasmussen et al, 2015). Dogs contracting plague by consumption of infected rodents and passing it on to human contacts seems possible with the tools of the Bronze Age strains. It might also be worth investigating the potential role of dogs in the beginning of the Great Manchurian Plague of 1910-1911, which focused on hunters who likely used dogs extensively. Indeed hunters in this region would feed sick marmots to their dogs believing that they could not contract the disease. Outbreaks of 100% lethal plague were not unknown among hunting families in Manchuria (Summers 2012: 122-124). Such a high mortality rate would suggest pneumonic plague.


Archibald, W. S., & Kunitz, S. J. (1971). Detection of plague by testing serums of dogs on the Navajo Reservation. HSMHA Health Reports.

Esamaeili, S., Azadmanesh, K., Naddaf, S. R., Rajerison, M., Carniel, E., & Mostafavi, E. (2013). Serologic Survey of Plague in Animals, Western Iran. Emerging Infectious Diseases, 19(9).

Gage, K. L., Montenieri, J. A., & Thomas, R. E. (1994). The role of predators in the ecology, epidemiology, and surveillance of plague in the United States, 20.Proceedings of the 16th Vertebrate. Pest Conference (W.S. Halverson& A.C. Crabb, Eds.) Published at Univ. of Calif., Davis. 1994.

Ge P, Xi J, Ding J, Jin F, Zhang H, Guo L, Zhang J, Li J, Gan Z, Wu B, Liang J, Wang X, Wang X, Primary Case of Pneumonic Plague in Marmata himalayana natural focus area Gansu Province, China, International Journal of Infectious Diseases (2014),

Gould, L. H., Pape, J., Ettestad, P., Griffith, K. S., & Mead, P. S. (2008). Dog-Associated Risk Factors for Human Plague. Zoonoses and Public Health, 55(0), 448–454.

Li, Y., Li, D, Shao, H., Li, H and Han, Y. (2016) Plague in China 2014 — All sporadic case report of pneumonic plague. BMC Infectious Disease. 16: 85.

Lin, Karen. (2014-07-02) Photo: Himalaya marmot eaten by wild dogs in N. Tibet. China Tibet Online.

Nichols, M. C., Ettestad, P. J., Vinhatton, E. S., Melman, S. D., Onischuk, L., Pierce, E. A., & Aragon, A. S. (2014). Yersinia pestis infection in dogs: 62 cases (2003-2011). Journal of the American Veterinary Medical Association, 244(10), 1176–1180. doi:10.2460/javma.244.10.1176

Rasmussen, S., Allentoft, M. E., Nielsen, K., Orlando, L., Sikora, M., Sjögren, K.-G., et al. (2015). Early Divergent Strains of Yersinia pestis in Eurasia 5,000 Years Ago. Cell, 163(3), 571–582. [Bronze Age cases]

Runfola, J. K., House, J., Miller, L., Coltron, L., Hite, D., Hawley, A., et al. (2015). Outbreak of Human Pneumonic Plague with Dog-to-Human and Possible Human-to-Human Transmission — Colorado, June–July 2014. MMWR. Morbidity and Mortality Weekly Report, 64(16), 429–434.

Salkeld, D. J., & Stapp, P. (2006). Seroprevalence Rates and Transmission of Plague (Yersinia pestis) in Mammalian Carnivores. Vector-Borne and Zoonotic Diseases, 6(3), 231–239.

Summers, William C. (2012) The Great Manchurian Plague of 1910-1911: The Geopolitics of an Epidemic Disease. Yale University Press.

Wang, H., Cui, Y., Wang, Z., Wang, X., Guo, Z., Yan, Y., et al. (2015). A Dog-Associated Primary Pneumonic Plague in Qinghai Province, China. Clinical Infectious Diseases, 52(2), 185–190. doi:10.1093/cid/ciq107

Wang, X., Liang, J., Xi, J., Yang, J., Wang, M., Tian, K., et al. (2014). Canis lupus familiaris involved in the transmission of pathogenic Yersinia spp. in China. Veterinary Microbiology, 172(1-2), 339–344. doi:10.1016/j.vetmic.2014.04.015

Grandes Chroniques de France The Death of Saint Louis.

The Schistosoma in the Reliquary

The 800th anniversary of the birth of Saint Louis, King of France, in 2014 provided an opportunity to obtain a sample of his relics for “scientific identification”. With all relics the chain of custody and its backstory are critical for evaluation. Most of Louis’ relics held in the Basilica of Saint-Denis  were destroyed during the religious violence of  sixteenth century Paris. Fortunately the process of preserving and transferring Louis home to France from the site of death on crusade in Tunis, North Africa left bits of him in several locations.  Part of the preservation process used at the time removed his intestines and other internal organs to be embalmed separately while the remainder of the body was boiled to clean the bones to return to Paris. The bones were enshrined in Paris, while the heart and some viscera were enshrined at the abbey of Monreale near Palermo by his brother Charles, King of Sicily, who oversaw the preparation of the body and its transport back to France.

13th century Reliquary of Saint Louis, Basicilla of St. Dominic, Bologna Italy. (Source: Photo of Georges Jansoone, public domain on Wikipedia)

During a stop over at Bologna en route to Lyon and then Paris, some of his viscera were removed and interned in the Basilica of Saint Dominic. In 1297 Louis, who had died on 25 August 1270, was officially canonized as Saint Louis of France.  A portion of these visceral relics were given for the consecration of the cathedral of Turin in 1895, and these were transferred to the cathedral of Versailles in 1985. It is from this visceral relic that the 2 g specimen was obtained for scientific evaluation.

Microscopic Examination

The plan is to do a full “medical and forensic anthropological analysis” of the remains. The first result released by Phillipe Charlier’s team is the discovery of a semicircular parasite viewed by Scanning Electron Microscope (SEM) analysis, identified as a male Schistosoma based on its size and morphology.  Schistomsoma are a sexually dimorphic flat worm, also known as a blood fluke, that inhabit the capillaries of the abdomen (mesentery or bladder plexus depending on species) and release their eggs into either feces or urine. The eggs hatch in fresh water and must pass through a fresh water snail before emerging as larvae that can inhabit a mammalian host. Only about 50% of the eggs produced actually exit the body.  The adult worms and eggs that do not reach the feces or urine can cause extensive inflammation resulting in granulomas and fibrosis (scar tissue) to the abdominal organs (liver, spleen, intestines, bladder) and the blood vessels of the abdomen causing an accumulation of fluid in the peritoneal cavity.  Eggs that do breach into the lumen of the intestine cause chronic blood loss into the lumen producing chronic bloody stools. In the worst cases the blood loss can cause anemia.

Saint Louis
Source: Charlier, Bouchet, Weil & Bonnet, 2015.

Compare to a SEM preparation of a modern (non-mummified) male Schistosoma:

A C-shaped male schistosoma; the smaller female resides in the canal. (Source: David Williams, Illinois State University made public domain, Wikipedia)

King Louis had not been in Tunis long enough for him to contracted schistosomiasis upon his arrival only a month before his death. When and where he contracted the flat worm infestation is open to more speculation.  Schistosoma have been observed in archaeological remains of one individual from 9th century France, but have not yet been commonly observed. Charlier et al. (2015) suggest that Louis’ previous crusade in North Africa between 1250 and 1254, spending some time imprisoned in Damietta, Egypt, is the most likely period for start of the infection. If this is true, then Louis would have had a chronic infection for about 20 years at the time of his death. Charlier’s team do not believe that Schistosomiasis contributed to his death.

So far they have not observed any other parasites in the sample. This is not necessarily surprising considering that they have not yet identified the anatomic source of the specimen. It is not possible to even guess at the anatomic source from the crumbling, blackened specimen pictured in their study (fig. 1). Their analysis is continuing.

Debating Saint Louis’ Cause of Death

As soon as the schistosoma report was published, the debate on the cause of Louis’ death began in the letters of Forensic Science, Medicine and Pathology (where the report was published). So lets begin with the best account of Louis’ death, and go from there.

Beyond skirmishing and entrenching the camp nothing was done, as King Louis was awaiting the arrival of his brother Charles of Anjou (now King of Sicily). Whilst they were waiting encamped, John Tristan fell sick, and died on board one of the ships on August 3rd. A few days later the Legate also died and many other persons, some of fever, some of dysentery. Philip, the King’s eldest son, fell sick with fever; and the King was taken with dysentery (the complaint to which he nearly succumbed in his first Crusade) and died on August 25th. (Guillaume de Nangis account in the Memoirs of Lord Joinville, Book 4, Ch. 4)

Strangely, the plague has traditionally been claimed as Louis’ cause of death. This is completely unfounded since the Black Death will not bring epidemic Yersinia pestis back to the Mediterranean for another 77 years! There is nothing in the account above to suggest plague. This has rightly been dismissed as Louis’ cause of death.

Eric Faure wrote a letter arguing that malaria was a possible cause based on reports of Louis’ history of tertian fevers dating back to the 1242. Faure suggests that Louis went on his first crusade in thanksgiving for surviving “cerebral malaria with a coma” after a relapse in 1244. Cerebral malaria is usually caused by Plasmodium falciparum, which is not a chronic (relapse causing) infection. If Louis suffered relapses of malaria contracted in France then it was most likely Plasmodium vivax, which rarely causes cerebral malaria. Whether or not Louis had cerebral malaria in the 1240s, this doesn’t really inform of his his health in 1270.  Faure also notes that some of the men on Louis’ last crusade had intermittent fevers suggestive of malaria. Faure reaches too far suggesting that the dysentery was a symptom of malaria. Gastrointestinal symptoms are possible but rare in malaria and usually then in children. Philippe Charlier responded with a letter dismissing Faure’s suggestion to look for Plasmodium in the remains, because they would not have caused Louis’ death. Following the report in Lord Joinville’s memoir (quoted above), Charlier reports in his letter that his team is now looking for evidence of bacteria, viruses or amoeba in the embalmed “intestines” that are more likely to be the cause of the “dysenteric syndrome” reported in “Louis and his court”.

I will be watching for the final report, but the idea of a single enteric pathogen being the cause of death may not really represent reality. Based on Joinville’s memoir is appears that the “court” was suffering from a variety of camp diseases found in most medieval armies on prolonged campaigns. In such a situation, co-infection is highly likely particularly with chronic parasites. Indeed, Louis was probably not the only one in camp with schistosomiasis lingering from previous travels.  Although I doubt malaria caused Louis’ dysentery, it is quite possible he was suffering from chronic malaria and that it contributed to weakening his health, making him more susceptible to other pathogens. Indeed co-infection with Schistosoma and Plasmosdium could have made him quite anemic.  It would still be worth knowing if Louis had an active malaria infection, even if Shigella or another enteric pathogen was the primary cause of death.


Charlier, P., Bouchet, F., Weil, R., & Bonnet, B. (Oct. 2015). Schistosomiasis in the mummified viscera of Saint-Louis (1270 AD). Forensic Science, Medicine, and Pathology, 1–2.

Faure, E. (Dec. 2015). The infections of Saint-Louis: possible involvement of malaria.[Letter]  Forensic Science, Medicine, and Pathology, 1–1.

Charlier, P. (2016). Neither plague nor malaria, but dysentery as a cause of death for St. Louis. [Letter]  Forensic Science, Medicine, and Pathology, 1–1.

The Memoirs of Lord Joinvilletranslated by Ethel Wedgwood, E-text. University of Virginia library

Louis IV of France, Wikipedia.

WHO fact sheet: Schistosomiasis

Schistosoma, Wikipedia

Michael Walsh, Schistosomiasis on the Infection Landscapes blog. See this page for the best description of the medical effects of schistosomiasis.