Category Archives: Zoonosis

Human Parasites of the Roman Empire

Last week photos of Roman toilets were splashed across the web breaking the news that the Romans were not a healthy as most people seem to have assumed. As with many public health interventions, the real value of a sanitation system is out of view (and out of mind) to most people. Its not the toilet that keeps us healthy; its the water treatment plant. Plumbing just moves waste with its microbes and parasites from one place to another.

Paleoparasitology specialist Piers Mitchell put the Roman public health system to the test by evaluating the evidence for human parasites in archaeological remains from before, during and after the Roman Empire. Comparisons before and after the empire are more difficult in North Africa and the Middle East because these areas had long standing sophisticated civilizations before the Roman empire. There is more clarity between civilizations in Europe since Celtic and Germanic societies did not have anything like Roman infrastructure. Contrary to his expectations, there were just as many parasites and ectoparasites in the Roman era as before or after.  In some cases the empire helped spread parasites across Europe. Relative amounts of parasites across times is difficult to ascertain for a huge variety of reasons. So while the same parasites were present, the degree of infestation would have varied by place and time period, and archaeology can’t reliably predict this.

The Roman achilles’ heel was their use of human waste for fertilizer and fecal contamination of rivers.  Human waste was added to the other manure and redistributed to farm fields and the watershed. What they could not have understood is that human waste is a greater risk for the transmission of human parasites and bacterial diseases. Mitchell also suggests that Roman bath water, that was rarely changed, could have transmitted worm eggs and other parasites. Aquaducts did bring in cleaner water to some of the larger cities but the system could be contaminated and not all Roman sites had access to water from aquaducts. Walter Scheidel (2015:8) has claimed that the city of Rome itself was an example of the”urban graveyard” effect with a very unhealthy population despite having a “heavily subsidized food and water supply”. Scheidel emphasizes the impact of malaria and gastrointestinal disease. We should also keep in mind that a large proportion of gastrointestinal disease would have been bacterial or viral.

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Second century Roman mosaic of foodstuffs

As the mosaic to the left shows, the Romans did change agriculture throughout the empire. They spread Mediterranean preferences for cereals and more fish and other aquatic food sources. Mitchell suggests that the Roman love for fish products, especially the fermented fish sauce garum, probably help spread fish tapeworms found throughout the empire. Many parasites and bacterial spores have evolved to withstand preserving methods like smoking, pickling, and osmotic preservation (like salting or sugaring).  Whipworm was the most common parasite found, but round worms and tape worms were also common. Lancet liver flukes were widespread and indicate the (presumably accidental) consumption of ants.  Antibody based detection (ELISA) has been able to identify Entamoeba histolytica that causes the usually endemic amoebic dysentery (as opposed to the epidemic bacterial dysentery caused by Shigella species). Although not strictly speaking parasites, Mitchell notes an abundance of evidence for flies around cesspits suggesting that they contributed to the spread of diseases associated with fecal contamination. He also notes that schistosomiasis has not been identified in Roman Europe, even though it has been found in medieval European remains.

Turning to ectoparasites, Mitchell found ample evidence of head lice, body lice, public lice, human fleas and bed bugs across the Romanized world. Human fleas (pulex irritans) have been particularly well preserved in Roman, Anglo-Scandinavian and medieval York in Britain. Mitchell notes that human fleas and body lice were present in over 50 archaeological layers at York. He concludes that “the Roman habit of washing in public baths does not seem to have decreased their risk of contracting ectoparasites, compared with Viking and Medieval people who did not use public baths in the same way” (Mitchell 2016: 6). Mitchell suggests that there were enough ectoparasites to support particularly lice transmitted diseases. He notes that Plague of Justinian was transmitted by fleas but is non-committal on the likely specific vector.

In examining the impact of the Roman empire, Mitchell notes that the transition from a wide variety of zoonotic parasites to those primarily associated with human fecal contamination had already occurred before the Roman expansion out of Italy. This shift is paralleled elsewhere and is tied to shift from hunter-gathers to settled agriculture. Whipworm, roundworm and amoebic dysentery were the primary parasites of Roman Europe, while the Romans seem to have made a lesser impact on North Africa and the Middle East where endemic zones of parasites were well established.

Malaria is the one parasitic disease I would have liked to see Mitchell discuss more. Mitchell notes that malarial aDNA has been found in Egypt and anemia possibly caused by malaria in Italy. He overlooks all the malaria work by Robert Sallares including malarial aDNA from Late Roman Italy and better anemia studies correlating with malaria have been done in Italy and Britain by Rebecca Gowland’s group. Yet, malaria is such a big topic that it would be hard to cover along with all the other parasites.

References:

Mitchell, P. D. (2016). Human parasites in the Roman World: health consequences of conquering an empire. Parasitology, 1–11. http://doi.org/10.1017/S0031182015001651

Scheidel, W. (2015). Death and the City: Ancient Rome and Beyond. Available at SSRN 2609651.

See also:

Hall, A., & Kenward, H. (2015). Sewers, Cesspits, and middens: a survey of the evidence of 2000 years of waste disposal in York, UK. In P. D. Mitchell (Ed.), Sanitation, latrines and intestinal parasites in past populations (pp. 99–120).

Summer reading

 

summer 2

The summer is officially over this week so its time for my quarterly reading update. I read a more eclectic mix of topics this summer than usual. These are just those that really stood out as being useful for my purposes. I hope you find something of interest!

Books

  • Gregory Aldrete. Floods of the Tiber in Ancient Rome. 2006.
  • Robert Sallares, Malaria and Rome: A History of Malaria in Ancient Italy, 2002
  • Nukhet Varlik. Plague and Empire in the Early Modern Mediterranean: The Ottoman Experience 1347-1600. Cambridge UP, 2015
MA Thesis

Katharine Dean. Modeling plague transmission in Medieval European cities. (2015, June 1). MA Thesis.  Oslo.

Papers

  • Kimura, H., Saitoh, M., Kobayashi, M., Ishii, H., Saraya, T., Kurai, D., et al. (2015). Molecular evolution of haemagglutinin (H) gene in measles virus. Scientific Reports, 1–10. doi:10.1038/srep11648
  • Scheidel, W. (2015). Death and the City: Ancient Rome and Beyond. Available at SSRN 2609651.
  • Smith-Guzmán, N. E. (2015). The skeletal manifestation of malaria: An epidemiological approach using documented skeletal collections. American Journal of Physical Anthropology, n/a–n/a. http://doi.org/10.1002/ajpa.22819
  • Sigl, M., Winstrup, M., McConnell, J. R., Welten, K. C., Plunkett, G., Ludlow, F., et al. (2015). Timing and climate forcing of volcanic eruptions for the past 2,500 years. Nature. http://doi.org/10.1038/nature14565

  • Kostick, C., & Ludlow, F. (2015). The dating of volcanic events and their impact upon European society, 400-800 CE (Vol. 5, pp. 7–30). Post-Classical Archaeologies.

  • Schats, R. (2015). Malaise and mosquitos: osteoarchaeological evidence for malaria in the medieval Netherlands. Analecta Praehistoricaleidensia, 45, 133–140.
  • Eisen, R. J., Dennis, D. T., & Gage, K. L. (2015). The Role of Early-Phase Transmission in the Spread of Yersinia pestis. Journal of Medical Entomology, tjv128–10. http://doi.org/10.1093/jme/tjv128

Ebola’s Chain of Infection

Chain of Infection A chain of infection is a method for organizing the basic information needed to respond to an epidemic.  I’ve gathered the best information I’ve been able to find. As the current epidemic is analyzed, there is no doubt some of the recommendations and basic knowledge will change.

The Ebola Virus (EBOV)

img8The Ebola virus is a Filovirus, an enveloped RNA virus containing only eight genes. Three of the five ebola virus species are highly pathogenic to humans: Zaire ebolavirus (Case fatality rate (CFR) 70-90%), Sudan ebolavirus (CFR ~50%) and Bundibugyo ebolavirus (CFR 25%). The 2014 epidemic is caused by the  Zaire ebolavirus.

Ebola attaches to the host cell via glycoproteins that trigger absorption of the virus. Once inside the cell it uncoats and begins replicating the eight negative sense RNA genes (seven structural genes and one non-structural gene). It initially targets immune cells that respond to the site of infection; monocytes/macrophages carry it to lymph nodes and then the liver and spleen. It then spreads throughout the body producing a cytotoxic effect in all infected cells. Death occurs an average of 6-16 days after the onset of symptoms from multi-organ failure and hypotensive shock.

Symptoms present 2-21 days after infection and the patient is contagious from the onset of symptoms.  Symptoms include a fever, fatigue, headache, nausea and vomiting, abdominal pain, diarrhea, coughing, focal hemorrhaging of the skin and mucus membranes, skin rashes and disseminated intravascular coagulation (DIC). In the 2014 epidemic, abnormal bleeding has only occurred in 18% of cases and late in the disease process.

The Reservoir

Fruit bats in Africa are believed to be the primary reservoir. Transmission between bats and other animals is poorly understood.

ebola_ecology_800px

Portal of Exit

Ebola leaves its reservoir by contact with body fluids of an infected animal, often by bushmeat hunters. The spill-over is usually very small with the vast majority of human cases being caused by human to human transmission.

Transmission 

Transmission between humans occurs by contact of skin or mucus membranes with the body fluids of an infected person. Viral particles are found in all body fluids: blood, tears, saliva, sputum, breast milk,  diarrhea, vomit, urine, sweat and oil glands of the skin, and semen. Ebola can be found in semen three months after recovery from an infection but transmission by this route is poorly understood. Viral particles are found in other body fluids for 15 days or less after the onset of symptoms. It lasts the longest in convalescent semen and breast milk. All fluids from dead bodies are highly infectious.

All materials touched by the infected person, body fluids, medical waste, and used PPE must be discarded and destroyed as infectious medical waste. Non-disposable items like rubber boots, furniture, and building structures must be professionally decontaminated.

Ebola virus is a Biosafety Level 4 pathogen and a category A bioterrorism agent along with other viral hemorrhagic fevers.

Portal of Entry

Ebola enters the human body through breaks in the skin, including micro-abrasions and splashes on mucus membranes. Personal protective equipment (PPE) includes full body coverage including hood, mask or face shield, a tight fitting respirator, boots or shoe coverings, and double gloving. A buddy system should be used for dressing and disrobing. Removing PPE is a point of frequent contamination and should be done with help from another robed person.

Vulnerable populations

The most vulnerable populations for ebola are defined by their occupation. Care givers in medical facilities are at the highest risk because the viral titers reach the highest levels in fatal cases shortly before death. Mortuary and burial workers are also at high risk. The infectiousness of the bodies means that the usual burial practices can not be done in any setting or country. Home caregivers and decontamination workers would also be at a higher risk.

Information is lacking on survival vulnerabilities such as age, gender, pregnancy, or pre-existing conditions. More information on these aspects should be available in the post-epidemic analysis of the current epidemic.

 

References and further reading:

Martines, R. B., Ng, D. L., Greer, P. W., Rollin, P. E., & Zaki, S. R. (2014). Tissue and cellular tropism, pathology and pathogenesis of Ebola and Marburg Viruses. The Journal of Pathology, n/a–n/a. doi:10.1002/path.4456 [in press]

Chowell, G., & Nishiura, H. (2014). Transmission dynamics and control of Ebola virus disease (EVD): a review. BMC Medicine, 12(1), 196. doi:10.1186/s12916-014-0196-0

Toner, E., Adalja, A., & Inglesby, T. (2014). A Primer on Ebola for Clinicians. Disaster Medicine and Public Health Preparedness, 1–5. doi:10.1017/dmp.2014.115

Bausch, D. G., Towner, J. S., Dowell, S. F., Kaducu, F., Lukwiya, M., Sanchez, A., et al. (2007). Assessment of the Risk of Ebola Virus Transmission from Bodily Fluids and Fomites. Journal of Infectious Diseases, 196(s2), S142–S147. doi:10.1086/520545

CDC: Ebola Virus Disease portal