All posts by Michelle Ziegler

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.


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 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

The Paleomicrobiology of Malaria Detection

Malaria is arguably one of the most influential infectious diseases in human history. Its been with us as long as we have been human, but as Teddi Setzer shows us in her recent review of detection methods, our abilities to find it in the past leaves a lot to be desired.

The standard method of looking for malaria involves searching for signs of anemia on the skeleton on the hypothesis that the anemia caused by malaria leaves these marks. This is not as clear as it might seem. There have been very few skeletal studies of modern people who have been diagnosed with malaria. There is no medical need; there are much more reliable methods of diagnosing malaria in a living person (or recent cadaver). So, it is unclear how often these lesions form in malaria patients. Other causes of anemia and even scurvy can cause the same or very similar lesions as well.  The number of malarial infections and/or relapses also effect bone changes. Plasmodium falciparium produces a short, virulent disease that may kill before bone changes develop. On the other extreme, a single P. malariae infection can relapse for life, although the anemia is not as severe.  Osteology must be correlated with other information to support the diagnosis. 

Cribra Orbitalia from Jess Beck’s blog Bone Broke

Cribra orbitalia and porotic hyperostosis are the two main indicators sought. Both are caused by bone marrow expansion in an attempt to compensate for the loss of red blood cells. Cribra orbitalia is pitting and extra bone growth in the orbits of the eyes, as seen in the photo.  Porotic hyperostosis causes pitting and thinning of the compact bone ‘shell’ that covers the cranial bones. A  correlation of nutritionally informed osteology with later epidemiology and mosquito incidence in England reviewed in a previous post shows that a convincing case can be made for malaria in ancient remains.

Detection of human genetic traits selected for by malaria such as the Duffy blood group, sickle cell trait, thalassemias, and glucose-6-phosphatase deficiency (G6PD) can with supporting information suggests that the population was once under selection by malaria. Balanced polymorphisms like sickle cell trait can remain in a population for centuries after the selection is gone (by either ecological change or by migration away from the malarious region). While there are some skeletal indicators of some hemoglobinopathies, human ancient DNA analysis would be a more secure method of diagnosis. Care has to be taken to distinguish skeletal changes made by malaria’s hemolytic anemia and the hemoglobinopathy anemias.

Ancient DNA detection of the malaria Plasmodium parasite has been disappointing. To date, only the tropical Plasmodium falciparium, that causes the most severe disease, has been detected by PCR. It is believed that attempts of detect the historically more common Plasmodium vivax have been stymied by the low parasite load in the blood.  The difficulty in finding vivax aDNA is a reminder that pathogens really do need to be in high concentrations within the sample to overcome degradation and be detected by PCR or sequencing technology. As far as I know, there have not been attempts to detect the other three human malarial parasites– Plasmodium ovale, Plasmodium malariae and Plasmodium knowlesi — by aDNA analysis.

Hemozoin crystals in the liver (Source: KMU Pathology Lab)

Modern medicine is devising an ever expanding array of tests for malaria diagnostics and prognostics. However, most of these tests all require fresh (soft) tissue or blood. Immunological methods have not been applied to malaria in archaeological material yet. The most promising detection method for malaria among the newer diagnostics is the detection of the iron containing waste product of the Plasmodium parasite hemozoin. When the parasite feeds on hemoglobin in the red blood cell, toxic iron waste products are processed into the biocrystal hemozoin and excreted into the tissues. In patients with reoccurring or multiple malaria infections, hemozoin will stain their bone marrow black and can be found in liver, spleen, brain and lungs. It can be detected microscopically (as seen above) or by mass spectrometer. Although some other blood parasites also excrete hemozoin, they can be distinguished from the malarial product. 

Despite the advances in diagnosis for existing malaria patients taking advantage of new methods and technologies, archaeological detection has not enjoyed the same success. Building a case for malaria in the past, must rely on an array of data with knowledge of ecology, vectors, and nutritional status of the population in addition to osteological markers of anemia. Hopefully, the detection of hemozoin will eventually be the key to opening up biological studies of malaria in the past. If hemozoin can identify malaria victims, then perhaps focusing the ancient DNA work on hemozoin positive remains will be more successful breaking through the firewall to malaria’s evolution and historical epidemiology. 


Setzer, T. J. (2014). Malaria detection in the field of paleopathology: A meta-analysis of the state of the art. Acta Tropica, 140, 97–104. doi:10.1016/j.actatropica.2014.08.010 (open access early editionfinal edition)

See also Jess Brek “Porotic Hyperostosis and Cribra OrbitaliaBone Broke, March 2014. 

Illustrations of the 1896-1897 Influenza Epidemic in Paris

1890 Influenza cartoon (Source: National Library of Medicine)
1897 Influenza cartoon (Source: National Library of Medicine)

This image has been used here at Contagions in various cropped versions as the header and avatar for several years now. I found a couple more related illustrations that are worth sharing and put the illustration in better context. This is an emergency tent hospital erected to handle the epidemic of 1897.  It certainly looks different from the outside as you can see below.

Source: National Library of Medicine
Source: National Library of Medicine

Based on the date of this newspaper header (12 Jan 1897), this must be illustrations of a lesser known epidemic in 1896-1897 that occurred between the pandemic of 1890 (Russian flu) and that of 1900.

Another view of the scene in the usual header here.

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