Plague Bacteria: The Condemned Live Longer

18. March 2011

In the 14th Century The Apocalyptic Horseman made a rich harvest: about a third of the population died of the plague. Although since then medical diagnostic and therapeutic progress has been achieved, the bacterium Yersinia pestis is not yet consigned to history.

The World Health Organization presents corresponding figures regularly. Related documented reports talk about the number of cases of the plague being up to 3000 each year, mostly in Africa, Russia, China, India, South and Central America. Only isolated cases are reported from the USA, primarily afffected are the regions Arizona, New Mexico and Utah.

Small bites, big impact

Besides the universally well-known rat, other rodents such as squirrels or prairie dogs represent a natural reservoir of the plague pathogen. Fleas then acquire their bacterial load by biting diseased, wild rodents. If the stomach-intestinal passage is clumped up with Yersinia, (Once the stomach-intestinal passage is clumped up …) the ever-hungry bloodsucker bites again and the next animal is infected. A new finding is that such fleas also use pets as a way station and turn up in the vicinity of settlements with high hygienic standards.

As the climate researcher Nils Stenseth of the University of Oslo found , the living conditions of the blind passengers keep worsening. He analysed weather data from the last 56 years. Due to the increasingly early onset of snow melt in the mountains, according to Stenseth, the humidity in the cave dwellings of rodents is continually dropping. This is a bad deal for the fleas, as they need a certain minimum moisture to survive. If the water content of the air rises due to local climatic events, the number of plague cases soars, as Stenseth vividly demonstrated with Pacific neighbouring states.

Struggle in the body

For an infection, the number of bacteria is critical. Using molecular biological techniques, David Engelthaler and Kenneth L. Gage of the U.S. Department of Health and Human Services were able to show the presence of around 100,000 Yersinia pestis germs in one flea. A few hours or days after a bite occurs in humans, symptoms such as headache, body aches and fever appear. Lumps arise, especially in the lymph nodes and lymph vessels. Once the pathogen has entered the bloodstream, it spreads out to all organs, and reaches the point of becoming a life-threatening sepsis via toxins.

The above-mentioned lumps and pneumonic plague are essentially caused by the same agent, the differences in the final analysis are not yet being understood. Via highly infectious sputum, the lungs of healthy people can be attacked and infected, something which is unlikely with bubonic plague. Unlike influenza viruses, Yersinia are, however, not very stable in the air, according to several studies. There is another macabre characteristic: Since untreated patients die very rapidly – the mortality rate being over 90 percent – large epidemics are unlikely. Considerably more benign is the abortive plague – it clears up after showing mild to moderate symptoms and gives the patient a degree of immunity.

Probe with multiple effects

The flea world and human world are biochemically poles apart. This makes things particularly tricky, so a plague bacterium essentially recognises where it is currently located. Rat fleas are a rather cool type of organism, and at 24 degrees body temperature Yersinia plays a “wait and see” game. The RovA protein serves as a thermometer, researchers at the Helmholtz Centre for Infection Research have found in different Yersinia species. That isn’t all it does; the protein also determines the nutrient and metabolic activity. “The function of RovA in this form is unique to bacteria,” says group leader Petra Dersch. “All the more surprising then was that RovA controls various processes as a thermometer and is self-regulating.” RovA facilitates penetration of the cells. After an infection, the 37 degrees Celsius brings the moment of truth for the bacterium. Since our immune system would recognise its telltale surface proteins rapidly, these are quickly disassembled by the bacteria. The intruder makes itself almost invisible to the immune system.


All the more important is an effective diagnosis. Well-equipped laboratories reveal Yersinia by their distinctive genetic material. Bacteriological identification is also possible. Especially in developing countries, however, there is a need for a quick and simple method. Braunschweig researchers for that reason bonded small magnetic beads onto a specific antibody that binds to surface structures of Yersinia. This reagent is mixed with a plasma sample of the patient on-the-spot. Professor Mahavir Singh of the Helmholtz Centre for Infection Research: “Within a diagnostic device, these complexes couple onto a specially coated surface and become exposed to a magnetic field. A detector then measures not only whether plague proteins are present in the solution, but can also determine their concentration.” The new system should also be deployable in remote areas without well-functioning health infrastructure.

Quick intervention

Because speed wins. Otherwise Yersinia infections are still fatal if medical staff do not recognise it in time. This is no surprise, as the initial symptoms of fever, headache and body pain to be expected with quite a few other diseases. With early diagnosis – and this is the crux – a plague-bacteria infection can with antibiotics be treated well. In such cases tetracyclines, sulfonamides, Streptomycin or Chloramphenicol have proven successful. A protective vaccine is also now available.

Let the dead speak

Looking back: Was Yersinia pestis really responsible for the great epidemics of the Middle Ages? Researchers had occasionally in the past also considered Anthrax or typhoid fever as bringers of evil. A group of anthropologists from Johannes-Gutenberg-Universität Mainz wanted to know precisely. The researchers organised skeletons from assumed plague burials in Germany, Italy, England, France and the Netherlands. Ancient DNA isolated from teeth or bones, together with immunological methods, found the guilty culprit to be Yersinia pestis. And not only that: “Our findings suggest that the plague was imported through at least two channels to Europe and then in each case an individual route was taken,” said Dr. Barbara Bramanti, Department of Anthropology. The surprise was that on the basis of 20 markers, neither the variants “Midevalis” or “Oriental” were discovered. Instead, the researchers tracked down two previously unknown varieties, one of which at least no longer exists. The other genetically matches a variant that was isolated from local plague outbreaks in Asia. With the data it was even possible to reconstruct some propagation paths: Already in 1347 the bacteria migrated from Asia via traditional trade routes to the French Marseille, then on through France to England. In the Netherlands another variant was exposed – which was evidence of an infection route via Norway and northern Germany.

The depicted scenario still has a blemish: The speed at which the epidemic moved through town and country can’t be reconciled with the cause being rats and their blind flea passengers. Vets have calculated a spread radius of up to 20 meters per week, but historical sources have concluded that the range was from 20 to 25 kilometers per week. One possible explanation comes from scientists at the University of Marseille. Didier Raoult, head of the Department of Clinical Microbiology, considers the body louse to be the evil culprit. The organism, after infection, deposits bacteria within its excretions for about two weeks, and so the disease could be transmitted via clothing. Hence it isn’t, according to Raoult, the migration of rats that was crucial to the Black Death. Instead, people themselves would have been responsible for transmission along the travel routes. This is a phenomenon which was at that time as relevant as it is today.

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1 comment:

Wolfram Seidler
Wolfram Seidler

Very interesting article !

#1 |

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