Category Archives: microbiology

Yersinia pestis found in human fleas, Madagascar 2013

Madagascar is consistently one of the top two countries in Africa (and usually the world) in cases of plague, caused by Yersinia pestis. For five years prior to January 2013, Madagascar registered 312 to 648 cases per year, with a majority being laboratory confirmed of which >80% were bubonic plague. Of the multiple reservoir species in Madagascar, the black rat (Rattus rattus) is the primary reservoir with Xenopsylla choepus being the main urban vector and Synopsyllus fonquerniei in rural areas.

After a nine case bubonic outbreak in the rural area of Soavina in the district of Ambatofinandrana (shown below), fleas were collected within and outside of five houses over three nights.


The team from the Institut Pasteur de Madagascar collected 319 fleas representing five genera; the most common being the human flea Pulex irritans (73.3%).  In this study, X. cheopis and S. fonquerniei were only collected outside of the houses. Pulex irritans was found only indoors where it made up 95.5% of flea species. Of the 274 fleas tested for Yersinia pestis, 9 pulex irritans were positive. These positive human fleas came from three homes, one of which had a confirmed case of human plague. None of the other flea species tested positive for plague.

Previous observations of pulex irritans in Madagascar suggest this flea may be responsible for domestic human-to-human transmission. High densities of human fleas were reported in plague outbreak villages in 2012-2013. Flea surveys on rats in Madagascar conducted over the last three quarters of a century show that pulex irritans are very rare on rats, suggesting it is not transmitting plague from rats to humans at least in Madagascar. Although pulex irritans are commonly called the human flea, they will feed on dogs and pigs  in addition to humans.  They have also been sporadically found on a variety of other mammals and birds, including rats.

Coping with human fleas as plague vectors will be a significant extra burden on the public health services of Madagascar. Ridding homes of human fleas can be a difficult task. It will however give plague researchers an opportunity to study pulex irritans as a vector in one of the top human plague producing countries in the world.

Within the last ten years, Madagascar has produced human plague cases from three different fleas and pneumonic transmission. With its diversity of plague reservoirs and now flea vectors, Madagascar is illustrating how deeply Yersinia pestis can penetrate and become entrenched in the environment.

Reference:

Ratovonjato J, Rajerison M, Rahelinirina S, Boyer S. “Yersinia pestis in Pulex irritans fleas during plague outbreak, Madagascar” [letter]. Emerging Infectious Disease. 2014 Aug [30 June 2014].http://dx.doi.org/10.3201/eid2008.130629

Wyrwa, J. 2011. “Pulex irritans” (On-line), Animal Diversity Web. Accessed July 01, 2014 at http://animaldiversity.ummz.umich.edu/accounts/Pulex_irritans/

What do you really want to know about the past?

Michelle Ziegler:

A post from my medieval history blog. I’d like to hear what Contagions readers think as well.

Originally posted on Heavenfield:

When you think about the past, what do you really want to know? Do you want to know what people thought and felt, their philosophy or understand their spin? Or, do you really want to know what really happened? What was their world really like, not what they said it was like? Sure we are all a little curious about both, but when push comes to shove, what do you want to know the most? Where will you invest your time?  These are really two very different approaches. I’ll soon be reviewing two books here that both look at nature in the Middle Ages and take opposite approaches.

The best example I have found of these diametrically opposed approaches is on medieval epidemics. Some historians will argue that it doesn’t matter what the disease was, all that matters is its demographic effect. Scientists will argue that you can’t really know…

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The Spotty History of Chicken Pox

For its extreme antiquity the virus that causes chicken pox, it has a surprising sparse documented history.  The earliest clear reference to the virus is actually to an emergence of its latent form as shingles, also called zoster. The ancient Greeks called it zoster after word for girdle, while shingles comes from the latin word cingulus (belt) both referring to the most common site of emergence along peripheral nerves of the back that wrap around the abdomen. There are many theories, but as far as I know, no one has successfully explained how it got the name chicken pox. It was not until histological and immunological investigations in the early twentieth century that the relationship between the primary phase infection, chicken pox (varicella), and the emergence of the latent virus as shingles (zoster) was confirmed.

Into the 18th century, chicken pox and smallpox were commonly confused as a severe and mild form of the same disease. There are subtle differences between the rashes than can distinguish them. Chicken pox produces watery pustules that concentrate on the head and trunk of the body, while smallpox lesions become hard and dimpled and are concentrated on the appendages.  Chicken pox lesions are sparse or absent from the palms of the hands and soles of the feet, while these areas are often heavily covered by smallpox lesions. But, both diseases can cause lesions anywhere in the body including internal cavities and both can leave deep scars.

Chicken Pox 1

They are also, of course, distinguished by their mortality rates. Smallpox has a mortality rate of around 30%, while chicken pox  has a mortality rate of less than 1%. However, pregnant women and immune compromised patients are at high risk for life threatening complications from chicken pox. The blisters can also develop secondary bacterial infections that can become life threatening. Unlike chicken pox, smallpox requires a constant supply of non-immune hosts to persist in a community.

 

Viral Lifecycle

The lifecycle of the varicella virus is ideal to persist in small communities over many generations without outside introduction. It is primarily transmitted as a respiratory virus, but it can also be transmitted by contact with fluid from the blisters. Both routes are critical. Respiratory transmission allows it to spread rapidly while contact with blisters transmission allows it to persist in the community (more on this below).

As the virus enters the body it replicates for 10 to 21 days before the chicken pox rash of virus filled blisters appears. Meanwhile, some of the virons are infecting the peripheral nerves where the virus becomes dormant (latent). A couple days before the rash appears people feel unwell with fatigue, headache and potentially a fever, and they become contagious by coughing or sneezing. By spreading the virus before the rash appears, they spread the virus far and wide before the disease is recognized and isolated. The blisters usually appear first on the scalp and on the trunk of the body with the number of blisters increasing with increasing age of the person. Young children can have as few as a dozen or less, while adults can have thousands of blisters. Over one to two weeks,  the immune system gains the upper hand and the pustules scab over. Once the rash is scabbed over, the person is no longer contagious. The length of time it takes for the rash to stop depends completely on the strength of the immune system.

The virus can remain dormant in the peripheral nerves for 50 years or more emerging when either the peripheral nerves become inflamed (often by injury) or immune suppression develops. It reemerges as shingles (zoster), a highly painful, high density group of blisters that break out along the line of the peripheral nerve they come from, usually spinal peripheral nerves. It will looks something like a whip mark of blisters wrapping around the body from the back to the front. Fluid from these blisters can cause chicken pox in non-immune people. This is a generational persistence strategy. In small communities, the virus persists by being transmitted from an elder’s shingles to children born after the last epidemic.

life long immunity usually follows recovery from chicken pox.  Young children who only have a few lesions in their first infection can contract chicken pox a second time. It is also possible for vaccinated people to develop a usually mild case of chicken pox. In the United States vaccine acceptance is high enough that many people under age 25 have never seen a case of chicken pox. There is little doubt that if vaccination coverage wains, chicken pox will quickly become endemic again.

Origins and Evolution

The ancestral  Varicella-Zoster Virus (VZV), that causes chicken pox and shingles, co-evolved with apes, hominids and humans. Along with VZV, its closest alphaherpesvirus relatives herpes simplex 1 (HSV1, ‘cold sores’) and herpes simplex 2 (HSV2, genital herpes) have a common ancestor that is approximately 120 million years old. If the age estimates for the herpes phylogenetic tree are accurate, the evolution of the alphaherpesviruses  (VZV, HSV1, HSV2) coincides with the split of Africa from the supercontinent Godwanaland.

VZV has the ideal lifecycle to persist in small, isolated groups of humans, allowing to easily survive through all three human epidemiological transitions. Latency and re-emergence in elders allowed the virus to survive in small hunter-gatherer groups, and continues to remain an advantage today. This process was observed in action on the small mid-Atlantic island of Tristan de Cunha where the population of about 200 people only experienced chicken pox outbreaks after an elder first exhibited shingles (Grose, 2012).

Phylogeny of VSV supports its origin in Africa before humans left the continent and subsequent spread through the world. Regionalism has likely occurred because VZV viruses undergo few replications per infection before they become latent so there is little chance for mutation or recombination between the clades (though it does occur).  Once many more sequences are available correlations between VZV evolution and human migration should become more clear.

The history of the chicken pox virus still has a long way to go. As a DNA virus, it is possible that it may be found in ancient DNA but as a virus with a low mortality rate, it will be extremely difficult to find specimens with a high enough viral copy number to detect. Those rare mummies found with pox scars should be tested for both the smallpox virus and varicella-zoster virus. Regardless we must be careful distinguishing smallpox and chicken pox in the historic record.

 

References:

Grose, C. (2012). Pangaea and the Out-of-Africa Model of Varicella-Zoster Virus Evolution and Phylogeography. Journal of Virology, 86(18), 9558–9565. doi:10.1128/JVI.00357-12

Schmidt-Chanasit, J., & Sauerbrei, A. (2011). Evolution and world-wide distribution of varicella–zoster virus clades. Infection, Genetics and Evolution, 11(1), 1–10. doi:10.1016/j.meegid.2010.08.014

Wood, M. J. (2000). History of Varicella Zoster Virus. Herpes : the Journal of the IHMF, 7(3), 60–65.

Centers for Disease Control and Prevention (CDC): Chicken Pox (Varicella) Information portal. Last updated February 26, 2014.

CDC, Varicella: People at High Risk for complications. Nov. 16, 2011.

Conger, Cristen.  “How Chicken Pox Works”  11 March 2008.  HowStuffWorks.com. <http://health.howstuffworks.com/skin-care/problems/medical/chicken-pox.htm&gt;  24 May 2014.