Posts Tagged 'disease'

Curious case of armadillo leprosy


Texans love all things armadillo. It is the state animal and Texas has become somewhat of a haven for hunting the small creature. In Louisiana and Texas, people hunt, skin and eat armadillos. Nothing exemplifies this all-things-armadillo attitude quite like the fact that barbecued armadillo and armadillo chili are popular delicacies in Texas. During the Great Depression Texans went as far as to stock their pantries with armadillos.

Every year, a significant number of people in southern United States walk into emergency rooms presenting with lesions of unknown origin. The lesions are quite clearly as a result of leprosy, but with some patients showing no history of foreign exposure (leprosy is not endemic to the United States) how they ended up with leprosy had always been somewhat of a mystery. Leprosy is rare in the United States, with only about 150 new cases reported each year — the majority of affected people lived or worked abroad in leprosy-endemic sub-tropical regions and may have acquired their disease there.

Leprosy is not highly infectious — caused by the slow-growing bacillus, Mycobacterium leprae, and transmitted via droplets from the nose and mouth of infected and untreated patients. It can cause nerve damage, leading to muscle weakness and atrophy, and permanent disabilities when left untreated.

It was in a lab in Baton Rouge, Louisiana that the case was first confirmed. Whole-genome resequencing of the leprosy bacteria from one wild armadillo and three US patients with leprosy revealed that the infective strains were identical. Infected armadillos had been reported across the southern United States, in Alabama, Arkansas, Louisiana, Mississippi, Texas, and Mexico, with several case reports have suggested that armadillos may be a source of the bacteria. The building body of evidence that these small animals act as a reservoir for the disease.

Even though leprosy is exceptionally rare in the United States, it seems exposure to armadillos in southern states is quite common. Authors publishing in the New England Journal of Medicine show that a single predominant strain is involved in most human and armadillo infections. Transmission is relatively easy, either direct or indirect, involving fomites. Although in this case the authors suppose it occurs most frequently through long-term direct contact with an infected host as the bacteria doesn’t last for long out in the environment.


Historically, leprosy had been hard to study. Very few animal models provided an adequate host for the disease. It grows vigorously in one animal — the armadillo, a fact discovered only in the 1970s at another federal laboratory in Baton Rouge. The nine-banded armadillo, Dasypus novemcinctus, is the only species of armadillo that occurs in North America, wondering north from Central America sometime during the early Pleistocene.

There was a time, before sophisticated experimental techniques, when the bacteria for leprosy couldn’t be cultured. Research, especially research that deals with combating infectious diseases relies heavily on being able to culture the infectious agent in a controlled environment. They tried experimentally to transmit the bacteria to other animals such as mice — but failed. Not being able to produce enough bacteria to be truly useful is always a setback for research. Add that to the fact that mice don’t live very long and human leprosy can be over the course of two decades.

Armadillo leprosy closely resembles the infection in humans — the lesions in its nerves was evidence of the armadillo as a suitable model animal.

Today, it is estimated that a third of the leprosy cases that arise each year in the United States almost certainly result from contact, in one form or another, with infected armadillos. Interspecies transfer of the disease is uncommon and inefficient, but within the armadillo species transmission is efficient.

What is becoming more and more evident is a complex problem — the ever increasing, incrementally advancing scourge of certain tropical diseases towards previously virgin areas, together with the fact that doctors have never seen these sorts of exotic diseases on a regular basis means there is frequent misdiagnosis. And as an estimated 70 percent of new emerging infectious diseases were known to have animal origins, perhaps it’s time to reflect and reframe the question.

The microbe that causes leprosy is a fragile one. It does not grow in laboratory petri dishes, and survives only a week or two in moist soils. Its presence in armadillos predates the fact we use it as a disease model. Ironically, armadillos would have acquired it from humans sometime in the last 400 to 500 years — sometime after colonization of the New World. Now they’re giving it back…

Image — source, source.


The Contagion of Violence…


When Professor Plum killed Dr Black, in the library, with the candlestick it was for no other reason than murder is a disease. Murder is infectious and the contagion of violence is everywhere.

Violence begets violence.Violence within nations and cultures. It occurs within families and between partners. It increases the risk of violence directed at children and increases the risk of the children behaving violently themselves. Violence within a community perpetuates and spreads. Children catch it from their parents, and parents can catch it from their children. Violence is highly contagious in all respects it seems.

It was a 2012 essay by L. Rowell Huesmann that sparked off a study, appearing in Justice Quarterly. A study with a simple premise and question; if homicide is infectious, it should diffuse through communities, infecting those susceptible, and that diffusion should be detectable. Much in the same way we can track the flu from year to year, we can track the spread of murder as an epidemic. It offers an interesting way of looking at murder and homicide.

Welcome to Newark, New Jersey. A city that houses roughly 277,000 people has a homicide and murder rate over three times greater than that of anywhere else in the US. There were 104 murders and 504 shooting victims in 2006 alone. Firearms were used in 71% of the 380 reported murders in 2011. Suffice it to say, Newark is not a safe place.

The study took a look at how murders and homicides moved and behaved over a 26-year period (1982 to 2008) across the city. Firearms and gangs were the infectious agents; spreading from within the centre of the city and spreading south-westerly over the course of nearly three decades.

Their main argument is that the way murders move across a community is not random. The elements required for disease to propagate itself may be relevant and can be applied to the movement of homicide. And if this is so, then it can be predicted and controlled.

If you take a look at a map of Newark it is hard to see a pattern. Homicides occurred in all parts of the city. Almost the entire city appears to be a hot spot for murder. But analysis over the decades suggest that there was expansion of overall homicides between 1982 and 2008 with a dip in 1997 and a sharp rise in 2000. And highlighted an area of the city (North and East) that seemed largely immune to the spread of homicide. Indeed, murder was on the move.

The criminal justice system seeks to prevent murder, but only after the fact — by deterring those that do it with the penalty that awaits them after the fact (jail and criminal prosecution). Indeed, police forces already have an eye out for certain hotspots within a location. Areas where violence is known to spark and ignite at any given moment. What they don’t know is where it will go next. The authors of the study model homicide as an infectious disease as simply a way to offer instructive understanding of how homicide works. The most telling application of this non-literal model is the fact that for homicide to spread as a disease, a population susceptible to transmission must be present. Just like every other infectious agent, except this time poverty and social inequality replace a population with no herd immunity.

Image — source

Zeoli, A., Pizarro, J., Grady, S., & Melde, C. (2012). Homicide as Infectious Disease: Using Public Health Methods to Investigate the Diffusion of Homicide Justice Quarterly, 1-24 DOI: 10.1080/07418825.2012.732100

After Sandy…

Before hurricane Sandy touched down on the east coast of America, it passed through the Caribbean, causing around 80 fatalities — 60 of them occurred in Haiti, 11 in Cuba, two in the Bahamas, two in the Dominican Republic and one in Jamaica.

Hurricane Sandy started life out over central America, nonchalantly, as a collection of winds that would eventually gather momentum, speed and energy. It began its non-discriminating path through the Caribbean, eventually to hit Puerto Rico and the Dominican Republic as well. As it hit Jamaica it was a category 1, destroying around 1500 hectares of farmland. In Cuba the next day it was a category 2, destroying banana, coffee, bean and sugar crops. Sandy destroyed roughly 30% of the nation’s coffee farms. Add to that the 200,000 damaged homes. The Bahamas archipelago was next, before it would set it sights on America’s eastern seaboard.

While most of the focus of western media centred on the damage Sandy caused in America, especially this close to a Presidential election; there were few news outlets that reported what had passed in the Caribbean — outside the death tolls and damaged infrastructure. Indeed, as it is becoming more and more apparent, it is always the blogosphere that provides an adequate source of information. Hurricane Sandy’s progression was followed by bloggers on the ground, giving another side of the story we don’t often get to see.

But it is in Haiti, a country that has yet to recover from tropical storm Isaac that hit in August of this year, as well as the earthquake of 2010, that felt the worst of Sandy’s wrath. 1.8 million people in Haiti are affected by the storm, according to the United Nations relief agency.

With everyone concerned with the numbers, damage, and brute destruction, there is the underlying problem that any disaster hit area has to deal with. Namely, the aftermath. It is the aftermath of the Caribbean region we must now think about. There will be the inevitable worry about food prices from this point on. Huge crop losses in southern Haiti raise famine worries.

Prime Minister Laurent Lamothe, after assessing the damage, said “Most of the agricultural crops that were left from Hurricane Isaac were destroyed during Sandy, so food security will be an issue.”

Three days of constant rain caused rivers to overflow and the floodwaters to rise. Most of southern Haiti is underwater. In the whole Caribbean region rainfall amounts as high as 250 millimeters were measured over eastern Cuba and some extreme southern areas of Hispaniola. Haiti experienced 20 inches. Port-au-Prince receives an average annual rainfall of 54 inches.

As the rains stopped the damage is only made worse to the tune of infectious diseases such as cholera. Haiti has been fighting a cholera epidemic since 2010. A cholera outbreak that has killed over 7400 people and left up to 600 000 sick across the country.

According to the Pan American Health Organization (PAHO) and the WHO, there is an increase in cholera cases in the south and south-east, where 49 cases and 9 deaths have been recorded.

The list of infectious disease outbreaks following natural disasters is long. Although, usually there are some that are more common than others. Diarrheal diseases, acute respiratory infections, malaria, leptospirosis, measles, dengue fever, viral hepatitis, typhoid fever, meningitis, as well as tetanus and cutaneous mucormycosis have all been documented as the incidence and magnitude of natural disasters increase.

Natural disasters and infectious diseases outbreaks represent a significant challenge. But they do not necessarily go hand in hand. Disasters do not transmit infectious diseases. But the risk of infectious disease is multiplied by the change in situation — populations displaced, overcrowding, limited access to food and water, and public health breakdown.

Haiti’s Prime Minister, Laurent Lamothe said “I am launching an appeal to international solidarity to come and help the population, to help support the completion of our efforts towards saving lives and property,”

Flood disasters are the most common natural disasters throughout the world, and diarrheal diseases are the leading cause of death from displaced populations living in camps. France has promised to rebuild seven destroyed bridges and Mexico has offered food. How Haiti deals with the aftermath of Sandy will be one to follow closely.

Image — source, source

Originally appearring in Australian Science

Arya SC, & Agarwal N (2012). Prevention and control of infections after natural disasters. Expert review of anti-infective therapy, 10 (5) PMID: 22702315

Kouadio IK, Aljunid S, Kamigaki T, Hammad K, & Oshitani H (2012). Infectious diseases following natural disasters: prevention and control measures. Expert review of anti-infective therapy, 10 (1), 95-104 PMID: 22149618

Panique au village: the revolution that caused an epidemic…

It boasts, struts, and flaunts with that kind of assurance that only comes from the mentality of knowing that you are right, and that even if you may be wrong, others will admire you for it. This is Paris.

Where other cities flowed and spilled out to occupy a space larger than its originality, Paris said enough is enough and contained itself. To this day only the “arrondissements” count. Anywhere outside “le périphérique” and you are demoted to “les banlieues”, with all the meaning that entails.

And so, with this in mind, we begin our story in 19th century Paris. Paris was suffering under the weight of its own self-importance. With an ever-increasing population, an almighty scourge was about to inflict itself on a population.

In the past, much like in the future, people will give it all up to live in cities. Immigrants from the countryside in search of employment came to Paris in their numbers — only to be met with the other side of urbanity’s progress.

The image of Paris was one only metaphor can convey. Paris was sick. So sick even the bourgeoisie avoided its inner ‘beauty’. By 1832 cholera would firmly appropriate this metaphor.

The story is one we could talk about in statistics. But the story of cholera in Paris in 1832 is one best talked about in revolutions (both scientific and social) and repercussions. The story of cholera in Paris is one that goes hand in hand with the mindset of Paris. The mentality and mindset of an entire city, right from its lofty bourgeoisie to its most lowly inhabitants.

Writers, academics, philosophers and the French societal elites became obsessed with poverty and the poor. We must remember that at this point in time not much was known about disease. Koch and germ theory were a few decades away. Thus poverty and its stench were written about and debated through this lense.

The perfect fictional disease goes something like this: the germ spreads in all directions, no safe place, no cure and no protection. It spreads when the diseased are still symptomless. Quarantine is the only escape — don’t let them in, not even your friend. Some are still in doubt of its existence — the naive will be the next to fall. Some call it forgiveness and some refer to it as God’s vengeance. The poor say the rich have the cure, the rich say the poor are the cause. Retired revolutionaries say it’s nothing more than a psychological war, invented by the press just to sell column inches. The nuns blame the whores and the whores blame the nuns. The scientists are lost without consensus. Some say it only infects the mind… the others say it steals the soul. The hobo on the street corner with the sign that reads “the end is nigh” knew it all along.

Translate that to 19th century Paris, and it ticks a lot of the boxes. Urban decay and a populus in panic. Immigrants were seen as symbols of such an urban decay. Poor and sick, not as a result of disease or poverty, but as a result of the victim’s own wrong doing. It is this mentality we must keep in mind when exploring 19th century Paris.

Then… cholera came to Paris!

Cholera attacked Paris with a discrimination that is hard to believe wasn’t personal — the disease claimed no other life outside of Paris in its early days. Passing through the countryside and with a single jump arriving in the nation’s capital. It first came to France in 1832 from England via Calais. March 15th was the first recorded case. Even with no railways at this time the disease moved remarkably quickly, taking only 11 days to traverse the 260 km to Paris. In March, 90 people died. In April it was 12,733. In 1832 the population of Paris was a meek 785,862 so this was no small portion of the damned and meek.

Like love, a new epidemic disease is most fatal in the first instance. Further epidemics of cholera would not leave as much of an imprint on the city. Due, in part, to the fact that Paris had learned its lesson.

The diseases came to a halt just as quickly and with as much verve as it had started. By July the worst of it was over and deaths were on their way down. Those that had fled the city looking for a safe place began to return. By September it was over. In total 18,402 people perished.

17 years would elapse before cholera yet again returned to Paris, by that time Haussmann had already recreated Paris in a Napoleonic image. The difference being that many districts had been demolished… to make way for light and air and space in the heart of the city. “Les grandes boulevards” being a symbol of this rebirth.

Haussman’s Paris was the much needed tonic for an ailing city. Slums, crammed, without air or light — people and animals living in the putrid flows of waste were now consigned to the history books. The proof was in the numbers — deaths per 100 000 inhabitants decreased at each successive wave of cholera epidemic in the 1800s across Paris.

The revolution that caused a disease

For three glorious days in 1830 there was revolution. The cholera epidemic of 1832 brought Paris right back to those three days. Social unrest as a result of the disease was not uncommon during 1832. Where some commentators saw the cholera epidemic as a direct result of revolution, others saw the two as evidence of an empire in decline.

Cholera and revolution were one and the same. Both hidden in plain sight until it was too late. Both unable to control. Both linked to indulgence and over-excess. Government’s preventive literature of the time distributed to the public about cholera cautioned Parisians to avoid “excesses of any kind.”

As a result, the disease was given a familiar face.

The official government report for the epidemic saw it necessary to look into the relationship between disease and revolt. Could civil unrest really cause or leave a populus more suceptible to disease? Is the fear and panic from political insurrection the same as the fear and panic from disease?

In the end, revolution, they put it, could not cause cholera. But as we have seen elsewhere — cholera can cause revolution.

Originally appearing in Australian Science

Kudlick CJ (1999). Learning from cholera: medical and social responses to the first great Paris epidemic in 1832. Microbes and infection / Institut Pasteur, 1 (12), 1051-7 PMID: 10617936

The clues to human uniqueness…

Over 2 million years ago, before the emergence of the genus Homo, within the rift valleys and savannah grasslands of Africa during the Pliocene period, a unique event took place. One that, with some hyperbole, admittedly, shaped the course of human evolution. The event was on a molecular scale but had its bearings on what we now call and search for as the “human condition”.

Ever since Darwinian evolution gave us an image of our nearest cousins (the chimpanzees, bonobos, gorillas and orangutans of the non-human hominids) we have been constantly searching for what it means to be human — that human condition — for what makes us unique. From an opposable thumb, to the way our brains work, to the simple fact we learnt to cook our food. All of these have been proposed — at one point or another and with various degrees of certitude — as the key to our humanity.

Now the indication lies not so much within us, but with our interaction with disease. In a paper published in the Proceedings of the National Academy of Sciences, researchers are circling in on another hypothesis. The suggestion that inactivation of two specific genes related to the immune system may have conferred selected ancestors of modern humans with improved protection from certain infectious diseases, and also lead to our divergence from our common ancestors.

Dr Ajit Varki and his team study the biology of sialic acids. What they found was that the inactivation of two sialic acid genes played a role in the course of human evolution. Two events at the genomic level that occurred before the emergence of modern humans in Africa.

Infectious pathogens interact with the different types of sialic acids on your cell surface. They are the target for a huge number of pathogens, and successful pathogens have evolved to be able to mimic the sialic acid coat to evade and dampen the human immune system. Look at this in an evolutionary context and what you get is an evolutionary arms race of sorts, with repeated re-invention of the microbes and pathogens that interacted with our ancestors.

Dr Varki and his team describe two sialic acids (Neu5Ac and Neu5Gc) — molecules that differ by a single oxygen atom — one of which was rendered nonfunctional by genetic events during hominin evolution. Across the range of non-human hominids both Neu5Ac and Neu5Gc exist. Uniquely, modern humans do not have Neu5Gc. Today we see the traces of this evolutionary event when we look at the disease-specific differences between humans and the great apes.

There are a large number of disease difference between humans and primates that are not explained by anatomical differences. HIV progression to AIDS is common in humans but very rare in apes, myocardial infarction is common in humans but rare in apes, and humans are susceptible to the malaria parasite P. falciparum whereas apes are resistant.

Falciparum is a recent disease as all the falciparum strains of the world come in one small clade in Africa, evolving from an older strain that had a preference to bind and infect via Neu5Gc. When early hominids evolved to get rid of Neu5Gc and have mainly Neu5Ac (possibly as a result of selective pressure from disease), and perhaps resulting in a potentially malaria-free period in time, until that is falciparum evolved to keep up.

The difference between Neu5Gc and Neu5Ac point to powerful evidence of how infectious diseases have shaped human origin. Researchers make the argument that changes of innate immune defense against invasive human pathogens, particularly those that are involved in neonatal life, would have exerted a powerful selection pressure on the reproductive success of our ancestors.

In a press release Varki noted that it’s probable that humanity’s evolutionary bottleneck was the complex result of multiple, interacting factors. “Speciation is driven by many things,” he said. “We think infectious agents are one of them.”

Image — source

Originally appearing at Australian Science

Wang X, Mitra N, Secundino I, Banda K, Cruz P, Padler-Karavani V, Verhagen A, Reid C, Lari M, Rizzi E, Balsamo C, Corti G, De Bellis G, Longo L, NISC Comparative Sequencing Program, Beggs W, Caramelli D, Tishkoff SA, Hayakawa T, Green ED, Mullikin JC, Nizet V, Bui J, Varki A, & NISC Comparative Sequencing Program Members (2012). Specific inactivation of two immunomodulatory SIGLEC genes during human evolution. Proceedings of the National Academy of Sciences of the United States of America, 109 (25), 9935-40 PMID: 22665810

Varki A (2010). Colloquium paper: uniquely human evolution of sialic acid genetics and biology. Proceedings of the National Academy of Sciences of the United States of America, 107 Suppl 2, 8939-46 PMID: 20445087

What had I twaught…

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