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Livestock bacteria are as old as the livestock they kill


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Aurochs were the ancestors of domestic cattle. Photo Marcus Sümnick

Animals were wilder then. Horns were longer, temperaments fiercer. These wild things had forever been free when humans took control of their flocks and herds, 10.000 years ago. Through careful breeding and rearing, the first pastoralists of the Near East moulded the beasts into more docile versions of their former selves. Over time, Bezoar became goat and auroch became cow. But it weren’t just the beasts that changed. Somewhere deep inside their lungs, invisible to the human eye, a wild bacterium became livestock disease.

Meet Mycoplasma mycoides. This bacterium has left a long and bloody trail through livestock history. Virulent strains of Mycoplasma raged around the world in the 19th century, killing millions of goats and cows. But the roots of Mycoplasma mycoides run deeper. In their paper, Anne Fischer and her colleagues show that the entire Mycoplasma mycoides cluster arose 10,000 years ago. Mycoplasma mycoides is as old as the livestock it kills.

A severe Mycoplasma infection begins with a cough, followed by a groan, a grunt and more coughing. Breathing becomes difficult and painful. Eventually, the cow or goat becomes listless and, in the terminal stage of disease, stops moving altogether. It just stands there, oozing mucus and saliva from its nose and mouth, until it dies. Untreated, the most deadly of Mycoplasma strains can slaughter herds within days.

Mycoplasma mycoides travels in the droplets that are released with every cough and breath. A goat or cow has to be to be in direct contact with the droplets from a diseased animal in order to contract the disease. This is not as rare of a occurrence as it sounds. All it takes to infect an entire herd is one infected animal in a tightly packed truck, stable or kraal. After a major outbreak amongst goats in South Africa, veterinary surgeon Duncan Hutcheon recalled the extraordinary speed at which the disease spread and animals died:

On 4 March 1881, the main flock began to show evidence of lung disease which spread rapidly. Some 700 goats died in the next 14 days. I was not sure at first that the disease could be contagious. I had no knowledge of any disease which could cause the death of so many goats so quickly.

The nineteenth century Hutcheon lived in was a golden age, as far as Mycoplasma mycoides was concerned. The livestock trade became global, while vaccination programmes were still in their infancy. Entire countries could be infected by a single animal. 50 years before Hutcheon described the outbreak amongst goats, a handful of cows in his country became infected by a Friesian bull, imported from the Netherlands. The disease soon swept through South Africa, killing 100.000 cows and oxen along the way.

A young Navajo woman tending to her sheep and goats.

To be fair, not every strain of Mycoplasma mycoides is a killer, and not every infection ends in death. The Mycoplasma family is large and most strains are not as lethal as Mycoplasma mycoides mycoides (for cows) and Mycoplasma capricolum capripneumoniae (for goats), the two strains that cause the contagious pneumonia described above.

Over the past few years, scientists have realized that the Mycoplasma mycoides family extends beyond its two most infamous members, but have so far failed to chart all the relationships between the different strains. To figure out who is related to whom, Anne Fischer and her colleagues collected 118 different strains from all over the world, and sequenced 7 of their genes. The collection features bacteria from all times and places, including strains isolated from African cattle in 1931, Rocky Mountain goats and Mouflons from Qatar.

Using the genetic differences between strains as a measure for their kinship, Fischer’s team reconstructed the entire Mycoplasma mycoides family tree. From this tree, the team concludes that the founding father of all Mycoplasma mycoides lived 10,000 years ago – around the same time pastoralists domesticated cattle, goats and sheep in the Near East. It’s easy to see how a lung disease would thrive better in a dense, human controlled herd, compared to a wild one. Animals are brought together in kraals, stables and around watering troughs, and if the herd is mixed, they are exposed to bacteria and viruses they haven’t encountered before.

No bacterial family is born out of thin air, not even a lung disease like Mycoplasma mycoides, so who where its ancestors? Was it indeed a wild bacterium, lurking in the lungs of the first wild beasts herded by man, as I suggested in the introduction? Fischer and her colleagues might have found a clue to that points in this direction. In their extensive collection of bacteria, they identified an unknown relative of the Mycoplasma cluster in several wild goats. This new species was isolated from Alpine ibexes in zoos and from a wild Rocky Mountain goat. The researchers are already sequencing its genome and characterizing its biochemical traits, to see what secrets about Mycoplasma mycoides‘ ancestry it holds.

The family tree of the Mycoplasma mycoides cluster. Horizontal axis represents time, in years. The entire cluster is 10,000 years old, but the two most virulent strains (M caprcicolum subsp capripneumoniae and M mycoides subsp mycoides) are much younger.

Mycoplasma leachii, a member of the Mycoplasma family that causes inflammation in the joints and udders of cows rather than pneumonia, has another interesting story to tell. Most strains formed distinct genetic populations. Not Mycoplasma leachii. The researchers discovered that this bug is of hybrid origin. Almost a third of its genes come from Mycoplasma that cause contagious pneumonia in cows, whereas the remaining two-thirds are from goat-specific strains. Since no Mycoplasma can survive without a host, the hybridization must have taken place within a single a single animal. Animals in mixed herds run the most risk of becoming infected by multiple strains. They are what the authors call “hybridization ovens”, baking new Mycoplasma mycoides variants in their co-infected bodies.

While Mycoplasma mycoides as a family might be as ancient as livestock itself, the two most contagious and deadly strains are much younger. The common ancestors of the strains that cause contagious pneumonia in cows and goats lived between 91 and 414 and between 56 and 490 years ago, respectively. I’m surprised that the authors make little note of this in their paper and wonder what could have favoured the origin and survival of these hypervirulent bugs in recent centuries. Herding made Mycoplasma mycoides – but what turned it into a killer?


Images:
Auroch by Marcus Sümnick
Navajo woman scanned by koiart71
Mycoides family tree from reference.
References:
Fischer A, Shapiro B, Muriuki C, Heller M, Schnee C, Bongcam-Rudloff E, Vilei EM, Frey J, & Jores J (2012). The Origin of the ‘Mycoplasma mycoides Cluster’ Coincides with Domestication of Ruminants. PloS one, 7 (4) PMID: 22558362

Lucas Brouwers About the Author: Lucas Brouwers is fascinated by evolution. He writes about science on his blog and for a Dutch daily newspaper. Follow on Twitter @lucasbrouwers.

The views expressed are those of the author and are not necessarily those of Scientific American.





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  1. 1. fthfth 3:45 am 10/10/2012

    Contagious bovine pleuropneumonia may be one of the most recently emerged animal bacterial disease and it was exported from Europe to other continents in the 19th century.

    A comment on
    Livestock bacteria are as old as the livestock they kill
    By Lucas Brouwers | May 14, 2012 |

    My comments will focus on the last sentence of this blog:
    Herding made Mycoplasma mycoides – but what turned it into a killer?

    The assertion in the first part of the sentence is not exactly what the study of Fischer et al. showed. This study showed that the mycoplasma mycoides cluster emerged about 10000 years ago. Domestication of ruminants also occurred at the same period. There is a correlation of timing (plus or minus the dating uncertainty, which may amount to thousands of years for both events) but not necessarily a cause-effect link, which is a completely different matter.
    When two events are occurring at the same time it is tempting to conclude that there is a causality link between the two but this is very often misleading and anyway very difficult to prove.
    (see http://stats.org/in_depth/faq/causation_correlation.htm )

    The question raised in the second part of the sentence is really interesting and the recent unraveling of complete mycoplasma genome sequences is shedding light on what may have happened, at least for Mycoplasma mycoides subsp. mycoides SC (MmmSC), the agent of contagious bovine pleuropneumonia (CBPP), a respiratory disease of cattle (Thiaucourt et al. 2011).
    The closest relative of MmmSC is M. mycoides subsp. capri (Mmc), which is usually found in goats. Mmc can be harbored as a simple saprophyte, in the ear canal for example, or may act as a pathogen inducing a variety of symptoms: mastitis, arthritis, keratitis and pneumonia. MmmSC has adapted to a new host, cattle, and specialized in lung infections. By doing so its genome has undergone a number of evolutions.
    It has first expanded in length with duplications of large DNA fragments and incorporation of mobile genetic elements such as insertion sequences. These insertion sequences have the ability to duplicate and transpose within bacterial genomes. The MmmSC genome contains about one hundred insertion sequence copies. Interestingly, one of these insertion sequences is similar to what can be found in the genome of another mycoplasma infecting cattle Mycoplasma bovis suggesting that MmmSC acquired that mobile element when it adapted to its new host.
    In parallel MmmSC genome has been rapidly decaying, finally losing a lot of the original Mmc coding capacity. For example it contains only 56 genes coding for lipoproteins, found at the surface of the bacteria, when Mmc contains 86 of these genes. In addition this decaying process can be evidenced by the high number of pseudogenes, ie: genes which are intact in Mmc but which are interrupted by frameshift mutations in MmmSC.
    What we see is a process of specialization to a very specific ecological niche. MmmSC is getting rid of a number of genes which are not absolutely necessary for its survival in its new environement. This deletion process is very rapid. At the same time it is acquiring new genes which may allow him to adapt better, in a much longer process.
    What is also really interesting is that this evolution process is very recent and took place within the last 300 years of evolution of this bug (Dupuy et al. 2012). To evaluate this duration we have focused our study on MmmSC genomes. We compared the full genomes of 6 of them and then selected 62 genes that could help us building a phylogeny (family tree) for this pathogen.
    Apparently the most recent common ancestor to all MmmSC strains appeared around year 1704. Most likely this event took place in Europe as CBPP was clearly described by a Swiss author, B. de Haller in 1773. This dating exercise allowed us also to evaluate when CBPP was introduced in Africa: around year 1814. Again the molecular dating is in complete agreement with historical data showing that CBPP was raging in central Europe, for example around Paris (Huzard 1798), at that period.

    The common ancestor to all M. mycoides subsp. mycoides SC strains appeared around year 1704 while the common ancestor to all African strains appeared around 1814 suggesting an importation from Europe.
    When CBPP was introduced in Africa, Fulani herdsmen tried to fight the disease with inoculation procedures which were similar to what was used to fight small-pox. In the case of CBPP this procedure can lead to the death of the animals except if this inoculation is made at the bridge of the nose. It then leads to the formation of “pseudo-horns” which were observed in Senegal around 1880 but which can still be seen locally in Africa. Finally CBPP gained a worldwide distribution through cattle trade after 1840.

    Nowadays, CBPP has been eradicated from most of developed countries and it persists mostly in Sub-Saharan countries where it causes heavily losses. Efforts are really needed at an international level to eradicate the disease and hopefully stop the evolutionary process of MmmSC once and for all !

    References
    Thiaucourt F, Manso-Silvan L, Woubit S, Barbe V, Vacherie B, Jacob D, Breton M, Dupuy V, Lomenech AM, Blanchard A, Sirand-Pugnet, P : Mycoplasma mycoides, from “mycoides Small Colony” to “capri”. A microevolutionary perspective. BMCgenomics 2011, 12:114.

    Haller B de: Mémoire sur la contagion parmi le bétail, mis au jour pour l’instruction du public. In. Berne; 1773: 32.

    Huzard JB: Mémoire sur la péripneumonie chronique ou phtisie pulmonaire qui affecte les vaches laitières de Paris et de ses environs. Paris: Madame Huzard, rue de l’éperon; 1798.

    Dupuy V, Manso-Silvan L, Barbe Vr, Thebault P, Dordet-Frisoni E, Citti C, Poumarat F, Blanchard A, Breton M, Sirand-Pugnet P et al: Evolutionary History of Contagious Bovine Pleuropneumonia Using Next Generation Sequencing of Mycoplasma mycoides subsp. mycoides “Small Colony”. PLoS ONE 2012, 7(10):e46821.

    Link to this

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