A Shining Mystery

Brucella abortus
(false colored).
Source: Veterinary
Laboratories Agency
(UK)

Who wouldn't agree how enormously gratifying it would be to make ecological sense of every lab finding, to see how the phenomenon being observed fits with the organism's life outside the lab. Sounds easy? Fat chance. Most of the time, we can only make guesses, and there are occasions when even a good guess eludes us. Here is a recent example. Brucella abortus, the agent of brucellosis in livestock and humans, has a light sensor, and the expression of some of its genes are controlled by light. Not being a phototroph and not living most of the time in a lit environment, this alone may be a surprise. But there is more to this.

The light sensor consists of a module in a histidine kinase, called LOV for light, oxygen, or voltage. The LOV protein domain contains approximately 110 amino acids and is associated with a light-sensitive flavin cofactor. That is not news because some 100 bacterial species are known to have LOV, and so do certain archaea, fungi, plants, and animals. What is news, however is that B. abortus responds to blue visible light in a most unexpected way: it increases its virulence. When grown in the light, B. abortus is ten times more virulent in a macrophage system than when grown in the dark or when its LOV function is eliminated through mutation.

How does light activate the virulence genes involved? Absorption of light by the bound flavin induces a conformational change in the LOV-histidine kinase protein, which, it is presumed, leads to alterations in the expression of virulence genes. B. abortus shares its LOV-kinase arrangement with another brucella, B. melitensis, with the plant pathogen Pseudomonas putida, and with a marine bacterium, Erythrobacter litoralis.

Cow. Source: Florida
Department of Health

What's the connection in the real world between light and Brucella virulence? This is a conundrum because these organisms are usually transmitted through milk and direct contact. Try as you may, it's not easy to make the case for more than sporadic contact of these organisms with light. Is light sensitivity an atavistic remnant of an ancestor with a different ecology? Is light a synonym for another natural stimulus? Is this mere happenstance? Most microbial environments are not exposed to sunlight, and most microbes lead a light-sheltered existence. The exceptional illuminated habitats are the aquatic environments of photosynthetic bacteria, the surface of plant leaves (the phyllosphere), crusts of soils, and some others.

Massive proliferation of Brucella
in a bovine macrophage.
Source: Texas A & M University

Several publications have had a field day with this story, snaring their readers with headlines such as "Bacteria See the Light." Science magazine commentators predict that microbiologists will start incubating their cultures under both light and dark conditions, which may well lead to an explosion of interesting data. We share this excitement and the sense of surprise. But let's own up to it, the function of light-sensing in these microbes does seem like a mystery.

It would be unfair to leave it at that. There is one B. abortus story that may quench our ecological/physiological craving. This organism has a special predilection for erythritol, a sugar found in the placentas of some mammals─specifically in those in which B. abortus causes abortion (e. g., cattle), but not in those where it doesn't (e. g., humans). There is probably more to this story, but it seems less inscrutable than the effect of light.

Comments

[Richard Ellis]

Just stumbled on this post. The neutrophil oxidative burst essential for the intracellular killing of phagocytosed organisms is capable of generating light, albeit of a low intensity. This could be the answer maybe as we know that B. abortus is predominantly an intracellular pathogen. It would be interesting to know exactly what virulence factors are upregulated.

[Anna M. Bond]

Brucellosis Infection
In Cattle

In cattle, brucellosis is primarily a disease of the female, the cow. Bulls can be infected but they do not readily spread the disease. The brucellosis organism localizes in the testicles of the bull and produces an orchitis (inflammation of the testicles), whereas in the female the organism localizes in the udder, uterus, and lymph nodes adjacent to the uterus. The infected cows exhibit symptoms which may include abortion during the last third of pregnancy, retained afterbirth, and weak calves at birth. Infected cows usually abort only once. Subsequent calves may be born weak or healthy and normal. Some infected cows will not exhibit any clinical symptoms of the disease and give birth to normal calves. The brucellosis organism is shed by the millions in the afterbirth and fluids associated with calving and aborting. The disease is spread when cattle ingest contaminated forages or lick calves or aborted fetuses from infected cattle. Outside the animal, the afterbirth, and aborted calves the brucella bacteria are easily killed by sunlight, high temperatures and drying; however, the brucella organisms are difficult to control while they are in the animal; there is no economical cure for a brucellosis infected animal.

[Fernando]

Thanks for the information!!!!!!!!!!!!!!!

[Rapidshare]

I completely agree with all that here is told
So you can find the information on it on my search resource
http://fileshunt.com

[Paul Orwin]

It's been a while since I commented (start of the term, blah blah) but I can't resist this one - one of the weirdest findings in a while, in my humble opinion.
I think it has to be an evolutionary remnant, because it makes no sense for Brucella to use light as a virulence trigger. An alpha proteobacterial plant pathogen might find it useful, though (according to Wikipedia, the 2nd chromosome might have evolved from the Agrobacterium megaplasmid). It might plausibly stay with Brucella over evolutionary time because it certainly wouldn't hurt to have an extra + regulator of virulence, and if it senses oxidative stress, it might plausibly play a positive role in virulence as well.

To play devil's advocate with myself, it could be that the LOV plays a role in fine tuning virulence (turning some genes on only in the lysosome?. It could also be part of a mechanism to distinguish between macrophage and free-living protozoan predators - this might still be in dark soil, but could plausibly be exposed to enough blue light (higher energy, penetrates deepest in opaque material) to induce.

I have to keep away from this distracting blog!!!