Getting Friendly with Bacteria Fall 2014

Don’t put me in a box–Iā€™m not Ā gram negative ORĀ positive. I am a diderm, meaning I have two membranes, like gram negative, but with some different stuff going on. I am a slow-growing (12-18 hour doubling time) microaerophile, with an optimal growth temperature of about 32 C. As for energy, I generate it exclusively from substrate-level phosphorylation. Like many parasites I rely on my hosts–serve me up some N-acetylglucosamine (NAG), please! Ā Iā€™m tiny, 20-30um long but only 0.2-0.3um wide. You canā€™t see me with a light microscope, but dark-field microscopy works, and of course a scanning electron microscope does the trick too.

As you can see in my family portrait above, I’m a spirochete. Which tells you a lot about me. Not really into long walks on the beach–too much air. More into moving around corkscrew fashion. My whole phylum is into it. One theory is that way of moving is an adaptation to viscous environments. I donā€™t remember though, that was before my time. A lot of bacteria just have their flagella waving around as if they are trying to flag down an antibody. Pretty dumb, as flagellar proteins are antigenic. My flagella is endo, itā€™s an inside job. You can call it an axial filament if you like. Iā€™m pretty sure it helps me evade some immune responses. Another potential virulence factor that Iā€™m really proud of is my 21 plasmids! The most of any bacteria. One time, they cultured me in the lab for a long time and I lost some plasmids. It made me less virulent. Coincidence? I think not. Youā€™re not impressed? Well, Iā€™m just getting started. I am about to get in your head. Your brain to be specific. Iā€™ve been known to hang out on the other side of the blood-brain barrier. Itā€™s a good hideout. The human immune response isnā€™t top-notch up there. Speaking of immune response, I can also change my surface proteins. That keeps them guessing long enough for me to get a nice chronic infection going. Oh, Iā€™ve also been witnessed going intracellular in lab cultures. So, I may be doing that in vivo too.

Even though I have that impressive CV it wouldnā€™t surprise me if you donā€™t know me by name. Iā€™m actually pretty infamous though. I cause Lyme Disease. In Europe they call it Lyme Borreliosis. I live in mice, but I also live in ticks and deer, and of course humans, and dogs, rats and birds too. Mice and deer are the main reservoirs though. As far as humans are concerned, Ixodes ticks are the gun, and the bullet is me.

My reliance on Ixodes ticks, who have a complex life cycle involving three different blood meals often from three different animal species, has drawn comparisons to the relationship between malaria causing Plasmodium and Anopheles mosquitos.

Come to think of it, pretty much everything about me is complex. Lyme disease, which I cause, has many potential ill effects on humans. In the first phase of infection, following the tick bite, a bullā€™s eye rash is produced, about 75% of the time. That is followed by flu-like symptoms. If antibiotics are taken at this time they are often effective in eradicating me. After that, if no effective treatment occurred, things can really start going downhill for humans. I can cause neurological problems such as facial palsy, severe headache, sensitivity to light and more. If the symptoms persist, that is an indication that I have achieved chronic infection. That often means similar neurological impairment with potentially increased severity. Some sufferers have also reported severe joint pain. One study supports that complaint by finding sequestration of me (B. burgdorferi) in the vicinity of joint cartilage.

Before I go must mention that there is tremendous controversy surrounding the symptoms and diagnosis of Lyme Disease. This is not helped by the fact that there is no single test that can reliably detect me. And when it comes comes to early detection that is of particular importance as chronic infection can be especially difficult to treat. Check out this scholarly article on the subject if you like. It states that ā€œclinical suspicion based upon well-recognized cardinal features of Lyme disease is still the most appropriate approach.ā€ In the absence of a sufficiently high index of suspicion, multiple tests, generally including a serological test, increase the likelihood of correct identification. The difficulty in detection has made it difficult to draw a direct link to many of the chronic symptoms of Lyme Disease, such as headache, joint pain, and fatigue. Furthermore these symptoms can be attributed to any number of causes. Anyway, this is real can of worms and I am more of a tick guy. I hope we can be friends. Especially Treponema pallidum , Leptospira interrogans and Spirillum minus. I haven’t seen you guys since that crazy rave!! Everyone else, Ā check out my references below.

http://textbookofbacteriology.net/Lyme.html

http://en.wikipedia.org/wiki/Lyme_disease

http://en.wikipedia.org/wiki/Lyme_disease_microbiology

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1248466/

http://www.newyorker.com/magazine/2013/07/01/the-lyme-wars

https://microbewiki.kenyon.edu/index.php/Borrelia_burgdorferi

Microbiology, An Introduction. 11th Edition. Tortora, Funke, Case

 

 

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