So it’s been two weeks since I last posted – and the reason is sort of ironic. On the one hand, there’s not been enough in a week to tell you about, and yet I’ve been so ridiculously busy that there’s not been a spare minute to write in.
How does that happen?
Well, unfortunately, bacteriology and immunology remain the full-time focus of my degree. This means that there’s an extraordinary amount of work to be done and things to be learnt, but there’s so little of it that might excite the casual blog-reader. But I’ll be damned if I don’t try anyway!
The last fortnight has explored the cycle of pathogenesis, from infection to resolution, and identified the distinct habits of some fairly famous microbes: Salmonella, Streptococci, Mycobacteria, Staphylococci and Chlamydia to name a few. At first glance, that looks like a pretty scary line-up, but I’ve discovered that a great many species in these genera have preferences for non-human hosts. And, interestingly, different bacterial species often cause different diseases in different host species.
Possibly the best example I can give is Chlamydia. Within this genera, C. caviae has a flare for conjunctivitis in guinea pigs, whilst C. suis has a habit of giving pigs pneumonia, and C. psittaci is a zoonosis that infects the lungs of both birds and humans. These are all separate from the infamous Chlamydia trachomatis, the STI that causes urogenital disease and blindness in humans. It’s this variety in disease that really lays bare the physiological differences between species. The differences in veterinary patients goes beyond whether they have hooves or paws. It goes right down to a molecular level, where cattle are indifferent to toxins that would knock you sideways, and substances pleasurable to humans are fatal in cats and dogs. Sorry, medics, this is where we like to take the intellectual high ground!
But I had my own bug-hunting to do when we were set our AB2 essay, with a question that required me to select three pathogens and discuss the way that they manipulate host cells. I moaned and I groaned, but at the end of the day, I can’t deny that it’s more than a little bit cool to discover the sneaky ways in which pathogens turn our own cells against us. Then again, the pleasure is extinguished somewhat by having to wade through academic papers to find out.
The lucky three that made it to my line-up were: Legionella pneumophila, Salmonella typhimurium and Human Papillomavirus (HPV). Contrary to what you might have anticipated, these are very much human diseases – but that’s where the research is!
My essay is long-winded and filled with TLR-4, CD14, LCVs, NF-kappaB, Cdc25A and ‘et al’s, which means that it’s not a pleasurable read. But there are some real gems of knowledge in there, which could really interest you. I’ll tell you what, if you’re really not interested (I don’t blame you), scroll down to the picture of the horse and go from there. For everyone else, here are some of the nifty things I learnt about my chosen pathogens:
- L. pneumophila allows itself to be ingested by immune cells to gain access, but then blocks the cell’s attempts to digest it – creating a protected little bubble
- it then pulls off heists on cell packages filled with useful stuff, that the cell was taking elsewhere
- these infected immune cells would rather die than be infected, but l. pneumophila prevents that too
- it then nicks degradative enzymes from the cell, and uses them to feed itself amino acids by breaking down host proteins
- S. typhimurium injects proteins that rearrange the host cell’s cytoskeleton (yep, cells have skeletons!) to force it into hugging the bacterium, then taking it in
- it then uses these proteins to build itself a skeleton ‘nest’ inside
- next, it gets a croggy on the cell’s little protein taxis to hitch a ride to the nucleus
- here, it steals cell packages like Legionella
- finally, it sends out a chemical alert to recruit immune cells into the gut, and releases proteins to force the host cell into pumping chloride into the gut lumen
- the combined effect creates terrible diarrhoea, which serves as (this is great) an effective route of faecal-oral transmission between hosts – ace.
- HPV is a virus that infects mucosal and epithelial cells, such as those in the vagina
- it has a little genome, but it can’t replicate this itself, so it uses host proteins
- but cells have mechanisms to shut down replication if it senses damaged DNA – and HPV DNA is foreign, which looks damaged to the host
- these mechanisms halt the cell cycle before S phase – where all the proteins the virus needs are created
- so HPV uses the cell’s own degradative enzymes to destroy the proteins that do the halting – which removes the brakes
- it then pushes the accelerator by having the cell express genes that drive the cycle forward
- as the cell enters the division phase, HPV puts a sudden hiatus on the cycle to allow the cell’s own machinery to spin out of control, causing damaging alterations to the DNA
- the result of damaged DNA and accelerated division: cancer
- not all strains do this, but if you’re a virus it’s the best way to ensure that you dominate a tissue, by creating huge masses filled with virus-infected cells
For a single-celled organism, this is pretty clever stuff. And this is the crux of my essay, except I didn’t use words like ‘croggy’. And I referenced no less than 48 papers by the people who actually spend their careers finding this stuff out – kudos!
This horse has nothing to do with the vet school, I met him 5 years ago on a countryside walk. But he makes a nice landmark for those less bacteriologically inclined, don’t you think?
But he is relevant, because I had the first of my horse practicals the other day. The school has its own set of teaching horses and, surprisingly enough, many new students haven’t handled horses before.
Anyone who knew me before I came here will know that horses had been a staple component of my week for as long as I can remember. Since moving in in September, however, this has been my first contact with them in 7 months!
Suffice to say they took us right back down to basics, and there was nothing new in this session for me. But just spending time with horses does plenty for the soul! This bunch had seen it all and were quiet, kind and affectionate. If only the sun had stayed out – the session had begun in warm Spring sunshine, which quickly retreated behind the clouds and left us slowly freezing in our wellies.
So, Crufts has just finished, and the Best in Show went to a very fluffy West Highland White. Unfortunately, I didn’t get to watch a great deal of it, but there’s one Best of Breed that I most definitely did hear about:
I’m not even opening this for debate, I’m just putting it out there. This is absolutely disgraceful, and a blatant failure of Kennel Club judges to make sure that animals of this conformation never make it to the show ring – never mind win Crufts Best of Breed.
There are many, many breeds that have undergone ridiculous inbreeding and changes in conformation that have resulted in debilitating and lifelong heritable conditions. But there have been promises made to tackle the crippling hip, pelvic, spinal and hindlimb damage found in GSDs with sloping backs.
The KC Breed Standards for GSDs clearly state, “Back between withers and croup, straight”, “roach backs undesirable and should be heavily penalised”, “effortless forward propulsion”, “absolute soundness of movement essential”, “hocks are strong and firm” and “rear pasterns are vertical”.
The bitch shown above fails on every single count. You can go to YouTube to watch her final against a dog who wasn’t a great deal better. Her gait is awkward, wobbly and hunched. This is not an animal whose genes should be passed on. And yet here she is, winning awards that will put her right in the middle of the breeding pool, passing on a legacy of pain and premature death.
This is a working type GSD (as opposed to the show type at Crufts). I don’t think I need describe the anatomy behind why this dog would be capable of “effortless forward propulsion” for hours on end. He’s built well to do his job.
Why do dogs need to be so grossly exaggerated? Surely, if ‘true to type’ dogs were the most desirable, then they should look as they did when they were first developed. The Crufts bitch certainly does not look capable of guarding herds of sheep day in, day out.
It was an immunology lecturer that told us only the other day that dogs are the most inbred species on the planet. And it didn’t surprise me in the slightest. There’s one heck of a lot of work to be done on improving canine genetics to prevent unnecessary suffering, and Give a Dog a Genome is trying to do just that – check them out!
In other, happier, news: my rectal gloves arrived! 100 rectal gloves – who could want for more? And, what d’ya know, they fit like…
…a glove – see you next week!
The Dogsbody 