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A bit of fun and a bit of science mixed in with a bunch of diseases gives us Disease Prone. A jargon-free look into the world's most interesting diseases.
James Byrne
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- September 14, 2011
- 06:05 PM
- 623 views
Peptidoglycan - The bacterial wonder wall
by James Byrne in Disease Prone
Quick, can you describe your grandparents? Staphylococcus aureus, or the Golden Staph, can and it is a single cell. If you couldn’t you should visit them more often. In any case, a very cool paper came out recently but before we can get there we need to begin by going backwards to explain a very important bacterial structure called peptidoglycan.... Read more »
Turner, R., Ratcliffe, E., Wheeler, R., Golestanian, R., Hobbs, J., & Foster, S. (2010) Peptidoglycan architecture can specify division planes in Staphylococcus aureus. Nature Communications, 1(3), 1-9. DOI: 10.1038/ncomms1025
van Heijenoort J. (2001) Formation of the glycan chains in the synthesis of bacterial peptidoglycan. Glycobiology, 11(3). PMID: 11320055
- September 9, 2011
- 01:51 AM
- 403 views
Acinetobacter baumannii the most opportunisitic-ist pathogen you know
by James Byrne in Disease Prone
A. baumannii does not mess around. As opportunistic pathogens go it’s pretty out there. An aerobic, gram negative, almost entirely antibiotic resistant (largely through passive mechanisms) bacterium that’s developing such a terrible reputation that it has picked up the nickname ‘Iraqibacter’, but that’s mostly because of the high proportion of A. baumannii infections in returned American troops.... Read more »
Mussi, M., Gaddy, J., Cabruja, M., Arivett, B., Viale, A., Rasia, R., & Actis, L. (2010) The Opportunistic Human Pathogen Acinetobacter baumannii Senses and Responds to Light. Journal of Bacteriology, 192(24), 6336-6345. DOI: 10.1128/JB.00917-10
McBride, M. (2010) Shining a Light on an Opportunistic Pathogen. Journal of Bacteriology, 192(24), 6325-6326. DOI: 10.1128/JB.01141-10
Reddy, T., Chopra, T., Marchaim, D., Pogue, J., Alangaden, G., Salimnia, H., Boikov, D., Navon-Venezia, S., Akins, R., Selman, P.... (2010) Trends in Antimicrobial Resistance of Acinetobacter baumannii Isolates from a Metropolitan Detroit Health System. Antimicrobial Agents and Chemotherapy, 54(5), 2235-2238. DOI: 10.1128/AAC.01665-09
Dijkshoorn, L., Nemec, A., & Seifert, H. (2007) An increasing threat in hospitals: multidrug-resistant Acinetobacter baumannii. Nature Reviews Microbiology, 5(12), 939-951. DOI: 10.1038/nrmicro1789
- August 2, 2011
- 08:57 PM
- 496 views
Antibiotics are good for more than just killing
by James Byrne in Disease Prone
As a community here @sciamblogs we decided to each cover something chemistry related on each of our individual blogs to coincide with the World Chemistry Congress taking place in Puerto Rico. This scared the bejeezus out of me as I’m a biologist, not a chemist, and I’ve never been brilliant at the textbook chemistry stuff from my undergraduate classes. Also, a wise biology teacher once told me that all chemistry is boring until it starts moving, then its biology.... Read more »
Falconer, S., Czarny, T., & Brown, E. (2011) Antibiotics as probes of biological complexity. Nature Chemical Biology, 415-423. DOI: 10.1038/nchembio.590
- July 28, 2011
- 07:56 PM
- 577 views
Can’t fall asleep? You don’t want to read this then.
by James Byrne in Disease Prone
Unlike narcolepsy, which has been shown to have genetic and environmental triggers insomnia seems to have no genetic component. The closest thing to a genetic insomnia is the ominously named fatal familial insomnia, which my old friend Thomas wrote about here.
A diagnosis of insomnia relies on the way the following questions are answered, “Do you experience difficulty sleeping?” or “Do you have difficulty falling or staying asleep?” You answer yes to either of those and you have insomnia.... Read more »
Reiner PB, & Kamondi A. (1994) Mechanisms of antihistamine-induced sedation in the human brain: H1 receptor activation reduces a background leakage potassium current. Neuroscience, 59(3), 579-88. PMID: 8008209
Roth T, & Roehrs T. (2003) Insomnia: epidemiology, characteristics, and consequences. Clinical cornerstone, 5(3), 5-15. PMID: 14626537
Jacobs GD, Pace-Schott EF, Stickgold R, & Otto MW. (2004) Cognitive behavior therapy and pharmacotherapy for insomnia: a randomized controlled trial and direct comparison. Archives of internal medicine, 164(17), 1888-96. PMID: 15451764
- July 16, 2011
- 05:46 PM
- 445 views
Narcolepsy…zzzZZZzzz…
by James Byrne in Disease Prone
Everyone knows what narcolepsy looks like from movies like the ridiculous display in Deuce Bigalow (one of the ‘adorable misfit bunch of suitors’) to other more subdued examples like Mike in My Own Private Idaho. Oh, and when I say that, I mean people know the stereotype of the instantaneous drop during dinner into a bowl of soup. What I really mean is that the stereotype isn’t the norm at all.... Read more »
Klein J, & Sato A. (2000) The HLA system. Second of two parts. The New England journal of medicine, 343(11), 782-6. PMID: 10984567
Mignot E. (2001) A commentary on the neurobiology of the hypocretin/orexin system. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 25(5 Suppl). PMID: 11682267
Maret S, & Tafti M. (2005) Genetics of narcolepsy and other major sleep disorders. Swiss medical weekly, 135(45-46), 662-5. PMID: 16453205
Zorick FJ, Salis PJ, Roth T, & Kramer M. (1979) Narcolepsy and automatic behavior: a case report. The Journal of clinical psychiatry, 40(4), 194-7. PMID: 422531
- June 26, 2011
- 01:37 AM
- 620 views
Soylent brown – “Shit burgers”
by thomastu in Disease Prone
Sorry again for the lack of activity on the blog. I am going pretty well on my thesis, thanks for asking. Anyway, I was drinking with a couple of friends of mine who are doing their PhDs in environmental health … Continue reading →... Read more »
He, X., Cheng, L., Li, W., Xie, X., Ma, M., & Wang, Z. (2008) Detection and distribution of rotavirus in municipal sewage treatment plants (STPs) and surface water in Beijing. Journal of Environmental Science and Health, Part A, 43(4), 424-429. DOI: 10.1080/10934520701795731
Fong, T., Phanikumar, M., Xagoraraki, I., & Rose, J. (2009) Quantitative Detection of Human Adenoviruses in Wastewater and Combined Sewer Overflows Influencing a Michigan River. Applied and Environmental Microbiology, 76(3), 715-723. DOI: 10.1128/AEM.01316-09
- June 24, 2011
- 07:25 PM
- 845 views
No door? No problem. T. cruzi uses the window to cause Chagas Disease
by James Byrne in Disease Prone
For invasive pathogens the only way to survive, and consequently make you sick, is to get inside your cells. This is a rough exercise as you have an immune system working everywhere in the body to prevent this and the cell to be invaded is none too happy with the idea either so invasive pathogens must use tricks.... Read more »
Jermy A. (2011) Parasitology: Adding insult to injury. Nature reviews. Microbiology, 9(7), 484. PMID: 21625249
Andrade LO, & Andrews NW. (2005) The Trypanosoma cruzi-host-cell interplay: location, invasion, retention. Nature reviews. Microbiology, 3(10), 819-23. PMID: 16175174
Fernandes MC, Cortez M, Flannery AR, Tam C, Mortara RA, & Andrews NW. (2011) Trypanosoma cruzi subverts the sphingomyelinase-mediated plasma membrane repair pathway for cell invasion. The Journal of experimental medicine, 208(5), 909-21. PMID: 21536739
- June 18, 2011
- 12:00 AM
- 809 views
Anti-cancer Fungi
by James Byrne in Disease Prone
Mycology, the study of fungi, is an often-overlooked member of the microbiology family. Having said that there are plenty of dedicated mycologists out there doing all sorts of cool stuff and plenty more fungal species doing all sorts of weird and wonderful things.... Read more »
King-Fai Cheng, & Ping-Chung Leung. (2008) General review of polysaccharopeptides (PSP) from C. versicolor: Pharmacological and clinical studies. Cancer Therapy. info:/
Luk SU, Lee TK, Liu J, Lee DT, Chiu YT, Ma S, Ng IO, Wong YC, Chan FL, & Ling MT. (2011) Correction: Chemopreventive Effect of PSP Through Targeting of Prostate Cancer Stem Cell-Like Population. PloS one, 6(6). PMID: 21674070
- June 11, 2011
- 01:05 AM
- 507 views
To Tattoo or Not To Tattoo
by James Byrne in Disease Prone
One of the things I didn’t realise about getting a tattoo the first time was just how much mess it makes and how much blood there is. It doesn’t make any sense really given that I was completely aware a bunch of needle were going to repeatedly puncture my skin but, honestly, I’d never really thought about the blood. I can assure you if I had known I probably would have wussed out.
... Read more »
Wagle WA, & Smith M. (2000) Tattoo-induced skin burn during MR imaging. AJR. American journal of roentgenology, 174(6), 1795. PMID: 10845532
Tope, W., & Shellock, F. (2002) Magnetic resonance imaging and permanent cosmetics (tattoos): Survey of complications and adverse events. Journal of Magnetic Resonance Imaging, 15(2), 180-184. DOI: 10.1002/jmri.10049
Hartwig, V., Giovannetti, G., Vanello, N., Lombardi, M., Landini, L., & Simi, S. (2009) Biological Effects and Safety in Magnetic Resonance Imaging: A Review. International Journal of Environmental Research and Public Health, 6(6), 1778-1798. DOI: 10.3390/ijerph6061778
- June 3, 2011
- 07:22 PM
- 3,124 views
Treating the Bends
by James Byrne in Disease Prone
ResearchBlogging.org
Last week I wrote about the Bends, a medical problem based in an understanding of physics that results in bubbles of (primarily) nitrogen in your blood if you move from one atmospheric pressure to another to quickly, typically surfacing from depth while diving too fast.
The therapy is actually very simple – take the person back to the depth they were diving at to force the bubbles to resolve into the blood. This immediately solves of the symptoms of the condition but is a little impractical to drive the diver back to the beach and drag them underwater. So, instead, we fake it.... Read more »
Vann RD, Butler FK, Mitchell SJ, & Moon RE. (2011) Decompression illness. Lancet, 377(9760), 153-64. PMID: 21215883
Acott, CJ. (1999) Oxygen toxicity: A brief history of oxygen in diving. South Pacific Underwater Medicine Society Journal. info:/
Clark JM. (1974) The toxicity of oxygen. The American review of respiratory disease, 110(6 Pt 2), 40-50. PMID: 4613232
- May 28, 2011
- 09:00 AM
- 1,133 views
Physics Medicine = The Bends
by James Byrne in Disease Prone
Arguably many diseases can be based in physics including heart disease, atherosclerosis and pretty much anything else to do with the pipes in your body but a disease known as ‘the bends’ or ‘decompression sickness’ invokes a bunch of physics laws and principles and then also requires a physics based treatment to deal with it.
... Read more »
Vann RD, Butler FK, Mitchell SJ, & Moon RE. (2011) Decompression illness. Lancet, 377(9760), 153-64. PMID: 21215883
- May 6, 2011
- 07:06 PM
- 443 views
Zombies Pt 2 (or how I distracted my students)
by James Byrne in Disease Prone
Last week I mentioned how my students sidetracked me in a tute regarding introductions to the origins of life and in particular the acronym HOMR standing for Homeostasis, Organisation, Metabolism and Replication by initiating a discussion of whether or not zombies technically were alive. Well, the following week they had a test that occupied half the allocated tutorial time so instead of letting them out early I extended the discussion to real world zombies.
After a little investigation it became clear that ‘zombism’ is a lot more common in nature than I expected. While not true zombies the examples I have below represent some of natures best approximation of living dead.
The first one I quite liked was The North American Wood Frog (Rana sylvatica), which undergoes an extreme return from the dead each year.
Sup? I'm just defrosting.
The winter hibernation in northern North America is very important because of how long and extreme it can be. To up the challenge the wood frog hibernates in the leaf litter and consequently freezes solid during winter. By solid I mean properly solid. The frogs can survive multiple freeze/thaw events as long as less than 65% of their water remains unfrozen. Freeze/thaw stops my experiments on bacteria from working but apparently these frogs are just fine. To survive the big freeze the frogs accumulate urea in the tissues and build enormous glycogen stores which breaks into glucose upon ice formation in the tissues. The soluble urea and glucose prevent ice formation and save the frogs. This phenomenal life cycle enables easier and early access to the natal ponds where eggs are laid and tadpoles develop and must leave before the thawing dries up the pools. So the question was posed, is a wood frog alive during winter hibernation? Technically it's dead, no heartbeat, no metabolism and yet it survives. Does this make it a reanimated corpse? Very spooky.
There are lots of zombie ant variations that I could go to but my two favourites are zombifying fungi Ophiocordyceps unilaterius, which zombifies Camponotus leonardi ants and Dicrocoelium dendriticum which zombifies Formic fusca (the European common black ant).
All ants are creepy up close (Photo Credit: D. S. Sikes)
O. unilaterius infects the worker ants via its respiratory system and quickly spreads throughout the ant's body. Importantly the fungus spreads into the brain and the result is the ant alters the way it responds the pheromone messengers.
The zombieness of this interaction does not come from the death of the ant but instead the ant’s loss of ant-ness. Infected ants leave the colony (and in some cases are removed by the colony members directly) and climb. The climbing is very important as the fungus can only grow at a particular temperature and humidity. The ant must locate these conditions based on the chemical instructions of the fungal controller. Once a suitable environment has been found the ant performs its final act, it climbs underneath a leaf and grips with its mandibles, never to let go. Why the underneath? Because the fungus is sensitive to UV light. The fungus continues to grow and kills the ant in the process eventually resulting in the emergence of fungal stalks covered in spores that are sprinkled on the ground near the ant colony that provided the last victim. Is the ant, which continues to satisfy HOMR (except for the ‘R’ that it never did that anyway), actually alive when the fungus takes over? Or is it an animated corpse?
Not as creepy as when they look like this though.
Similarly the Formica fusca have to deal with the mind-controlling pathogen Dicrocoelium dendriticum also known as the Lancet Liver Fluke. The adult flukes reside in the livers of cattle and other grazing mammals and its eggs are released in the faeces of that animal. The eggs sit happily in the poo until consumed by snails. Once eaten the flukes drill into digestive tract of the snail where they develop into juvenile flukes. Obviously the snail would prefer that this didn’t happen and so attempts to wall the flukes of in cysts. It is these cysts that are eventually released by the snail.
The cysts are left behind in the snail trails, which are harvested by the F. fusca and as such this is how they get infected. Similarly to the activity in the snail most flukes get caught up in cyst but one fluke navigates to a bundle of nerves in the ants oesophagus and from there it controls the ants activity.
As the night air cools the infected ants leave the colony and ascend the grass blades and clamp down on the tops with their mandibles and waits. If nothing happens during the night the ant decends in the morning as the temperature rises and it rejoins the colony. However, occasionally a grazing animal will eat the ants along with the grass allowing the infective process to start all over again. Again is this ant alive during the day but a reanimated corpse at night?
Loner ant waiting to be consumed.
Like the fungus and fluke before it the pathogenic barnacle Sacculina is a mind controller but this barnacle has an even more sinister side. Sacculina are castrating parasites of crabs and their lifecycle is as fascinating as it is weird. A female Sacculina will find and attach to a crab exoskeleton and then move around on its surface looking for a gap through which it can invade. It then ejects its own hard shell as it invades the crab’s interior. Once beneath the skeleton the Sacculina infiltrate all parts of the crab but specifically have activity at the genitals of the crab. The male crabs are castrated and rearranged to become females and the female’s egg sack is infiltrated and becomes Sacculina’s new home.
In its new home the parasite prevents the crabs natural molting and regrowing of limbs, as this is not nutritionally beneficial to the parasite, which prevents the crab from growing and repairing damage. Over time a male Sacculina finds the lady Sacculina in its crab host and fertilises her eggs inside the crab. The crab is further manipulated to develop nurturing characteristics and behaves exactly like a pregnant lady crab should. Once ready to be released the crab follows its normal birthing behaviour of climbing to a high rock, massaging her egg sac... Read more »
Costanzo JP, Lee RE Jr, & Lortz PH. (1993) Glucose concentration regulates freeze tolerance in the wood frog Rana sylvatica. The Journal of experimental biology, 245-55. PMID: 8409827
Andersen, S., Gerritsma, S., Yusah, K., Mayntz, D., Hywel‐Jones, N., Billen, J., Boomsma, J., & Hughes, D. (2009) The Life of a Dead Ant: The Expression of an Adaptive Extended Phenotype. The American Naturalist, 174(3), 424-433. DOI: 10.1086/603640
Jones JL, Kruszon-Moran D, & Wilson M. (2003) Toxoplasma gondii infection in the United States, 1999-2000. Emerging infectious diseases, 9(11), 1371-4. PMID: 14718078
PHILLIPS, W., & CANNON, L. (1978) Ecological observations on the commercial sand crab, Portunus pelagicus (L.), and its parasite, Sacculina granifera Boschma, 1973 (Cirripedia: Rhizocephala). Journal of Fish Diseases, 1(2), 137-149. DOI: 10.1111/j.1365-2761.1978.tb00014.x
Tarry, D. (2009) Dicrocoelium dendriticum: The Life Cycle in Britain. Journal of Helminthology, 43(3-4), 403. DOI: 10.1017/S0022149X00004971
- April 8, 2011
- 10:45 PM
- 867 views
Yes We C(r)an(berry)!
by James Byrne in Disease Prone
That title is awful I know but I'm tired. Cut me some slack :) I ran into a something that I have heard about before but assumed was rubbish and never really looked into it properly. A friend of mine insisted it was the case so I looked it up and I have to say, I was a little surprised.
So this is what cranberries look like. I never knew.
Cranberry juice is apparently very good at prevent urinary tract infection, particularly in women. There have been a few studies approaching it from different angles but, disappointingly, the studies all use different types of cranberry product, different doses and dosing techniques but despite all this the message seems to be pretty clear. Cranberries prevent urinary tract infections kicking in.
Before we can consider how this occurs its important to define what we are talking about. Urinary tract infections or UTIs are generally caused by a strain of Escherichia coli called Uropathogenic E. coli (UPEC) and it gets there by moving from the colon…ew. For this reason men rarely have to worry about them while they can be a chronic problem for women around the world, however the insertion of urinary catheters is a major risk factor for both genders. Clinical symptoms include burning sensation during urination and cloudy urine but these are only really evident once the bacteria have ascended the urethra into the bladder causing urethritis and cystitis respectively. If you want to feel real pain however let the little bastards work their way into your kidneys where kidney infection (or pyelonephritis) results in the above symptoms plus back pain and fever and the possibility of systemic spread.
So the first step in the infective process is generally stable colonisation of the colon. This step is often overlooked but without a source of UPEC it’s hard to get a proper infection going. The next step is invasion of the vaginal microbiota. Not an insignificant task since the vaginal niche is normally fully occupied by lactobacilli and other innocuous strains. Only once this has occurred can the UPEC ascend the urethra.
Having ascended the urethra the UPEC are not in the free and clear because the bladder and urethra have a formidable barrier to infection, the waterfall of flushing, cleansing urine that washes away all in its path. To overcome this UPEC have developed powerful adhesins, proteins used adherence of the bacterium to a surface and in this case specifically to the urinary epithelial tissue.
Adhesins are found in most pathogenic bacterial species but the array and strength of the UPEC adhesins is staggering. Among the most important adhesins produced by the UPEC are the pili. Pili are hair-like structures on the bacterial surface that are often capped with sticky (in the molecular sense) ends that facilitate adhesion. Importantly for UPEC possessing three different sticky caps (S, P and Type 1 pili) increases the chances of binding.
The S pili tend to be more important for adhesion outside of the gentio-urinary tract and so may play a part in systemic spread. In the urine however these pili bind the mannose filled protein uromodulin. Because of this S pili are called mannose sensitive pili and its thought that the ability to bind uromodulin, the most abundant protein in urine, possibly results in bacterial clumping and this allows a better opportunity for the P and Type 1 pili to do their thing. These two pili are responsible for the binding in the urethra and bladder.
Initially the Type 1 pili bind mannose sugars on the surface of the bladder cells allowing the bacteria to get some traction on the bladder/urethra walls before the P pili bind to a different sugar group to cement the interaction. The ability of P pili to bind non-mannose sugars has earned them the alternative title mannose resistant pili whereas type 1 pili are grouped with the mannose sensitive S pili.
The pili are the hairy bits on the picture of E. coli. The paper this pic is from is referenced at the bottom.
Once adhered to the host surface the UPEC can invade the epithelial cells but the bladder’s defence against this is to kick those invaded cells into the urine. A good defence strategy but it may contribute to tissue damage in the urinary tract when infections are recurrent. Also it seems some bacteria can prevent this expulsion of the cell they have invaded and in doing so remain as a reservoir of infection out of the way of the immune system and most antibiotic treatments.
Invasion does not always occur and instead some UPEC strains are able to release toxins directly onto the host epithelial surface due to the close interaction between bacterium and host. These toxins, as well as one of my boss’s favourite little molecules lipopolysaccharide (LPS) cause the inflammation that goes with the UTI.
So that’s the UTI side of things but where does Cranberry juice come into this story?
Cranberries (Vaccinium macrocarpon if you don’t mind) together with blueberries and Concord grapes constitute the only native fruit species to the US and Canada. Bet you didn’t know that, or maybe you did but I didn’t. In any case often the best way to work out what the native flora is capable of you have to look back to the indigenous peoples and, surprise surprise, Native Americans have known about and utilised the medicinal properties of cranberries for many years. Commonly used in different preparations to treat blood disorders, stomach issues, liver trouble and fevers.
By the 1880’s people were trying to work out what was doing what with cranberries and some German researchers found benzoic acid in cranberries. Then as now it was known to be a potent antiseptic and was included in a number of medicines and topical anti-bacteria treatments. This observation set researchers down the wrong path from the get go as the real power of cranberries lies in other activities of other compounds.
Continuing research into the antibacterial properties of cranberries found the benzoic acid was converted to hippuric acid, another antibacterial agent that also has a role in acidifying the urine. Everyone thought they were onto a winner. A powerful antibacterial compound excreted in the urine because you ate some cranberries. This is open and closed right? Well…
Could I be any clearer... Read more »
Raz, R., Chazan, B., & Dan, M. (2004) Cranberry Juice and Urinary Tract Infection. Clinical Infectious Diseases, 38(10), 1413-1419. DOI: 10.1086/386328
Gross, L. (2006) Bacterial Fimbriae Designed to Stay with the Flow. PLoS Biology, 4(9). DOI: 10.1371/journal.pbio.0040314
BODEL PT, COTRAN R, & KASS EH. (1959) Cranberry juice and the antibacterial action of hippuric acid. The Journal of laboratory and clinical medicine, 881-8. PMID: 13801916
Sobota AE. (1984) Inhibition of bacterial adherence by cranberry juice: potential use for the treatment of urinary tract infections. The Journal of urology, 131(5), 1013-6. PMID: 6368872
- April 2, 2011
- 07:58 PM
- 919 views
Exploding Head Syndrome - No pun required
by James Byrne in Disease Prone
This is an old post from my previous blog. Recently it has been seeing a lot of activity so I thought I'd play around with it a bit and re-post it here. Enjoy :)
Sometimes when searching for disease to write about a wonderful thing happens. The clouds part, cherubs descend, angels play intricate harp-based musical compositions, and a beam of light illuminates the link to a wonderful disease. This happened to me the other day, and now, without further ado, let me introduce you to Exploding Head Syndrome. Best. Disease. Name. Ever.
Acute Exploding Head Syndrome sufferer (screenshot from the 1981 movie Scanners)
Okay so heads don’t actually explode but sufferers seem to experience a simulated explosion in the form of an incredibly loud noise coming from inside their own head. This sound can take many forms from ringing and screaming to, of course, explosions. One patient even described the preceding whistle of dropping bombs, the explosion of shells, and then complete silence, similar to an experience she endured as a child during the Blitz in London.
Exploding Head Syndrome is related to equally terrifying syndromes called ‘ice-pick headache’ and ‘needle in the eye syndrome’ but each of those have a pain component where Exploding Head Syndrome doesn’t (I can’t help capitalising Exploding Head Syndrome, it just feels like it should carry capitals).
The syndrome itself is described as “harmless but frightening” for sufferers. I guess the sensation that your head is about to explode isn’t pleasant but frightening doesn’t seem to be enough of a word to describe the torment.
Just to up the scare factor of this syndrome it seems to be associated with sleep. In a case study published in the British Medical Journal a woman described her attacks as…:“Being wakened by a sudden bang in the head, as if my head was bursting with a flash of light over both fields of vision, after which I would be dazed for a split second" [and then would] "Come round, terrified, my heart thumping. There was no pain, just a frightening sense of explosion.”Wow.
So what’s happening? Nobody has any idea. It isn’t auditory because deaf sufferers have been reported. It’s not linked to random nerve firing (often reflected in a condition called myoclonic jerks). It’s not linked to epilepsy. It’s not linked to migraines.
So we can’t understand what causes it, we have no idea what’s happening, we can’t say what might trigger it, it doesn’t seem to correlate with any associated conditions, apart from sleep – there’s only one thing missing here. Can we cure it? Of course not, what are you, stoopid?
There have been some reports that sedatives help but also, confusingly, apparently so do stimulants. Anti-depressants apparently help but not in all cases. The best bet for treatment seems to be to let it go away on its own. Many recorded cases had an acute onset where every night’s sleep was disrupted at least once and over a month to years the attacks became less frequent until they appeared to stop altogether.
I guess sufferers can take heart that if nothing else, being diagnosed with an Exploding Head makes for pretty interesting dinner party conversation!
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Listerine - Insensitive to Exploding Head Syndrome sufferers since 1914
Chakravarty, A. (2008). Exploding head syndrome: report of two new cases Cephalalgia, 28 (4), 399-400 DOI: 10.1111/j.1468-2982.2007.01522.x
Evans RW, & Pearce JM (2001). Exploding head syndrome. Headache, 41 (6), 602-3 PMID: 11437900
Kallweit U, Khatami R, & Bassetti CL (2008). Exploding head syndrome--more than "snapping of the brain"? Sleep medicine, 9 (5) PMID: 17709298
Pearce JM (1989). Clinical features of the exploding head syndrome. Journal of neurology, neurosurgery, and psychiatry, 52 (7), 907-10 PMID: 2769286... Read more »
Chakravarty, A. (2008) Exploding head syndrome: report of two new cases. Cephalalgia, 28(4), 399-400. DOI: 10.1111/j.1468-2982.2007.01522.x
Evans RW, & Pearce JM. (2001) Exploding head syndrome. Headache, 41(6), 602-3. PMID: 11437900
Kallweit U, Khatami R, & Bassetti CL. (2008) Exploding head syndrome--more than "snapping of the brain"?. Sleep medicine, 9(5), 589. PMID: 17709298
Pearce JM. (1989) Clinical features of the exploding head syndrome. Journal of neurology, neurosurgery, and psychiatry, 52(7), 907-10. PMID: 2769286
- March 11, 2011
- 06:24 PM
- 946 views
Capsular Polysaccharide and Pneumococcal Disease
by James Byrne in Disease Prone
A paper came out as an ePublication ahead of print this week looking at the capsular polysaccharide of Streptococcus pneumoniae. Want to know how I know? I wrote it :)
Insert stock photo of pneumo. Check.
It seems a little wrong to blog my own paper but in reality more people will read this blog entry than will read the paper itself, and that’s fine. Its relevance is very narrow and the work very preliminary but really it’s the drive behind the work that is important. So lets talk about Streptococcus pneumoniae (aka the pneumococcus or simply pneumo) for a second to set the scene.
Pneumo is a big deal. It is responsible for roughly a million deaths in children under 5 around the world every year and is such a problem in the developing world its one of the bugs that Bill and Melinda Gates have taken a personal dislike to.
This data is taken striaght from the WHO website. The only modification is I have added Streptococcus pneumoniae as a separate bar. Deaths caused by pneumo make up approximately 2/3 of all lower respiratory infections. I colour coded the bars for some reason for another post, I cant remember the key... #badblogger
Despite being such a huge killer it’s actually a very common bacteria. Every single person on Earth probably has it right now, so in that respect it’s not a great killer but at the same time, it doesn’t want to be. If you kill the host you destroy your home and food source so pneumo is happily carried in populations without causing disease, for the most part.
I have spoken about pneumo like there is only one kind of pneumo but that’s as silly as saying there is only one kind of human. An important common characteristic is that the outside of each pneumo, similarly to humans, doesn’t always look the same. In humans, differences in skin colour, texture, etc allows us to tell people apart, for pneumo however it’s the chemical composition of a structure called the capsule which encases the entire bacterium.
This capsule has, roughly, 90 different common variations and the distributions of these variations (referred to as serotypes) change depending on geographical region, age and community.
The important thing about the capsule is its job. The bacterium uses the capsule to hide from the host immune system, which is what generally triggers an immune response, and so allows the bacteria to persist asymptomatically in the naso-pharynx.
But as I hinted before pneumo doesn’t always sit happily in the naso-pharynx…
Generally during some other infection the pneumo will descend into the lungs and cause pneumonia, from which the bacteria derives its name. Approximately 30% of pneumonia patients will develop bacteremia as the bacteria use the lung damage to gain access to the blood. Once in the blood the bacteria can move all around the body and cause all sorts of disease but importantly they can cause meningitis (inflammation of the meningies in the brain) and this occurs in approximately 30% of bacteraemic patients.
Pneumo relies on its capsule to hide from the immune system during pneumonia, bacteraemia and meningitis (collectively called the invasive pneumococcal disease of IPD’s), but what if you take the capsule away? It turns out the immune system can ‘see’ the bacteria very easily without its capsule and so un-encapsulated bacteria can sit in the naso-pharynx but if they try to cause trouble the immune system can knock them out very easily.
This is where my work comes in.
Now it’s true that we can treat pneumo with antibiotics and we have two vaccines against pneumo but its still a massive problem. Something in the order of 60% of all clinical isolates show some level of antibiotic resistance with up to 10% showing resistance to 4 or more common antibiotics. The vaccines we have are also of limited use as one doesn’t work in children, where most of the disease occurs and the other doesn’t have enough ‘serotype coverage’ to be effective throughout the entire world.
To compensate for this my lab looks at alternative vaccines and that protective capsule layer. My work has really been to investigate how the biosynthesis of this layer is regulated and look for potential to break the regulation and in doing so prevent capsule formation and the invasive potential of the pneumococcus.
The regulation of capsule biosynthesis is achieved through a dynamic phosphorylation cycle that essentially acts like a switch.
This model was developed by my supervisor based on extensive mutagenesis work.
This is the current working model of the regulation. On the left we have the capsule being synthesised. The details are a little much for here but ‘C’ is a protein embedded in the membrane, it interacts with ‘D’, a tyrosine kinase. A tyrosine kinase is an enzyme that adds a chemical group called a phosphate to something else. In this system it actually adds that group to itself and when it does it forces itself to change shape. This altered shape in ‘D’ (represented on the right of the diagram) is thought to either change ‘C’s’ shape as well or the change is simply relayed through ‘C’ to the outside of the cell and production of capsule stops. Instead when ‘D’ is phosphorylated any complete capsule is stuck to the cell wall. As this process is not a one way switch we need to return to the left of the diagram and this is achieved due to the activity of ‘B’ which is able to remove phosphate groups from ‘D’.
For what was published in the paper we (or rather I) performed some mutagenesis on ‘C’ that resulted in it not being able to relay the change in shape of ‘D’. This resulted in switches jammed on to the left or the right but incapable of changing.
Importantly other mutants that have been constructed with an inability to switch capsule biosynthesis properly are unable to cause disease. Our hope however is to reach a point where we know enough about this system that instead of relying on a mutation in ‘C’ to give us a switching defect we might be able to design a drug or inhibitor that blocks ‘C’ activity in vivo. But that’s 5 – 10 years away.
I think I’ll just write this and my other experiments up into my thesis, then worry about the rest of the work that needs doing…
References... Read more »
Byrne JP, Morona JK, Paton JC, & Morona R. (2011) Identification of Streptococcus pneumoniae Cps2C Residues that Affect Capsular Polysaccharide Polymerisation, Cell Wall Ligation and Cps2D phosphorylation. Journal of bacteriology. PMID: 21378192
Morona JK, Miller DC, Morona R, & Paton JC. (2004) The effect that mutations in the conserved capsular polysaccharide biosynthesis genes cpsA, cpsB, and cpsD have on virulence of Streptococcus pneumoniae. The Journal of infectious diseases, 189(10), 1905-13. PMID: 15122528
- February 18, 2011
- 10:11 PM
- 1,115 views
Third hand smoking - Can we ban this poison already?
by James Byrne in Disease Prone
I’m not going to write a post on why smoking is bad, it’s too obvious and if you don’t understand why then your probably never going to find this post anyway. I’m not even going to talk about second hand smoking, ie. blowing your death cloud at me on the street. Again it’s obvious why it’s bad and may even be worse than smoking the cigarette itself as second hand smokers don’t get the benefit of a filter. No, this post is about third hand smoking, a fun new way smokers can harm those around them long after they have butted out.
Yeah. That looks healthy.
I want to say here I don’t hate smokers, just smoking. That position will change however if you smoke near my food or drink or blow smoke directly at me. If you do that I’m going to nerd rage and you will take both barrels from someone who has spent the last decade in biomedical science. Just a warning…
The terms first, second and third hand smoke describe where the smoke came from. First hand smoke goes directly from the cigarette into the smokers lungs, second hand smoke comes from the exhaled smoke or smouldering end of a lit cigarette into a non-smoking persons lungs and third hand smoke is the contamination and subsequent consumption of items in an environment after the cigarette has been extinguished.
As the smoke dissipates and becomes invisible we tend to forget about it but cigarette smoke is full of fine particulate matter that then settles on everything in the local environment. Subsequent cigarettes layer particulate on top of previous layers and so a build up occurs. The smaller the area you smoke in the quicker the build up, for example the worse place seems to be the car.
Sleiman et al. (2010) looked at the formation of carcinogens on surfaces by looking at the interaction of nicotine and nitrous acid (found in the air) and found that if they left a cellulose pad in a smokers car to absorb third hand smoke and react with the air they could collect known carcinogens. In total they found 11 different carcinogens including, wait for it, polonium-210!!!
Even the cigarettes are sad.
Of course smokers also carry around third hand smoke on their skin and clothes so they too are also a walking, talking source of contamination.
The harm in third hand smoke is exaggerated in children, which of course is excellent. Children have higher respiration rates and so take in second hand smoke faster but also crawl around on the ground and put things in their mouths which are covered in third hand smoke residues. That’s not anecdotal either, children consume up to 20 times the amount of dust that adults do and when third hand smoke residue is present children get the brunt of the exposure.
At this stage no specific diseases have been linked to third hand smoke exposure but it is only a matter of time. In 2006 the US Surgeon General stated that there is no-risk free level of tobacco exposure and with more than 250 identified dangerous chemicals in each cigarette that’s a bit of an understatement. Prolonged second hand smoking is now associated with all sorts of respiratory conditions and cancers. Given that third hand smoking was only first described in 2010 it wont be long till we identify associated problems with cigarette residue exposure. Given the exposure to children is exaggerated many are tipping currently unexplained developmental impairment as a serious consequence of third hand smoking.
So how do we deal with third hand smoke? Easy actually. Beg, plead, cajole and support everyone you know to quit. Clean all your surfaces regularly, particularly around children and quit! Seriously, please quit.
This blog is a no smoking area.
ReferencesAvol EL, Gauderman WJ, Tan SM, London SJ, & Peters JM (2001). Respiratory effects of relocating to areas of differing air pollution levels. American journal of respiratory and critical care medicine, 164 (11), 2067-72 PMID: 11739136
Sleiman M, Gundel LA, Pankow JF, Jacob P 3rd, Singer BC, & Destaillats H (2010). Formation of carcinogens indoors by surface-mediated reactions of nicotine with nitrous acid, leading to potential thirdhand smoke hazards. Proceedings of the National Academy of Sciences of the United States of America, 107 (15), 6576-81 PMID: 20142504... Read more »
Avol EL, Gauderman WJ, Tan SM, London SJ, & Peters JM. (2001) Respiratory effects of relocating to areas of differing air pollution levels. American journal of respiratory and critical care medicine, 164(11), 2067-72. PMID: 11739136
Sleiman M, Gundel LA, Pankow JF, Jacob P 3rd, Singer BC, & Destaillats H. (2010) Formation of carcinogens indoors by surface-mediated reactions of nicotine with nitrous acid, leading to potential thirdhand smoke hazards. Proceedings of the National Academy of Sciences of the United States of America, 107(15), 6576-81. PMID: 20142504
- February 4, 2011
- 06:14 PM
- 770 views
Flooding and disease
by James Byrne in Disease Prone
I’m not sure what the coverage has been like overseas but most of the east coast of Australia has been hit pretty hard. First there were biggest floods Australia has seen for a VERY long time that started in Queensland and continue to affect the east cost of Australia. Then, instead of letting Queensland off the hook for a few weeks nature hit the coast with a cyclone THE SIZE OF THE U.S.A. that might move so far inland that it could dump rain into my state, which is a desert, halfway across our island continent.
A map showing Tropical Cyclone Yasi superimposed over the USA / news.com.au
While all of this was occurring I was thinking about what kind of diseases we can expect in flood damaged towns. Luckily, nothing has surfaced and this has been attributed to the integrity of the water supply being maintained (against all odds it should be added) but it could have been so much worse.
Floods can potentially increase the transmission of water and vector transmissible diseases. A vector transmissible disease is the fancy way of saying an infection that spreads between humans but requires an intermediate host, a vector. Malaria is a vector transmissible disease due to the requirement of mosquitoes for example.
Rates of diarrhoea (including cholera and dysentery), respiratory infections, hepatitis A and E, typhoid fever, leptospirosis, and diseases borne by insects are often seen to increase in flood affected areas. However it has also been observed that the increased rates are often small unless water supplies are contaminated or significant portions of the population are displaced causing crowding in the remaining safe areas.
Of particular importance during floods is leptospirosis. This disease (known by lots of names with my personal fav being Rat Catcher’s Yellows) is caused by a spirochaete (kind of bacteria) called leptospira that is commonly found in rodent urine. In floods rodent populations explode and of course rodent urine gets mixed into the water. The leptospira can then catch a free ride to your insides though open wounds (plenty in a crisis) or directly onto your airways or gastrointestinal system. Once there the disease goes through two phases, the first of which is annoyingly general flu-like symptoms but the second phase, separated by a brief period without symptoms, sees the development of meningitis, jaundice and renal failure.
Vector transmissible diseases are generally only a problem if flood waters become still. The initial flow of water will generally wash away any established breeding sites for insects like mosquitoes but after the flow water tends to pool and with lots of water comes lots of mosquitoes. Malaria is always the concern with flooding but previous major floods have resulted in outbreaks of dengue and West Nile Fever so it very difficult to predict what will happen. Luckily, it seems that despite all the extra water its actually the change in human behaviour (sleeping outside, temporary break in disease control and overcrowding of disaster centres) that is the major issues. This is lucky because changes in human behaviour can always be modified with experience of disaster situations.
The final concern many have about disease spread during disasters and particularly flooding is the danger posed by corpses. The Queensland floods took many lives and there were concerns that these individual tragedies could result in the spread of disease. Corpses actually pose very little threat as most agents in a body will die very soon after the host itself with the notable exception of HIV which can persist for up to a week. The major problem is if death occurred due to cholera or haemorrhagic fever both of which were not reported in the Queensland floods.
Flood-waters even got into the CBD
The Queensland floods and the continued devastation of Australia’s east coast (there have been reports of a monsoon in Victoria now as well) have been traumatic but it could have been much worse. The water supply staying safe for the majority of the crisis has undoubtedly saved thousands of lives and so while our hearts must go out to all those effected our thanks should go to the volunteers who helped in any way they could, including those charged with protecting the precious water supply and the medical staff who protected a state during a phenomenal crisis.
References
WHO: Flooding and communicable diseases fact sheet
Ohl, C. (2000). Flooding and human health BMJ, 321 (7270), 1167-1168 DOI: 10.1136/bmj.321.7270.1167
Howard MJ, Brillman JC, & Burkle FM Jr (1996). Infectious disease emergencies in disasters. Emergency medicine clinics of North America, 14 (2), 413-28 PMID: 8635416... Read more »
Ohl, C. (2000) Flooding and human health. BMJ, 321(7270), 1167-1168. DOI: 10.1136/bmj.321.7270.1167
Howard MJ, Brillman JC, & Burkle FM Jr. (1996) Infectious disease emergencies in disasters. Emergency medicine clinics of North America, 14(2), 413-28. PMID: 8635416
- January 25, 2011
- 06:51 PM
- 884 views
The Australia Antigen
by James Byrne in Disease Prone
I feel a little left out some times on the internet as many (but certainly not all) of my bloggy friends are English or American. So, just to fill you in, the 26th of January is Australia Day and it commemorates the landing of our first fleet in 1788 and the planting of the British flag in what was then known as New Holland and is now known as Sydney Cove, New South Wales, Australia. Most people celebrate the day with a public holiday, a beer or two, a barbi and the TripleJ Hottest 100.
We will get back to the Australiana theme in a moment but I want to take it down a notch first by talking about Hepatitis B virus.
Hepatitis diseases are not limited to those induce by viruses. In fact hepatitis just means inflammation of the liver from hepat(o)- for liver and –it is meaning inflammation of. This has led to the common misconception that the Hepatitis viruses (A, B, C, D, E) are related to each other, they’re not, but they do all cause liver inflammation. In fact according to the Balitmore Classification of viruses they fall in completely different families. Furthermore the run of letters, which also suggest relatedness, simply describe the order in which the viruses were identified.
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The Baltimore Classification describes the lifecycle of all viruses based on their genome structure. Protein is produced based on the mRNA sequence so that’s why all lines flow back to mRNA.
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While all are problematic in their own way for this post we are interested only in Hepatitis B virus (HBV), arguably the biggest problem in the (not) family of hepatitis inducing viruses.
How big a problem is HBV? Well, approximately 2 billion people worldwide are infected, greater than 350 million people are in the chronic phase of infection and its estimated that a quarter of these people will die of liver cancer or other complications directly caused by HBV.
Like many viruses encased in a membrane (a so called enveloped virus), HBV requires body liquid exchanges to transmit from person to person but is not necessarily picky as to which liquid and transmission has been observed by blood exchange, sexual contact and even maternal-foetal exchange across the placenta.
HBV disease is very well characterised and follows a fairly generalised route. Following transmission the viruses work their way into the blood stream and eventually find their way into the liver where they can attach and enter liver cells. Once inside the cells the virus and its components are very stable and viral replication kicks in resulting in huge numbers of virus being produced and seeking out new liver cells. This infection stage can last up to 6 months with almost no symptoms beyond generalised flu-like symptoms or a touch of jaundice.
Following initial viral replication there are three outcomes are possible. Best case scenario, you mount an early, strong and effective immune response that removes all the virus from your system. Worst case scenario #1 (short term), you develop a form of acute hepatitis called fulminant hepatitis which is caused by your immune system reacting too strongly and liquifiying your liver in an attempt to remove the virus resulting in a quick death. Worst case scenario #2 (long term), your immune response is slow or weak and the virus persists resulting in a chronic infection. An interesting little side note here is that if you are a child your chances of developing chronic hepatitis B skyrocket to 95% compared to the 5% chance to adults and at this stage we really don’t understand why.
So your either fine, dead or a time bomb and chronic sufferers can look forward to a life of medications attempting to prevent death. Having said that some chronic HBV patients go on and live lives free of complication or further symptoms but most end up with either a passive or active form of liver destruction depending on whether you show any symptoms or not respectively.
The destruction of the liver is immune mediated which mean the virus doesn’t actually kill liver cells but its presence activates the immune system inducing it to kill any cell with virus. As the liver can regrow your left with constant cell death and constant cell renewal but it all comes at a cost, scars. Scars in tissues are called scar tissue (duh) or more accurately fibroma. Fibromas are a problem as they impair organ function and when you develop too many the organ starts to die as blood cannot flow to all parts of the liver or promotes the liver to overcompensate and regenerate faster leading to cancer – hepatocellular carcinoma.
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Pic courtesy of my good friend Thomas Tu from the wonderful blog Disease of the Week. In unvaccinated hosts this is the pathway through HBV infection.
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So what can we do about HBV? Currently your best option is vaccination. Its pretty cheap (for me it was any way), very safe and really effective. As well as being the best option, its kind of the only option as all the anti-viral drugs currently available do not ‘cure’ the virus, they can only act to freeze or pause it. When you stop the drugs the virus un-pauses. As I will most definitely talk about at a later date vaccines are ... Read more »
Blumberg, B. (1984) Landmark article Feb 15, 1965: A "new" antigen in leukemia sera. By Baruch S. Blumberg, Harvey J. Alter, and Sam Visnich. JAMA: The Journal of the American Medical Association, 252(2), 252-257. DOI: 10.1001/jama.252.2.252
Lee WM. (1997) Hepatitis B virus infection. The New England journal of medicine, 337(24), 1733-45. PMID: 9392700
- January 21, 2011
- 06:13 PM
- 1,012 views
Halitosis - Your mouth smells like arse
by James Byrne in Disease Prone
Sometimes I'm going to write about rare cancers or blood diseases and sometimes I’m going to write about bad breath. That’s just the way I roll.
Halitosis literally means “condition of the breath” and has many causes and just as many home remedies. Original therapies (and by original I mean 1550 BC) like heavily herb infused wines didn’t remove the bad breath but like mints and other modern treatments they just attempted to cover the bad smell with something more pleasant.
Halitosis isn't limited to humans. Ever smelt a dogs mouth?
Halitosis can be divided into two distinct problems, transient halitosis (morning breath) and chronic halitosis. While the difference between these conditions is the time frame of affliction both have the same root cause. Sulphur.
A study by Suarez et al. looked at what caused the odour in people with morning breath and found that the unique smells produced by people were due to three sulphurous gases combining into a malodourous mixture. The gases, hydrogen sulphide (smell of rotting eggs), methanethiol (smell of rotting cabbage) and dimethylsulphide (which has a slight sweet smell), were present in varying quantities between participants giving them all bad morning breath.
The sulphurous gases are produced by bacterial build up in the mouth and in particular on the tongue. During the night your production of saliva drops significantly and with less saliva bacterial numbers increase dramatically. Saliva has a number of jobs in the mouth related to bacterial load but its three main roles are to acts as a tidal wave to wash bacteria out of the mouth, to inhibit bacterial growth using various chemical components and participate in the killing of bacteria by carrying parts of the immune system into the mouth. But less saliva equals more bacteria and consequently, bad breath.
Given this it wasn’t surprising that the treatments that Suarez et al. found good immediate treatments of halitosis (I say immediate because as saliva production increased the bad breath went away naturally) where mechanical scraping of the tongue. Specifically brushing of the teeth with toothpaste did nothing but brushing of the tongue with water was much more effective. Eating a dry bread roll was also very effective as it scraped across the tongue, removing bacteria.
The best treatment was a mouthwash of 5mL of 3% hydrogen peroxide – guess why. This treatment killed huge umbers of bacteria and immediately dropped the concentration of the sulphurous gases, which stayed low for hours afterwards.
While rare there are a few conditions that produce halitosis that has a non–oral origin but they are extraordinarily rare and halitosis is but one of a bevy of symptoms that the patient would possess.
Foetor hepaticus, or the ‘breath of the dead’, is seen in people with late stage liver failure. It is caused by the passage of thiols from the blood into the lung. These compounds are normally removed in the liver but as the liver shuts down thiols remain in the blood and can escape into the lungs. Apparently distinct from typical halitosis foetor hepaticus smells of sweet faeces.
Another condition, known as trimethylaminuria is also known as fish odour syndrome. People suffering from trimethylaminuria lack the metabolic enzyme Flavin containing monooxygenase 3 which breaks down trimethylamine to trimethylamine oxide. The result is that trimethylamine builds up in the blood and is removed in the urine, sweat and breath. Despite its name an odour of fish is rare and most sufferers just have an unusually strong and sometimes unpleasant odour.
So if you have halitosis, but don’t have late stage liver failure or metabolic disease, you can treat your bum breath with breakfast and mouthwash if you pedantic. So no excuse for blowing it in my face on the train from now on!
Reference Suarez FL, Furne JK, Springfield J, & Levitt MD (2000). Morning breath odor: influence of treatments on sulfur gases. Journal of dental research, 79 (10), 1773-7 PMID: 11077993... Read more »
Suarez FL, Furne JK, Springfield J, & Levitt MD. (2000) Morning breath odor: influence of treatments on sulfur gases. Journal of dental research, 79(10), 1773-7. PMID: 11077993
- January 7, 2011
- 07:02 PM
- 830 views
Jumping Frenchmen of Maine Syndrome
by James Byrne in Disease Prone
Well I’m back! I’m not going to pretend like you missed me but I hope your glad to see another post out of me. I did a bit of writing during my time off to build up a bit of a backlog so hopefully I can keep posting regularly for a while. Anyway, without any further ado…
Jumping Frenchmen of Maine Syndrome
Best. Disease. Name. Ever.
This disease was first observed in 1878 by the neurologist Dr. George Miller Beard, a guy I will definitely talk about again, in French-Canadians, lumberjacks and presumably some French-Canadian lumberjacks living in northern Maine. So that explains the “Frenchman” and “Maine” parts but lets look at what makes this a “Jumping Syndrome”.
This is the famous jumping Frenchman Patrick de Gayardon. He has nothing to do with this story. Left Right.
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This syndrome is due to an exaggerated startle reflex resulting in uncontrolled jumps commonly but can also manifest as spasms throughout the body. The startle reflex is very important and forms part of the ‘fight or flight response’ normally.
Essentially a startle (which by definition has an auditory component) has three major neurological routes in the brain that have a number of effects. First, the auditory nerve fibres stimulate the cochlear root neurons (CRN) that form the first part of the central nervous systems auditory processing. Following this stimulation the CRN’s stimulate the nucleus reticularis pontis caudalis cells (PnC) located in the Pons (part of the brainstem). Finally the input into the Pons results in stimulation of motor neurons, particularly to the head and neck and the spinal cord. This results in the jerking response aimed at orientating you to the source of the startle while also priming your body for a response.
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Left shows brain side on with exposed brain stem and pons are highlighted while right shows the dorsal view of the brain stem (dorsal means back, think about the location of the dorsal fin on a dolphin) with the CRN highlighted.
One thing that I think is important to point out is how fast this all is. The time taken from the detection of the stimulus to the first muscles to react (in your jaw) is roughly 14 milliseconds! The last muscles to react (unsurprisingly in your feet and legs) receive stimulation after only 400 milliseconds!
Jumping seemed to not be the only unusual response in the Jumping Frenchman. Some exhibited echolalia (one of my favourite words and albums) or echopraxia. Others yelled, spasmed or hit out and another observation was made that confused matters further. Some jumpers would inexplicably follow commands given alongside their stimulus including one man who was startled whilst being given an order to throw causing him to launch the knife in his hand across the room. This was observed to be repeatable and the sufferer was ordered to throw a bunch of objects including a pipe he had just finished packing.
Researchers have looked for something in this community to explain this unusual stimulus response. This isolated community exhibits all the hallmarks of a population that might result in mutations that could develop and persist. Lending credence to this possibility were Beard’s original observations that the jumpers were confined to family groups but so far no genetic analysis has show a causal link to the condition.
These studies have suggested a different cause. In particular the work of the Saint-Hilaire’s which involved videotape evidence of a number of sufferers seems to suggest the response is psychological, not neurological, and may have been brought on by positive re-enforcement of this unusual behaviour in the small community.
Whatever the cause the disease still has a funny name. Almost feels like it should have been a Monty Python sketch if you ask me.
References
Saint-Hilaire MH, Saint-Hilaire JM, & Granger L (1986). Jumping Frenchmen of Maine. Neurology, 36 (9), 1269-71 PMID: 3528919
Saint-Hilaire, M., & Saint-Hilaire, J. (2001). Jumping Frenchmen of Maine Movement Disorders, 16 (3), 530-530 DOI: 10.1002/mds.1080
... Read more »
Saint-Hilaire MH, Saint-Hilaire JM, & Granger L. (1986) Jumping Frenchmen of Maine. Neurology, 36(9), 1269-71. PMID: 3528919
Saint-Hilaire, M., & Saint-Hilaire, J. (2001) Jumping Frenchmen of Maine. Movement Disorders, 16(3), 530-530. DOI: 10.1002/mds.1080
Howard R, & Ford R. (1992) From the jumping Frenchmen of Maine to post-traumatic stress disorder: the startle response in neuropsychiatry. Psychological medicine, 22(3), 695-707. PMID: 1410093
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