When the wind blows

.. the cradle will rock. So the rhyme goes, reminding us that the elements are indiscriminate in their destructive actions. At the time of writing Tropical Cyclone Iggy lingers off our shore, still a little undecided on if and where to make landfall.

TC Iggy

The Australian Bureau of Meteorology website provides a useful introduction to cyclone climatology. The northwest WA coast is the most cyclone-affected coastline in Australia. The annual averages are:

• 5 tropical cyclones form off the northwest coast
• 2 cyclones come ashore
• 1 of these will be severe, most often in March or April

Making tracks

Cyclone tracks vary considerably, some making U-turns or even loops. However, BOM notes that there is a preferred route starting in a south westerly direction, then turning more southerly and eventually south easterly when they travel as far south as the Pilbara.

The link with melioidosis

The path cyclones follow has been a matter of interest to the Micrognome for some time because of the link between melioidosis and severe weather in northern Australia. His team noticed there was a correlation between the direction cyclones took in a given year and the number of cases of severe disease.

Cyclone dynamics

Cyclone physics is complex and reflected in the variability of their destructive effect, wind speed, rainfall and duration. In general, BOM notes four main stages in the life-cycle of a tropical cyclone: formative, immature, mature and decay. We noted that the years when more cases occurred were years in which cyclones made landfall over the Northern Territory then followed a south westerly track. Years with cyclones approaching exclusively from the West and making landfall over the Kimberley or Pilbara coast were not bad years for severe melioidosis.

The fluid dynamics of interaction between a cyclone and the land it passes over  are most definitely complex. An added level of complexity is the rainfall that occurs in the cyclone’s decay stage. This looks like it may explain some of the excess cases observed in the NT.

At least we can predict cyclones like TC Iggy are unlikely to cause extra cases of melioidosis, while the likes of TC Carlos (see moving image) are a different kettle of fish.

Melioidosis info sources

• melioidosis clinical guideline
• the treatment of melioidosis
• melioidosis, a disease of surprises

The Aftermath of the Western Australian Melioidosis Outbreak.

The 1997 outbreak of septicaemic melioidosis in a remote northwestern Australian community marked a watershed in public health microbiology response to bacterial infections in regional WA. This was the first time we attempted to put a scratch team together to provide immediate disease control measures, on-site environmental microbiology assessment and follow up with molecular epidemiology. This post looks at the aftermath of the melioidosis outbreak.

Much has been learned in almost a decade and a half since the event; most notably the role of the drinking water supply as a means of distribution of the causal agent, Burkholderia pseudomallei. Though we still don’t know exactly what the final means of exposure was, the disease control measures introduced in a hurry just before Christmas 1997 and the additional measures rolled out when we identified contamination of the water treatment installations a year later appear to have worked. There have been no further septicaemic cases attributable to exposure after the original outbreak in the last decade. It therefore looks like we may have stumbled upon an unexpected method of melioidosis control. Certainly not the only effective method, but at least it’s a start.

The other big insight has been the potential for occasional long distance movement of the causal agent, B. pseudomallei as a result of severe weather events. We’ve known for some time that severe weather in northern Australia coincides with an increased occurence of melioidosis cases, but the incidental observation that peak years for the infection in WA are when tropical cyclones approach the state from a landward direction. At this point the association is based on 10 years’ data generated as a result of disease notification in WA. It will be interesting to see how this shapes up over a longer period.

Disease notification has already alerted us to possible effects of climate change on the epidemiology of melioidosis. It should also allow monitoring of the results of agricultural and mining development in the State’s north. Clearly we need to keep a close eye on the impact of industrial cultivation of rice in the Kimberley, since melioidosis is a disease of rice farmers in Southeast Asia. Mine sites and other large scale industrial developments significantly alter soil conditions and bring workers into contact with the soil. This may also change the melioidosis risk in tropical WA.

Carefully organised and effectively targeted surveillance will help pin-point the risk and deliver disease workable control measures. Lessons learned in the aftermath of the 1997 melioidosis outbreak may bring wider benefits to the booming norther part of the State.

About melioidosis.

References:

• The Aftermath of the Western Australian Melioidosis Outbreak.

MicroGnome, 6-JUN-11.

5 key points on fever in international travellers (clinical problem)

• a travel history should be obtained from anyone with a febrile illness
• malaria should be excluded in anyone with a fever who has been in a malaria-endemic area recently
• then consider dengue & other arbovirus infections if there has been mosquito exposure
• do not forget the neglected bacterial tropical infections: enteric fever, leptospirosis, scrub typhus & melioidosis
• do not forget to ask about potential risk for sexually-transmitted infections & HIV/AIDS

6^th World Melioidosis Congress, Jupiter’s,  Townsville,  1^st-3^rd December, 2010.  

Highlights

Identifying and unravelling the known unknowns in melioidosis epidemiology. Bart Currie.  Melioidosis is a major cause of disease in Thailand, Malaysia, Singapore and Northern Australia. In Cambodia there are significant differences within the country e.g. not many cases in Phnom Penh, but a lot in rural locations such as Siem Reap. Global spread with introduction into SE Asia, is believed to have occurred during the last Ice Age. There are unexplained locations such as Aruba, East and West Africa, Madagascar and desert locations such as Arizona. Dissemination has been proposed via animals or plants and soil, but long range transfer via human travel or by birds has not yet been demonstrated. Environmental determinants have been identified e.g. rice paddies, exotic animals, bore water supplies, sports fields and savannah grasses and landscape changes are not been documented and used to develop predictive maps. Genome analysis has shown evidence of horizontal gene transfer from other bacteria including other Burkholderia species that co-habit with Burkholderia pseudomallei, and identified over 100 gene islands. But it still remains to be seen whether B. pseudomallei is a true biothreat agent or an environmental opportunist. In recent reviews of NT culture positive cases, 14% had fatal infections but none of these were previously healthy. It is still not clear whether there is a subset of really nasty strains among the clinical variants such as those responsible for neurological infection.  The mode of infection is believed to be mainly inoculation, though severe weather is thought to cause a shift in favour of inhalation. The global extent of environmental B. pseudomallei is not known, nor its means of long distance spread, nor the environmental drivers of bacterial load.

Development of Ceftazidime resistance by Burkholderia pseudomallei following human infection associated with large scale gene deletion. Narisara Chantratita. B. pseudomallei was isolated from a patient with multiple splenic abscesses who failure therapy. The isolate had a Ceftazidime resistant phenotype (MIC > 256 ug/mL), was nutritionally variant and produced filamentous forms. It only grew on Ashdown’s agar, and not on other solid media. MLST genotyping indicated that it probably developed from the original B. pseudomallei isolate. A comparative genomic hybridisation array showed a 71kb deletion of 49 genes on chromosome 2 associated with penicillin binding protein.

Glibenclamide is anti-inflammatory and associated with reduced mortality in patients with septic melioidosis. G Koh

Glibenclamide is anti-inflammatory and associated with reduced mortality in patients with septic melioidosis. Gavin Koh. In NE Thailand the majority of patients with septicaemic melioidosis have diabetes, but interestingly there is a reduced risk of death, contrary to expectations based on the diabetic mouse model. Careful epidemiological analysis showed that the survival benefit was restricted to patients receiving glibenclamide who had a 50% reduction in risk. The precise mechanism of action is unclear but there is no direct inhibition of B. pseudomallei growth. However glibenclamide was shown to reduce inflammasome assembly-related gene expression in polymorphonuclear leukocytes.

Melioidosis in Cambodia: clinical and epidemiological data in 58 patients. Erika Vleighe. The first work on melioidosis in Cambodia was reported in 2008 by Wuthiekanun and colleagues who studied the epidemiology of an apparently emerging infection. There were then two documented clinical cases. Prospective studies on melioidosis have identified 58 cases since then, mainly from southern lowlands and particularly in diabetic farmers. 11.5% blood culture isolates in the Prince Sihanouk Hospital grew B. pseudomallei. A high proportion of septicaemic cases developed septic shock.

Reservoir for melioidosis in Townsville city. Anthony Baker. Melioidosis cases in Townsville cluster around Castle Hill. An environmental sampling method was developed but due to Taq polymerase inhibition, direct NAA was abandoned in favour of an initial culture step followed by PCR. Systematic sampling was planned in transects, taking 50g soil at 30cm depth. A maximum of 114 CFU/mL B pseudomallei was recorded. Run off at W and SW from Castle Hill gave 14/16 PCR positive locations. A totl of 10 MLST types were found, with multiple sequence types in single water samples.

Utility of culture in the molecular era for the diagnosis of melioidosis. Vanaporn Wuthiekanun. In Thailand there has been an increase in melioidosis incidence from 9 to 20 per 100,000 population. Direct immunofluorescence is not commercially available. LAMP and conventional PCR methods based e.g. on the TTSS cluster have low sensitivity due to the low number of bacterial cells present.  Therefore we need to reconsider the role of culture and confirmation of identity by phenotypic methods such as API 20NE. From 1997-2006 2243 culture positive infections were followed. Blood cultures were collected on admission and after 10 days. 956 patients died (43%). The bacterial count was greatest is pus samples and lowest in blood cultures. The presence of B. pseudomallei in urine was associated with a poor prognosis, but only 24% patients with a positive MSU had urinary symptoms. A positive throat swab was 100% specific, but only 36% sensitive.Only 2 patients in more than 2000 had a Ceftazidime resistant strain on admission and in vitro antibiotic resistance developed in only 25.

Defining the true accuracy of diagnostic tests for the diagnosis of melioidosis using Bayesian latent class models. Direk Limmathurotsakul. The problem with diagnostic tests for melioidosis is that the gold standard is imperfect. The true sensitivity of tests for melioidosis is unknown, Hypothetical assessment suggests an apparently poor specificity and thus severe bias. Bayesian analysis has been applied to diagnostic tests for several decades. Given three tests (culture, IHA, IgM ELISA) applied to a single patient population, a mathematical model was developed, using Markov Chain Monte Carlo and a random walk with WinBUGS. A Bayesian latent class model predicts 60% sensitivity for blood culture and 70%  for IHA. ELISA has a lower predicted sensitivity but much higher predicted specificity. Is this hypothetical or actual? Culture should probably not be used as a gold standard test.

Molecular basis of antibiotic resistance mechanisms in Burkholderia pseudomallei: lessons for rational melioidosis therapy. Herbert Schweizer. Effective antibiotic therapy needs to take account of intrinsic and acquired mechanisms of antibiotic resistance. A series of tools compliant with Select Agent regulations have been designed. Two main mechanisms of resistance operate: PenA, a class A beta-lactamase, and BpeEF-OprC, an efflux pump belonging to the  resistance-nodulation-cell division superfamily (RND). PenA acts on beta-lactams including Ceftazidime. Some efflux pump mutants have reduced susceptibility to a specific therapeutic agent on exposure to subinhibitory concentrations of Trimethoprim or Doxycycline, so that resistance becomes dependent on the other antibiotic. Inhibitory combinations should be discouraged. Meropenem is preferable to Imipenem.

Burkholderia mallei and Burkholderia pseudomallei genomic analysis, evolution and insights into pathogen virulence. Paul Keim. The genome of B. pseudomallei is more than twice the size of Staphylococcus aureus, has two chromosomes and a high GC ration. It is difficult to sequence. The Sanger Centre’s work on B. pseudomallei K96243 provided a critical resource. Gene islands are easy to locate from the GC ratio. If a bacterial genome is clonally propagated, genomic diversity is driven by mutation. B. pseudomallei achieves diversity by lateral gene transfer including from other bacterial species e.g. Yersinia-like chemotaxis factor genes.10-15% difference between genomes corresponds to adaptation to different environments. In B. pseudomallei the extent of recombination contributing accessory genes beyond the core genome is extreme, and differs between Australian and SE Asian strains. A novel system of analysis has been developed around obligatory orthologous SNPs.

B. mallei, on the other hand, has fewer additional genes on new strain genomes. This is a closed and cloistered genome. It has a 0.84 consistency index, suggesting clonal propagation. However, there has is still some genetic variation due to an explosion of IS elements consistent with specialisation. Genome decay relates to adaptation or inhibition. B. pseudomallei, by comparison, has a promiscuous genome.

One instance of B. pseudomallei evolution has been noted involving a eight year series in an animal model. Involving two missing regions, and a 200kb deletion. This may be similar to the natural process in B. mallei. There will be intra-host neutral variation. Hypermutable regions are subject to genetic decay. Selected variation is likely to be a very rare event. E.coli O157:H7 has a highly clonal, specialised genome with little evidence of horizontal gene transfer. The problem with next generation sequencing that relies on autoassembly is in seeing something new.

A genomic survey of positive selection on Burkholderia pseudomallei provides insights into the evolution of accidental virulence. Tannistha Nandi.  B. pseudomallei shows evidence of a complex co-evolutionary process. Adaptation has resulted from a range of selection pressures, possibly contributing to the emergence of virulence. B. pseudomallei genomes were sequentially analysed: SNPs, indels (minor fractions) and SNP microgenome variations corresponding to geographic location. A positive selection process led to selection of a range of adherence, membrane functions and stress response. A proportion of the core genome is subject to functional selection, leading to accidental pathogenesis.

Association of soil properties, landscape position and causative agent with melioidosis case distribution in Townsville, North Queensland. Maree Corkeron. Spatial clusters of melioidosis occur around the Ross River. Statistical analysis of clusters and their relationship to five key soil landscape types including Piedmont slopes, undulating uplands & alluvial plane deposits. Analysis included clay abundance, mineral content, pH and topography. The landscape model shows depressions, flats, slopes and crests. Cases were located more with flats, than depressions, slopes or crests, contrary to expectation based on depth and waterlogging.

Effects of landscape change ecology upon Burkholderia pseudomallei in the Top End of Australia. Mirjam Kaestli. B. pseudomallei has been associated with disturbed soils in gardens. Organic and NPK fertilisers are both associated with increased B. pseudomallei counts. Analyses at test sites have included soil moisture, clay content, urea, soil pH and organic fertiliser. An association has been made with invasive mission grass. Hotspots have been determined that correlate with introduced Tully, Paspalum and Mission grass varieties. It remains to be seen whether bacteria and grasses prefer the same environment or have a specific association. However, fluorescent in situ hybridisation shows B. pseudomallei outside the stomata and in the root hairs of grasses in vitro. Wild rice, however, was not affected.

Notes by the MicroGnome, 1-3 DEC 2010.

It’s that time of year when all are on the move, and most have caught a bad dose of LETICE (Leave Early Today Is Christmas Eve). We hear it’s been so bad this year with the run-up to a four day holiday that government departments have been granting special LETICE Leave. This could be made a lot worse if there are outbreaks of RELATED (REturn Late After The End of December) disease.

The MicroGnome is glad to report that all those who were travelling away from gnome have safely reached their intended destinations. Whether or not you believe in climate change, Father Christmas or other explanations for global catastrophe, southerners have had to skirt floods while travelling north and northerners have had to brave ice and snow while travelling south. Both contingents may have to grapple with seasonal infections of greater importance than LETICE or RELATED disease. The northern winter is a great time for respiratory infections and particularly pandemic influenza (H1N1/09), which can cause severe pneumonitis or set the scene for a secondary staphylococcal pneumonia. The corresponding period in northern Australia is the wet season when melioidosis peaks. This year should be a big season thanks to floods and a high level of cyclone activity.

• Western Australia
• Northern Territory
• Queensland
• New South Wales

With those sober thoughts, we wish you all a Happy Christmas and look forward to your comments in our second year of blogging.

The MicroGnome.

The closing stages of this year has been marked by a flurry of activity in the priobe universe.

• We recently marked the passing of the Frank Fenner, whose work on the eradication of smallpox was probably his most valued contribution in a long and highly productive career as a virologist. He was still contributing to professinal meetings until shortly before his death.
• Last week saw the 6th World Melioidosis Congress; a meeting that brought together infectious disease physicians, microbiologists, immunologists, epidemiologists and other melioidistas to review progress in this steadily growing corner of priobiology.
• We also heard from NASA scientists about a fascinating species of extremophile bacteria capable of metabolising Arsenic. While some may have been disappointed that the announcement was not an actual extraterrestrial species (unless you count aquatic environments as extra-terrestrial), the discovery has excited the attention of bacteriologists who were quick to grasp the significance of a self-sustaining metabolism that could effectively utilise alternative (toxic) substrates. Some possibilities there for bioremediation, perhaps.
• Then in this corner of the globe we presented data on the decline in Mycobacterium bovis infections. Could this be a public health success story?
• And finally, the MicroGnome has been preparing to travel with a purpose again. More on this in the next MicroGnotes.

5th December, 2010

Legend has it that in the dim and distant mists around the dawn of time a tiny typing (sic) error let to the term “whole gnome sequencing” being substituted for “whole genome sequencing”. Nothing more than a slip of the key (or single nucleotide deletion), and quite easily missed at the initial proof reading stage. The rest, as is painfuly evident from this Blog, has been put down to history.

Courtesy D Ussery, Biocentrum.

But after that brief historical preamble, now is the time to note the publication of several draft bacterial genomes from the genus Burkholderia. The fifteen reported in this paper include 5 from the WA group, including the WA outbreak strain Burkholderia pseudomallei NCTC 13177, the persistently mucoid phenotype B. pseudomallei DM 97, the Brazil outbreak strain B. pseudomallei BCC 215, a B. thailandensis from Northern Australia and the very first B. ubonensis to be fully sequenced, also from WA.

These 5 bacteria bridge several critical divergence points in the proposed phylogeny of the genus Burkholderia and therefore illustrate why we are beginning to wonder whether the origins of the disease-causing Burkholderias lie in northern Australia.

For pseudomalleiologists and other wrinklies, could WA be near the root of all evil?

Socrates

Notes for last week’s four-lecture marathon can be found via the following links:

• Epi 1:  travel-associated infection risks: Tropical medicine masterclass, CDC Yellow book
• Epi 2: Priobes & the principles of aetiology: Principia ætiologica paper
• Diagnostics: identification & characterisation of biological agents of disease. Sepsis detectives, introduction to language of infection, substantives, verbs
• Melioidosis resource centre

Additional support materials are available to members of the University of Western Australia through WebCT.

The MicroGnome was busy in Queensland last week, revisiting his roots in soil microbiology at the 19th World Congress of Soil Science. His lecture on environmental aspects of melioidosis can be found on the Priobe Net via this link.

Other recent material on melioidosis and its corresponding priobe can be found either here on the Priobe Net or the MicroGnome site.

An editorial on melioidosis was posted recently by our colleagues at Life in the Fastlane.

Happy digging!

Make no mistake about it: our battle is with the germs. The front line is particularly volatile and liable to change in the immediate future. Here is an approximate view of the forces of infection ranged against us, subject to change on the arrival of more up to date disease intelligence.

The symbol conventions used follow the principles of campaign maps. You can see how thinly dispersed health units are in the northwest, compared to the disposition of immediate disease threats.

Those threats include arbovirus infections and neglected bacterial diseases, which you can follow on the Priobe Net and Life in the Fast Lane. Whitmore’s bacillus is particularly notable for its ability to lay low for many months and resurface when the conditions are right, to produce severe illness or less acute infection in pockets of disease activity throughout the Kimberley.  Leazar’s personal infection is unknown in this region, but other flavi-, alpha- and assorted other arboviruses are a potential mosquito-borne threat. The build-up of an unprotected civilian population in this region presents a possible vulnerability to the endemic infections of the area. Forewarned is forearmed.

No. Just for once this isn’t about mapping a microbial genome. This is where you can find some disease distribution maps for the infections we’ve already covered on the road to the FACTM pt 1 exam.

Try these out for size, making note of your answers as you go.

Download (PDF, 581.04KB)

The correct answers can be found via these links:

• neglected bacterial infections
• arbovirus infections

Happy hunting.

Once again melioidosis is in the news. Queensland Health’s Dr Jeff Hanna has highlighted the melioidosis hot spot recently identified in the vicinity of Townsville, and Darwin melioidosis export Prof Bart Currie fronts up on the ABC’s 7.30 Report tonight.

Changing climate conditions in the north, particularly in the northwest, are thought to be responsible for some of the apparent increase in cases that can be blamed on severe weather events. But occupational activities as diverse as expansion of farming, the mining industry and even the local film industry could all contribute to an increase in meaningful encounters with a contaminated environment, and therefore subsequent cases of infection.

For a recent on-line review on melioidosis, see Life in the Fast Lane.

The μGnome got out his set of paintbrushes today to refresh a set of disease maps for the forthcoming tropical medicine breakfast session at Sir Charles Gairdner Hospital.

Gone are the neat little red outlines carefully added to world map outlines. This is the genuine graffiti version in block colour – world distribution of scrub typhus and melioidosis, as of May, 2010.

The stand-alone maps will appear on the Priobe Net shortly.

Download (PDF, 618.35KB)

What’s the connection between Ena Sharples; the hairnet helmeted doyenne of Coronation St and tropical medicine? Coronation St afficionados would be hard pressed to place the sullen rows of back-to-back brick terraces with the humid tropics.

The explanation will be unveiled during next Tuesday’s tropical medicine breakfast in the Emergency Department seminar room at Sir Charles Gairdner Hospital.

You may glean a shrew idea if you take a look at the lecture notes before Tuesday.

Download (PDF, 830.79KB)

For those following the FACTM pt 1 series, the next instalment is just around the corner, if you’re planning your diary for next week. The face-to-face session will take place at the later time of  7:30am next Tuesday (25th May) in the ED seminar room at Sir Charles Gairdner Hospital, and will run for an hour in its usual two topic format.

Next week’s session is open to junior medical staff and there will be a light breakfast as usual. The MicroGnome apologises for not having the unit notes ready in time for this post, owing to an encounter with arboviruses in Queensland earlier this week. He assures you that the lecture material will meet the usual standard, and was inspired by recent fieldwork in tropical Australia.

Tuesday’s units will cover Leptospirosis, Melioidosis and Scrub Typhus; three infections prevalent in the Australian tropics. Reading for this unit includes:

• Leptospirosis – Oxford Handbook of Tropical Medicine p694
• Manson’s Tropical Diseases p1161 ff;
• Melioidosis – Oxford Handbook p700, Manson p1127 ff
• Scrub Typhus – Oxford Handbook p687, Manson p 885 ff.

Sorry to disappoint you if you were looking for an item on infectious diseases and the hygiene hypothesis or evolutionary biology.

This is a timely reminder from fellow micrognauts and their supporters in the Northern Territory of Australia. They note that the bacterial cause of melioidosis (Burkholderia pseudomallei) is alive and well in Darwin and other parts of the Territory. In fact this year (2010) is looking particularly bad from the figures they have collected so far: 72 known cases and 10 deaths from melioidosis, mostly occurring in vulnerable people with underlying diseases known to predispose to this infection.

Figures for northern Queensland and Western Australia have yet to be published, but weather conditions across northern Australia this year are grounds for believing that the number of cases will be up in all three northern jurisdictions.

The most recent edition of Geographical, the magazine of the Royal Geographical Society, features a series of articles on the theme of water shortage. Not only does the editor single out Australia for special mention of its challenging water supply problems, but sunny old Perth is singled out for special mention on the featured world map of water shortage.

The Atlas of Water, 2nd edn, Black & King

The map was reproduced from Black & King’s Atlas of Water. The μGnome has a soft spot for maps, probably because of their ability to depict complex aspects of our environment in ways that can be used to explain the geographic distribution of infectious diseases.

Water is clearly a big issue in Australia. Perhaps surprisingly, not only because there isn’t enough in the South. In the northwest, we get so much that agriculture is expanding prodigiously to exploit the increased annual rainfall. This change in northern climate has been substantial, and may be starting to have an impact on the pattern of tropical infections that connect with the environment – melioidosis and arbovirus infection, to mention two.

Is the climate putting us at greater risk of other infections? The issues are complex, and surveillance correspondingly difficult. Perhaps we are developing a septic climate, and maybe that make the μGnome a climate septic. These issues need careful analysis, dispassionate consideration and sustained debate in order to develop a robust appreciation of the main drivers. There are clearly alternative explanations for changing patterns of environmental infection such as direct anthropogenic change, resulting from local anthropogenic alteration to the habitat microbes an humans cohabit.

The majority of the global ecosystem is rural and therefore managed by rural communities whose emerging infections are often seen as a footnote to the range of diseases that challenge wealthier urban communities. The μGnome wonders whether changing patterns of neglected tropical diseases among neglected rural populations might serve as an indicator of long term environmental stress. The series of articles in Geographical paint a bleak picture of what’s happening to some of those populations. Maybe it’s time to take closer look at geographic distribution of environmental infections and ask whether any changes could be explained by large scale environmental stress.

From the little planes buzzing around like angry bees over Perth this weekend (Red Bull air race), you wouldn’t have guessed that the skies over Europe are still; airlines fearing the effects of volcanic dust on their airframes. Perth skies were clear on a beautiful autumn day, apart from small puffs of smoke released by the Red Bull competitors.

It’s all a bit apocalyptic: empty skies above Heathrow, nothing on the radar. There is a large European no-fly zone , with many operators cancelling flights. The effects are expected to continue for months; the more visible results of the huge plume of volcanic ash currently drifting over Europe.

Health authorities in the UK have predicted that the effects will be short lived. But will they? The μGnome notes that experts differ on the risk from volcanic ash when it starts to settle. The WHO has advised that people with respiratory disorders may be at risk until the air clears.  And then there are more subtle indirect effects, through reduction of visible and ultraviolet light. The immediate health effects of volcanic ash are described in a useful website here.

There has been a lot of  interest in the effects of ultraviolet light on bacteria recently. There are even suggestions that seasonal variations in UV may explain the winter predominance of invasive pneumococcal infection, and the summer predominance of melioidosis [1,2]. So when volcanos billow ash [3], water vapour and SO2 into the atmosphere, their UV blocking effect might have a knock-on effect on bacterial infection. The next few months should provide us all with a natural experiment. We watch the Beeb with interest [4].

Further information

1. pneumococcal infection and UV light: Let the sun shine in
2. melioidosis and UV susceptibility
3. Vulcanology 101
4. BBC reports on Icelandic volcano ash cloud

autumn skies over Perth, WA

Life in the fast lane, Jim, but not as we know it …

precordial thump has just posted a series of thumbnail sketches of pneumonia, complete with a series of questions. A good revision exercise on the range of clinical presentations you may encounter, aetiology, and antibiotic choice.

Go on; test your knowledge. You know you want to.

Here are a few questions to tickle the grey cells while you kick back and prepare for another week battling germs. You might even want to use the comment option to fire back dot point, short notes style answers:

1. Give a brief account of the Burkholderias
2. Explain the differences in virulence among Burkholderia species
3. Describe recent changes in the epidemiology of melioidosis
4. Why is melioidosis often considered a tropical disease?

Have a look around the site for clues before you finalise your answer.

μgnome, 20th March