Myiasis

Dermatobia larva, ca. 1cm long

Infestation of skin by fly larvae, which feed on living or dead tissue

There are three main variants of this condition: cutaneous, body cavity and accidental myiasis

1   Cutaneous myiasis

• bloodsucking, in which larvae attach to the skin and either bite or suck blood: Auchmeromyia, Tabanidae, Therevidae
• furuncular, in which larvae penetrate skin to make boil-like lesions: Cordylobia, Dermatobia, Wohlfartia
• creeping, in which larvae tunnel in the epidermis without completing their life cycle: Hypodermatinae, Gasterophilinae
• wound/traumatic, in which larvae develop in wounds: Calliphoridae, Fanniidae, Muscidae, Phoridae, Sarcophagidae

2   Body cavity myiasis

• nasopharyngeal, lung, auricular & ophthalmomyiasis in which eggs or larvae deposited in cavities: Calliphoridae, Oestridae, Phoridae, Sarcophagidae

3   Accidental myiasis

• intestinal, in which larvae ingested or enter via rectum: Anisopodidae, Calliphoridae, Drosophilidae, Fanniidae, Muscidae & others
• urogenital in which adults attracted to infected tissue or clothing: Anisopodidae, Calliporidae, Fanniidae, Muscidae and others

Larva of Dermatobia hominis, the cause of furuncular cutaneous myiasis in man, cattle, dogs, other mammals and some birds in Central and South America.

D. hominis is occasionally seen in international travellers from outside the region. Dermatobia belongs to the Cuterebrinae sub-family of the Oestridae family of Diptera. Their larvae have bodies with strong, evenly distributed spines and posterior spiracles with a lot of small, serpentine slits.

A small nodule with a central breathing pore develops around the larva at the site of penetration. These swelling usually last for a few weeks, before the mature larva emerges and drops to the ground to pupate.

Reference:

Hall MJR, Smith KGV. Diptera causing myiasis in man. Ch 12. ed Lane RP, Crosskey RW. Medical Insects & Arachnids. Chapman & Hall, London, 1993. ISBN 0 412 40000 6.

Micrognome, October, 2011

Leishmaniasis:  5 point summary of highlights, further details in leishmaniasis module of Tropical Medicine teaching series

• parasitic infection transmitted by the bite of a sandfly
• distinct skin, mucocutaneous & visceral forms of infection are known
• leishmaniasis is present in one or more of its forms in the Indian Subcontinent, the Middle East & Mediterranean rim, Central and South America
• some cutaneous lesions can be treated conservatively
• laboratory confirmation of diagnosis requires specialist pathology services

Dengue: 5 point summary of highlights, further details in arbovirus module of Tropical Medicine teaching series

• viral infection of humans spread via Culicine mosquitoes
• in rare cases may prove fatal
• clinical features may not distinguish dengue from other infections
• dengue can be acquired in tropical Australia
• no antiviral treatment is effective against dengue

Malaria: 5 point summary of highlights, further details in malaria module of Tropical Medicine teaching series

1. commonest fatal parasitic infection worldwide
2. prevented by avoiding bites from malaria-bearing Anopheles mosquitoes
3. all international travellers to malaria-endemic zone with fever on their return have malaria until proven otherwise
4. malaria cannot be completely ruled out by a single, one-off blood test
5. first line treatment recommended for uncomplicated malaria is based on an ACT-containing regimen unless good reason for choosing otherwise

Trop Med revision in a day? Who said it can’t be done.

Oxford Handbook of Tropical Medicine, 3rd edn

Here are some on-line resources to assist you:

1. Expedition medicine
2. Malaria
3. Fever in an international traveller
4. Arbovirus infections
5. Diarrhoeal disease
6. Enteric fever
7. Neglected bacterial diseases
8. Pneumonia
9. Snake bite
10. Envenomation
11. Leishmaniasis

Self assessment questions:

Clinical scenarios

Key information sources:

• WHO neglected tropical diseases
• CDC Yellow Book on travel health
• Oxford Handbook of Tropical Medicine
• Manson’s Tropical Diseases

It’s not that often the MicroGnome gets to see Leishmania promastigotes wiggling their little tails, but this week was the exception. Here they are, tiring a little after a couple of hours’ exertion in NNN media:

You can find more information on the group of diseases known as leishmaniasis via a previous post on Leishmaniasis and the parasites that cause it.

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.

The first thing you notice on your way into the Bairo Pité Clinic is a small collection of very grubby vehicles; some held together by stickers from sponsors and other aid organisations. Not a bit like the clean white UN Prados and Land Cruisers that line the streets of Dili, these vehicles take clinic staff and visiting volunteers to outreach clinics well beyond the city’s edge.

When your eyes adapt to the relative gloom under the awnings, you see a gaggle of prospective patients waiting their turn for an appointment with Dr Dan. Dan Murphy’s personality looms large in the Bairo Pité Clinic, an NGO that provides a large slice of the acute health care in Dili. An American physician, Dr Dan sees at least 250 patients per day and has dealt with over 500 at times of great need.  His tall stature, commanding presence and sharp clinical acumen attract a stream of visiting medical students and junior doctors who join his daily clinical rounds for a regular dose of teaching on the run.

It isn’t long before you start to hear the rattling, productive cough that afflicts many of the clinic’s patients. When asked what the commonest medical complain was, Dr Dan replied that it was without any doubt tuberculosis. You don’t need surveillance data to work out that TB is a huge problem here. But with only acid fast stains available and no concentration or culture methods, laboratory-confirmed aetiology of pneumonia is an unimaginable luxury.

Not just TB. So many of the other conditions seen are either primary infection or the consequences of infection. A snapshot from just a couple of days at the Bairo Pité Clinic included malaria, pelvic inflammatory disease, HIV/AIDS, infective endocarditis, post-rheumatic heart disease mitral stenosis, meningitis, soft tissue abscess and tropical ulcers. Tragically, many of these conditions were easily recognisable because they had been allowed to run their course by patients who lacked the means to do anything about it. Further compounding this sorry tale were the family groups represented by several members attending the same TB clinic.

I was there with a colleague from the Lab Without Walls Foundation, looking at the feasibility of establishing clinical laboratory support for detection of several tropical infectious diseases. We flew in with various bits of portable lab gear in a small collection of air freight boxes, hoping to show the potential for direct molecular analysis of clinical samples in a clinic without much pathology support.  We knew there was no culture, but did not know exactly what else had already been done.  One thing we were clear about was the need to hose down unrealistic expectations. We were very careful to explain that we were not there to make a diagnosis or to replace an existing conventional approach.

Our planned programme was simple but ambitious. In four days we would run a series of molecular tests at a rate of one type per day: septicaemia, tuberculosis, malaria and PID. We took additional back up for genetic fingerprinting of tuberculosis bacteria, and for identification of other mosquito and tick-borne diseases (dengue, Japanese encephalitis and scrub typhus). But someone mischievous had other plans. First of all, a public holiday was called for the first two working days of the visit, bringing about a modest change of plans and a change of location for our lab work. Secondly, the party mood spilled over to delay our start by a day, and lastly the return to work on our last working day was accompanied by a series of power cuts. Power outages caused run failures on each item of equipment we used, requiring repetition of tests, a great deal of ingenuity and a monumental dose of patience.

In spite of it all, and quite possibly because of it, we had good reason to join the party mood at the end of our working week. The reason we felt an urgent need to pop a bottle of champagne was successful demonstration of the bacteria that cause tuberculosis in clinical samples, starting from scratch. Every bit as exciting (for crazy bug hunters) was the detection of malaria by our in-house molecular method in samples that had been checked and declared negative by standard microscopic examination. Evidently, the molecular (PCR) method is more sensitive than blood film examination. What of the other tests? Time and power supply didn’t allow us to complete our preliminary work on these tests during the deployment. Development will have to continue back at the Western Australian home base. Those celebrations will have to wait until the next Lab Without Walls project deployment.

You have to wonder what health expectations the youngest generation of Timorese have. It is clear to anyone involved in international health development how much could be achieved with a small fraction of the resources at our disposal in Australia. There is another thought nibbling away at the back of the mind – with the right tools and the community support, it might just be possible to eradicate at least one of the headline infectious diseases within a generation. A worthy goal that could be brought a step closer by your support.

More detailed reports on how the work was done will follow: travel reading [FEVER, Sonia Shah, 2010].

MicroGnome’s correspondent in Dili, December 2010.

Lab Without Walls project 2010/Dili/01 is supported by

Now that the MicroGnome can reliably get lecture notes onto this Blog, here is the Malaria series for students of tropical medicine:

the London School of Hygiene & Tropical Medicine

No, not a reference to lyrics from the Waifs. More a matter of ruminating over the consequences of a flying visit to the UK capital; home of the London School of Hygiene and Tropical Medicine. The London School is the larger of the two remaining British centres of tropical medicine and maintains R & D collaborations with partner centres round the world; a truly international centre in more ways than one. The MicroGnome was there to plan yet more field research and deliver a lunch-time talk on the field applications of molecular microbiology [Field Apps LSTM 2010], and was rewarded with a day-long feast of medical microbiology with fellow micrognauts.

Also on the London itinerary was the map reading room at the Royal Geographical Society‘s Kensington Gore site. Think modern university library but switch maps for books. Heaven must have a map room. Micrognome was on a quest for early depictions of tropical Western Australia. He was rewarded by maps from the original John Forrest expedition to the Kimberley and Canning’s survey for the eponymous stock route,. It is so easy to view physical geography through Google Earth or with the aid of a GPS receiver; data which becomes obsolete every times the geosatellite passes by. Not for us the sheer hard, footslogging of travelling survey teams. Which makes the hand drawn survey maps all the more impressive. This may only be the surface with marginal notes on the topography and its flora. But these early geographical surveys are records of systematic exploration, and an expanding state economy. They provide us with time, date and location markers for the start of movements of livestock and other traffic which may have contributed to the distribution of zoonotic and environmental diseases. 

London is a complex city with many faces, and much to occupy the traveller beyond the headline tourist attractions. It brings to mind the sort of list you can probably find somewhere on the Net: 

you know you’re in London when:

• you recognise those old buildings from the label on a sauce bottle
• you hear a clock chime the hour and think it’s the lead in to the news
• the skyline has appeared in the Bill, Spooks and countless other series shown on the ABC
• they warn you to ‘Mind the Gap’ even when it’s only a couple of centimetres
• you can find your way round underground better than you can on top
• there’s a coffee shop, sandwich chain and old world pub on every street
• and the suburbs have names that must have been introduced by early Australian settlers

Clinical Case of the Febrile Returned Traveller

Ms A, a 23 year old aid worker who has just returned after half a year overseas. She spent six months on aid work in the Amazon region and had a two week holiday in Mozambique on her way home. She took no travel health precautions before or during her travel.

She developed fever and profuse diarrhoea on her last day in Mozambique, and went straight from the airport to the Emergency Department.

On initial examination she was alert and oriented, but unwell and dehydrated with a pulse of 120 and a blood pressure of 90/60. She had diffuse abdominal tenderness and a mildly enlarged spleen. Her chest was clear.

Q1. What is your differential diagnosis?

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The initial investigations were:

• Hb  100
• WCC  8.6
• Plts  25
• Na  135
• K  4.8
• Ur  13.7
• Cr 149
• Stool microscopy – no parasites seen

These blood investigations produced this result.

Q2. What are these investigations ?

Show answer

Q3. What is the result?

Show answer

Q4. What other widely available investigation would give a rapid confirmatory result?

Show answer

Q5. What treatment would you commence?

Show answer

The patient had a very stormy course.

• she was given 8L iv crystalloid in the first 24h, iv artesunate (SAS Category A, requiring informed consent), and exchange transfusion (6 units packed cells)
• despite this, she deteriorated and went into multiple organ systems failure and DIC, requiring 29 days in intensive care
• she was discharged from hospital, having lost 8/10 toes to necrosis

Additional resources

• other clinical problems
• malaria revision
• malaria files
• seafood poisoning & toxins

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.

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.

Manson’s Tropical Diseases. 22nd edn. Ed GC Cook, AI Zumla. Elsevier, 2009. ISBN 978-1-4160-4470-0

When a medical textbook reaches its 22nd edition, it has clearly become an institution. Manson’s Tropical Diseases has become one of the leading sources of authoritative opinion on tropical medicine in the English-speaking world. The most recent edition goes well beyond the standard fare of tropical infectious diseases to cover the challenges of other medical specialties in the tropics and a collection of non-infective conditions. This diverse range of topics has been presented to a consistently high standard; a notable editorial achievement for a topic with such breadth. 89 chapters are divided into 12 sections and supplemented by on-line material in a series of 5 appendices. It adds up to 1783 pages of carefully crafted professional writing.

From recent use [FACTM on-line modules; Malaria & Arbovirus Infections] I have been particularly impressed by Nick White’s magisterial chapter on malaria and David Smith’s group’s review of arbovirus infections. Both chapters are examples of lucid prose that is a pleasure to read for reading’s sake. They are also one of reasons Manson’s Tropical Diseases has sustained its success over so many editions, through making the familiar read as new while making the genuinely novel accessible to a wider audience. The editors have achieved this difficult balancing act by retaining many of their chapter authors from the 21st edition.

Manson’s Tropical Diseases is recommended further reading for the FACTM pt 1 exam.

Sections: underlying factors in tropical medicine, symptoms and signs, system-oriented disease, related specialties in the tropics, environmental/genetic disorders, viral infection, rickettsial infections, bacterial infections, mycotic infections, protozoan infections, helminthic infections, ectoparasites.

The satirist, Jonathan Swift (1667-1745) wrote in 1733 that “Hobbes clearly proves, that every creature lives in a state of war by nature.” While the arboviruses and their mosquito vectors can hardly be described as leviathans, they continue to have an impact on the health of many millions living in the tropics.

The Arbovirus Infections unit for FACTM pt 1 study is now complete. Lecture notes for both modules (FACTM Arbo 1, and FACTM Arbo 2) can be found via this site. The live version takes place in the Emergency Department seminar room, Sir Charles Gairdner Hospital,  at 06:50hr next Tuesday (11th May, 2010). Further details on the Calendar function of this site (right hand contents bar). Sources of supplementary information on arbovirus infections can be found on the Priobe Net.

No, this post has nothing to do with deception, mendacity or plain lying.

This is about the group of mosquitoes that includes Aedes aegypti; that carrier of yellow fever and dengue. A. aegypti has lyre-shaped markings on the upper surface of its thorax, black and white legs and is one of the most successful Culicine mosquitoes. Its close relative, Aedes albopictus, sometimes known as the “Asian tiger mosquito”, has a silver stripe along the length of its thorax. Both are featured in the lecture notes on Culicine mosquitoes, which form a part of the FACTM pt 1 Arbovirus infections.

So there you have it: ‘borne lyre’ is a helpful little mnemonic that links the arthropod borne (arbo-) viruses with the Aedes group, and A.aegypti, in particular.

Download (PDF, 715.69KB)

Not only is today ANZAC Day; it’s also the day we note the achievements and continuing challenges of the Rollback Malaria campaign – World Malaria Day.

To mark the occasion, the Lancet has run a special feature edition on malaria.

The μGnome has nailed his colours to the mast in our FACTM pt 1 malaria series. Here is a short summary; highlights of the malaria unit.

Download (PPT, 910KB)

Oxford Handbook of Tropical Medicine. Eddlestone M et al. 3rd edn. Oxford University Press, 2008. ISBN 978-0-19-920409-0

42 contributors. 22 chapters. 843 pages

This small textbook has been recommended by the Australasian College of Tropical Medicine as an essential core text for those studying towards the Part 1 Fellowship exam. There is good reason for this recommendation. This small, easily portable volume provides a comprehensive and authoritative guide to this area of clinical medicine. Its contents go well beyond the inner circle of tropical infectious diseases, envenomations and nutritional disorders to include tropical paediatrics, mental health, multisystem diseases and covers topics relevant to other areas of general medicine, obstetrics and gynaecology.

Guidance is practical and details of drug administration and other key aspects of acute patient management are plentiful.

This is the third edition, and contains a series of updates to the previous editions including new material on non-infective conditions such as heat stroke and altitude sickness. There is quite a bit of integration through cross-referencing and supplementary coverage in other chapters. For instance, the well-crafted chapter on Malaria (Ch 2) might have the last word on the infection, but there is also a well-made reminder about malaria in the chapter on multi-system infections (Ch 18: p668). Indexes can serve this function if you have the time to be methodical, but any busy clinician will tell you that pressure of work will rarely allow you that luxury. Well thought out contents and information layout are at the heart of a useful clinical handbook. As always, the proof of the pudding is in the eating, and in this case the Oxford Handbook stays on my desk, close to the phone. It gets used most days; more often than the authoritative Manson’s Tropical Diseases.

But no textbook is perfect. If I were asked to make any recommendations for the fourth edition I’d bring the contents list forward. Page ix buries the all-important contents between acknowledgements and a list of colour plates. Unfortunately the grey page markers do not line up with the contents list on p ix or the back cover. But these are cosmetic criticisms. The heart of this book is made of gold.

Oxford Handbook of Tropical Medicine, 3rd edn

No, it’s not the latest climate change, though we have had some odd weather recently.

This is the start of postgrad Tropical Medicine training on the QEII campus. For those thinking about the Fellowship of the Australasian College of Tropical Medicine part 1 exam, or preparing for other medical college fellowship exams that have a tropical medicine component, teaching commences on Tuesday 13th April at 6.55am prompt. The first four units will be on malaria, two of which will be covered in the first session [Malaria 1, Malaria 2]. The remaining two will be in a fortnight’s time. Remote and Rural Medicine can use the on-line materials for distanced learning.

There will be a light breakfast for those who can get there in time next Tuesday. If coming along, you might want to use the powerpoint files to take notes.

• Malaria 1

Show Malaria 1 Presentation

• Malaria 2

Show Malaria 2 Presentation