I digress. Blister Beetles!

Recently had a patient pitch up after an afternoon in the garden, she had been gardening when a bug fell down her top and she squished it and carried on gardening. After an hour or so she noticed the area stinging and checked to find a red area. She had a shower and noticed that the stinging was  a little less but when the area blistered she came to the acute clinic.

Pt was happy to share her story but as she had squished the bug on her “Décolletage” she wasnt so keen to have photos taken and shared with the word. So here is a nice US Marine with a blistering injury from a bug:

blister beetle

So Blisters from Beetles:

There are a few types of bugs that cause blistering eruptions and/or dermatitis.

The most widely know are the Meloidae family from which comes the Spanish Fly. The Meloidae are known as blister beetles in many parts of the world. They are so named because they cause a painful blistering eruption within 2-3hours of exposure.

A few blister beetles:


Black_blister_beetleLytta-vesicatoria spanish fly



Paederus beetles also cause a dermatosis and blistering but this generally occurs 24-72 hours after exposure. These have been having a recent resurgence in research as they are common in Iraq and have caused outbreaks in a number of American Army camps there. These lead to the 2007 report attached.


Depending where you are in the world these beetles have a variety of illnesses named after them. If you are in Africa and squish one and wipe you face you may contract “Nairobi eye or Kenya fly dermatitis” In India Paederus beetles also cause seasonal outbreaks. 

 In New Zealand Oedemeerida (the false blister beetles) are more common and famously caused an outbreak of blisters in soldiers near Auckland  in the 1980s. 74 Soldiers erupted with dermatitis after night exercises. An epidemiologists dream! Investigation lead them to the Thelyphassa lineata (Fabricius) after ruling out a number of other causes. Its ability to produce the reaction was tested on some willing participants (Medical Students)

So how do these little bugs cause such a wonderful bullous eruption and dermatitis. Both Melodiae and Oedemeerida produce Cantharidin which is a potent blistering agent. The male beetles produce all of the cantharidin and gift some to the females after mating. Male beetles secrete cantharidin from their joints so they dont need to be squashed to cause exposure and dermatitis. Wonderfully we dont know the exact biomechanical means of its production within the beetles. I also dont like to tell people where presents for my SO come from. Cantharidin is a very potent toxin with a LD50 of 0.5mg per Kg in humans. The most common animals poisoned by blister beetles are horses as the beetles commonly live in alfalfa and other green feed.

Paederus beetles have a more complex but better understood production of their toxin Pederin. The females in this case have  a symbiotic relationship with a Pseudomonas which produces the toxin. This is in turn deposited into the eggs and larvae. Further toxin is ingested when beetles eat the shell of their egg after hatching. Paederus dermatitis takes longer to reveal itself often 24 hours before discolouration which then goes on to blister.

Treatment: The best treatment is prevention, simple things such as removing beetles rather than squashing them. One prevention in Iraq was moving the night guards further from the light towers which attracted the beetles. With Cantharadin patient will usually have washed themselves as the burning is an early symptom. With Paederus they often only present well after the toxin has been spread and absorbed, these patients show classical Kissing signs where skin surfaces have touched eg: elbow flexures. Once the dermatitis is established the best treatment is topical steroids but if the case is severe oral antihistimines and even antibiotics have some benefit.

Blister beetles have been used for centuries and despite their toxicity people took them as an aphrodisiac. In roman times (wake up @eleytherius)  Livia Drusilla a great schemer of Rome attempted to poison visitors with cantharidin. Hoping they would act in a manner which they would later regret and allow her to blackmail them. (Its unclear if this was succesful) Cantarella which is the combination of Cantharidin and arsenic was reportedly the poison taken by Juliet to appear dead (We know how succesful that was)



http://www.ncbi.nlm.nih.gov/pubmed/2189910 Oedemerid blister beetle dermatosis: a review. Nicholls DS, Christmas TI, Greig DE.

Christmas TI, Nicholls D, Holloway BA, Greig D. Blister beetle dermatosis in New Zealand. N Z Med J. 1987;26:1515-1517 (paper copy)

When you think you see a dog but maybe it’s just spots.

Had this patient come in whilst on nights.

82 y/o female presented with chest pain.

Previously had CABG >15 years ago following presentation with “unstable angina”. which resolved her angina, nil since them.

Sudden onset chest and back pain and maybe between shoulders. not really a tearing quality but different to her pre CABG angina. pain wasn’t severe but enough to get her to come in. Felt her normal self otherwise.

Not on any medications.

Tachycardia 105. BP 108/64. (bilaterally)  Normal ECG sinus.

She looked pretty good TBH. sore but not “sick, sick”

Given GTN with no real change in pain. but settled with a push of morphine.

Istat troponin was negative.

Off for a CXR.

Was willing to say the mediastinum looked wide and the radiologist agreed that the aortic contour looked a bit funny.  We discussed presentation and decided that CT was indicated. I pushed for the scan as my gestalt was telling me there was something unusual about this patient.

Obviously there’s dissection from “top to bottom” as a colleague described it.

Formal report came back as extensive type A dissection extending from aortic root to abdominal aorta. There is no adjacent soft tissue reaction and no high density material on the unenhanced scan. These findings strongly suggest this is a chronic dissection.The false lumen is thrombosed in several locations and patent in others Major arch branches are patent.

Summary: extensive chronic aortic dissection with aneurysmal dilatation.

So my patient was now pain free, with an “old” dissection and lowish BP. Her tachycardia had settled after the CT. With discretion being the better part of valor I admitted her to the ward overnight. Repeat troponin in the morning was negative. She also had a D-Dimer added (no one confessed to this) which was negative. Discharged home.

I saw this patient recently in GP clinic and her BP remains low, no further episodes of pain. 

This was my first experience of when aortic dissection isn’t “aortic dissection” Anyone else had a similar case?

 Great discussion of Aortic dissection from LITFL: http://lifeinthefastlane.com/2010/09/die-like-a-king/

Leptospirosis in Aotearoa

 I recently had a patient a 42 yo dairy farmer who had not been right for a week. Flu like symptoms, headache and lethargy.

He was a “good keen man” a deer hunter who brought home steaks with respectable frequency. His partner had bullied him to the clinic. He had been unwell enough to take to bed which his partner reported was most unusual. Usually fit and well with ono PmHx. Being summer and his symptoms he earned a leptospirosis serology test.

Which came back as positive with a significant titre.

Treatment for  symptomatic cases here is oral doxycycline and follow up to see if symptoms resolve.

#FOAMed and Leptospirosis

After looking around I found the Excellent talk from Dr Lane (ICU Queensland) http://www.intensivecarenetwork.com/index.php/icn-activities/icn-podcasts/393-39-lane-on-tropical-microbiology But his experience didnt fit with mine. Are kiwis just tougher than those weak australian soldiers he sees? or is there some other factors effecting the cases we see?

Also the Adventure doc blog had an article: http://adventuredoc.net/2008/12/29/leptospirosis/

Firstly what the hell is leptospirosis?

To quote professor wikipedia Leptospirosis (also known as Weil’s syndrome, canicola fever, canefield fever, nanukayami fever, 7-day fever, Rat Catcher’s Yellows, Fort Bragg fever, black jaundice, and Pretibial fever) is caused by infection with bacteria of the genus Leptospira

Have I heard of that?

Leptospirosis was in the news in 2010 when british olympic rower Andy Holmes passed away after contracting the disease.

How does it present?

“Lepto” can present like just about anything from a mild flu like illness to a severely sick patient with hepato-renal syndrome and meningitis.

Natural history of leptospirosis

Usually patients will have the initial phase with flu like symptoms For many this is all the patient will experience but for some this is resolves and they then have a second phase of illness. This is more severe and may include hepatic failure (Weil’s disease) and renal involvement.

So how common is it?

Worldwide it is one of if not the most common zoonotic disease.

Leptospirosis is a notifiable disease in NZ so we have good records of when lab tests come up positive.

New Zealand has between 80-140 confirmed cases a year, this is about three quarters of the positive lab serology results. (more on this later)

Making leptospirosis not common but not rare. So it falls into that BS category of “Maintain a high index of suspicion” Now im pretty sure there isnt a suspicion index but you will see it from time to time. (if you look)

Which leads to the question of who gets it? meatworksdeer













Meat workers, esp those who “pull kidneys” or work the offal line. Deer hunters and farm workers are other high risk groups.

Risk in NZ

Over the years there has been a number of vaccination campaigns in cattle, pigs and now they are trialing deer vaccines to reduce the carriage of leptospira in herds. Despite this amongst herds some animals remain positive/carriers. Around 70% of beef herds, 40% of sheep and 80% of deer herds have leptospira. This is highest amongst farms which graze both cattle and deer.

These figures lead to an estimated exposure of 8-25 leptospirosis carrying carcases per day for a meatworker.

Why is it not everywhere? Are we missing cases?

Waikato epidemiologists feel it is likely we have significant underreporting. The serological evidence that many people are infected and clear the leptospira without significant illness. Currently the ELISA has a low sensitivity and it is felt that serology is better for clinical diagnosis. The culture may take a number of weeks to become positive. To be eligible in NZ for Accident compensation corporation funding/payments you must have appropriate symptoms and a rise in your serology titer of 4 fold. It seems a safe bet that we are missing a number of cases.

Leptospirosis mortality:

In contrast to Dr Lanes Queensland experience deaths from leptospirosis are quite rare in New Zealand with one every few years.  New Zealand appears to have slightly different endemic strains of leptospira. Also the soldiers are likely exposed to rodent urine vs that of bovines. Rat urine is more commonly infected with the more virulent strains of leptospira. A final thought from me about deaths from Leptospirosis: As deaths are reduced by immunomodulation perhaps the soldiers who are often being exposed for the first time to these antigens vs the meat workers who have a chronic exposure simply do not have the same immune overreaction?

 So how did the patient do?

My patient improved over the following few days but took a couple of weeks to “come right” This was defined as  being able to spend a couple of days staking deer in rough terrain and delivering me some venison steaks!

vension steak


Paul Lane, ICU (Queensland) http://www.intensivecarenetwork.com/index.php/icn-activities/icn-podcasts/393-39-lane-on-tropical-microbiology

A new dawn of leptospirosis in New Zealand“Turning prevalence to incidence”
C Heuer et al. http://epicentre.massey.ac.nz/acvsc/scwk_08/Heuer_050708.pdf

Professor Wikipedia et al. http://en.wikipedia.org/wiki/Leptospirosis



I was working nights and had that sorta grumbly tummy you can get where your just not right but nothing to worry about. Took a couple panadol and carried on. Slept alright the following day but pain was getting bit more so did what most doctors do and took some codiene and carried on.

Nightshift was ok few to see but not super busy. But as it carried on i started feeling worse. hot and cold. got up from chair and felt light-headed and very nauseated. Night nurse declared i was white as a sheet and was in no state to see patients. Thankfully one of the other docs who was oncall nipped in to finish my shift.

He put me in a sideroom and had a bit of a look at me. “could be your appy but you knew that didnt you?”

So had an ok sleep for a couple hours. woke up and had bloods.

 [blackbirdpie url=”https://twitter.com/keeweedoc/status/264277584647446529″]


Cool local ultrasonographer goes “you know we never really get a good view of these. lays probe on and there is an appendix.

Abdominal pain

Abdominal pain

Appendix was reported as “likely normal, some increased vascularity, clinical correlation is required”

Bloods showed mild neutrophilia and CRP of 56

Chat with surgeon went like this “Want it out?”


“Lets do that then”

[blackbirdpie url=”https://twitter.com/keeweedoc/status/264174442844925952″]


I have failed the #FOAMed team in that the nurse in theatre struggled with my phone so the video of my intubation is rubbish. =(

 Post op went pretty well, bit tender but got on with things.

Sympathy flowed from my medical friends…

[blackbirdpie url=”http://twitter.com/keeweedoc/status/264285319539609600″]

 Finally big thanks to everyone who was involved in my care.



Clinical Details
Nil. (Surgeons!)

Appendix 50x10mm with fragment of mesoappendix 45x9mm.  Serosa is congested
and the wall is focally haemorrhagic and firm.  (mp/1/r; HEBL)

Sections show appendix with extensive mucosal ulceration and a moderate
transmural acute inflammatory infiltrate, consistent with acute

Appendix:  Acute appendicitis

A quick ECG from my mummy

Got sent this ECG by my Mum who is a kickass emergency nurse and midwife.

She saw a young man who came in after a syncopal episode.  Thoughts on the ECG?

Update October 17:

So had a few comments and thoughts on twitter and here people are pretty onto it with this one.

My thoughts:looking at the ECG,

Sinus rhythm rate of 60.

V1/V2 and maybe V3 have what i would agree look like Epislon waves. T waves are not inverted.

High voltage ECG but difficult to accertain in a skinny young male.

QTC is 390 but the QRS in V1-V3 is not widened.

So we have a young mane with syncope our concern is hypertrophic/arrthmogenic cardiac disease in this case ARVD (Arrhythmogenic right ventricular dysplasia)

First a bit more on ARVD,

ARVD is a genetic defect that causes fibro/fatty change in the myocardium. It predominantly effects the right ventricle.It has an incidence of  1/1000 with a male predominance, from 1/3 to 1/2 of cases are familial. For those working in Italy apparently it has a much higher incidence possibly as high as 40/1000. It is a major cause of cardiac death/sudden death in children and young adults.

The diagnosis is made Via ECG findings, Family history, ECHO +/- endomycardial biopsy

Diagnosis of ARVD: requires 2 major criteria and one minor.

Major Criteria

Minor Criteria

Touch more about Epsilon waves apparently can be caused by other diseases of the right ventricle, including right ventricular infarction, infiltration disease, and sarcoidosis which might also produce the pathological substrate required for production of epsilon waves.

Outcome of the case:

Patient was referred to the tertiary ED who happily took the patient. They were admitted under cardiology and patient had an ECHO which showed no concerning features! Bloods were all normal. Kept on telemetry and discharged home with follow-up. I am unsure if they are planning on going to Biopsy or not at this stage.