Mycoplasma genitalium #GPCMEsouth

Edward Coughlan is a sexual health physician at Christchurch hospital. He recently spoke at both GPCME south and to the training registrars. His first talk was on Mycoplasma genitalium and had the title “The new black” which reflects the sexual health worlds recent interest and research going on around M. Gen.

So lets start at the very beginning which is apparently a reasonable place to start.

Mycoplasma genitalium was first isolated from men with urethritis in 1980 by – Tully,Talyor-Robinson- Lancet 1981;1:1288-91 (might need to check in a library to find this it’s the building you use to get free wifi) M. Gen. Is very small with 582,970 base pairs  in a circular chromosome,coding for 521 genes. Has no cell wall. But is very adherent to the urinary tract. It has a flask like shape see the photo from 1981 publication and electron microscope images.

 

Mycoplasma Genitalium flask

This was followed by a lull whilst the technology caught up. Once PCR arrived the studies have shown that  M. Genitalium is a major cause of non-gonococcal urethritis. range is variable from 10-20% depending on population group making it the most common after chlamydia. Currently the gold standard test is nucleic acid amplification technique (NAAT) this can be done from urine or swabs.

Now when I mentioned M. Gen. on Twitter a reasonable number of people thought this was the sexual health physicians making our lives hard or the diagnosis is irrelevant as the treatment is the same.

See discussion: https://twitter.com/MDaware/status/368223586315550720

 But recent studies have looked at this and the 1g stat dose of azithromycin which was shown to be 95% effective in the earlier studies has  dropped to lower than 80% in the last large case series. But more importantly those who don’t respond to the initial 1g dose have a very low cure rate of 30-40% if the azithromycin stat dose is repeated. The results for doxycycline are much worse with higher initial resistance patterns around 70%. The current 1g “Z-Pack” and go approach is selecting for resistant strains of M. Gen.

As recurrent Non-gonococcal non -chlamydial urethritis are the patients most likely to have M. Gen these are the patients we should be testing. So how can you prevent its resistance? using a 500mg stat dose followed by 4 days of 250mg worked well for 95% of patients. Which leaves you with a small group 1 in 20 who are resistant.

So what then? Pharmac has just approved Moxifloxacin special authority for Azithromycin resistant M. Gen. SA funding is for a 7 day course of 400mg daily. This is for NAAT confirmed M. Gen. after failing the long azithromycin course.

In short if you are treating patients for urethritis you should know about M. Gen. If someone has recurrence of their Urethritis then you should be thinking about it and testing and if they have “treatment resistant” Non-gonnococcal non-chlamydial  urethritis M. Gen. should be your first thought.

References:

Wikstrom  STI 2006 82 ;276 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2564707/

 
Bjornelius STI 2008, 84,72-76 http://sti.bmj.com/content/84/1/72.abstract
 

  

 
 
 
H Sen Yew et al. J Clin Microbiol. 2011 April; 49(4): 1695–1696.  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3122813/
  
 

GP CME South 2013 #GPCMEsouth

This week I shot down to Dunedin for the NZ medical associations CME conference.

top_banner2013

It was a great event and had a huge variety of talks and informal Q+A sessions.

See programme here:

http://www.gpcme.co.nz/south/programme.php

It was a little lonely on the twittersphere (#GPCMEsouth) but the teams from Canterbury health laboratories and New Zealand Doctor magazine keep me company.

The social media talks were well attended and in the plenary sessions others spoke about the need for doctors to have more information in the public realm. I did have the slight embarrassment of being called out at the #SoMe talk as a “serious tweep” and “blogger” (Thanks Barbara!)

Our wee kiwi GP conference managed to generate 224,403 Impressions! which was quite cool and It was really nice to get lots of messages from those who enjoyed the info flowing onto their timelines. Symplur here

Many of the presenters have been kind enough to let me write about their talks and include a few pearls in a longer format than 140 characters.

So over the next few weeks I should have a few interesting talks to cover and hope to share a few learning points and help solidify my thoughts as well.

Depression in the elderly #GPEP1

We recently had a talk on depression in the elderly. I Thought I would try to compress it down into a couple of pages for those who are interested.

Forgive me the length and the clichéd photos.

First rates:

Old people have lots of friends who die, they are lonely, they can’t do the things they used to. Therefor they must be more depressed, right?

Yes and no:

Rates of depression are stable at around 3% of the more youthful and the older population. This is when using the DSMIV criteria.

But if you take 100 older folks and put them in front of a psychiatrist they will usually have 10 pts who they feel are depressed tho many wont meet the criteria. What is it the specialists are seeing that makes them feel this patient is depressed?

Most would argue they are seeing suffering, burden of disease. The illness effect upon them, chronic pain, reduction in function, social withdrawal often mimic depression. Will discuss this a little more later.

This is reflected in the statistics of depression in multiple settings: Those at home have the lowest rates, It increases across the spectrum from rest homes in independent units, to rest home inpatients to the final and highest risk group those in hospital.

In fact if you follow the elderly around a time of loss most do very well exactly the same as younger people with a period of grief and slow improvement. A patient was quoted as saying “I suffer aloneness, I am no depressed” Which is an interesting sentiment and worth thinking about when dealing with these patients.

 

So onto the diagnosis, this can be difficult as depression is a line on a spectrum.

As with any disease we need to decide where this is.

Most diseases we make the diagnosis on one major factor: Impairment of function does it cross this line.

We then add in some time factor : Duration or persistence.

Then we look at specific symptoms, we may count them (4-5 of 9)

We may look for special symptoms, psychosis, suicidal thoughts

We consider cognitive effects, slow thinking

physical effects, psychomotor retardation or agitation, sleep, weight gain/loss.

another common symptom is a spiritual one, those who are believers in a  certain faith often feel separated from god. those who are atheists or agnostic may explain they feel somehow disconnected from a greater purpose.

In short we are looking for Aaron Becks triad. (Nothing to do with JVPs and low BP) Of negative thoughts of self, others and the future. In short, Im miserable, other people are crap and its never going to get any better.

This gives us our diagnosis of depression from there we have some subtypes.

Bipolar: sometimes high, hypomanic/manic
Anxious: anxiety predominant symptoms
Agitated: irritable, psychomotor agitation, pacing, fidgeting.
Psychotic: psychotic symptoms.

In New Zealand we often hear about the high rates of suicide in our youth esp our maori and pacific youth. But the highest rates of all groups are white males over 80 years. There are not many of them but their numbers are growing rapidly. Sadly this is considered one of the harder groups to engage with. They have the highest rate of completed suicide, they chose lethal methods. 

Illness and depression: as i mentioned earlier in the elderly there is an interplay between physical illness and their depression.

This interplay is  bidirectional. We know diabetics BSLs go haywire if their mood is low.

Some very interesting studies have been done on mortality and morbidity post myocardial infarction and the patients mood. A diagnosis of depression at the time of MI increases your mortality 2-3 fold over the following year! This is provided you survive the first 3 days. Having low mood doesn’t seem to effect your massive aneurysmal wall rupturing but does increase your PVC rate.

Another illness that needs to be considered is the possibility that their mood disturbance is a first symptom of a neurodegenerative disease. In some studies upwards of 20% of patients who develop Parkinson’s disease are diagnosed the year before with depression. This is before any outward signs are present. It has been shown to proceed dementia and often complicates the diagnosis.

Another important discussion is around the patients alcohol intake. We know that alcohol is a depressant and the best treatment for low mood in the context of abuse is to reduce intake. The elderly are quiet drinkers, occult drinkers. Very different to teenagers who get pissed punch someone or crash a car. It’s a good thing to question each time you seen an older person with falls. But why do they hide it so much? Simply society is much more accepting of young idiots getting drunk than old folks who should know better. I wonder if the phrase “Dulce et decorum est pro-ethanol morti? ” is pretty close to the truth.

So what should we do with the elderly who can’t stop drinking? we accept that younger alcoholics cant and work on harm minimization. They get their vitamins and thiamine. Which leads to how much to give via what route? Oral thiamine is so poorly absorbed I believe the correct molar dosage is a shitload. You need to give it IM. We happily give B12 to patients and other meds but need to make this change.

Ok after that sidetrack

We have made our diagnosis what tests should we order?

Tests fall into two groups, those that we can treat and hope their depression improves and those for ongoing treatment.

The treatable ones, B12 and Folate go together often low in the elderly good to check and be sure. Thyroid function (TSH) might see the odd hypothroid and depression presentation in your career. Calcium, we all remember the, stones, groans and psychic moans.

then some for the future: ECG, you need a baseline for comparison, most of our drugs are going to have some QT concerns. LFTs not a bad test for the future again can be changed by our meds.

Treatment:

First agent: This is really a bit of a toss-up. Tricyclic antidepressants are better in a trial setting but SSRIs do better in the real world. This really comes down to compliance which is most effected by side effects.

SSRI win out for me, As I havent had a trip to Hawaii for a conference im still using citalopram over escitalopram but some would argue the decreased risk of QT mischief is worth the increased cost.

Second line I would use TCA and specifically Nortiptyline, reasonable in regard to H/L does take a some fiddling to get the dosage up but has milder withdrawal than others

Third option in NZ is Venlafaxine, you can have it funded if you have trialed both SSRI and TCA. worth reminding people of the withdrawal and the need for a washout period before starting this.

Other therapies.

Something for anxiety and or sleep?

New Zealand has seen a massive surge in the use of Quetiapine. Many call it Vitamin Q with tongue firmly in cheek. It is good for ruminant thoughts and is sedating. But its no better than Benzos for falls risk, No antipsychotic ever made anyone smarter and many dont tolerate its side effects.

“Grandmas little helper” Benzos have gone well out of fashion in the elderly, people are concerned about dependence and risks of well just about everything being increased. Our psychogeriatricain was arguing that they are very well known drugs, we know the side effects, we know most people dont become dependant and that using them for a short period they are very effective for sleep/sedation.

 

Finally we discussed when to refer to tertiary services.

We came up with 3 reasons:

1. Assessment, you just aint sure of the diagnosis, would like a second opinion.

2. Treatment knowledge/Actual therapy, do you not know what to do next or can you not access it.

3. Access to rehab, one of the most common referrals, the loss of function from their illness is enough to require inpatient or outpatient rehabilitation and increased services.

So there is my wall of text on depression in the elderly if you made it to here well done, will try make the format more digestible in the future.

 

References:

Depression post myocardial infarction: http://circ.ahajournals.org/content/91/4/999.short and http://www.psychosomaticmedicine.org/content/66/6/814.short