MFF0082: Google

Up popped Joseph Mortimer Granville. Granville lived from 1833 to 1900. He was English and he is best known as the inventor of the electric vibrator.


It’s Monday 4 September 2017

Welcome to Spring, or if you’re in the Northern Hemisphere, Autumn.

Thank you for listening and thank you for watching Medical Fun Facts

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Last week I asked for feedback. I didn’t get much, but that’s okay. A friend on Twitter suggested gunt and for those who are not familiar with that word, you can either look up Urban Dictionary or think FUSA, or fatty upper pubic area.

Rather than share experiences with gunt, I opened the Google search engine and typed in “famous medical people last name starts with G.”

Up popped Joseph Mortimer Granville. Granville lived from 1833 to 1900. He was English and he is best known as the inventor of the electric vibrator.

He invented it not as a device for sexual pleasure but for the relief of muscle aches. In fact, it’s said he eschewed what he called the misuse of his invention for the treatment of what was then called hysteria or a wandering womb under the belief at the time that doctor induced paroxysm could cure insomnia, irritability, nervousness, or “excessive moisture inside the vagina”.

Anyway, I’m not sure that Granville and electric vibrators are necessarily a good topic for discussion on Medical Fun Facts. Instead, the letter G could also represent Google or Dr Google. I’m not a fan of the term “Dr Google”. It’s become popular and made more popular by journalists looking for a catchy vacuous phrase. It’s become common for people to open the Google search engine and type in various symptoms they may or may not be suffering. The search engine’s algorithms are so good that within fractions of a second a long list of possible diagnoses is provided. In some situations, if the inquiry was made intelligently, the list could function as a provisional diagnosis along with a differential diagnoses list too. The difficulty is that medicine is more than symptoms. Signs that a doctor elicits are important, medical, family and cultural history are important. We should never forget a patient’s sexual and travel history either. A good medical practitioner will always run through her or his mind a broad classification starting with infectious, neoplastic, endocrine, psychiatric, neurological, immunological, and hæmatological systems. I would argue, that physical examination is vital in the vast majority of situations.

While using a search engine may help a patient get some idea, I think the best way to use a search engine like Google is after seeing the doctor and learning more about the diagnosis. I know many people will disagree and feel that I’m disempowering them, I’m not. I’m looking at this from a medical perspective. Quite often when a patient presents with a large amount of researched information, an internal bias may have formed, it’s really important that such biases are recognised and accounted for in the assessment and diagnostic process. This is especially true if the patient has explored online forums where people share stories of their illnesses. This is known as confirmation bias.

There will always be stories of patients being more educated than their doctors and the fact that if it were not for their own painstaking research, the illness may never have been diagnosed. I’m not discounting those experiences for a second. On the other end, there are patients convinced they have an illness only to realise after a sign has been elicited or a pathology test has been performed, that the symptoms fit something else entirely. Medical practitioners are also real time risk managers, we have to be able to instantly weigh up the product of likelihood and consequence, we have to determine if a risk is acceptable or not and if not, we need a risk treatment to ameliorate the risk. The likelihood component of risk, with risk being the product of likelihood and consequence, is something that we learn in medical school and hone throughout our careers. As much as I love the Gregory House approach, in truth, common things are common and the best-placed person to understand likelihood is usually a well read and experienced medical practitioner rather than a search engine like Google. That said, I’m sure the software engineers are working on clinical support algorithms to rival the best clinicians.

So I have some questions for listeners.

  • Have you used a search engine like Google to make a self-diagnosis?
  • Did this approach help?
  • Would you recommend Google before or after seeing your general practitioner or family physician?
  • Do you think I’m too old fashioned and paternalistic in my thinking or am I on the money?

Please leave your answers in the comments section of the show notes or on the Facebook page or on YouTube.

If you have any questions or comments please let me know. If I’ve said anything incorrect I welcome correction. I’ll catch you next week for episode 83. Something beginning with the letter H. Send me suggestions.
Thank you, and good night.

You can find me on Twitter and Facebook. Please follow me on Twitter and like my Facebook page.

MFF0081: Polling my audience

So I’m wondering, what next? I still enjoy what I do, so it’s not like I’m unhappy and am going to stop. I would, however, like to get some feedback on what I can do to improve engagement. So I’m polling my audience (hmm that sounds a bit rude).


Hello, and welcome to Medical Fun Facts, it’s episode 81 and I’m taking a poll.
It’s Monday 28 August and as this show drops I’m in a teleconference for work. It’s one of the great things about podcasting, I can record a show the weekend before and schedule it to come out in iTunes, Stitcher and YouTube every Monday evening at 7 pm Canberra time.

This week’s show is a little different and little shorter, not that these shows are terribly long. I like to keep them to around the 5 minute mark so I can get across a few facts and maybe one or two fun lines without wasting anyone’s time.

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Since I started Medical Fun Facts in 2016, I’ve been gratified by the people in real life who have mentioned they have listened to a show or two. I know I have a few loyal subscribers and when I look at the analytics, I know there is a small core of people who at least visit the blog and spend a minute or two reading what is written. I know there are people who have subscribed and listen to the podcast via iTunes and Stitcher, but I really have no idea of the exact numbers.

The numbers for YouTube are much lower. For some videos, I’m the only person who watches. That’s okay though. I persist with YouTube, not because it’s my focus but because I find editing easier when I’m doing it with video.

You see, before I started video recording the podcast, I was using a USB microphone (a Blue Yeti) and editing each show in a program named GarageBand® in my MacBook. I have very little knowledge about sound and audio so my editing has been based on what I could learn from YouTube videos. When I moved to video recording, I used a Sony mirrorless camera with a microphone attached and then I edit the video in a program named Final Cut Pro X®. I find the audio from that to be easier and cleaner to edit than when I’m using a dedicated audio program. It’s odd I know. Anyway, in Final Cut Pro X I can export audio and video as well as audio only. I do both and upload a show to YouTube as well as the podcast through the blog which has an RSS feed into iTunes and Stitcher.

What I’ve also noticed since starting the podcast/blog/YouTube channel is that I get very little engagement via the blog comments section and any social media I push the show out to including Facebook, Twitter and Google+.

I think part of the problem is because the blog is hosted on Squarespace®. As a website platform it’s great and easy to use. As a blogging platform, it’s not as flexible as WordPress. The native comment capability isn’t that easy so that’s why I use a third party comment provider, viz., Disqus®. There are some hoops to jump through to write a comment, but the one thing it does well is virtually eliminate spam.

So I’m wondering, what next? I still enjoy what I do, so it’s not like I’m unhappy and am going to stop. I would, however, like to get some feedback on what I can do to improve engagement. So I’m polling my audience (hmm that sounds a bit rude).

  • Do you have any suggestions for me to improve engagement?
  • Are you happy with things as they are?
  • Does anything I do really annoy you?

I’ll be back to going through the alphabet next week in episode 82, it’ll be something starting with the letter G. The last time I did something on the letter G it was on Ghon, as in Anton Ghon back in episode 21. Feel free to check it out.

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MFF0080: Influenza

Yes, lung butter, that’s a colloquial expression for phlegm. I’d love to know if any listeners not in Australia are familiar with the term lung butter. Please let me know in the comments.


Hello and welcome to Medical Fun Facts Episode 80
It’s Monday 21 August 2017

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I’m sorry if my voice is really flaky but that’s what this episode is all about. More about that later.

So what about the letter F. Well F is for a word I really don’t like using in public discourse. Can you guess what word I’m thinking of?

Of course, it’s the word Flu. As much as I like Star Trek and especially the character of Data in The Next Generation, my reason for not liking contractions of words isn’t the same as Data’s. I think for proper names, we shouldn’t shorten them. For one thing, it dismisses the significance and it also sounds childish. The same is true when I hear people contract the name of one of my favourite diseases from Melioidosis to Melio! It doesn’t sound right.

So back to Influenza, yes, that’s the proper disease name. As I alluded to, part of the problem is that the term Fluin common parlance has come to mean anything but Influenza. People use it now to describe almost any upper respiratory tract infection or URTI. I also hear people use the term Stomach Flu to describe gastroenteritis or what is more likely just a colitis which is causing some diarrhoea.

Now, don’t get me wrong, I’m not railing against a great Australian tradition of shortening names of things and people. For example, rather than Gary, I get called Gaz or Gazza or Gus. People named Lawrence may get Laz or Lazza. People with red hair may get called Blue. Likewise, upper respiratory infections used to be called a lurgy or a wog. But now, the latter is deemed politically incorrect. As an aside, when I was a boy, Mum told me that WOGmeant Wise Oriental Gentleman so I was keen to be called a Wog rather than the Greeks and Italians at school.

So I don’t have Influenza at the moment. I was immunised earlier this year with this season’s quadrivalent vaccine. That said, it could have failed and I could have an aborted infection. More likely though I’ve been infected with another respiratory virus or viruses. Yes, it’s possible to be infected with more than one.

This year we’ve seen a good spike in reported cases of Influenza. This has been evident in the officially collected statistics from jurisdictional and Australian Government sources. What we’ve also seen is a good spike in laboratory confirmed diagnoses of respiratory viral infections. On Fridays when I’m practising medicine in ACT Pathology, I get to authorise the molecular microbiology reports and this last Friday was huge. I can only imagine what it’s like in private pathology practice.

What I’ve also noticed is an increase in reports where we diagnose more than one respiratory viral pathogen.

I’ve snipped part of a screen shot from a report I authorised on Friday. You can see we reported three viral pathogens in the one specimen.

Respiratory panel

For people in Canberra, I know a lot of us have been enduring this low grade viral infection which has been manifesting as a persistent cough which is keeping us up at night so we feel like zombies with brain fog during the day. There aren’t the usual paranasal congestion symptoms of a common cold and the head ache we’re experiencing is more to do with the cough than the infection itself.

While this podcast is very clear about not offering any medical treatment advice, all I can say is that rest and fluids and waiting it out is what it will take. I know some people worry about secondary bacterial infections, but you really should notice a change in symptoms, e.g., developing a mild fever or an increase in lung butter or symptoms of sinusitis.

Yes, lung butter, that’s a colloquial expression for phlegm. I’d love to know if any listeners not in Australia are familiar with the term lung butter. Please let me know in the comments.

If you disagree with anything in these podcasts or if you would like to voice a different view, please feel free to write a comment. If I have said something incorrect I welcome correction. Please also feel free to share your comments on social media.

You can find me on Twitter and Facebook. Please follow me on Twitter and like my Facebook page.

MFF0079: Enteroviral infections II

The term aseptic effectively means bacteria-free rather than microorganism-free. Unlike the bacterial causes of meningitis mentioned before, viral and fungal meningitis is mostly subacute as well. By that, I mean, rather than fulminating in less than 24 hours, aseptic meningitides tend to take longer than 24 hours to develop. Patients tend to feel unwell with a fever and a slowly worsening headache. They may also take longer to develop the signs of inflammation of the meninges, such as neck stiffness or nuchal rigidity and pain when looking into the light or photophobia.


It’s Monday 14 August 2017.

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Last week I did part I of enteroviral infections. I’m recording parts I and II on the same day because I’m going to be busy on the weekend 13 and 14 August. So, to recap, enteroviral infections are caused by enteroviruses, or viruses in the genus Enterovirus. These are very small RNA viruses in the family Picornavirdidae (pico=small so small RNA viruses). There were traditionally four major groups with polioviruses being in a single group, but now each enterovirus serotype is given a number, e.g., EV71. Apart from the polioviruses you may have heard about coxsackieviruses, echovirsues, and rhinoviruses. Within the genus Enterovirus there are 12 species, viz., Enterovirus A to Enterovirus J and Rhinovirus A to Rhinovirus C. The polioviruses PV1, PV2 and PV3 are found in Enterovirus C. Common clinical syndromes caused by enteroviruses include: Poliomyelitis Polio-like disease Aseptic meningitis Nonspecific febrile illness Hand foot and mouth disease Pericarditis and/or myocarditis Acute conjunctivitis Herpangina Encephalitis Diabetes Mellitus type 1

Last week I briefly described hand, foot and mouth disease. Tonight I want to describe aseptic meningitis. Aseptic meningitis is an old fashioned term used before we really knew a lot about the causes of meningitis and when most serious meningitis was caused by bacteria like pneumococci, meningococci, Hæmophilus influenzæ and Streptococcus agalactiæ. With the advent of HIV infection and AIDS, fungal meningitis also became more common and better described.

The term aseptic effectively means bacteria-free rather than microorganism-free. Unlike the bacterial causes of meningitis mentioned before, viral and fungal meningitis is mostly subacute as well. By that, I mean, rather than fulminating in less than 24 hours, aseptic meningitides tend to take longer than 24 hours to develop. Patients tend to feel unwell with a fever and a slowly worsening headache. They may also take longer to develop the signs of inflammation of the meninges, such as neck stiffness or nuchal rigidity and pain when looking into the light or photophobia.

The other reason why the term aseptic is used is because traditional bacterial culture methods will not reveal the ætiological agent. Even in 2017, viral culture is not commonly performed. My clinical virology friends like to point out that they pioneered molecular microbiology well before simple bacteriologists like me thought about using genetic techniques let alone whole genome sequencing.

So the most common cause of viral or what we used to call aseptic meningitis are enteroviruses. The clinical illness progresses over a few days to a really severe headache and body aches and pains. You’ll want to keep the doors and windows covered to prevent sunlight hurting your eyes and you will not want to make any sharp movements because your head and body feels so delicate. So long as you rest and keep your fluids up, most of the time you will recover with no sequelæ. Unfortunately, some patients will progress to more severe meningitis and even to encephalitis or inflammation of the brain.

If you disagree with anything in these podcasts or if you would like to voice a different view, please feel free to write a comment. If I have said something incorrect I welcome correction. Please also feel free to share your comments on social media.

You can find me on Twitter and Facebook. Please follow me on Twitter and like my Facebook page.

 

MFF0078: Enteroviral infections

Hand, foot and mouth disease shouldn’t be confused with foot and mouth disease. Foot and mouth disease is an animal disease and we don’t have it in Australia. In fact, our Department of Agriculture and Water Resources has a large focus on keeping FMD out of Australia. The FMD virus is also a security sensitive biological agent in Australia’s pathogen security scheme.


It’s Monday 7 August 2017.

Thanks for subscribing and listening to Medical Fun Facts.

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Last week I did Dengue virus and Dengue fever. Tonight, as we progress again through the alphabet I thought about enteroviral infections.

This is going to be a two-part show because I’m not going to be able to record a show next week.

So, enteroviral infections are caused by enteroviruses, or viruses in the genus Enterovirus. I find the taxonomy of enteroviruses to be really confusing. The easy to remember facts are that these are very small RNA viruses in the family Picornavirdidae (pico=small so small RNA viruses). There were traditionally four major groups with polioviruses being in a single group, but now each enterovirus serotype is given a number, e.g., EV71.

Apart from the polioviruses you may have heard about coxsackieviruses, echovirsues, and rhinoviruses.

These viruses mutate rapidly and frequently recombine.

Within the genus Enterovirus there are 12 species, viz., Enterovirus A to Enterovirus J and Rhinovirus A to Rhinovirus C.

The polioviruses PV1, PV2 and PV3 are found in Enterovirus C.

Common clinical syndromes caused by enteroviruses include:

  • Poliomyelitis
  • Polio-like disease
  • Aseptic meningitis
  • Nonspecific febrile illness
  • Hand foot and mouth disease
  • Pericarditis and/or myocarditis
  • Acute conjunctivitis
  • Herpangina
  • Encephalitis
  • Diabetes Mellitus type 1

Hand, foot and mouth disease shouldn’t be confused with foot and mouth disease. Foot and mouth disease is an animal disease and we don’t have it in Australia. In fact, our Department of Agriculture and Water Resources has a large focus on keeping FMD out of Australia. The FMD virus is also a security sensitive biological agent in Australia’s pathogen security scheme. Hand, foot and mouth disease though is relatively common in Australia and mainly affects children. HFMD is caused by the coxsackievirus group and is generally mild in nature. HFMD starts as a red dotty rash that goes on to ulcerate and form blisters. The blisters can occur in the mouth and on the tongue as well as on the soles of the feet and palms of the hands. The blisters normally last about seven days.

Sometimes children can have a mild fever and in rare circumstances, a subacute viral meningitis may occur.

HFMD is spread by the faecal-oral route. Enteroviruses live in the human gut and can be found in abundance in faeces.

Good hygiene, especially hand hygiene is important in preventing the spread of the disease. You know when you’re in the toilet, wash your hands, even if you’re a bloke and you only went to void your bladder. Your penis is close enough to your anus to have faecal flora on it no matter how long or how clean you think it is.

Next week I’ll discuss one more enteroviral infection.

If you disagree with anything in these podcasts or if you would like to voice a different view, please feel free to write a comment. If I have said something incorrect I welcome correction. Please also feel free to share your comments on social media.

You can find me on Twitter and Facebook. Please follow me on Twitter and like my Facebook page.

MFF0077: Dengue virus infection

There is no specific treatment for Dengue fever. It’s important not to use drugs that inhibit platelet aggregation like aspirin and nonsteroidal antiinflammatory drugs.

I’ve seen two patients die while infected with Dengue virus. Unfortunately, one patient was given a nonsteroidal antiinflammatory drug which lowered his platelet count to 8 and he bled out. In my mind that was an avoidable death.


It’s Monday 31 July 2017.

Last week I did Cryptococcus. Tonight, as we progress again through the alphabet I thought about Dengue fever and Dengue virus.

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The Dengue virus is in the genus Flavivirus which also includes Zika virus and Yellow fever virus. The Dengue virus is a single-stranded RNA virus transmitted to humans by mosquitoes. Dengue virus is also known as an arbovirus or arthropod-borne virus.

Unlike some other Flavivirus infections, human infection with Dengue virus, Yellow fever virus and Zika virus are not incidental because when infected, our cells produce enough replicated virus for a mosquito to carry it to other humans without the need for other animals to be involved.

Within the species Dengue virus, five serotypes exist.

Until a few hundred years ago, the Dengue virus was transmitted within nonhuman primates and Ædes mosquitoes, with humans as a dead-end host. Now, the transmission cycle is exclusively between these mosquitoes and humans.

Dengue fever is the disease caused by Dengue virus. The disease occurs after a mosquito carrying Dengue virus bites a human and infects the human through the bite site. Symptoms begin to appear between three and fourteen days after infection. The usual symptoms include fever, headache, vomiting, muscle and joint pain, along with a skin rash. It usually takes a week before a patient begins to feel better. In a small number of patients, the disease progresses to Dengue hæmorrhagic fever. Dengue hæmorrhagic fever is characterised by bleeding, an abnormally low platelet count, and blood plasma leakage. When the patient’s blood loss is extreme and their blood pressure falls dramatically, the patient is said to be in Dengue shock.

While infection with one of the five serotypes typically confers life-long immunity to that type and partial immunity to the other types, when infection occurs with another serotype, the complex immunological reactions are thought to give rise to Dengue hæmorrhagic fever as a complication of the less severe Dengue fever.

Several methods have been devised to reduce infection. These include simple measures to avoid mosquitoes plus some vaccines which are currently being investigated. In Australia, work is being done on biological control measures including the use of the bacterium Wolbachia. The notion being that Wolbachia infected mosquitoes are resistant to infection with Dengue virus.

Diagnosis is often made clinically in the tropics and subequatorial areas where Dengue fever and the mosquitoes that carry Dengue virus are endemic.

Patients often have nausea and vomiting plus a low white cell count, and clinical evidence of a low platelet count like petechial hæmorrhages. The earliest changes in laboratory test parameters include a low white blood cell count.

Specific diagnostic tests include direct detection of the NS1 protein or Dengue virus antibodies. PCR tests are also available.

There is no specific treatment for Dengue fever. It’s important not to use drugs that inhibit platelet aggregation like aspirin and nonsteroidal antiinflammatory drugs.

I’ve seen two patients die while infected with Dengue virus. Unfortunately, one patient was given a nonsteroidal antiinflammatory drug which lowered his platelet count to 8 and he bled out. In my mind that was an avoidable death.

If you disagree with anything in these podcasts or if you would like to voice a different view, please feel free to write a comment. If I have said something incorrect I welcome correction. Please also feel free to share your comments on social media.

You can find me on Twitter and Facebook. Please follow me on Twitter and like my Facebook page.

MFF0076: Cryptococcus

In the old days before we had good quality agglutination assays and serological assays as well as PCR, the old-fashioned way to diagnose cryptococcal meningitis was to look for a halo around a classically shaped yeast in an India ink preparation of cerebrospinal fluid. India ink is a simple black ink composed of fine soot particles which is combined with water.


It’s Monday 24 July 2017.

Last week I finished off Bordetella. Tonight, as we progress again through the alphabet I thought about Cryptococcus.

I fear this week’s podcast will be a little flat. I made an error with the lighting and made the decision to still record video and audio, but the YouTube show will be a still image with some scrolling text in parts.

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Cryptococcus means hidden sphere in Greek. It is the name given to the yeast phase while its filamentous sexual phase is known as Filobasidiella. The type species is Cryptococcus neoformans and it is best known for the capsule which is a virulence factor and rich in mannose and glucuronic acid.

There is another species which is found mostly in Africa and Australia, viz., Cryptococcus gattiiC. gattii has an association with gum trees also known as eucalyptus trees. So, in non-native environments, outbreaks of C. gattiican be found when gum trees are planted in non-native areas, e.g., Canada. This was seen when Acquired Immunodeficiency Syndrome caused by the Human Immunodeficiency Virus was at its peak. Cryptococcosis was a common AIDS defining infection and the isolation of C. gattii occurred in places where gum trees, especially river red gum trees have been planted.

Clinically most infections are of the lungs and patients present with fever and a dry cough. In immunocompromised patients, e.g., patients being treated for a malignancy, the yeast can cause a subacute or chronic meningitis with headaches, vision problems, and confusion.

In the old days before we had good quality agglutination assays and serological assays as well as PCR, the old-fashioned way to diagnose cryptococcal meningitis was to look for a halo around a classically shaped yeast in an India ink preparation of cerebrospinal fluid. India ink is a simple black ink composed of fine soot particles which is combined with water. Note it is not Indian ink, it is India ink. Apparently, India ink was invented by the Chinese. The halo is caused by the presence of the capsule. Occasionally, you may also see yeast cells when microscopically examining cerebrospinal fluid in a Fuchs-Rosenthal counting chamber.

Growing Cryptococcus in culture and identifying the yeast to a species level is easily performed in most competent microbiology medical testing laboratories.

In pulmonary disease, Cryptococcus species can also be diagnosed in histopathological slide preparations stain with silver stain or Periodic acid-Schiff.

Not only are trees a reservoir for these yeasts but the faeces of birds like pigeons can act as a good reservoir and reinforces the value of cleaning pigeon faeces from public spaces and not encouraging flocks of pigeons near hospitals.

The good news is there is no person-to-person transmission. The risk is in inhaling the fungal elements from the environment.

If you disagree with anything in these podcasts or if you would like to voice a different view, please feel free to write a comment. If I have said something incorrect I welcome correction. Please also feel free to share your comments on social media.

You can find me on Twitter and Facebook. Please follow me on Twitter and like my Facebook page.