“We have a lady with puerperal fever. She’s 2 days post-delivery and pretty unwell. Critical Care are reviewing her now and we’d like some advice about the best antibiotics to give her” said the Obstetrics Registrar.
 
Excellent thought the Microbiologist; they’re being proactive about a serious problem.
 
“If she’s not allergic to anything then IV Benzylpeniciilin and Clindamycin. Have you looked for retained products and done a DNC?” asked the Microbiologist.
 
“She’s really unwell, we don’t really want to take her to theatre. We might damage the uterus” replied the Registrar.
 
“She’s unlikely to improve if you don’t,” said the Microbiologist sympathetically. “You need to remove as much infected material as you can. I know it sounds brutal but it’s really important”.
 
“Okay,” said the Registrar sounding doubtful, “my Consultant is with the patient at the moment so I’ll go and tell them what you have advised. Thanks for your help.”
 
The Microbiologist put down the phone and put down his pen. Time to visit the obstetric ward and see what is going on…
 
What is the cause of puerperal fever?
Puerperal fever is caused by the bacterium Streptococcus pyogenes, also known as the Group A beta-haemolytic streptococcus. The bacterium can be either introduced from the mothers own flora, the attending healthcare professional or even from a contaminated environment. The bacterium then causes inflammation in the genital tract and ascends into the uterus causing what is known as endometritis (inflammation of the uterus).
 
The history of puerperal fever
Puerperal fever has an important historical context in the world of infection control and microbiology. Back in the 1700s and 1800s puerperal fever was a leading cause of maternal death. Puerperal fever was particularly common in “lying-in wards” (a room where women were confined in childbirth), especially those which were staffed by “accoucheurs” as the Doctors practicing in the “new field of obstetrics” were known; “accoucher” in French means ‎“to give birth”, or to “go into labour”.

In context, this “realisation” is all-the-more remarkable as the cause of puerperal fever was still unknown and many “experts” believed puerperal fever was caused by toxic miasmas (bad air), imbalance of the four humours or even excessive build-up of faeces in the mother’s bowel!
 
But it’s what Semmelweis did next that really makes him stand out. He put in place procedures to ensure that all doctors entering the wards washed their hands in a dilute chlorine solution and the effect was dramatic. When he compared the clinic where hand washing was in practice with a clinic where it wasn’t he saw the mortality had dropped from 12% to 3%!

​So Semmelweis was hailed as a hero and his handwashing practice immediately adopted all across the World…?! Not exactly, in fact no he wasn’t and neither was handwashing. His ideas went against the current opinion and dogma of the medical profession. Not only that, but many Doctors took offence at the suggestion that “their hands were dirty” and “that they were the cause of the disease” (reminds me a bit of trying to implement hand-hygiene even today!). Semmelweis was in fact ridiculed and rejected, he was sacked by the Vienna Hospital (partly because of political unrest relating to Hungary) and he had to move to Budapest.
 
Unfortunately Semmelweis’ story does not have a happy ending. He continued to try and convince people of his ideas with no success. In 1865 he suffered a breakdown and his “colleagues” had him forcefully committed to a “mental institution”. It is thought that he was beaten by guards, put in a strait jacket and locked in a darkened cell. He died 2 weeks later due to sepsis from an injury he sustained, during the scuffle, to his right hand... ironically it was probably the very bacterium he had spent his career trying to control, Streptococcus pyogenes!
 
Nowadays we refer to Semmelweis as the “Father of Infection Control” because he was the first person to show that close attention to hand hygiene reduces rates of infection. An amazing piece of work and Semmelweis is now rightly recognised for what he did, even if at the time he was treated so badly.
 
How does puerperal fever present?
Puerperal fever presents with fever during labour or up to 10 days after delivery. It is associated with severe abdominal pain and offensive bloody vaginal discharge. Often patients appear a lot sicker than the clinical findings in the genital tract, with tachycardia, hypotension and sepsis.
 
Any swabs taken from the vagina or placenta, as well as blood cultures, usually grow S. pyogenes, although endometritis itself can be caused by numerous other bacteria. It is the severity of the presentation that is the usual clue to this being S. pyogenes.
 
How should puerperal fever be managed?
Puerperal fever due to S. pyogenes is an obstetric emergency. Treatment consists of source control, antibiotics and supportive care with fluids and antipyretics etc.
 
Source control is the most important aspect of the management of puerperal fever. Patients often have retained products of conception (RPOC); these are bits of placenta still within the uterus. The location and nature of RPOC makes the infection difficult to treat and antibiotics less effective so these RPOC need to be removed, usually in a procedure with the unpleasant name of a dilatation and curettage (DNC). This should be done as soon as possible and can be life-saving.
 
Infection with S. pyogenes is often severe and requires the antibiotics IV Benzylpenicillin and IV Clindamycin to treat it. I tend to use both together because Benzylpenicillin kills the bacterium and Clindamycin interferes with the bacterium’s ability to produce toxins which makes the combination particularly effective.
 
Puerperal fever due to S. pyogenes is also an urgently notifiable disease. Public Health England will trace all household members and consider giving antibiotic prophylaxis, or eradication therapy, in order to prevent any further cases of infection caused by this aggressive bacterium, e.g. cellulitis, tonsillitis, septic arthritis and even necrotising fasciitis.
 
By the time the Microbiologist got to the obstetric ward (in our modern hospital scenario not the 1840’s “lying–in” ward!) the Consultant Obstetrician had already advised the operating theatre team of the need to do an emergency procedure.
 
With excellent source control, antibiotics and Critical Care support the patient made a full and speedy recovery and was soon back home with her new baby; a relief to all concerned. Fortunately there were no further cases on the obstetric ward but even so everyone continued to pay close attention to washing their hands…
 
If you’re interested in knowing more about the history of puerperal fever and Semmelweis there’s a nice little, easy to read, book called “The Doctor’s Plague” by Sherwin B. Nuland which is very good.
 
…I’m off to catch up on Charité season 2!

Happy Valentine's Day! The Love Virus is in the air...
“Chinese media are showing hardworking hero stories, it's Jeong Jae Pung’s wedding anniversary … ‘come home soon’ his sign says [according to the BBC reporter] … his wife is a nurse looking after virus patients and contact with the outside world is forbidden…” (BBC News at 10, 13/02/2020)

So what’s wrong with this picture?
The nurse is on a mobile phone wearing her PPE outside of the hospital, according to the UK’s guidelines it should be removed inside the patient’s room and why is she using her mobile phone?!

This breaches Infection Control policy in so many ways; leading to contamination of the hospital and the wider environment and also exposes this person and their family to the virus. She might as well not bother wearing the PPE at all.

This picture is so crazy it deserves a caption competition, no prizes, just the kudos for being the wittiest reader of the bug blog!
​
Add your caption below or on Facebook :-)

It’s all over the news; a new deadly plague is spreading across the World in an unstoppable wave of death and disease! Cities are falling, governments are collapsing, mass panic and chaos are ensuing… or at least that’s what the media would have us believe about the novel coronavirus from Wuhan in China. Gosh, it’s reminding me of the game of Pandemic!

What is 2019-nCoV?
2019-nCoV (originally known as Wuhan Virus) is in the coronavirus family along with SARS Virus (Severe Acute Respiratory Syndrome) and MERSCoV (Middle-Eastern Respiratory Syndrome Coronavirus). Both of these viral infections caused a stir Worldwide due to a relatively high mortality in those affected, even though the incidence remained very uncommon. SARS was particularly nasty once it got established in crowded hospitals as many of those affected were actually the healthcare workers looking after the patients. The cynic in me also thinks they caused a stir because they had catchy acronyms which allowed the media to present popular horror stories to frighten the public into watching more news stories…!
 
There is emerging evidence from researchers analysing the genetic sequence that suggests 2019-nCoV is a “recombinant virus between the bat coronavirus and an origin‐unknown coronavirus … [with a] snake the most probable wildlife animal reservoir”. As is the case with most new coronaviruses there is an animal source; SARS was from horse-shoe bats, MERSCoV from camels (“Camel Flu”, as I like to call it), and countless other new infections in animals such as swine acute diarrhoea syndrome, mouse hepatitis virus and even ferret systemic coronavirus! I particularly like the idea of Ferret Fever…
 
What is the current situation?
As of the 5th February the World Health Organisation have reported 24,554 confirmed cases of 2019-nCoV; 24,363 in China (16,678 from Hubei Province where Wuhan City is located) and 191 from the rest of the World; almost all cases outside of China had a travel history to China. So far only 2 cases have been detected in the UK out of 414 tested.
 
There have been 492 deaths (all in China, except 1), and those that have died had severe co-morbidities that would predispose them to a high mortality from any viral respiratory infection. The mortality is therefore currently around 2% but remember, in the initial stages of an outbreak the epidemiology is skewed towards severe cases as widespread surveillance for mild or asymptomatic cases has not yet been done; the overall mortality will be lower than this.
 
Okay, so on the face of it, this does sound bad but let’s just take a breath and try and bring some context to this. Hubei Province has a population of about 60 million, almost as big as the UK (65 million); which means the incidence of 2019-nCoV infection in Hubei is about 1 in 3,500, and in China with a population of about 1.4 billion the incidence is 1 in 60,000.
 
Let’s compare this to something more familiar, “common” influenza. In the USA this influenza season (2019/2020) there have been 19 million cases of flu, 180,000 admissions to hospital and 10,000 deaths. If we extrapolate these figures to China then there have been about 760,000 cases of influenza with 40,000 deaths so far this year which significantly dwarfs the situation with 2019-nCov.  Even in the UK there are 2-3,000 deaths a year from influenza. Influenza is still a much higher risk to public health in the UK than 2019-nCoV.
 
What has China done about 2019-nCoV ?
In my opinion the response from the Chinese authorities has been amazing. They have been quick to implement strict quarantine measures and quick to share information with the WHO and the global community. This has meant that diagnostic tests have been rapidly developed and vaccines are already being worked on. I doubt any other country in the World could have achieved this. They have even built a 1000 bed hospital in 10 days; in contrast in September 2019 the Health and Social Care Secretary Matt Hancock announced the UK will spend £2.8 billion on 6 new hospitals to be built in 5 years!
 
The Chinese authorities were also quick to close Huanan Seafood Wholesale Market in Wuhan City where poultry, snake, bats, and other farm animals were being sold. But as of the 1st January this year it was increasingly clear that the outbreak was no longer due to the exposure at the seafood market; there was evidence that 2019-nCoV could also spread from human-to-human.
 
How does 2019-nCoV infection present?
Like most coronaviruses, 2019-nCoV infection presents with a flu-like illness; fever, cough, sore throat, shortness of breath. The key aspect is the travel history i.e. has the patient potentially been exposed to 2019-nCoV … if not then it’s not the 2019-nCoV.
 
The current case definition for infection is:
 
Severe acute respiratory infection requiring admission to hospital, with clinical or radiological evidence of pneumonia, or acute respiratory distress syndrome
OR
Acute respiratory infection of any degree of severity (including at least one of: shortness of breath, cough or sore throat)
AND
In the 14 days before the onset of illness:

• Travel to mainland China OR
• Contact with confirmed cases of 2019-nCoV, defined as:

1. Living in the same household, OR
2. ​Direct contact with the case or their body fluids or their laboratory specimens, or in the same room of a healthcare setting when an aerosol generating procedure is undertaken on the case OR
3. ​Within 2 metres of the case in any other setting not listed above, for any length of time
   

If anyone fits this case definition then they should be discussed immediately with the local Duty Microbiologist or Infectious Diseases Physician, who will liaise with the local Public Health England Health Protection Team.
 
How is 2019-nCoV diagnosed?
The current sample types required from patients in the UK with possible 2019-nCoV are:

• Viral nose and throat swab OR nasopharyngeal aspirate (NPA) for PCR
• Sputum OR bronchoalveolar lavage (BAL) for PCR
• 5ml Clotted blood (1ml for children <12 years old) for antibody testing (acute and convalescent 14 days later)

 
Testing should be discussed with the local Public Health England Health Protection Team before sending samples to the Reference Laboratory; this should be done by the Duty Microbiologist or Infectious Diseases Physician.
 
REMEMBER to take samples for all “normal” respiratory infections as well as those required for 2019-nCoV, your patient is far more likely to be ill from a “usual” condition. Note: local laboratory testing for Influenza Virus as well as other causes of pneumonia should be undertaken in a Category 3 facility, which is normal protocol.
 
Dealing with the media and public concerns
I returned from holiday to find a free newspaper on the train saying “deadly virus” and was travelling next to two young men wearing surgical masks! No one even mentioned the virus in Fuerteventura!
 
So what about the concern for bringing “our” citizens home from China? I’m not convinced this was entirely driven by health advice. Putting asymptomatic people on an aeroplane with others is OK as the virus (as with all respiratory viruses) is transmissible through droplets; no droplets on hands or in the air (sneezing and coughing) means no virus risk. However it does place all these people in close proximity with others who have a high risk factor for exposure, so if someone on board the aeroplane becomes symptomatic all on board are then at risk of further exposure. I suspect this evacuation was more political and media led. As for the “all must leave” message, well the WHO currently advise against the application of any travel or trade restrictions on China.
 
The other story that caught my eye regarded the transferring of asymptomatic people in a coach from the evacuation aeroplane to their quarantine facility. A member of the transporting team could clearly be seen in full PPE next to the “unprotected” coach driver. The PPE was unnecessary; remember it’s the symptomatic patients who spread the virus. It was poor practice to be in PPE as all PPE should be removed after assessment of a patient, be it within the patient’s room or anteroom. If the PPE is contaminated wearing it on a coach around the country or around the hospital clearly puts more people at risk and is against advice.
 
In contrast the PHE infection control advice that “all transfer staff should wear full PPE and maintain a 2 metre PPE protection zone around the patient and their equipment” (see PPE below) is recommended for confirmed symptomatic patients and enables the staff member to be able to respond to the patient’s needs if required, can you imagine trying to explain that “the patient was chocking but we delayed our treatment as we had to put on our PPE!”?
 
So will a surgical face mask help me on the underground? No, normal surgical face masks do not filter air and will not stop someone inhaling anything! Why wear them in surgery then?!? A surgical mask stops contamination from skin and sweat from the surgeon “dropping” onto the surgical site and should prevent the surgeon touching their nose and mouth during the procedure! Why are patients asked to wear these face masks during transport across a hospital (see PPE below)? The patient should wear a ‘surgical mask’ if this can be tolerated to prevent large respiratory droplets being expelled into the environment by the wearer, essentially it’s the same as the “coughing into a tissue” advice given to the public with Influenza Virus.
 
Of course people get concerned, it’s only natural, but playing into these fears (especially fuelled by the media) is not helpful.
 
How is 2019-nCoV treated?
There is no specific treatment for 2019-nCoV. Patients require good supportive care with fluids and ventilator support.
 
Infection Control Precautions
It is important to keep in mind that all of the current strategies for dealing with 2019-nCoV, including the current infection control precautions, are to try and prevent it becoming established in the population like influenza.
 
Human-to-human transmission of 2019-nCoV can occur, and has been demonstrated in this outbreak. By far the most important method of spread is respiratory droplets so hand hygiene is critical. This was the same for SARS and MERSCoV where the main factor related to the spread of infection in hospitals was how close did you get to the patient, i.e. were you in an area where respiratory droplets would land (within 2 metres) and therefore be contaminated by the patient?
 
All travellers from Hubei Province are expected to self-isolate themselves within their own homes for 14 days whether they have symptoms or not; travellers from other areas of mainland China should isolate themselves if symptomatic. If they develop any of the symptoms of 2019-nCoV infection they should ring NHS 111 for advice rather than attend their GP practice or local hospital. NHS 111 will arrange for the patient to be assessed in the appropriate setting. A symptomatic patient attending a healthcare setting unannounced will put other people at risk of infection.
 
Infection control within the home - all exposed and symptomatic patients should “catch it, bin it, kill it” using tissues when coughing or sneezing. The virus is likely to only survive about 15 minutes on a tissue, like other respiratory viruses. Then the person should wash their hands with soap and water.
 
A summary of the infection control requirements in hospital is in the table, for more details see the current guidance from the Department of Health.

It is slightly trickier in primary care. Patients should be asked about travel history via phone if possible or at reception as part of triage. If someone has a travel history that suggests a risk of infection then they should be asked to stay at home and wait for a telephone consultation, or if in the surgery directed to a room on their own, away from other patients. They should not use the usual waiting room. If however risk comes to light during the consultation then the doctor should withdraw from the room, close the door and wash their hands with soap and water. Evaluation of the patient should ideally continue via telephone from outside of the room. Once this has been done then discussion with the local microbiology or infectious diseases services should take place to decide if assessment and investigation is required. For more details see the current Department of Health guidance for Primary Care.
 
So rather than go back to bed and hide under the duvet I think I’m just going to stop watching the news and only read the bulletins from WHO or Public Health England to get my outbreak information from now on… although perhaps I should have stayed on holiday for a few weeks longer until all of this settled down… now there’s an idea!
 
In other news today, a Briton has claimed the Guinness World Record for the largest onion bhaji ever made; the media headline is likely to be something like “Panic as National mango chutney shortage after over production of a gargantuan Indian side dish!”

“I’ve got a tricky one for you” said the Respiratory Consultant.
 
“Go on then, tell me what you’ve got” replied the Microbiologist, knowing from previous experience that this would indeed be a tricky case, but looking forward to his colleagues challenge.
 
“I’ve got an elderly chap who has bronchiectasis and I have been treating for an exacerbation without much luck. In fact he’s getting worse. Despite 2 weeks of different IV antibiotics his CT shows progressive cavitation. He has lost a lot of weight over the past couple of months and unless we come up with something I think I’m going to lose this battle”
 
As the discussion went on the Microbiologist started to look at the patients past results. The one bacterium that stood out as being a bit unusual was Mycobacterium abscessus which had grown a few times over the past year in various sputum samples.
 
“Mmmm, what do you think about the M. abscessus?” asked the Microbiologist. “It sounds like this may be more significant than we’d normally give it credit for.”
 
“I’m glad you say that, I thought the same, but didn’t want to influence your thoughts” replied the Respiratory Consultant.
 
“Mmmm, I have only rarely seen it cause clinical disease, although it’s improbable, it is possible, so let me check the latest literature and I’ll meet you on the ward and we’ll go from there” said the Microbiologist already opening a large tome of reference text, muttering to himself …this isn’t going to be covered in Microbiology Nuts & Bolts!!

What is Mycobacterium abscessus?
Mycobacterium abscessus is a non-tuberculous mycobacterium that is normally found in the environment throughout the World. In fact there are 3 subspecies of M. abscessus (abscessus, bolletii and massiliense) but most labs tend to just think in terms of M. abscessus. At the end of the day the bacterium’s full name doesn’t really matter too much.
 
I tend to think of M. abscessus as in a group of mycobacteria which I call the “rapid growing mycobacteria”. This is because, compared to other Mycobacteria spp., M. abscessus grows relatively quickly; within a week in liquid culture. Even when I started in microbiology, in the days before liquid culture when mycobacteria were grown in square glass jars on slopes of Lowenstein-Jensen media, M. abscessus was regarded as being a quick grower. It used to take around 2-4 weeks compared to the usual 8-12 weeks of other Mycobacteria spp. I include M. abscessus, M. fortuitum, M. chelonae, M. smegmatis and M. mucogenicum in my categorisation of rapidly growing Mycobacteria spp.  What really matters, regardless of its speed of growth, is whether a culture is significant and needs treatment or not. I have rarely seen any of the rapidly growing Mycobacteria spp. causing clinical disease and therefore if I’m honest I often tend to forget about them! But just maybe our culture might be significant; it has grown a few times in earlier sputum samples, so it might not just be a coloniser.
 
How does infection with M. abscessus present?
M. abscessus does have the potential to cause infections of the respiratory tract, but usually only in people with some form of underlying lung disease such as cystic fibrosis, bronchiectasis or emphysema.
 
Respiratory infection presents with:

• Cough - often present for months or years
• Fever
• Weight loss
• Haemoptysis (coughing up blood)
• Shortness of breath
• Chest x-ray changes – interstitial or alveolar infiltrates or cavitation

 
Other, less common, clinical manifestations of M. abscessus infection include:

• Lymphadenitis – enlarged painful lymph glands, often in the neck
• Disseminated infection – multiple subcutaneous nodules or abscesses in immunosuppressed patients
• Skin and soft tissue infection - single or multiple abscesses or sinuses, similar to disseminated infection but in an immunocompetent patient
• Musculoskeletal infection – following direct inoculation of mycobacteria into the skin, bone or joint either from trauma or surgery
• Prosthetic device infection – infections of prosthetic joints, pacemakers and tympanostomy tubes (also known as grommets) have been described
• Post-operative infection – this has been described after all sorts of procedures including laser eye surgery, cosmetic surgery and even cardiac surgery, and has often been linked to the use of non-sterile water at some stage during the procedure

 
How is M. abscessus infection diagnosed?
The key to making a diagnosis of M. abscessus infection is, as often the case, firstly to consider it and then take the right microbiological specimens.
 
For respiratory infections, sputum or bronchoalveolar lavage specimens should be taken. As it is fairly common to find M. abscessus as a colonising bacterium, multiple samples (at least 3 sputums over several weeks) need to be positive in a patient with a consistent clinical infection and chest x-ray changes before making the diagnosis.
 
For non-respiratory infection biopsies should be taken from the lesions and cultured. A positive culture from this type of specimen is less likely to be due to colonisation, and if from a normally sterile site then a positive culture proves the diagnosis.
 
M. abscessus in the UK is usually grown in liquid culture in a system like the Becton-Dickinson Mycobacterium Growth Indicator Tubes (BD MGIT), but there are other types of system available. BD MGIT is an automated incubator system, similar to a blood culture incubator, which contains a liquid culture media, growth supplements and antibiotics to suppress non-mycobacterial bacteria. As mycobacteria grow in the tube they use up the available oxygen which then allows a fluorescent compound in the bottom of the tube to fluoresce telling the incubator that the culture is positive. The tube can then be taken out, stained with auramine or Ziehl-Neelsen (ZN) stain and identified by PCR and tested for antimicrobial sensitivity (usually at a reference laboratory). Liquid culture is one of my Top 3 most significant advances in microbiology since I started in the speciality back in 2001.
 
How is M. abscessus infection treated?
Treatment of M. abscessus infection is difficult, not least because it is resistant to the conventional anti-tuberculous drugs such as Rifampicin, Isoniazid, Ethambutol and Pyrazinamide. Also treatment involves prolonged courses of potentially toxic antibiotics, so you definitely want to be sure of the diagnosis before you start down this path. Any abscesses should be drained and infected prosthetic material should be removed whenever possible.
 
Treatment of M. abscessus infection should be under a Respiratory Physician or someone who has experience of treating such infections.
 
Traditionally Clarithromycin has formed part of the treatment of M. abscessus however recently an inducible resistance gene for macrolides has been found in M. abscessus subspecies abscessus and subspecies bolletii. This is a nuisance because it means that whilst the bacterium might test sensitive in vitro it will become resistant in vivo during treatment. Sneaky huh?! All strains of M. abscessus should therefore have sensitivity testing before starting on treatment, including looking for the inducible macrolide resistance gene.
 
The current British Thoracic Society (BTS) guideline for the treatment of M. abscessus is:

​These drugs can be toxic, and because the treatment course is so long, patients should be monitored closely, including regular  assessment of kidney, liver, hearing, balance and bone marrow function (on initiation of treatment and then at least monthly).
 
The mortality from M. abscessus infection in those completing treatment is about 15% which is very high.
 
Armed with the latest BTS guidelines the Respiratory Consultant and Microbiologist had a long chat with the patient. They explained the infection, the treatment and all of the difficulties in its year-long management; this was going to be some New Year’s resolution for the patient to comply with treatment! Eventually between the three of them they agreed a plan of action. The patient was started on the initial phase cocktail of antibiotics and soon began to feel a bit better. After 6 weeks he had gained weight and was well enough to go home. The plan was to continue to treat for a further 11 months and see how things went, but it was a good start…
 
How are your New Year’s resolutions coming along? Our New Year’s resolution was to stop spending money on vets bills but apparently Guacamole (our ginger moggy) didn’t get the memo and has broken the resolution already…!

Yes really this is made with bacteria on agar…amazing isn’t it?! This was the 2018 winner of the American Society for Microbiology agar art contest, "The battle of winter and spring," by Ana Tsitsishvili. It is staggeringly good! Every time I see this it takes my breath away. 

Now some people see agar art as a waste of resources, time and money… but I think they are wrong. In order to produce something this incredible you have to know so much about bacteria and fungi, how they appear in different environments, how different agar affects them and how they interact with each other.

Personally I think every microbiology lab should run an agar art contest every year… maybe I should start this locally… anyway back to the art…
 
To produce a picture on agar out of bacteria and fungi you need to exploit a number of criteria such as organism colour, texture, colonial size and type of haemolysis as well as using inhibition to create various effects. Okay, it helps to be artistic as well (and I’ll show you my attempt at the end… prepare to laugh, it’s not in the ASM league!).
 
Colour
Colour can be used in two main ways either the bacterial pigments or changes that occur in the agar itself.

​Some bacteria and fungi commonly isolated in clinical microbiology laboratories produce specific colours:

• Staphylococcus aureus – golden colour (hence the name aureus, the Latin for golden)
• Serratia marcescens – red (one of the theories as to why statues of the Virgin Mary can “cry blood”; it’s thought to be this Gram-negative bacterium growing on the statues!)
• Pseudomonas aeruginosa – various colours possible including green, blue, reddish brown (P. aeruginosa produces chemicals called pyoverdin - green, pyocyanin - blue and pyorubin – reddish brown)
• Coagulase negative Staphylococcus spp. – normally “boring” white (common contaminant) but great for making snowflake artwork
• Micrococcus luteus – lemon yellow (common contaminant)
• Rhodococcus equi – salmon pink (can cause severe infections in HIV positive patients and in horses causes foal fever)
• Rhodotorula spp. – red (this is the red waxy mould you sometimes see growing in showers)
• Chromobacter violaceum – purple (C. violaceum produces a pigmented antibiotic called Violacein which is a deep purple colour)
• Aspergillus niger – black (the spores of this fungus are black; it is an opportunistic pathogen)

 
These artists’ creations below use just one bacterium, S. marcescens (red) but I'm not sure what Mike Wazowski (Monster Inc.) is made of but I hope you agree the effect is quite striking!

​Another way to exploit colour in the laboratory is to use an indicator agar; these types of agar produce a particular colour that allow you to spot specific bacterial species:

• Blood agar – alpha and beta haemolysis of blood can give interesting art potential (alert! alert! the word interesting in a microbiology blog!!!); alpha haemolysis (e.g. Viridans Streptococcus spp.) gives a green colour whereas beta haemolysis (e.g. Streptococcus pyogenes) causes clear zones of complete haemolysis around the colonies
• Cysteine Lactose Electrolyte Deficient (CLED) agar is normally turquoise but goes yellow when bacteria ferment the sugar lactose to produce an acid, e.g. Escherichia coli, Klebsiella spp.
• MacConkey agar is normally an orange/red but goes bright pink when bacteria ferment the lactose in the agar, e.g. Escherichia coli, Klebsiella spp.
• Xylose Lysine Deoxycholate (XLD) agar is normally a rich red but some bacteria produce indole creating black colonies, e.g. Salmonella spp. and Proteus mirabilis

​In this example the CLED agar has been used to give a background turquoise colour for the water in which this microbial Koi carp is swimming... Unsurprisingly this is 2019 winner of the American Society for Microbiology agar art contest, brilliant hey!?
 
Using chromogenic agar is a way of taking colour to the next level!
This type of agar contains colourless compounds called chromogens which can be split by specific enzymes or chemicals to produce a pigment. The choice of chromogen can be used to detect an enzyme or chemical specific to a bacterial species and therefore the bacterial species itself. These types of indicator agar are used as screening agars for certain bacteria (e.g. MRSA agar) or to detect, quickly and cheaply, a limited array of bacterial species in a specific sample (e.g. UTI agar). Chromogenic UTI agar is especially good for agar art as different bacteria give different colours all on the same agar plate, it’s a bit like those wash-over colouring books you got as kids!

​On this agar (Chromagar Orientation) specific bacteria give particular colours:

• E. coli = dark pink to reddish
• Enterococcus spp. = turquoise blue
• Klebsiella spp., Enterobacter spp., Citrobacter spp. = metallic blue
• Proteus mirabilis = brown halo
• Pseudomonas aeruginosa = cream, translucent
• S. aureus = golden, opaque, small
• Staphylococcus saprophyticus = pink, opaque, small

 
If you get it right with chromogenic agar, the variation of colours can be stunning:

​BUT if you really want to get creative, start to use Texture!
It’s not just the colour of microorganisms you can creatively exploit, but their texture as well. Some bacteria are smooth, some are crinkled, some have a glassy appearance, others are mucoid and slimy and some eat into the agar itself creating a concave appearance to the art.

• Smooth – Staphylococcus spp.
• Crinkled – Actinomyces israelli
• Glassy – Bacillus spp.
• Mucoid – Pseudomonas aeruginosa
• Slimy – Klebsiella pneumoniae
• Eats agar – Eikenella corrodens

You can even use a Staphylococcus spp. and add hydrogen peroxide to activate the enzyme catalase, producing water, oxygen and foamy beer!

​Fungi are even more textured, especially the moulds such as Aspergillus spp., zygomycetes and dermatophytes. These are raised and fluffy and can be very dramatic. Just look at the volcano agar art below; a specific fungal agar has been heaped up and then cultured with the mould Cledosporium spp. to give the mound a rocky appearance… pure genius, it came 3rd this year in the American Society for Microbiology agar art contest.

​Hold yourselves back, let’s consider - inhibition
The final type of criteria that could be used to create agar art is the ability of microorganisms to inhibit each other. Most antimicrobials actually come from microorganisms and the truly great agar artists use these naturally occurring antimicrobial compounds to create clear zones between coloured colonies or to get colonial edges to heap up and change shape. Some of this is extraordinary; in the example below the yeast Saccharomyces cerevisiae is used in two forms, one producing an antifungal which inhibits another S. cerevisiae creating a clear zone with heaped up blue edges… wow!

​So there you have it; lots of different ways to produce agar art using different bacteria and fungi. But it’s not as easy as it seems. The entrants to the ASM agar art competition are truly fantastic, I think you’ll agree. Most of us can only aspire to produce such amazing results BUT the knowledge behind creating agar art is the fundamental knowledge of microbiology. It’s about an intimate knowledge of the microorganisms we deal with every day.
 
Okay, it might seem frivolous and a waste of energy and resources but is it? Is all the knowledge gained a waste? I don’t think so… take a look at my agar art! Ermmmmmm… at least it’s recognisable!!! … “Is it a multi-eyed alien?” No it’s a Christmas tree!!! OK it’s certainly not going to win any competitions!?

​In the meantime take a look at the ASM site for previous entrants some are truly amazing, and watch the video about how to make agar art.

Here’s a festive selection of agar creations from the Internet to inspire you… so you think you could do better?! Post your images up on our Facebook page for us all to see and comment on… (please respect decency standards! It’s not clever to make a phallic object using salmon pink Rhodococcus equi and Pseudomonas aeruginosa brown blobs!!!)

It’s that time of year… no, not Christmas! In our house it’s Dentist time! While training I was told by a wise veterinary friend that “Doctors shouldn’t treat pets or teeth; they’re not vets or dentists…” and after a course of “stored-up” Metronidazole hadn’t helped my “sensitive tooth” my routine check-up visit has turned into “a repair appointment”. I should have taken my friend’s excellent advice…my issue was not an infection and my abilities in dental diagnosis are clearly lacking! However as Microbiologists we are allowed to consider the causes of dental infections and how they might lead to patients needing antibiotic treatment or even being admitted to hospital.
 
“What time did you go to the Dentist?”
 
“Two thirty” (Ha ha Tooth hurty, tee hee!)

What types of dental infections are there?
There are two main types of dental infections; local (dental caries and gingivitis) and systemic.
 
Dental disease is very common Worldwide. In the developed World it is estimated that 25% of adults aged 20-64 years have untreated tooth decay and 17% of those 65 years and over have no natural teeth!
 
It’ll come as no surprise that we humans have two sets of teeth during our lifetimes. The first set is known as deciduous teeth because we lose them in childhood (they fall like deciduous leaves from trees); they are also known as baby or milk teeth. Teething is the term often used to describe the time when deciduous teeth are appearing. During my time in paediatrics I remember reading a fantastic study (reference below), of hundreds of children, looking at the symptoms of teething to see if there were any patterns and the conclusion was that the only consistent thing that teething causes is the presence of teeth! Our 20 deciduous teeth start to appear from about 6 months old until we are about 2 years old, and we them lose them between 6 and 12 years of age. Our 32 permanent adult teeth appear as we lose our deciduous teeth.
 
Structure of a tooth

Okay basic tooth anatomy time (and it has to be basic, to keep in line with the rest of his anatomy knowledge – Editor Chief-in-Charge). The bit of the tooth that sticks up from the gum is called the crown and is covered in enamel, the hardest structure in the human body, under which is the dentin layer. The roots of the tooth anchor the tooth and extend into the bone of the mandible for the bottom teeth and the maxilla for the upper teeth. Within the space between the root and the bone is the periodontal membrane and cementum (tooth cement) which joins the tooth together and allows a bit of movement in the tooth’s socket to help to protect it from being bashed about whilst biting and chewing.
 
The inside of the tooth is called the pulp and this contains the blood vessels and nerves supplying the tooth. The soft tissue surrounding the tooth at the level of the gum is known as the gingiva.
 
How do dental infections start?
Dental infections start as a result of plaques of bacteria on the surface of the tooth. If the plaque is on the surface of the tooth above the gingiva it leads to dental caries, if it is beneath the gingiva it causes gingivitis and periodontal inflammation.
 
Untreated infections can extend along the areas of least resistance to cause deep infections in the bones of the maxilla or mandible or in the soft tissues of the mouth, face and neck.
 
What bacteria cause dental infections?
The bacteria that cause dental infections are usually part of our normal mouth flora. Yep, these are what are known as endogenous infections; our own flora is attacking us!
 
Within the mouth, different bacteria prefer different locations:

• Tongue and inside the cheek – Streptococcus salivarius and Veilonella spp.
• Tooth surface – Streptococcus sanguinis, Streptococcus mutans and Actinomyces viscosus
• Gingiva – Fusobacterium spp., Prevotella spp. and anaerobic spirochaetes

 
Dental infections are usually polymicrobial; multiple bacteria are acting together to cause the infection. Dental plaque has been studied for hundreds of years, ever since Antonie van Leeuwenhoek (the inventor of the microscope in the 1670s) first started to examine his own dental plaque. So far over a 1000 species have been identified in dental plaque, although some are more pathogenic than others, and some may even be innocent bystanders.
 
The most pathogenic bacteria in the mouth in terms of dental infections are:

• Dental caries - Streptococcus mutans is the only bacterium consistently found in dental caries
• Gingivitis – predominantly associated with anaerobic Gram-negative bacilli (Prevotella intermedia, Capnocytophaga spp, Finegoldia magna and Peptostreptococcus spp.)​
• Periodontal inflammation – mixed anaerobic Gram-negative and spirochaete bacteria (Porphyromonas gingivalis, Prevotella intermedia, Aggregatibacter actinomycetemcomitans, Tannerella forsythensis and Treponema denticola)

Don’t you just love bacterial names?! I particularly like Treponema denti ”cola”… especially as I was always told Coca Cola would rot my teeth… (and probably did!)
 
What factors allow normal flora to attack teeth?
So there must be more to dental infections than just the bacteria because if it was just down to the bacteria they would attack our teeth all the time.
 
Diet plays a major role in dental infections. The bacteria causing these infections produce acid from dietary sugars (especially sucrose) and are perfectly happy living at the lower pH that is caused, so they can continue producing more acid. The acid produced demineralises enamel which in turn allows bacteria to penetrate the tooth causing further demineralisation and so on. Eventually bacteria get inside and the tooth becomes inflamed and starts to be destroyed! Smoking also predisposes to gingival infections by damaging the soft tissue of the mouth.
 
The mouth tries to fight back by:

1. Being bathed in saliva (which is pH neutral, supplies calcium to help re-mineralise the tooth and contains antibacterial compounds such as lysozyme)
2. The tongue “brushes” the teeth removing food
3. By producing a protein film on the tooth’s enamel, this sterile coating called the “acquired pellicle” creates a barrier to acid.

 
However, a diet high in sugar and acid (like our modern diet of fizzy drinks and chocolate) will overwhelm these defences and dental infections will occur.
 
How are dental infections treated?
Most times you visit the dentist you are not prescribed antibiotics. Common dental procedures include:

• Closer attention to tooth cleaning, and occasionally specialist toothpaste products and antiseptic mouth washes are used in the treatment of plaque formation and gingivitis.
• Fillings (technically called restorative therapy) to treat dental caries, where the infected material is removed and replaced with a tooth-like compound.
• Root canal filling is when infected pulp material is removed and cleaning out the root before repairing the tooth with a tooth-like compound.

 
Fortunately it isn’t necessary to kill every bacterial species involved in a dental infection, the mouth’s own defences are good enough once the underlying issue is resolved, which is good as we have already discussed that there are possibly over 1000 species involved!
 
So only the most problematic or pathogenic need to be taken care of, if an abscess has formed, often as a result of ignoring a simpler problem, then a 7 days course of oral antibiotics is usually required. Typical antibiotics include Amoxicillin, Metronidazole and occasionally Co-amoxiclav. These all target the normal anaerobes that cause dental abscesses. An alternative for penicillin allergic patients would be Clindamycin. Once the abscess has settled down “surgical” correction of the underlying problem with a filling or root canal work is necessary to prevent it reoccurring.
 
How to prevent dental infections
There are a number of things we can do to reduce our risk of developing dental infections:

• Regular dental check-ups (at least yearly) and twice yearly visits to the hygienist to spot problems before they become too bad
• Brush our teeth twice a day – but not within 30 minutes of eating or drinking acidic food or drink!
• Floss between our teeth at least once a day
• Reduce the amount of sugary foods and fizzy drinks we consume
• Stop smoking

 
However, this is easier said than done for some of us and most of us have at least one weakness that predisposes us to dental infections. For me it’s the sugary food… I love chocolate! For the Editor Chief-in-Charge that means getting out of bed and brushing her teeth before she is served her breakfast!
 
But hold on! It’s nearly Christmas and that means sweets, chocolates and fizzy pop!!! Oh no… what am I going to do?! I know… brush more carefully, floss diligently and don’t tell my Dentist ​:-)​

Reference:
Symptoms associated with infant teething: a prospective study, Macknin ML1, Piedmonte M, Jacobs J, Skibinski C. Pediatrics. 2000 Apr;105 (4 Pt 1):747-52.

The Microbiologists were out having their Christmas curry together when the oncall phone twitched into action. Looking around the table, under pulled crackers and wrapping paper, the oncall Microbiologist (the only one not drinking!) took the call while the others ordered some more drinks and food… It was a noisy gathering as Microbiologists don’t get out much…
 
The waiter looked expectantly to take more drinks orders….
 
“I’m sure she said a mango lassie, I’ll get her one …yes… one mango lassie please and five cobra beers and another taka dahl, thanks”. The waiter scuttled off.
 
“I ordered you the mango lassie” said the (tipsy off duty) Microbiologist
 
“Why did you get me a lassie?” asked the oncall Microbiologist.
 
“You said mango lassie while on the phone… when we were ordering more drinks… didn’t you!?!”
 
“No… that was the Med Reg from the Royal Free, saying they thought one of contacts of the Dutch Lassa fever cases might be transferred to us for follow up and thought we’d like to be aware, as it was in the news and may cause us a call or two if the local media get to know!”… continuing… [and huffing]  “Really… its 10:30 on Friday night, I do not need to know this oncall, but everyone wants their minute of fluster and fame!!” … “Mango lassie…?! You lot need a hearing test or less Cobra beer!” said the oncall Microbiologist.
 
“5 Cobras and a mango lassie…” said the waiter with impeccable timing!
 
The Microbiologists crumpled in laughter and thanked the waiter who just looked puzzled and said he’d bring over the dahl.

The Critical Care ward round was moving slowly. It was a Monday and so most of the patients were new to everyone, including the Microbiologist.
 
The next patient was a middle aged woman who had been intubated and ventilated but who looked otherwise pretty well. [You get a feel for how unwell a patient is just by standing at the end of their bed and observing; equipment, medications, drains and tubes, as well as the colour and appearance of the patient are all clues.]
 
“This lady has Guillain-Barre Syndrome, so no infection issues” said the Critical Care Registrar moving past the end of the bed.
 
Guillain-Barre Syndrome is a rare neurological syndrome of progressive weakness that usually recovers with supportive care. It is thought to be autoimmune in nature.
 
“How did she present?” asked the Microbiologist doing his normal “I’m looking for trouble” kind of thing.
 
Humouring the Microbiologist the Registrar explained that the patient had presented with progressive difficulty swallowing and speaking following an episode of diarrhoea and vomiting. She had become so weak they had needed to ventilate her.
 
“This sounds like sausage poisoning” said the Microbiologist

"Why do we give broad spectrum antibiotics like Benzylpeniciilin, Gentamicin and Metronidazole to babies with necrotising enterocolitis [NEC] when their gut is sterile?" asked the Neonatal Unit [NNU] Registrar.
 
It was the middle of the NNU multidisciplinary ward round.
 
"Pardon?" said the Microbiologist, caught red-handed reaching for a second chocolate biscuit and suddenly feeling self-conscious as everyone turned to stare at him.
 
"Babies are born with a sterile gut so when they develop NEC why do they need antibiotics; surely there are no bacteria to cause a problem". The Registrar restated his question again but with more clarity.
 
The Microbiologist recognised the question was being rephrased; he obviously looked like he did not understand what was being asked! It was actually a very good observation of the Microbiologist! But it was an even better question thought the Microbiologist…so it needed a good answer…
 
Fortunately the Microbiologist was on the ball, and in fact was armed with the latest research provided by the NNU Pharmacist only a few weeks earlier.
 
Hopefully everyone knows where babies come from... but do you know where babies gut bacteria come from? Read on...