After a prolonged COVID-induced hibernation, Mycoplasma pneumoniae is back in NZ. Over the past couple of months there have been a sprinkling of cases throughout NZ picked up on respiratory panel testing by PCR in diagnostic laboratories, including my own.

I can hardly remember the last time I saw a Mycoplasma pneumoniae infection. It was definitely pre-COVID. The low Ro of Mycoplasma pneumoniae infection meant that transmission was brought to an almost instantaneous halt by the introduction of Non-Pharmaceutical Interventions (NPIs or “lockdowns”) following the emergence of the COVID pandemic.

Over the past year or so, it has started making a comeback worldwide. It has taken longer than other pathogens to return post-COVID, and as described in this interesting article in the Lancet, this is likely due to various factors such as the slow generation time (6 h), long incubation period (1–3 weeks), and relatively low transmission rate of Mycoplasma pneumoniae. It has returned later than most in New Zealand, likely due its geographical isolation and relatively sparse population.

In a (slightly perverted) way I am glad it is back. It is a very interesting bug! It is one of the smallest known bacteria, at only 300nm. It lacks a cell wall, which is why you cannot see it on a Gram stain. It is also why Mycoplasma infections do not respond to beta-lactam antibiotics. It most commonly causes respiratory infections but also has the ability to affect a wide range of organ systems, either by direct invasion or autoimmune reaction. This is eloquently summarised on this table.

It is sometimes referred to as a cause of “walking pneumonia” which can be a little misleading as it is certainly well capable of causing hospitalisation in both adults and children.

As for the “fried egg”, this refers to its phenotypic appearance on culture media (e.g. Hayflick media). Of course, fried eggs have not really returned as virtually nobody these days (and certainly no diagnostic labs in NZ) culture for Mycoplasma pneumoniae, with the mainstay of diagnosis now being PCR and to a much lesser extent, serological testing. Having said this, there is some evidence that Mycoplasma serology is more sensitive than PCR, likely due to delayed presentation to Health Services.

With the worldwide resurgence of Mycoplasma pneumoniae, the other thing to consider is whether the re-emerging strains are macrolide resistant.  This is difficult, due to the lack of laboratories culturing for Mycoplasma pneumoniae. However, assays are now being developed to look for the key rRNA mutations coding for macrolide resistance directly from clinical samples. It is certainly something we will need to think about both from a treatment and surveillance point of view.

Which is the optimal sample type for (molecular) diagnosis of Mycoplasma pneumoniae? There does not seem to be a lot of literature on this topic and it probably depends on the clinical presentation of the disease. If presenting as an upper respiratory tract infection, which it can do, then throat or nasopharyngeal swab is likely to be best.  For pneumonia then sputum or BAL are probably optimal.

So, Mycoplasma pneumoniae is back, and because of this, we need to start thinking about it again as a differential diagnosis in our patients. Its return has however, made my job a little more interesting…

Michael