There have been many reports of unusually high case counts of pneumonia in children and some of this appears to be related to Mycoplasma pneumoniae. Some are calling this white lung syndrome. h/t to @celestial_bean_ for this list of different locations.
The review article Infection with and Carriage of Mycoplasma pneumoniae in Children provides an excellent background on this problem (Meyer Sauter et al., 2016).
An eight-year study beginning in the 1960s in Seattle found carriage rates that varied between endemic (2%) and epidemic (35%) periods (Foy et al., 1979). One study found that 21% of asymptomatic children carried M. pneumoniae in their upper respiratory tract at a single study site (Spuesens et al, 2013). In a separate study, 24% of children with pharyngitis were found to have M. pneumoniae on testing as well (Esposito et al., 2014).
A 2023 study of children with recurrent respiratory tract infections found that 68% carried M. pneumoniae (Koenen et al., 2023). Why is this rate doubled of that a few years ago? Could COVID be a driving factor?
This organism is more likely to cause severe disease in an immunocompromised host (Yacoub et al., 2016). One problem is that colonization may not drive a mucosal antibody response (de Groot et al., 2022). I have a number of studies linked on this page indicating immune system damage from COVID.
Think of the immune system as a chemical defense system against pneumonia. Another defense system is mechanical. “Mucociliary clearance (MCC) is the primary innate defense mechanism of the lung. The functional components are the protective mucous layer, the airway surface liquid layer, and the cilia on the surface of ciliated cells. The cilia are specialized organelles that beat in metachronal waves to propel pathogens and inhaled particles trapped in the mucous layer out of the airways.” (Bustamante-Marin and Ostrowski, 2016).
In a hamster model, “SARS-CoV-2 infection is followed by a severe loss of cilia.” (Schreiner et al., 2022). Part of the mechanism of spread to other cells in the respiratory epithelium has been described and illustrated (Su et al., 2023).
The mechanism of the loss of cilia has also been described (Fonseca and Chakrabarti, 2022).
This damage can clearly be seen in both transmission and scanning electron microscopy.
The authors also showed the impact of infection on the ability of the cilia to sweep away low density 30 µm-sized polystyrene microbeads. The first video is of mock-infected cells where “beads deposited on mock-treated epithelia moved generally in the same direction, consistent with coordinated beating of the underlying cilia.”
“In contrast, beads deposited on infected epithelia were mostly immobile or showed randomly-oriented limited movements, indicating an impairment of the mucociliary clearance function.”
It’s clear that both immune system dysfunction and respiratory epithelial damage could be contributing to the M. pneumoniae problem in the pediatric population. The question then becomes one of why this seems to be surging now. Could it be that a new variant is driving this? The answer seems that this seems to be a distinct possibility. “Omicron variants dramatically accelerate spread via the ciliary transport/microvilli reprogramming pathway, which explains the increase in its attack rate compared to previous variants.” (Wu et al., 2022).
What variants do the impacted countries have in common currently? 23F (EG.5) and its sublineages (HV.1 is one of them).
This variant is also dominant in Ohio…
…as well as Massachusetts.
However, the HV.1 sublineage seems to be what is becoming dominant in the US which correlates with the M. pneumoniae cases. It’s interesting that the EG.5 is dominant in the world.
Of course, this could all be correlation with the variants. It’s possible that there is ascertainment bias and that much of the pneumonia in pediatric populations is a combination of COVID, RSV, influenza, and M. pneuomoniae which are all on the rise. Even more concerning is the possibility that this is a new virus. The rapid rise in cases would certainly suggest that. It’s also worth learning about the concepts of sufficient and necessary causes in epidemiology if one has that level of interest in this topic.
Mainly though, I hope to impress on people that COVID not only is a causal pathway for a number of chronic diseases, but I think I’ve made a case that it is also causal for infectious diseases as well, with a special focus here on respiratory ones. We need to be doing far more to protect children.
