Ah, Rhodococcus equi, I can't say that I have missed you...


It is that time of year unfortunately when foals are old enough for Rhodococcus equi to rear its particularly ugly head.  If this was an easy condition to diagnose and treat, we would all be better off.  But it isn’t, and it isn’t likely to be any time soon.

Originally known as Corynebacterium equi, R. equi was first proposed as a cause of purulent pulmonary disease in foals in 1923 by Magnusson.  Since that time we have come to know a lot more about it, and how it doesn’t just take up residence in the lungs, but can go about anywhere it wants in a foal.  The list of problems besides pneumonia in foals is long: abdominal abscesses, growth plate infections, submandibular lymph node abscesses and even bone infections are reported.  Adult horse disease also occurs but is rare.  Other species can be affected, and of great importance is R. equi infection of immune compromised humans.

There isn’t anywhere far enough away to run from trouble, and the same goes for R. equi.  Unless you are a penguin in Antarctica (the only continent where it is not found) you are going to come up against it sooner or later.  It is a free living soil saprophyte (feeds on dead material), with some strains adapted to infect horses courtesy of a small circular piece of DNA called a plasmid (more on those later).  Some of these R. equi have the added bonus of enjoying the contents of a horse’s colon, where they can happily live while they get spread around.  Once in the soil, they are one step away from being in the dust that gets inhaled.  As you increase the density of horses and handle them in drier conditions you get more dust.  Suffice to say, where there are horses, there is likely R. equi.

Traditionally infection was thought to be by ingestion, but Inhalation of virulent bacteria has turned out to be a very important means of transmission between infected and susceptible foals, and is now thought to be the main route of infection.  Complicating matters greatly, it is now known that healthy foals on endemic farms exhale virulent R. equi meaning these outwardly normal foals may harbor and spread the organism in the absence of clinical problems.  This has significance in the transmission and persistence of disease on endemic farms.

While there are non-pathogenic R. equi out there in the soil, the infectious ones have a special surface protein (vapA) that allows them to attach to cells and enter, escaping the immune system.  This protein is encoded by the plasmid.  Bacteria can swap this plasmid amongst themselves, meaning previously non-infectious R. equi bacteria can become problematic to the foal.  Once inside they can also survive the usual bacteria killing process within the infected cell.

So why are young foals so susceptible?  It is all to do with how their immune system develops.  It is not quite as good as an older horse in some respects, being unable to deal with intracellular infections as efficiently early in life, around the time R. equi infection occurs which is thought to be within the first few weeks.  As the organism is widespread in the soil, neonatal foals are potentially exposed from day 1 and this is ongoing, so it is nearly impossible for a foal to avoid exposure.  It’s basically a race: time taken for the foal to develop effective immunity against constant exposure to infection which hopefully is not sufficient to overwhelm the neonatal immune system.

Group some horses together, kick up some dust, throw in some young foals and away it goes.  A significant amount of disease is present by the time infection announces its arrival, with the onset of clinical signs often rapid and in some cases overwhelming giving you little time to respond.  So all in all, R. equi is quite sneaky really.

Next time I talk about R. equi I’ll mention the ways in which it can show up in your foal.

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