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In my first year at medical school I went to a lecture on cellulitis, and it is a testament to my ignorance – and the number of magazines that I read – that I thought it was going to be an in-depth scientific look into the problem of orange-peel thighs. A serious medical approach to skincare – how sophisticated and French! The first slide went up: a photograph of someone’s leg. From ankle to knee it was flushed bright red. “Dolor . . . rubor . . . calor . . . tumor,” said the lecturer, reciting the Latin names for the four cardinal signs of inflammation (pain, redness, heat, swelling). My neighbour had drawn a leg and was busy cross-hatching it in red biro. “Cellulitis is an infection of the skin’s deepest layer: does anyone know what that’s called?” asked the lecturer. The students at the front raised their hands. My neighbour added a shoe to the bottom of his sketch.
The outermost layer of our skin is called the epidermis. The next layer down is the dermis, which is a bit thicker (although even at its densest, such as the skin covering the back, it’s still only 3mm deep, about the depth of a piece of pre-sliced cheese). If bacteria gain access to the epidermal layer, they can cause an infection called erysipelas. Like many illnesses that are now viewed as relatively minor, it was far more serious in the days before antibiotics – the utilitarian philosopher John Stuart Mill died of it. If bacteria get all the way down into the dermis, they can cause cellulitis. It is not easy to distinguish between the two conditions, although erysipelas tends to affect the face and alter the texture of the skin’s surface; in cellulitis the overlying skin is usually smooth despite the presence of inflammation.
In both cases, a warm, tender, red area develops, which can enlarge rapidly. I spent much of my first year as a doctor drawing round patches of cellulitis (the illness is common among hospitalised patients: they are relatively immobile, which affects their lymphatic drainage, and they have relatively depleted immunity, making them less able to fight off invading bacteria). We would visit the patient, trace the edge of the cellulitis and date it. The next day the redness had often breached the boundary: untreated, it would continue to spread, and we sometimes saw thin red lines radiating out of the infected area as the bacteria tracked along the lymph vessels. We got used to seeing patients with concentric ink circles on their shins, like the age rings on a tree trunk, showing the progress of the infection.
It’s not that difficult for germs (usually staphylococci or streptococci) to access the skin’s deeper layers. A tiny scratch or an insect bite is enough; hospital interventions carry an obvious risk. Unappetising though some feet are, it is a mistake not to examine them, too. Even athlete’s foot can provide an entry point for bacteria. If you are fit and well, your body’s defences will often quash any invading microbes before they multiply enough to cause infection. But if your immune system is compromised in any way – by chronic illness or medical treatment – you’ll be more vulnerable, as is anyone with poor circulation, such as smokers, diabetics and the obese.
Most of the time we can treat erysipelas and cellulitis. We use antibiotics, which usually work (they will need to be intravenous if the infection is widespread or making you unwell). Unfortunately, doctors are generally not strict utilitarians: and so we have prescribed antibiotics for all kinds of non-bacterial illnesses, too, fostering the rise of resistant bacteria, and cellulitis that spreads almost faster than you can colour with a pen.
Sophie Harrison is a hospital doctor in South Yorkshire. This column appears fortnightly
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