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Pyrexia: the fever response
ОглавлениеSince the core temperature of the body is maintained at around 37°C, many human pathogens have adapted to replicate fastest at this temperature. During infection their numbers can grow exponentially, placing the body at risk of systemic infection and potentially sepsis and septic shock. Fortunately, the human body can respond by increasing body temperature to help slow down pathogenic replication. When leukocytes (white blood cells) begin to fight infection by trapping and killing pathogens, they release a small protein called interleukin-1 (IL-1). IL-1 can initiate a fever response by binding to receptors on the hypothalamus (Dinarello, 2015).
In response to IL-1 the hypothalamus releases a chemical called prostaglandin E2 (PGE2) which functions to shift the set point of the hypothalamus up from 37°C to 38–9°C. This increases the temperature of the body and takes it outside the favourable range for bacterial and viral replication, and as a result the rate of infection will slow. A fever response also allows more rapid trapping and killing of pathogens by leukocytes, some of which function more efficiently at these higher temperatures. Unfortunately, the other cells within the body are now outside of their optimal temperature range and their enzymatic activity slows; as a result, during a fever response we suffer malaise, feeling very ill and lacking in energy.
A normal fever response of 38–9°C is generally regarded as being healthy and beneficial to the body since it slows pathogen growth and speeds up killing, but when the fever response goes beyond 39°C, e.g. 40°C and beyond, this can be dangerous since cellular enzymes may be denatured and life-threatening convulsions can occur. Most non-steroidal anti-inflammatory drugs, e.g. aspirin, are very effective at reducing fever and function by blocking the production of PGE2 in the hypothalamus, thereby preventing the set point being shifted upwards.
To further your understanding of pyrexia, read through Prisha’s case study.