Lots of microorganisms can survive in remarkably difficult conditions – bacteria can bloom in hot springs at 80°C, archaea live around hydrothermal vents reaching a toasty 113°C, while viruses can survive in the Arctic sea ice. For human pathogens, only when they infect their desired host do they encounter perhaps the harshest environment of all: the bloodstream. Blood is chock full of cells, all jostling around, flowing at speeds varying between millimetres per second in narrow capillaries to metres per second in large arteries. When a foreign organism enters the bloodstream, the immune system registers the invader and scrambles an armed response unit. Very few organisms can survive this attack, but some do so by constantly and randomly changing into different disguises. One example is the African trypanosome, a single-celled parasite that is transmitted to humans in the bite of the tsetse fly, makes its home in the bloodstream, and causes the disease known as African trypanosomiasis. Trypanosomes in the blood are constantly covered in antibodies and immune complement proteins designed to explode foreign intruders out of existence, yet they are able to persist in this hostile environment with no adverse effects.
So how exactly do these parasites survive in their host? And does it have something to do with how they move through the bloodstream? Trypanosomes actively and persistently move through the circulation using a locomotive propulsion system consisting of a single tail, known as a flagellum, which beats at a regular frequency. They exploit the presence of densely packed donut-shaped red blood cells, seen above, to achieve maximum speeds, creating a hydrodynamic drag that allows the parasite to remove attached antibodies and therefore dodge normal pathogen clearance pathways. As they travel, their asymmetrical body smoothly rotates, allowing the flagellum to probe the blood vessels they’re travelling through in three dimensions, making it easier to navigate through the crowded physical microenvironment. In response to mechanical cues, trypanosomes are also able to rapidly adjust the direction in which their flagellum beats, so when they get stuck in narrow areas, they can switch into reverse and manoeuvre free. This is an important capability, since part of the trypanosome life cycle requires movement out of the blood through tissues and into lymph and cerebrospinal fluid. Such ingenious mechanical adaptations to the fixed and crowded habitat of the bloodstream probably represent a genetically programmed trait that ensures survival in the host.
Heddergott N, Krüger T, Babu SB, Wei A, Stellamanns E, Uppaluri S, Pfohl T, Stark H, & Engstler M (2012). Trypanosome motion represents an adaptation to the crowded environment of the vertebrate bloodstream. PLoS pathogens, 8 (11) PMID: 23166495
Very interesting article. Reminds me of work from a former colleague of mine (Dave Smith) who has done similar analysis of sperm swimming (see http://web.mat.bham.ac.uk/D.Smith/?path=Publications)
That’s a very good point, and the author’s of this paper drew similar parallels with regards to spermatozoa. The speeds they measured their trypanosomes moving at were equivalent to those reached by mammalian sperm, and they both showed similar responses in how they changed the use of their flagellum in environments of higher or lower viscosity. It appears that nature is happy to conserve well-engineered designs.