WARNING: This is not sci-fi, but a story based on scientific theories of bacterial and immune behavior.
Previously on Tetanus and Little Miss Muffin: Little Miss Muffin’s hand has been infected by a spore of Clostridium tetani. C. tetani, now in an oxygen-free environment inside her healed-over wound, is replicating and has released the toxins tetanospasmin and tetanolysin.
Chapter 3: Attack of Tetanospasmin.
As the bacterial infection grew within Miss Muffin’s hand, her bloodstream dispersed the tetanospasmin protein through her body. Tetanospasmin was not just an abstract blob, it had a definite structure and components. It is classified as an A-B toxin, meaning it is a toxic protein composed of two main chains where the A chain is “active” and works enzymatically and the B chain does the “binding.” When tetanospasmin was released from C. tetani, a special enzyme cleaved the tetanospasmin into two parts that were held together by a couple of sulfur atoms and some cute chemical “noncovalent” forces (1).
The flow of blood brought the tetanospasmin to a neuron. The much heavier B chain of the toxin attached to a receptor on a neuron’s membrane. This is not just any receptor, for only certain molecules fit certain receptors – a molecular lock and key. The light A chain was then internalized into the neuron and migrated via the axon subway to the central nervous system. At the spinal cord, tetanospasmin irreversibly attached to a junction of neurons designed to inhibit undesirable muscle contraction (tightening). The toxin blocked the release of gamma-aminobutyric acid (GABA) from a neuron. This GABA, although unknown to Miss Muffin, was essential to her ability to relax muscles. If many more of these appalling toxins came to the spinal cord and blocked the release of GABA, Miss Muffin’s muscles through her body would continually contract against each other. This torturous existence could very likely lead to death.
Chapter 4: Miss Muffin Fights Back.
A Y-shaped molecule drifted to the site of Miss Muffin’s nail puncture, as many Y-shaped molecules have, and as many more have drifted through her blood stream during her life. At the end of the two branches of the Y was a “binding site” of a particular shape and chemical reactivity. The binding site lightly touched a tetanospasmin molecule. It bound tightly, and wouldn’t let go.
Some time ago, Miss Muffin received three vaccinations to immunize against the triad of diphtheria, tetanus, and pertussis (DTP). Each vaccination included a particular toxoid, which was a disabled form of tetanospasmin unable to permanently bind to neurons, and thus unable to prevent the release of those important GABA molecules. Her T and B white blood cells noticed these toxoids. Through a complicated series of chemical signal swaps, the T and B cells agreed the B cells should amplify the production of antibodies against this tetanus toxoid, the afore-mentioned Y-shaped molecules. After some time, the quantity of these anti-tetanus toxoid antibodies decreased, but Miss Muffin was boosted with another DTP vaccination, and the number of antibodies skyrocketed and stayed high. Another booster shot was given and amped the production a wee bit more. They drifted in her blood stream and waited.
The tetanospasmin at the infection site was similar in molecular appearance to the tetanus toxoid of the vaccine. The drifting antibodies discovered the vile tetanospasmin at the wound site, and latched on. These quiet heroes neutralized the malevolent ones.
And what of the tetanolysin? It fastened to cholesterol molecules anchored in the exterior membranes of nearby cells and, with the aid of the traitorous cholesterol, formed a ring-shaped pore in the membrane (2). Numerous other tetanolysins incorporated pores in the ever-weakening cell membrane, destroying the cell’s integrity and allowing undesired substances in and precious ones out. The cell eventually lysed into a worthless mass.
Meanwhile, although C. tetani replicated inside the oxygen-deprived wound, various soldiers of Miss Muffin’s immune system noticed its presence and obliterated it. These little fighters included various other antibodies against the Gram-positive C. tetani, natural killer cells, neutrophils, and macrophages. That story is for another day.
- Murray Patrick, Ken Rosenthal, George Kobayashi, and Michael Pfaller. Medical Microbiology, 4th Ed. St. Louis, Mosby, Inc, 2002.
- Rottem S, Groover K, Habig W H, Barile M F, Hardegree M C. Transmembrane diffusion channels in Mycoplasma gallisepticum induced by tetanolysin. Infect Immun. Mar 1990; 58(3): 598–602. PMCID: PMC258507
About the author:
Theresa Adams graduated from Washington State University, Pullman, with a BS in Microbiology. She is married to a handsome guy named Ethan and has two little boys who are not aware of the of term “germs” and instead are occasionally reminded of “icky microbes.” She agrees with King David, that we are “fearfully and wonderfully made,” Ps. 139:14.