Bacterial toxins

Due to the action or breakdown of bacteria, toxic substances (toxins) are released into the environment. Such substances are capable of damaging, and in some cases even killing, the host. The ability to harm a host is called toxicity and is part of pathogenicity. It either acts directly or contributes to other pathogenicity factors.

Due to the action or breakdown of bacteria, toxic substances (toxins) are released into the environment. Such substances are capable of damaging, and in some cases even killing, the host. The ability to harm a host is called toxicity and is part of pathogenicity. It either acts directly or contributes to other pathogenicity factors.

Toxins in general
Chemically, toxins are antigenic proteins that are neutralized (blocked) in the human body by specific antibodies. Boiling inactivation is also possible, they are so-called thermolabile. Toxins can also be turned into toxoids that are used for active immunization.

The toxicity of bacterial toxins produced within the body depends on their concentration and the susceptibility of the host. Toxins can also be introduced into the body from the external environment (eg in food - botulinum toxins, enterotoxins ). These toxins depend not only on their concentration, but also on their absorption and resistance to digestive enzymes.

The mode of toxic action is characteristic of individual toxins (diphtheria, tetanus, botulism, cholera). Symptoms of clinical toxin disease are generally called toxinoses.

Bacterial toxins act on the host in two ways. The first is the reaction with the membranes of eukaryotic cells, which they damage. Hence, this group of toxins is referred to as cytolytic. The second way is the binding of the toxin to a specific receptor on the cell. By binding, the toxin penetrates into the cytoplasm, where it affects physiological mechanisms.


 * According to the target organs, we can divide toxins into
 * neurotoxins (botulinum toxin, tetanospasmin);
 * enterotoxins (choleragen, E. coli toxins);
 * dermonecrotoxins (diphtheria, staphylococcal alpha toxin);
 * cytotoxins (Clostridium difficile);
 * cardiotoxins (diphtheria, streptolysin O);
 * capillary toxin (B. anthracis);
 * hemolysins, leukocidins;
 * superantigen toxins (Streptococcus pyogenes, toxic shock syndrome toxin).

Exotoxins
Toxic bacterial proteins, secreted into the producer's environment. They are used in diseases caused by G + bacteria. Exotoxins are released from the bacteria into the environment during their growth.

Exotoxin genes are stored primarily on plasmids or on temperate bacteriophages. As a result, bacteria are not essential for life, but are useful for their survival and spread.

Penetrating enzymes (factors)
Hydrolytic enzymes that disrupt the intercellular mass. It is used for invasion (so-called invasion factor), to gain nutrients and energy. These enzymes include, for example, hyaluronidase, elastase, DNase, streptokinase (dissolves blood clots).

Cytolytic enzymes (cytolysins)
Toxins interact with the membranes of eukaryotic cells, which they damage. Chemically, these are phospholipases. Membrane disruption can also occur through the formation of pores.

Hydrolysis of phospholipids by phospholipases C and D removes the polar group from the phospholipids. This destabilizes the membrane and lyses the cells. Examples of such bacteria are Clostridium perfringens, whose alpha toxin is phospholipase C. It causes intravascular hemolysis in myonecrosis or intravascular coagulopathy. Another example is sphingomyelinase (beta-hemolysin) in Staphylococcus aureus.

Toxins that form pores in the membrane are elongated molecules. They integrate into the membrane, creating channels through which water penetrates. This membrane disruption is non-enzymatic. An example is Staphylococcus aureus alpha-toxin. Another example is streptolysin O, which is produced by Streptococcus pyogenes. Streptolysin disrupts the membrane of the granules inside the neutrophils. Another pore-forming toxin is Listeriolysin O, made by Listeria monocytogenes, which helps the bacterium escape from the phagosome.

Toxins affecting cell physiology
They do not kill cells directly, they modify their functions. ADP-ribose binds to the regulatory components of adenylate cyclase, which increases the concentration of cAMP. Increased cAMP concentration causes Cl- and water secretion and inhibits Na+ absorption. This will cause fluids to leak. Toxins therefore cause diarrhea (cholera toxin, thermolabile E. coli enterotoxin). Another example is Bordetella pertussis (pertussis toxin). It affects the level of cAMP in neutrophils. This will reduce chemotaxis and motility.

Inhibition of proteosynthesis
Intracellular toxins that cause subsequent cell death. The toxin has two components. The A (active) component is toxic, the B (binding) component binds to a specific cell membrane receptor. Binding will allow the toxin to endocytose into the cell. Enzymatic activation occurs inside the cell. Toxins cause the transfer of the adenosine diphosphate ribosyl group from NAD to the target molecule (elongation factor 2 - diphtheria toxin). This stops proteosynthesis, which causes cell death.

Neurotoxins
They act as peptidases. It acts at nerve synapses on proteins that are responsible for releasing neurotransmitters. These are tetanus toxin and botulinum toxin.

Tetanus toxin (tetanospasm) is a toxin that is formed by Clostridium tetani. Bacteria are present in the digestive tract of animals. With the droppings of these animals, they get into the soil, where they sporulate. Spores enter the human body when the infected soil comes into contact with an open wound (most often deep injuries). Spores in the wound germinate (ideal conditions - heat, humidity, anaerobic environment). Bacteria begin to produce toxins. They penetrate the blood and lymph into the nerve cells. Along their axons, they can reach the CNS (motor neurons). In the CNS, they can disrupt transmission on inhibitory neurons, where they inhibit GABA release. Continuous stimulation with excitatory neurotransmitters causes muscle cramps, and thus respiratory arrest, heart failure, and subsequent death.

Botulinum toxin is a toxin of Clostridium botulinum. It is probably the most effective poison known - the LD 50 is 10 ng/kg. Bacteria multiply in uncooked food. Heat treatment destroys the bacterium itself, but the toxin remains. It usually causes serious fatal poisoning. It is most often present in canned food (bacteria form gases → bulging can), especially meat (sausage poison).

From the intestinal mucosa, it enters the PNS through the blood. It acts on the neuromuscular discs, where it blocks the release of acetylcholine. It causes polio. If it attacks the respiratory muscles (diaphragm), death can lead to suffocation.

Superantigens
A subset of exotoxins that are able to induce polyclonal T-cell activation (mitogens). They bind to T-lymphocytes and macrophages. After binding, they induce an overall defense response (release of large amounts of cytokines). This contributes to the development of autoimmune diseases. They increase the sensitivity to the action of G− endotoxins. Examples are staphylococcal enterotoxins (food poisoning) and Streptococcus pyogenes superantigens (pyrogenic fever toxins).

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