Bacterial Toxins PDF

Bacterial Toxins: Description Toxins produced by [microorganisms](https://www.longdom.org/peer-reviewed-journals/microorganisms-2929.html) such as bacteria, fungus, protozoa, dinoflagellates, and [viruses](https://www.longdom.org/peer-reviewed-journals/viruses-25440.html) are known as microbial to...

Bacterial Toxins: Description Toxins produced by [microorganisms](https://www.longdom.org/peer-reviewed-journals/microorganisms-2929.html) such as bacteria, fungus, protozoa, dinoflagellates, and [viruses](https://www.longdom.org/peer-reviewed-journals/viruses-25440.html) are known as microbial toxins. Many microbial toxins promote infection and disease by causing direct damage to host tissues and causing the immune system to malfunction \[(https://www.longdom.org/open-access/a-brief-note-on-bacterial-toxins-92562.html#1)\]. Bacterial toxins are classified as exotoxins or endotoxins. Exotoxins are produced and actively released, whereas endotoxins remain in the bacteria. Exotoxins are also bacteria specific; for example, diphtheria toxin is only produced by *Corynebacterium diphtheriae* bacteria and is essential for the diphtheria disease. Endotoxins are lipopolysaccharide or lipooligosaccharide molecules found in outer plasma membrane of Gram-negative bacteria. Exotoxins are proteins with enzymatic activity that interfere with host cells. *Botulinum* toxins, Clostridial toxins, Tetanus toxin,* Staphylococcal* toxins, Cholera toxins are some of the bacterial toxins examples. **Botulinum toxins** *Botulinum* neurotoxins (BoNTs) are protein neurotoxins made by the* Clostridium* bacteria \[(https://www.longdom.org/open-access/a-brief-note-on-bacterial-toxins-92562.html#2)\]. BoNTs are presently being examined extensively for their potential to help with chronic inflammatory disorders including acne and multiple sclerosis, as well as for cosmetic purposes. The* botulinum* toxin, which is produced mostly by *Clostridium botulinum*, is the world\'s most toxic chemical. **Botulism** is a rare and potentially fatal [illness](https://en.wikipedia.org/wiki/Illness) caused by [botulinum toxin](https://en.wikipedia.org/wiki/Botulinum_toxin), which is produced by the bacterium [*Clostridium botulinum*](https://en.wikipedia.org/wiki/Clostridium_botulinum). The disease begins with weakness, blurred vision, [feeling tired](https://en.wikipedia.org/wiki/Fatigue_(medical)), and trouble speaking. This may then be followed by weakness of the arms, chest muscles, and legs. Vomiting, swelling of the abdomen, and diarrhea may also occur. The disease does not usually affect [consciousness](https://en.wikipedia.org/wiki/Consciousness) or cause a [fever](https://en.wikipedia.org/wiki/Fever). **Mechanism of action**: toxin is released by bacteria, coats pre-synaptic axonal ending membranes, is endocytosed (or forms pores that allow toxin entry) and prevents exocytosis of Ach from vesicles to the synaptic cleft = no excitation of post synaptic neuron or effector (skeletal muscles, sweat glands etc.). Flaccid paralysis that is progressive and results in respiratory failure **Tetanus toxins** *Clostridium tetani *produces tetanus toxin (TeNT protein), which causes tetanus. Tetanus is a paralytic disease that affects neonates and non-immunized persons worldwide. Tetanus toxin is produced by* Clostridium tetani*, a spore-forming bacteria found in soil. Tetanus is present in manure, soil, and dust and enters the body of organisms through wounds or [skin](https://www.longdom.org/peer-reviewed-journals/skin-29065.html) breaks. Tetanus causes spastic paralysis by interfering with the transfer of glycine and γ-aminobutyric acid from inhibitory interneurons in the spinal cord. When tetanus toxin enters the body, it is taken up by cholinergic nerve endings that move axonally into the brain and spinal cord, causing disruption of the motor function. Tetanus is a harmful toxin with a wide range of symptoms that can be prevented by vaccination/immunization. **Mechanism of action:** The mechanism of TeNT action can be broken down and discussed in these different steps: First, binding in the peripheryal neurons, then [Retrograde axonal transport](https://en.wikipedia.org/wiki/Axoplasmic_transport) to the CNS [inhibitory interneurons](https://en.wikipedia.org/wiki/Interneuron) and finally [Transcytosis](https://en.wikipedia.org/wiki/Transcytosis) from the axon into the inhibitory interneurons. The final goal of TeNT is to interfere with exocytosis of the neurotransmitters [γ-aminobutyric acid](https://en.wikipedia.org/wiki/Gamma-aminobutyric_acid) (GABA) and [glycine](https://en.wikipedia.org/wiki/Glycine). GABA inhibits motor neurons, so by blocking GABA, tetanus toxin causes violent spastic paralysis. The consequence is dangerous overactivity in the [muscles](https://en.wikipedia.org/wiki/Muscle) from the smallest sensory stimuli, as the damping of [motor reflexes](https://en.wikipedia.org/wiki/Motor_reflex) is inhibited, leading to generalized contractions of the agonist and antagonist musculature, termed a \"tetanic spasm\". **Staphylococcus toxins** Although S. aureus usually acts as a [commensal](https://en.wikipedia.org/wiki/Commensalism) of the human microbiota, it can also become an [opportunistic pathogen](https://en.wikipedia.org/wiki/Opportunistic_infection), being a common cause of [skin infections](https://en.wikipedia.org/wiki/Skin_infection) including [abscesses](https://en.wikipedia.org/wiki/Abscess#Classification), [respiratory infections](https://en.wikipedia.org/wiki/Respiratory_disease#Respiratory_tract_infections) such as [sinusitis](https://en.wikipedia.org/wiki/Sinusitis), and [food poisoning](https://en.wikipedia.org/wiki/Food_poisoning). Pathogenic strains often promote [infections](https://en.wikipedia.org/wiki/Infection) by producing [virulence factors](https://en.wikipedia.org/wiki/Virulence_factor) such as potent [protein](https://en.wikipedia.org/wiki/Protein) [toxins](https://en.wikipedia.org/wiki/Exotoxin), and the expression of a [cell-surface protein](https://en.wikipedia.org/wiki/Protein_A) that binds and inactivates [antibodies](https://en.wikipedia.org/wiki/Antibody). [Deoxyribonuclease](https://en.wikipedia.org/wiki/Deoxyribonuclease), which breaks down the DNA, protects *S. aureus* from [neutrophil extracellular trap](https://en.wikipedia.org/wiki/Neutrophil_extracellular_traps)-mediated killing. *S. aureus* also produces [lipase](https://en.wikipedia.org/wiki/Lipase) to digest lipids, staphylokinase to dissolve fibrin and aid in spread, and [beta-lactamase](https://en.wikipedia.org/wiki/Beta-lactamase) for drug resistance. S. aureus is one of the leading pathogens for deaths associated with **antimicrobial resistance and the emergence of [antibiotic-resistant](https://en.wikipedia.org/wiki/Antibiotic-resistant) strains, such as [methicillin-resistant S. aureus](https://en.wikipedia.org/wiki/Methicillin-resistant_Staphylococcus_aureus) (MRSA).** The bacterium is a worldwide problem in [clinical medicine](https://en.wikipedia.org/wiki/Medicine#Clinical_practice). Despite much [research and development](https://en.wikipedia.org/wiki/Research_and_development), no [vaccine](https://en.wikipedia.org/wiki/Vaccine) for S. aureus has been approved. Toxins produced by S.aureus strains include enterotoxins, which induce food poisoning, exfoliative toxins, which cause scalded [skin](https://www.longdom.org/peer-reviewed-journals/skin-29065.html) condition, and Toxic-Shock Syndrome Toxin (TSST), which causes toxic shock syndrome. These are classified as super-antigens. **Mechanism of action**: Staphylococcal enterotoxins (SEs) produced by Staphylococcus aureus work by binding to receptors on T cells and major histocompatibility complex (MHC) class II proteins. This binding activates the immune system, causing a massive release of cytokines and causing inflammation. Many of these cause gastroenteritis that is self-limiting, characterized by vomiting and diarrhea 1--6 hours after ingestion of the toxin, with recovery in 8 to 24 hours. Symptoms include nausea, vomiting, diarrhea, and major abdominal pain **[Exfoliative toxins](https://en.wikipedia.org/wiki/Exfoliatin) **are exotoxins implicated in the disease [staphylococcal scalded skin syndrome](https://en.wikipedia.org/wiki/Staphylococcal_scalded_skin_syndrome) (SSSS), which occurs most commonly in infants and young children. It also may occur as epidemics in hospital nurseries. The [protease](https://en.wikipedia.org/wiki/Protease) activity of the exfoliative toxins causes peeling of the skin observed with SSSS. **Superantigens** can induce [toxic shock syndrome](https://en.wikipedia.org/wiki/Toxic_shock_syndrome) (TSS). Toxic shock syndrome is characterized by [fever](https://en.wikipedia.org/wiki/Fever), [erythematous rash](https://en.wikipedia.org/wiki/Erythema), [low blood pressure](https://en.wikipedia.org/wiki/Hypotension), [shock](https://en.wikipedia.org/wiki/Shock_(circulatory)), [multiple organ failure](https://en.wikipedia.org/wiki/Multiple_organ_dysfunction_syndrome), and [skin peeling](https://en.wikipedia.org/wiki/Desquamation). Lack of antibody to TSST-1 plays a part in the pathogenesis of TSS. **Cholera toxins** Cholera is a potentially fatal infection caused by toxigenic Vibrio cholerae, which is spread through the fecal-oral route via food or water contaminated with the Vibrio cholerae. The intestines are the target of V.cholerae, which secretes cholera toxin (CT). It is an exotoxin and powerful enterotoxin that targets G-proteins, forcing intestinal [cells](https://www.longdom.org/peer-reviewed-journals/cells-53612.html) to discharge large amounts of water and electrolytes into the lumen. **Cholera** is an [infection](https://en.wikipedia.org/wiki/Infection) of the [small intestine](https://en.wikipedia.org/wiki/Small_intestine) by some [strains](https://en.wikipedia.org/wiki/Strain_(biology)) of the [bacterium](https://en.wikipedia.org/wiki/Bacteria) [*Vibrio cholerae*](https://en.wikipedia.org/wiki/Vibrio_cholerae). Symptoms may range from none, to mild, to severe. The classic symptom is large amounts of watery [diarrhea](https://en.wikipedia.org/wiki/Diarrhea) lasting a few days. [Vomiting](https://en.wikipedia.org/wiki/Vomiting) and [muscle cramps](https://en.wikipedia.org/wiki/Muscle_cramps) may also occur. Diarrhea can be so severe that it leads within hours to severe [dehydration](https://en.wikipedia.org/wiki/Dehydration) and [electrolyte imbalance](https://en.wikipedia.org/wiki/Electrolyte_imbalance) and sometimes, death. Symptoms start two hours to five days after exposure **Mechanism of action:** When consumed, most bacteria do not survive the [acidic](https://en.wikipedia.org/wiki/Gastric_acid) conditions of the [human stomach](https://en.wikipedia.org/wiki/Stomach). The few surviving bacteria conserve their energy and stored [nutrients](https://en.wikipedia.org/wiki/Nutrient) during the passage through the stomach by shutting down [protein](https://en.wikipedia.org/wiki/Protein) production. When the surviving bacteria exit the stomach and reach the [small intestine](https://en.wikipedia.org/wiki/Small_intestine), they must propel themselves through the thick [mucus](https://en.wikipedia.org/wiki/Mucus#Digestive_system) that lines the small intestine to reach the intestinal walls where they can attach and thrive. Once the cholera bacteria reach the intestinal wall, they no longer need the [flagella](https://en.wikipedia.org/wiki/Flagellum) to move. The bacteria stop producing the protein [flagellin](https://en.wikipedia.org/wiki/Flagellin) to conserve energy and nutrients by changing the mix of proteins that they express in response to the changed chemical surroundings. On reaching the intestinal wall, *V. cholerae* start producing the [toxic proteins](https://en.wikipedia.org/wiki/Exotoxin) (CT) that give the infected person a watery diarrhea. This carries the multiplying new generations of *V. cholerae* bacteria out into the drinking water of the next host if proper sanitation measures are not in place. Once within the small intestine the CT binds to membrane receptors and is endocytosed into the cell. Several steps occur that result in the efflux of Cl- ions from the cell. Na+ follows along with H2O into the intestinal lumen to maintain electroneutrality and osmotic balance. This leads to a massive secretion of water and electrolytes into the gut, causing diarrhea and vomiting  **Conclusion** The majority of the food poisoning outbreaks are caused by both gram positive and gram negative bacteria. Exotoxins from bacteria can be enterotoxic, cytotoxic, hemolytic, or neurotoxic. Bacterial enterotoxins are responsible for a variety of gastrointestinal symptoms, including diarrhoea. Bacterial enterotoxins are responsible for production of various types of gastrointestinal manifestations like diarrhea. Some bacterial toxins are very potent and are relatively easy to produce and are classifies as bio-threat agents. Ex: Botulinum neurotoxins. Bioassay methods, immunological assays, molecular techniques and cell cultures are used to detect the bacterial toxins.