A toxin is a specific substance, often a metabolic product of an organism that damages the host. Toxins can even induce disease in the absence of the organism that produced them. Diseases that result from the entrance of a specific toxin into the body of a host are called intoxication. The term toxemia refers to the condition caused by toxins that have entered the blood of the host. Toxins produced by the organisms can be divided into two main categories: exotoxins and endotoxins.
• Integral part of the cell wall of Gram-negative bacteria. Released on bacterial death and in part during growth. Release is not required for biologic activity.
• Formed only by Gram-negative bacteria
• Lipopolysaccharides. Lipid A portion is responsible for toxicity.
• No specific receptor.
• Moderately toxic. Fatal to animals in large doses.
• Relatively heat stable. Toxicity is not destroyed above 60°C for hours.
• Weakly antigenic. Antibodies are protective.
• Not converted to toxoid.
• Synthesis directed by chromosomal genes.
• Usually produce fever in the host by release of interleukin-1 and other mediators.
• Excreted by living cells
• Produced by Gram-positive and Gram-negative bacteria
• Usually bind to specific receptors on cells
• Highly toxic. Fatal to animals in very small doses
• Relatively heat labile. Toxicity destroyed over 60°C
• Highly antigenic. Stimulate formation of antitoxin. Antitoxin neutralizes the toxin
• Converted to toxoid by formalin. Toxoid is nontoxic but antigenic. Toxoids are used to immunize, e.g. tetanus toxoid
• Usually controlled by extra-chromosomal genes, e.g. plasmids, phage gene
• Usually do not produce fever in the host.
Based on the structure and physiological activities, exotoxins are categorized into neurotoxins (nerve tissue), enterotoxins (intestinal mucosa) and cytotoxins (tissues).
Based on the mode of action they are categorized as
• Toxins that act from cell surface Toxins bind to the cell surface receptors and stimulate intracellular signaling pathways. Example, superantigens.
• Membrane damaging toxins They disrupt the integrity of plasma membrane.
Two subtypes of this type of toxins are
I. Channel forming toxins Alpha toxin of Staphylococcus aureus inserts itself into the host cell membrane via open channels called pores.
II. Toxins that enzymatically damage the membrane Alpha toxin of Clostridium perfringe, which causes gas gangrene. The toxin has phospholipase activity which enzymatically damages the membrane by removing the charged polar head groups from the phospholipids.
iii. AB toxins These are intracellular toxins. The toxic B-subunit attaches itself to the target regions on cell membranes and the A-subunit enters through the membrane and possesses the enzymatic activity that affects internal cellular bio-mechanisms. A-subunit lack binding and cell-entry capability whereas B-subunits bind to target cells but are non-toxic and biologically inactive. Toxins by cholera, pertussis, shigella, tetanus, botulinum, anthrax and heat labile enterotoxin from E.coli produce this type of toxins.
Before pathogens can grow and cause a disease, they must first gain access to the tissues. There are several sites that act as the portals of entry for pathogens into the host. Some pathogens have specific portals of entry. For example cold viruses enter the host through the mucous membrane of the eye and upper respiratory tract, whereas pathogens responsible for causing sexually transmitted diseases enter through the mucous membrane of respiratory and reproductive tract along with mucous membrane of the eye and the upper respiratory tract.
• Skin acts as a barrier to infections.
• Tetanus occurs when the bacterium Clostridium tetani enters the wound of respiratory tract.
• Air containing droplets of infectious material is breathed in.
• Mycobacterium tuberculosis causes tuberculosis. It is an intracellular bacterium that prefer to infect macrophages.
• Vibrio cholerae causes cholera when drinking water is infected with faeces.
• Salmonella enteritis causes food poisoning when eating undercooked food.
• These organisms are resistant to acidic conditions in the stomach.
• Acid protects against microorganisms by providing a hostile environment.
• Transmission by vectors (Example malaria via Plasmodium parasite when mosquito vector takes blood).
• Direct entry through the intact skin (Example Schistosomiasis where the larval stage schistosome burrows through the skin of the feet).
Viral nucleic acids re-programme the cell operations to serve the goals of a viral replication. The specific symptoms of a viral disease are due to the type of cell infected and damage caused. There are four sequential phases of entry process; attachment, penetration, biosynthesis and assembly. Their release however depends upon their type.
Attachment The protein coat of the virus envelope binds to the protein receptors present on the host cell membrane.
Penetration The virus envelope fuses with plasma membrane and the virus capsid and then the nucleic acid enters host cell. Capsid disintegrates and the nucleic acid is released.Biosynthesis The copies of viral nucleic acids are replicated. Viral nucleic acids are used to synthesize new capsid proteins by employing organelles of host cell.
Assembly The newly synthesized capsid proteins and viral nucleic acid molecules are assembled into new viruses.
Release The viruses with envelop acquire their envelopes as they are released from their host cell.
Some viruses do not immediately follow the sequence of events described. Instead, there is a viral integration that takes place. Before producing viruses, the viral nucleic acid becomes a part of the host cell‘s DNA. This integration remains within the host cell‘s DNA for the life of cell.