뒤로Microbial Mechanisms of Pathogenicity
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Pathogenicity is the ability of a microorganism to cause disease.
Virulence is the degree of pathogenicity of a microorganism.
Mucous membranes, skin, and parenteral route (direct deposition into tissues via injections, bites, wounds).
The respiratory tract via inhalation is the most commonly used portal of entry.
Pathogens use adhesins (ligands) to bind to receptors on host cells, such as glycocalyx, fimbriae, or viral spikes.
Capsules (glycocalyx around cell wall) impair phagocytosis, helping bacteria evade immune response.
M protein (resists phagocytosis), Opa protein (attachment), and mycolic acid (resists digestion by phagocytes).
Coagulases, kinases, hyaluronidase, collagenase, and IgA proteases.
Pathogens alter surface antigens to evade host antibodies, making immune response ineffective.
Invasins rearrange host actin filaments causing membrane ruffling, allowing bacteria to be engulfed and move between cells.
Biofilms resist antibiotics and phagocytosis, contributing to 65% of infections by shielding bacteria with extracellular polymeric substance.
Siderophores are proteins secreted by pathogens to bind iron more tightly than host proteins, aiding bacterial growth.
Exotoxins are proteins secreted by bacteria that destroy host cells or inhibit metabolism; they are highly specific and often lethal.
A-B exotoxins have an enzyme (A) component and a binding (B) component that facilitates entry into host cells.
These toxins lyse host cells by disrupting plasma membranes, e.g., leukocidins kill leukocytes, hemolysins kill erythrocytes.
Superantigens cause intense immune responses by releasing cytokines, leading to fever, nausea, shock, and sometimes death.
Endotoxins are lipid A portions of LPS from gram-negative bacteria, released during bacterial death or multiplication.
Fever, chills, weakness, aches, disseminated intravascular coagulation, and endotoxic shock.
LAL assay detects endotoxins by clotting blood cells from horseshoe crabs in presence of endotoxin.
Incorporation of a prophage changes bacterial characteristics, such as toxin production, increasing pathogenicity.
Viruses hide intracellularly, use host receptors for entry, alter antigens, and may methylate viral RNA to mimic host RNA.
Visible changes in host cells caused by viral infection, including cell death, inclusion bodies, syncytium formation, and chromosomal damage.
Alpha and beta interferons protect neighboring cells by inhibiting viral protein synthesis and inducing apoptosis in infected cells.
Production of toxic metabolites, allergic responses, proteases, capsules preventing phagocytosis, and mycotoxins like aflatoxin.
By digesting host cells, growing inside phagocytes, and antigenic variation.
Use host tissue for growth, produce large masses causing damage, and release waste products causing symptoms.
Neurotoxin saxitoxin produced by dinoflagellate algae accumulates in mollusks, causing poisoning when consumed by humans.
Respiratory tract (coughing, sneezing), gastrointestinal tract (feces, saliva), genitourinary tract, skin, blood, and arthropod bites.