Microbial Mechanisms of Pathogenicity

Adhesins are molecules found on the surface of bacteria that help them stick to host cells. They're like tiny hooks that grab onto the host's cells.

Adhesins can be found on various bacterial structures, such as the glycocalyx (sticky outer layer), pili (hair-like projections), fimbriae (similar to pili) and flagella (tail-like structures).

Adhesins bind to receptors on host cells. These receptors are usually sugars, and they can vary between cell types.

A capsule is a protective layer that surrounds some bacteria. Capsules are made of polysaccharides (sugars) and help bacteria evade the host's immune system.

Capsules prevent phagocytes (immune cells) from engulfing bacteria by blocking their attachment to the bacterium's surface.

Shigella sonnei can move from one cell to another by polymerizing actin, a protein that helps cells move.

Shigella sonnei can escape from the vesicles that host cells use to engulf foreign invaders.

Dysentery is an inflammation of the intestines caused by bacteria like Shigella. It is characterized by severe diarrhea and abdominal pain.

These medications block the formation of prostaglandins, which are chemicals that cause fever.

Endotoxins released from Gram-negative bacteria trigger a life-threatening drop in blood pressure, leading to shock. This is called endotoxic shock.

Macrophages release tumor necrosis factor (TNF) after engulfing Gram-negative bacteria. TNF damages capillaries, leading to fluid loss and decreased blood pressure.

This bacteria releases IL-1 and TNF, which disrupt the blood-brain barrier, allowing phagocytes and bacteria to enter the nervous system.

The LAL assay detects the presence of endotoxins in drugs, medical devices, and body fluids. It utilizes the clotting properties of amebocytes from the horseshoe crab.

A heat-resistant and acid-resistant protein produced by Streptococcus pyogenes that mediates attachment to the host and helps the bacteria resist phagocytosis.

Hair-like appendages found on the surface of some bacteria that help them attach to host cells.

An outer membrane protein used by Neisseria gonorrhoeae to attach to and gain entry into host cells.

Waxy lipids found in the cell walls of Mycobacterium tuberculosis that help the bacteria resist phagocytosis.

An enzyme that coagulates fibrinogen in blood, forming a clot that can protect bacteria from phagocytosis.

An enzyme that breaks down fibrin, a component of blood clots, allowing bacteria to spread.

An enzyme that breaks down hyaluronic acid, a substance that holds body cells together, allowing bacteria to spread.

An enzyme that breaks down collagen, a fibrous protein found in connective tissue, aiding bacterial spread.

An enzyme that breaks down the IgA antibody, a protein that helps protect the body from pathogens.

The ability of some pathogens to change their surface antigens, making it harder for the body's immune system to recognize them.

Proteins secreted by some pathogens to bind iron in the host's body, enabling them to obtain this essential nutrient for growth and reproduction.

Proteins like lactoferrin, transferrin, ferritin, and hemoglobin that carry iron in the human body. Some pathogens can bind to these proteins to acquire iron.

Poisonous substances produced by certain microbes that can harm the host.

The ability of a microbe to produce toxins.

The presence of toxins in the bloodstream.

Diseases caused by the presence of microbial toxins, not by bacterial growth.

Toxins produced inside bacteria and released into their surroundings.

Antibodies produced by the body to provide immunity against exotoxins.

Inactivated exotoxins that no longer cause disease but still stimulate the production of antitoxins in the body.

The damage caused by pathogens as they metabolize and reproduce, leading to the rupture of host cells and the release of pathogens.

Staphylococcus and Streptococcus produce toxins like Streptolysin O and Streptolysin S, which can break down cell membranes. Trypanosoma cruzi and Listeria monocytogenes also release toxins that disrupt cell membranes, specifically phagolysosomes and plasma membranes.

Superantigens are bacterial proteins that trigger an extremely strong immune response. They bind to T cells, causing them to multiply rapidly and release a massive amount of cytokines.

The excessive release of cytokines by T cells due to superantigens leads to a variety of symptoms, including fever, nausea, diarrhea, and potentially more severe complications.

Endotoxins are produced by Gram-negative bacteria. They are part of the bacterial cell wall (LPS) and are released when the bacteria die and their cell walls break down.

Lipid A is the part of the lipopolysaccharide (LPS) in Gram-negative bacteria that acts as the endotoxin. It's the toxic component responsible for triggering the immune response.

Endotoxins trigger macrophages to release large amounts of cytokines, which can be harmful in high concentrations. This can lead to symptoms like fever chills, weakness, aches, shock, and even death.

Endotoxins can activate blood clotting proteins, leading to the formation of small clots in capillaries. These clots can block blood flow, potentially causing tissue damage.

Disseminated Intravascular Coagulation (DIC) is a serious condition that occurs when widespread blood clotting takes place throughout the body, leading to organ damage. It can be triggered by endotoxins.

The ability of a microbe to cause disease by overcoming host defenses. It's like the microbe's strength in fighting the host's immune system.

The degree of pathogenicity of a microorganism - how strong it is at causing disease. A highly virulent microbe can cause severe illness with a small number of organisms.

The ways microbes enter the body, like through the respiratory system (nose/mouth), skin, or GI tract (mouth/anus).

Infectious Dose - the amount of microbes needed to cause disease in 50% of a population. A lower ID50 means a pathogen is more easily spread.

Lethal Dose - the amount of toxin needed to kill 50% of a population. A lower LD50 means the toxin is more potent.

Molecules on pathogens that bind to host cells, allowing them to attach like tiny hooks. This is the first step in infection.

Pathogens can evade phagocytosis by hiding from immune cells, forming capsules, or producing enzymes that break down immune system cells.

Damage caused by pathogens directly, like when they multiply and burst host cells.