Tetanus toxin, botulinum toxin, lethal factor of anthrax toxin, and scalded skin toxin.
They determine the infectious dose and the ability to evade host defenses.
Streptococcus pneumoniae.
They protect bacteria from host immune defenses like antibodies and neutrophils, and impede wound healing, leading to chronic wound infections.
LD50 is the number of organisms needed to kill half of the hosts, while ID50 is the number needed to cause infection in half of the exposed hosts.
The organism's ability to produce various virulence factors.
Transplacental transmission of Treponema pallidum.
1. Incubation period, 2. Prodrome period, 3. Specific-disease period, 4. Recovery (or convalescence) period.
Many exotoxins have an A-B subunit structure, where the A subunit has toxic activity and the B subunit binds to specific receptors on human cells.
Listeria monocytogenes.
ADP-ribosylation.
It catalyzes the addition of ADP-ribose to elongation factor-2 (EF-2), inactivating it.
It is particularly important in virulence.
T. pallidum (causative agent of syphilis) and prions (infectious proteins).
They degrade collagen and hyaluronic acid, allowing bacteria to spread through subcutaneous tissue.
Protease that cleaves desmosomes in skin.
If it causes disease.
Cows.
Through a tick bite (Ixodes).
Legionella pneumophila.
By inactivating elongation factor-2 (EF-2), it inhibits protein synthesis.
Human-to-human, as well as from nonhuman sources like soil, water, and animals.
It is the time between the acquisition of the organism (or toxin) and the manifestation of symptoms, which can vary from hours to weeks.
Transmission from an external source into the portal of entry.
Enterotoxin acts as a superantigen.
Direct contact through intimate contact or passage through the birth canal.
Specialized structures called secretion systems.
Pathogens like Salmonella typhi can be isolated from patients who are not manifesting symptoms.
It must be isolated free from all other organisms and grown in pure culture in vitro.
It blocks the release of the inhibitory neurotransmitter glycine by proteolytic cleavage of releasing proteins.
Endotoxins are not actively released from the cell, whereas exotoxins are.
Virus (V).
Protozoa (P).
Ingestion of drinking water.
Fecal-oral transmission, where bacteria excreted in human feces are ingested in food or water.
Humans.
Exotoxins are produced by both gram-positive and gram-negative bacteria, while endotoxins are only present in gram-negative bacteria.
1) Activating macrophages to produce IL-1, TNF, and nitric oxide; 2) Activating the alternative pathway of complement; 3) Activating tissue factor.
Soil.
Bacterium (B).
Genital herpes.
Certain species of gram-positive and gram-negative bacteria.
Yersinia pestis.
Interrupting the chain of transmission.
Streptococcus agalactiae (group B Strep).
Watery diarrhea; its labile toxin stimulates adenylate cyclase by ADP-ribosylation, and stable toxin stimulates guanylate cyclase.
Quorum sensing, which allows bacteria to coordinate the synthesis of proteins based on their population density.
Adherence (colonization) to mucous membranes, usually by bacterial pili.
Clostridium tetani (Bacterium).
The number of organisms exposed to a person and the virulence of these organisms.
Fever and inflammation.
Different strains produce different exotoxins, leading to varying symptoms like watery or bloody diarrhea.
Invasion of tissue, toxin production, and immunopathogenesis.
Salmonella typhi.
It ADP-ribosylates the G i factor, inactivating it and thereby stimulating adenylate cyclase.
Fungus (F).
Gonorrhea.
Exotoxins have high toxicity (fatal dose on the order of 1 μg), whereas endotoxins have low toxicity (fatal dose on the order of hundreds of micrograms).
Pili.
Lyme disease.
Domestic animals.
Endotoxin.
E. coli O157: H7 strain.
Inhibits glycine release.
Endotoxins are an integral part of the cell wall of gram-negative bacteria.
Urethritis.
Virus (V).
Polysaccharide capsule.
A matrix formed by bacteria consisting of various polysaccharides, proteins, and nucleic acids.
Corynebacterium diphtheriae inactivates EF-2 by ADP-ribosylation.
It ADP-ribosylates the Gs factor, activating it and stimulating adenylate cyclase.
Bacterium (B).
Rickettsia rickettsii (Bacterium).
Clostridioides difficile.
By binding to the Fc region of IgG, preventing activation of complement.
The organism must be isolated from every patient with the disease.
By providing protection from phagocytosis or enabling survival against nonspecific host defenses like stomach acid.
Ingestion of contaminated meat.
It inhibits protein synthesis in enterocytes by removing adenine from 28S ribosomal RNA.
Fungus (F).
