Bacterial Pathogenicity Flashcards
Pathogenicity ?
The ability to cause diseases
Virulence?
the severity or harmfulness of a disease or poison
Infecting dose ?
the number of microorganisms required to produce infection
Phases of bacterial pathogenicity
- Adhesion and colonization
2.Invasion of host tissues and pathogen replication - Production of toxins
- Immunopathogenesis
Quorum sensing?
Quorum sensing is the regulation of gene expression in response to fluctuations
in cell-population density. Quorum sensing bacteria produce and release
chemical signal molecules called autoinducers that increase in concentration as a function of cell density.
Invasins?
The chemicals that r used by enterobacteria that make the cell membrane of the host to take up the bacteria
Hydrolytic enzymes ?
Bacterial extracellular enzymes can act on human tissues at the site of infection, playing a role in tissue injury and spread of pathogens( hyaluronidase, DNAse, collagenase, coagulase, neuraminidase)
Exotoxin?
Is a toxin secreted by bacteria and possesses an enzymatic activity that induces damage in the host cell
Endotoxin ?
Component of outer layer of bacteria
LPS in gram negative and teichoic acid in gram positive
What do endotoxins bind to?
They bind Toll-like receptors
Endotoxin and the pyrogen in response ?
The macrophage Engulfs the bacteria, bacteria release toxins which make the macrophage release IL-1 which go to the hypothalamus through blood and cause the fever
Dissemination of LPS can trigger____?
Septic shock
levels of virulence:
low, moderate, high, extremely high
a pathogen must be able to:
- enter a host
- find a unique niche
- avoid normal host def
- replicate fast
- cause an injury
What are bacterial adhesins?
Bacterial adhesins are cell-surface components or appendages of bacteria that facilitate adhesion or adherence to other cells or to surfaces
Hyaluronidase:
Produced by staphylococci, streptococci and clostridia,
depolymerizes the connective tissue by hydrolyzing hyaluronic acid
DNAse:
Produced by Staphylococcus aureus, strains, degrades DNA.
Collagenase:
Produced by clostridia, breaks down collagen
Coagulase:
Produced by S. aureus, produces a typical enzyme whose
coagulase is able to convert fibrinogen to fibrin. So producing a fibrin clot
that can protect the bacteria cells from host defenses. Also the same
microorganism is able to produce enzyme capable of dissolving fibrin
clots
Neuraminidase:
Cleaves sialic acid that is present in host mucin,
glycolipids, and glycoproteins
Streptokinase and Staphylokinase:
Produced by Streptococci and
Staphylococci, they act on plasminogen by catalyzing its transformation
into plasmin. That is like this enzyme capable of dissolving the cell
building blocks
Hemolysins, Phospholipases and Lecithinases:
Can act on cells near the
site of infection or far away. They’re also produced by Streptococci and
Staphylococci like Streptokinase and Staphylokinase (hemolysins and
phospholipases) also clostridia (lecithinases). Cytolitic exotosins are called
if act far away from the site of infection
sigA Protease:
Cleaves human sigA1 antibodies(important defense mechanism for hosts) in the hinge region to release the Fc portion from the
Fab fragment
The endotoxin is released by?
the lysis of the bacterial cell
monomeric toxins(superantigens) are able to bind to antigen-presenting cells, act as polyclonal stimulators of T cells causing __________?
massive cytokine release ( IL-1, IL-2,
TNF-α and Interferon γ ) with systematic effects such as shock
Examples of
superantigen exotoxins are
enterotoxin and toxic shock syndrome toxins of
Staphylococcus aureus, streptococcal pyrogenic exotoxins (SPE) of
Streptococcus pyogenes. Symptoms are similar to endotoxin ones(severe
shock)
The exotoxin is usually made by 2 subunits:
A (active) domain and B (binding) domain
active one is responsible for the pathogenicity and binding is responsible for the binding to the receptor
Cholera toxins act on _______?
intestinal epithelial cells
Cholera toxin A-1 subunit, after dissociation from B subunit, bind to and ADP ribosylates the GS-alpha subunit of adenylate cyclase in the cell membrane,
leading to an___________________
increase in intracellular concentration of cyclic AMP. The increased intracellular cyclic AMP concentrations in
villus cells mainly inhibit the uptake of NaCI and water. So the result is
dehydration
examples of Exotoxins Altering Intracellular Cyclic AMP Concentration
Health-labile toxin of Escherichia coli (LT)
Pertussis toxin: Has two toxins that act in increasing intracellular concentration of
cyclic AMP with two diverse mechanisms.
While toxins with intrinsic adenylate-cyclase activity independently synthesize
cyclic AMP: cyclosis from Bordetella pertussis EF from Bacillus anthracis.
Clostridium tetani and Clostridium botulinum neurotoxins exert their effect
at ______________
neural sites, they cause diseases like tetanus and botulism. These are
diseases whose clinical manifestations are due to only exotoxins
What causes the infection in tetanus?
The spore of tetani
Both
____________ toxin and ________ toxin act by blocking the release of neurotransmitters
at the synaptic site. These neurotoxins cause paralysis.
botilinum and tetanus
Bacterial ability to face host defenses:
a. Antiphagocytic factors: Polysaccharide capsules and surface proteins
(interference with complement C3b deposition, oxinizing factor present in
body fluids)
b. Survival in professional phagocytes
c. Escape by specific humoral immunity
what is Opsonophagocytosis?
is the engulfment, by macrophages and other phagocytic
cells like neutrophils, of bacteria opsonized (opsonines are macromolecules that
cover the microorganism, increasing radically the efficiency of phagocytosis since
they are recognized from receptors present on the membrane of phagocytes),
with antibodies and/or complement proteins. Thus, microbial cells in the blood or
within a specific tissue that become coated with IgG are soon recognized by
patrolling macrophages and neutrophil
Capsule polysaccharides and surface proteins interfere with complement C3b
deposition by binding serum factor H so that ______________
accelerates the degradation of C3b, contrasting the opsogenic ability, so
bacteria are protected from phagocytosis.
which bacteria when englobed by the phagocytes enzymatically lyse the phagosome membrane and multiply in the nutrient-rich host cell cytoplasm?
Listeria, Shigella
which bacteria remain in the phagosome and replicate even in professional
phagocytes. Known mechanisms for avoidance of the killing action of
phagolysosome include: prevention of phagosome, lysosome fusion, block
of acidification to the optimum pH for digestive enzyme activity, production
of enzymes (catalase, superoxide dismutase) that neutralize the
phagocytes’ oxidative burst?
Salmonella serotype Typhi, Mycobacterium
tuberculosis
examples of Escape by specific humoral immunity:
Molecular mimicry: the epitopes on the bacteria are similar to the ones of the host cells
bacterial antigenic variation: constantly changing antigens
______________ are distinct genetic elements on the chromosomes
of a large number of bacterial pathogens. PAIs encode various virulence factors
and are normally absent from non-pathogenic strains of the same or closely
related species
Pathogenicity islands (PAIs)
what do Pathogenicity islands (PAIs) do?
encode virulence factors and other accessory proteins, but no essential proteins.
Pathogenicity islands are transferred ________________ through plasmids or
transposons
horizontally
Most of the parasites are not __________ but __________
pathogens, commensals
__________ is the main protozoan disease. It was
the second infectious disease after
tuberculosis, before COVID pandemic.
Malaria
In sporozoan, asexual multiplication occurs by a process of multiple fission
termed ___________
schizogony. The nucleus of a trophozoite divides into several parts,
forming a multinucleated schizont. The cytoplasm then condenses around each
nuclear portion to form new daughter cells, or merozoites, which burst from their
intracellular location to invade new host cells
