Ch 15 Microbial Mechanisms of Pathogenicity Flashcards
What are the steps of virulence?
Gain access to the portal
Attach to the host
Be present in sufficient numbers
Evade host defenses
What are the portals of entry?
Skin Mucous membranes Respiratory - easiest most frequent GI tract Genitourinary tract Conjunctiva
What is special about biofilms?
Quorum sensing has different behavior than alone
What is coagulase?
a bacterial enzyme that brings about the coagulation of blood
What is kinase?
An enzyme that breaks down fibrinogen clots
What is collagenase?
Collagenases are enzymes that break the peptide bonds in collagen. They assist in destroying extracellular structures in the pathogenesis of bacteria such as Clostridium. They are considered a virulence factor, facilitating the spread of gas gangrene.
What is IgA protease?
An IgA protease is a highly specific enzyme that cleaves amino acid sequences of certain proteins. The natural substrate of IgA proteases is immunoglobulin A.
What is a capsule?
A extra wax layer in a cell wall.
Increases virulence by impairing phagocytosis.
What is antigenic variation?
Antigenic variation refers to the mechanism by which an infectious agent such as a protozoan, bacterium or virus alters its surface proteins in order to evade a host immune response.
How are cell walls damaged?
Using the hosts nutrition - chelate iron
Damage immediate vicinity
Produces endo/exo toxins
Induces hypersensistivity
What is a toxin?
A poisonous substance that contributes to pathogenicity.
What is toxemia?
Toxin in blood
What are cytokines?
small proteins that are important in cell signaling.
What are superantigens?
They cause non-specific activation of T-cells resulting in polyclonal T cell activation and massive cytokine release. SAgs are produced by some pathogenic viruses and bacteria most likely as a defense mechanism against the immune system.
What is the A and B in A toxin and B toxin?
Active enzyme
Binding enzyme
Differentiate exotoxins from endotoxins
Exotoxins————————–Endotoxins
Released from inside———-Released from cell wall
Gram pos————————–Gram neg
A-B toxins————————–Lipid A
Destroyed at 80 deg———–Can withstand autocliving
Not fever producing————Fever producing
Neutralized by antitoxin——-Not neutralized
Small lethal dose—————-Large lethal dose
What is septic shock?
Septic shock occurs when bacterial sepsis, in response to infection, leads to dangerously low blood pressure.
Dilation of blood vessels.
What is cytopathic effect?
Structural changes in host cells that are caused by viral invasion. The infecting virus causes lysis of the host cell
What is lysogeny?
The fusion of the nucleic acid of a bacteriophage with that of a host bacterium so that the potential exists for the newly integrated genetic material to be transmitted to daughter cells at each subsequent cell division.
What is the cytopathic effect of? Poliovirus - Enterovirus Warts - Papilomarvirus Measles - Morbillvirus HIV - Lentivirus
Cytopathic Effect Emterovirus - Cytocidal Papilomarvirus - Acidophilic inclusions Morbilvirus - Cell fusion Lentivirus - Destruction of T cells
What do the following do? Fungi Protozoa Helmiths Algae
Fungi - mold, toxic ergot
Protozoa - eat’s host’s food, giardia
Helminths - waste products, elephantiasis
Algae - red tide
List the mechanisms of pathogenicity
Portals of entry
Penetration or evasion of host defenses
Damage to host cells
Portals of exit
List portals of exit
Respiratory
GI tract
Genitourinary tract
Name the types of exotoxins
A-B toxins
Membrane-disrupting toxins
Superantigens
What is lipid A?
An endotoxin from the lipid portion of an Gram negative cell wall
What is the cytopathic effect?
Killing viruses
What is meant by the parenteral route?
Punctures or openings in the skin allow microbes to gain entry. Other than the mount and alimentary canal.
What is the meaning of a high WBC count and low WBC?
High WBC: bacterial infection
Low WBC: viral infection or pneunomia
What causes diphtheria?
Bacteria
Second step of fever?
LPS released from Gram-negative
