Lecture 33 - What Makes a Bacterium Pathogenic Flashcards
Which is NOT an immune component encountered by a bacterium upon first exposure?
a. IgM
b. Mucus
c. Neutrophil
d. Macrophage
c. neutrophil
Which bacterium is acid-fast?
a. E. coli
b. bacillus
c. mycoplasma
d. mycobacterium
d. mycobacterium
Which bacterium is perfectly happy at 4 degrees Celsius?
a. E. coli
b. Listeria
c. Leptospira
d. salmonella
b. listeria
which is the MOST common leukocyte in an abscess?
neutrophil
self-replicating genes in bacteria are called
plasmids
which is an example of a slow-growing bacterium
a. leptospira spp.
b. escherichia coli
c. listeria monocytogenes
d. mycobacterium tuberculosis
d. mycobacterium tuberculosis
parasite
an organism that lives in association with and at the expense of an animal host
primary pathogen
a microbe that WILL cause disease if exposed
opportunistic pathogen
an organism that CAN cause disease under certain circumstances
saprophyte
organism that normally inhabits inanimate environments shared with animals
commensal
organisms that do not cause harm to the host
what are the first innate immune defenses that a microbe encounters?
- mucus, sebum, tears
- low/high pH
- mucociliary escalator
- IgA, complement
- epithelial barrier
- sentinel cells (mast, macro -, and dendritic)
Pathogenicity
ability to cause disease
Virulence
degree of pathogenicity, clinical signs
Virulence factor
products produced by the pathogen that facilitates pathogenesis
host
animal affected
host-specificity
range of species that can be infected and affected by the pathogen
what were Koch’s postulates?
- present in all cases
- agent isolated and propagated outside the host
- produces original disease in host
- re-isolated from experimental infection
Virulence factors are either _____ or _____
synthesized; structural
what do virulence factors allow for?
- colonization (adhesins)
- invasion (invasins)
- evasion
- suppression
- acquisition of nutrients
pathogenicity islands
clusters of genes that code for virulence determinates
virulence plasmids
clusters of self-replicating extrachromosomal genes encoding virulence
what are the 7 steps in pathogenicity
- exposure
- adhesion
- colonization
- invasion
- evasion of host defenses
- damage to host tissue
- +/- transmission
what are the main modes of exposure
- ingestion
- inhalation
- inoculation
what are adhesins? give examples
proteins on the surface that help with attachment
fimbrial proteins or pili
what are host receptors that bacteria attach to
fibronectin
sialic acid
how do commensal bacteria keep pathogenic bacteria from attaching
they block receptor sites and secrete toxic substances that prevent pathogens from colonizing
Describe enterotoxigenic e. coli
- diarrhea in young animals/people/travelers
- bind receptors in the mucus layer via fimbrial attachment
- secrete heat labile and stable enterotoxins that disrupt cell membrane transport
- disrupt chloride channels
What are invasins responsible for
cytoskeletal arrangements
describe the “zipper” mechanism
- infection - bacteria w adhesin finds target cell
- receptor binding - adhesion binds to surface cell receptors
- membrane engulfment
- endosomal trafficking
describe the “trigger” mechanism
- infection - bacteria w T3SS finds target cell
- effector injection - T3SS punctures the target cell
- membrane ruffling
- endosomal trafficking
Describe enterohemorrhagic E. coli pathogenesis
- carried by cattle
- invasin called intimin
- attaching and effacing lesions cause bloody diarrhea
- humans are more susceptible to shiga toxin
A bacterium that do not normally cause disease in or help its host is called a
commensal
A bacterial PRODUCT that generally causes disease in the host is called a
virulence factor
Adhesions can be found on
pili
what are the 4 mechanisms of spread
- direct
- lymphatic/blood
- organ architecture (bronchial tree, bile ducts, nerves)
- within phagocytes
describe Burkholderia mallei pathogenesis
- gram-negative, aerobic, facultative intracellular rods
- primary lesion in upper airways/skin
- spread via lymphatic within macrophages
what are the 6 host defense evasion mechanisms
- firm attachment
- prevention of mechanical removal
- avoidance of phagocytosis
- impairment of phagocytic function
- degradation of antibodies/complement
- alteration of blood supply
how do bacteria prevent phagocytic degradation
- make toxins/proteins that kill phagocytes
- block opsonins
- produce capsule that “hides” microbe
- inhibit fusion of microbe-containing phagosomes w/ lysosomes
- help escape into the cytoplasm
- antioxidants block phagolysosomal killing
describe mycobacterium tuberculosis pathogenesis
- host-adapted and slow-growing
- phagocytized but prevents phagolysosomal generation
- can reactivate
describe listeria pathogenesis
- Gram-positive, facultatively intracellular rod
- foodborne pathogen
- grows at cooler temps
- can be transmitted by peripheral nerve endings to the CNS
- can translocate the intestine, use ActA to polymerize host actin and avoid immune response
what is contained in abscesses
neutrophil, extracellular bacteria
what enzyme is responsible for the production of pus-like liquid
myeloperoxidase
Describe staphylococcus pathogenesis
- gram-positive, “grape-like” clusters, facultative anaerobes
- common on skin and mucus membranes
- penicillin resistance common
- methicillin-resistant (MRSA) common to hospitals
what is a granuloma
focal aggregate of large, epitheliod macrophages
what type of bacteria causes granulomas
intracellular; mycobacterium
Describe the pathogenesis of Johne’s Disease
- mycobacterium
- a chronic, contagious disease in ruminants that affects the small intestine
- lamina propria of villi expanded due to macrophages
what is a biofilm
self-produced matrix of an extracellular polymeric substance
which mechanism of immune evasion does Mycobacterium tuberculosis use
phagosomal maturation inhibition
how does listeria spread from cell to cell while AVOIDING the immune response
polymerizing host actin
what is the most concerning characteristic of biofilms
bacteria can exchange antibiotic resistance genes
