BID Chapter 11

Endospores

Dormant bacteria that is coated with thick layer of peptidoglycan; Highly Resistant (temp, desiccation, UV, pH, phages)

Desiccation Tolerance

Lack of water; Contains amino acids (glycine beta, Trehalose, L-glutamate) that uptake water, EPS holds onto environmental water, Osmo protectant to combat DNA stress and degradation

Biofilm

Extremely resistant to phagocytosis, antibiotics, and mechanical displacement

4 stages of biofilm development

1.      Adhesion: finding a home

2.      Aggregation: secreting extracellular matrix/glycocalyx

3.      Maturation: forming the film

4.      Dispersal : continuous release of new microbes

Pathogen Mucus invasion strategy

degrade mucous layer (hydrolases); GI tract has less mucus (M cell Crypts);

SigA

Used to degrade the GI tracts M cell Crypts. allowing for epithelial colonization

Defensins

Natural antibiotics; binds to negatively charged surface of bacteria and disrupts membranes

Alpha Defensins

Produced my neutrophils

Beta Defensins

Makes capsules to protect membranes from defenses, OR alter surface change, Microbial protease; Produced by epithelial cells in skin, airways, and GI

Lactoferrin

Iron Limitation for Mucosal sites

Transferrin

Iron Limitation for Serum, induced by IL-6, produced in the liver

Ferritin

Iron Limitation for intracellular iron storage

Heme

Contains 70% of the body’s iron (Iron Limitation)

Siderocalin

iron scavenging molecule that microbes produce to compete with host cells

Gram-positive strategy against Iron Limitation

released hemoglobin on red blood cell mediated lysis through toxins; bacteria can bind to released hemoglobin through proteins or directly

Gram-negative strategy against Iron Limitation

Has 2 walls, Transferrin through two different transporters

Pili/ Fimbriae

Finds glycolipid/protein to stick to, creates specificity to what the bacteria can bind to; Primary means of adherence; Longer thicker surface structures of the bacteria

P Pili

Type IV Pili

Curli Pili

Chaperone-Usher (P) pili Structure

PapA/FimA, has tip protein that is excreted first, PapG

Curli Pili Structure

CsgA; Doesn’t need chaperone, the physiologic change with auto assemble

Type IV Pili Structure

PilE; Type 2 Secretion System Dependent

Sortase

makes a surface for the Gram-Positive bacteria for cell wall adhesion

Gram-Negative Adhesion

tethers the pili with periplasm

Nonfimbrial adhesions

In g+; Binds to extracellular matrix/ connective issue; hair-like protrusions similar to pili

Afimbrial Adhesins

promotes cell invasion (InlA + InlB)

MSCRAMMs

Staphylococcus aureus form of adhesin; does not have pili, but instead finds components and proteins of the hosts matrix to bind to

Host mimicry

Sialic Acid can make capsule out of sialic or hyaluronic acid to look like it is apart of the host tissue

Escaping from the phagosome

Produce toxins (LLO) that disrupt, degage, or make holes in host membrane

Cell-to-Cell spread

Listeria directs their own endocytosis can manipulate the actin cytoskeleton

Actin-base motility

able to push themselves around and to neighboring cells

Legionella

Removes proteins necessary for membrane fusion with lysosome (LAMP-1 and LAMP-2); Stops acidification in lysosomes, multiplies, ruptures phagosome, lyses host cells and escapes

Mycobacterium

Recruits host proteins to surface of phagosome, does not fuse with lysosomes, bacteria prevents acidification and has reduced oxidative burst; decorates phagosome with TACOs prevents fusion

Salmonella

Actin rearrangements and grows into pseudopods for salmonella, makes self-made vacuoles within the epithelial cells

Brucella

Only replicates upon acidification of vacuoles directing it to the ER (I’m on an acid trip; get me to the ER)

SOD + Kat Prx

takes something damaging to bacterial membranas and converts it to water

Resist Ros and No

reactive oxygen species are the primary watt he oxidative bursts kills bacteria