Microbiology Unit 1 – Flashcards

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Mutualism
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Benefits the host.

microbes in human gut (enterobacteria)

aid in digestion

train immune system

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Commensalism
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Microbe benefits, no help or harm to host usually

e.g. staphylococcus epidermis (lives on skin and eats sluffed off cells)

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Parasitism
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Microbe benefits, host is harmed

Types:

Primary pathogens

Opportunistic pathogens

Commensal pathogens

Chronic pathogens

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Primary pathogens

 

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Cause disease in otherwise healthy host

e.g influenza

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Opportunistic pathogens

 

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only cause disease when the health of thehost is compromised.

e.g. pathogenic fungi- pseudomona aeruginosa (cystic fibrosis, burns susceptible)

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Commensal Pathogens
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lie dormant for a while, eventually cause disease

e.g. mycobacterium tuberculosis

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Hall marks of bacteria
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single celled

binary fission for replication (replicate DNA, split)

Cell wall (peptidoglycan)

No nucleus

single circular chromosome

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Hallmarks of viruses
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obligate intracellular pathogen/parasite(need another cell to live)

enclosed by a membrane/protein coat

variety of nucleic acids for genome:

dsDNA, dsRNA, ssRNA, ssDNA

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Obligate intracellular pathogen/parasite
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needs another cell to live
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Hallmarks of Fungi
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eukaryote

cell wall (chitin)

heterotroph (all rely on braking down organic matter)

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Parasite
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eukaryotes:

protozoa

helminth (worms)

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Koch's Postulates
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1. microorganism should be found in organisms suffering from disease, but not in healthy organisms

2. Microorganisms must be isolated from infected organism and grown in pure culture.

3. implant into healthy organism

4. should be able to reculture organism from the infected individual.

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disease that Koch tested
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Woolsorter's disease (bacillus anthrasis)

 

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Life Cycle of bacillus anthrasis 
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1. Spores in environment 

2. spores enter host

3. spores germinate, spread

4. bacteria fight immune system, cause disease

5. host dies spores re-enter environment 

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steps for all pathogens
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1. reservoir

2. attachment entry

3. replication and spread

4. fight immune system

5. exit

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Innate immune system
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 all components that fight a pathogen the same way every time (no memory)

1st line of defense

 

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addaptive immune system
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all components capable of learning.

host takes advantage of unique aspects of pathogens to destroy them.  

e.g. viral pathogens (RNA replication process)

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1st physical barrier
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skin: epidermis is outermost (continually renewing)

outermost cornified dead layer is barrier to most organisms

can enter through cuts in skin, digestive system, lungs, use of additional organisms, hair follicles

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2nd physical barrier
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Mucous membranes:

continuous secretion of mucous (keeps pathogens away from cells, eg goblet secreting cells in villi of pancreas)

cillia: wave particles out of lungs and up esophagus.

stomach: low pH, degrading enzymes

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Chemical barriers
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1. anti-microbial peptides

2. anti-microbial proteins (larger, 3ary struct)

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anti microbial peptides
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AKA defensins

short +charged, amphopathic

forms pores in cell walls of bacteria, lyses

selective for bacteria

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anti-microbial proteins
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larger, tertiary structure

e.g. lysozyme (degrades peptidoglycan), albumin

RNAase (contra viral genomes)

lactoferrin: soaks up iron from bacteria (need iron to grow)

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types of antimicrobial proteins (aka serum)
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1. heat stable (antibodies), due to disulfide linkage

2. heat labile (compliment)

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serine protease cascade
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one protein is cleaven into two, one of which cleaves another, etc.

used in clotting

results in inherant amplification

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Alternative pathway
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study it!
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classical pathway
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study it!

 

uses antibodies

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opsonization 
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covering a bacteria in protein
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lectin pathway
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mannose/fructose pattern on bacterial surface is bound by manosbinding lectin (MBL)

triggers compliment cascade

MBLs recognize pathogens based on surface protein

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monocyte
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originate in bone marrow, resides in blood

gives rise to macrophage or dendritic cell

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macrophage
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tissue resident

long-lived

part of liver but originate in bone marrow

"Street sweepers" eat everything not supposed to be there 

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neutrophil
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short-lived, live in blood

respond to infection

contain granulocyte (dense vesicle of protein, anamirobial peptides, lysozyme)

 

Also called Polymorphonuclear cells (PMN)

lobed nucleus allows neutrophil to squeeze into tight places

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actin monomer
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microfilament
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rate limiting step of actin polumerization
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nucleation (initiation of polymerization)

actin dimer is hardest to form, after that its down hill

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how does actin polymerization gain directionality
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actin:atp is active form, actin:adp is inactive form

Arp2/3 is a nucleating protein, binds 3 actin polymers (overcomes rate limiting step)

Postive feedback: Arp2/3 binds to side of actin chain and initiates new chain, "webbing effect"

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CR1
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compliment receptor, involved in phagocytosis
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How does actin polymerization cause phagocytosis?
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phagocyte can bind to surface antibodies or compliment.

ARP2/3 activated near binding site, membrane curves around bacteria, additional receptors bind.

rapid polymerization, envagination

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PIP3 kinase
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phosphorylates PIP2 into PIP3, first stem in phagocytic binding of chemoattractants
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PIP3
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leads to the activation of Rho in actin activation during phagocytosis
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Rho
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small GTPase regulating actin assembly
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GAP
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GTPase activating proteins, inactivate GTP
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GEF 
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Guanine nucleotide exchange factor

Rho-lipid modification

activates Rho:GTP

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Rho:GTP
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activated Rho, recruits N-Wasp (promotes binding of ARP2/3, polymerization away from the binding site)
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FC receptor
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phage receptor for antibodies bound to bacteria
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respiratory burst
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metabolic process, exposes the phagolysozome to "reactive oxidative species"  
NADPH oxidase complex removes elctron from NADPH, creates O2-. (superoxide) which is converted to H2O2 (highly destructive) 
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abcess
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location where neutrophils and bacteria fighting it out
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two cytosolic components released by dead neutrophils
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1. protein: calprotectin

2. DNA chromatin forms extracellular trap

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purpose of calprotectin release by dead neutrophils
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4 ca2+ bound to, when released, Ca2+ is gone, calprotectin acts as metal sponge, absorbs Zn and MN (many bacteria and fungi need these to survive)
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purpose of DNA chromatin release by dead neutrophils
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creat neutrophil extracellular trap (NET) which traps bacteria
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4 types of granulocytes
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Neutrophil (esp. contra bact)

eosinophil (contra parasites)

basophils (allergy)

Mast cells (in tissue, release histamine)

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function of histamine
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causes inflammation:

capillaries swell, allow neutrophils to spueeze through tissues, diffusion of necessary chemicals

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systeic inflammation
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shock: entire circulatory system swells.  blood volume lost to internal organs.  
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anaphlactic shock
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high increasein histamine.

treat with epinephrine (contraction of vasculature) eg epipen.

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APCs
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professional antigen-presenting cells

work with adaptive immune system

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two types of APC's;
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macrophage

dendritic cell

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PAI
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Pathogen associated immunostimulant

any molecule made by pathogen that is not made by the host and which the host uses to detect infection

e.g small molecules, repeating patterns (PAMPs)

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three effects of PAI
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inflammation

recruitment of phagocyte

phagocytosis

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N-formylated peptides
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PAI;

unique tRNA for initial methionine start codon in bacterial transcription

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lipopolysaccharides (LPS)

;

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important PAI in gram negative bacteria:

the outer leaflet of the outer membrane of gram negative bacteria is composed of LPS

variation in LPS structure among bacteria, but all share common core.

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Toll-like receptors
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receptors in macrophage for PAIs
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TLR-4
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receptor for LPS, activates many down stream effects, notably NFkB
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LTA
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PAI

anchored in membrane, giant polymer protrudes through cell wall

fx: adherence, negatively charged

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TLR-2
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binds LTA
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Bacterial DNA
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serves as PAI

bacteria has ;CpG motife. ;In euk, cytosine methulated in fifth position, bacteria is normal.

;

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TLR-9
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recognizes CpG in bacteria
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RNA in pathogen as PAI
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used to recognize viruses

normal Euk RNA: mRNA, tRNA, rRNA

primarily single stranded

Double stranded in viruses (reovirus)

immune system recognizes dsRNA

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TLR-3
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recognizes double stranded RNA in viruses
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flagellum as PAI
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protein flagellin ("motor" structure)

;

TLR5 recognizes flagellin

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TLR-5
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recognizes flagellin (protein in bacterial flagellum)
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cytokine
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molecule released from one cell population that have an effect on themselves and/or other cell pop.s

;

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interleukins
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cytokine important for growth and differentiation of the immune system.

;

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chemoattractant
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recruits PMN cells (neutrophils)
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TNF alpha
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cytokine, made by macrophage, endothelial cells

results in inflammation, stimulates phagocytosis

by itself is responsible for gram negative sepsis

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IL 8
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cytokine, produced by macrophage, epithelial, endothelial cells

PMN chemotaxis (signal to neutrophils)

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Interferon gamma (IFN gamma)

;

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primarily made by T-cells (adaptive immune system)

signal to activate macrophage (wants signal for T cell swallows bacteria but doesn't kill cell outright until it gets IFN gamma from T cells)

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P-selectin
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protein with lectin domain, binds carbohydrate on PMN, forming weak connection.

selectin anchored to actin filament in cytosol.

during blood flow, neutrophil rolls along endothelial surface.

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cytotoxic T cell
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kills intracellular pathogen
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helper T cell
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helps B and T cells fight extracellular pathogens
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bacillus
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rod shaped bacteria
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coccus
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round ball shaped bacteria
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Staphylococcus aureus (kingdom, phylum, class, genus, species)
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bacteria, fermicute, bacillus, staphylococcus, aureus
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staph aur gram + or-?
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gram positive
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metabolism of staph aur?
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facultative anaerobe
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purpra fulminans
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"purple lightning" 

cutaneous hemorrhages and necrosis in kids and youth

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S. aureus (gram stain, shape)
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gram positive cocci
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group A streptococcus (gram stain and shape)
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gram positive cocci
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group B streptococcus

(gram stain and shape)

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gram positive cocci
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coagulase negative staph (gram and shape)
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gram + cocci
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enterococci (gram and shape)
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gram + cocci
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Neisseria (gram and shape)
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gram neg cocci
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listeria (gram and shape)
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gram + bacilli
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Clostridium (gram and shape)
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gram+ bacilli
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corynebacterium (gram and shape)
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gram + bacilli
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mycobacterium (gram and shape)
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gram + bacilli
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Nocardia (gram and shape)
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gram + bacilli
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e. coli (gram and shape)
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gram - bacilli
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Klebsiella (gram and shape)
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gram - bacilli
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pseudomonas (gram and shape)
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gram - bacillus
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proteus (gram and shape)
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gram - bacilli
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salmonella (gram and shape)
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gram- bacilli
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yersinia (gram and shape)
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gram- bacilli
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Brucella (gram and shape)
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gram - bacilli
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enterobacter (gram and shape)
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gram - bacilli
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Haemophilus (gram and shape)
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gram - bacilli
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bordatella (gram and shape)
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gram - bacillus
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moraxella (gram and shape)
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gram - bacilli
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Francisella (gram and shape)
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gram - bacilli
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campylobacter (gram and shape)
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gram - bacilli
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three classes of spirochetes
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tremonema

leptospira

borrelia

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treponema pallidum
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syphilis

spirochete

can't gram stain

can't culture

STD

chronic infection (takes decades to progress to tertiary)

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dx of treponema pallidum
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general serology

specific serology (antibodies for Lipoprotiens)

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mycobacterium TB
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chronic infection

obligate aerobic

non gram staining

acid fast (stains mycolic acid)

facultative intracellular pathogen

high lipid content, waxy and hard to penetrate

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drug that can be used for acid fast bacteria
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isonizid: blocks mycolic acid synthesis
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types of bacteria that form spores
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clostridium and bacillus
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chlamydia
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obligate intracellular

persistant chronic infections

non gram staining

can be stained with silver

human reservoir common

STD and ocular infection

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elemental body vs. reticular body
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EB: extracellular (infectious)

RB intracellular (replicating)

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mycoplasma
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no cell wall (no gram stain, no cell wall antibiotics)

shape changs

smallest bacteria

growth is fastidious and requires media with sterols

slow growth

 

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rickettsia
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obligate intracellular

polymerize actin

geographically diverse

no culture

zoonotic

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how does ehrlichia block cellular digestion by phagosome?
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blocks fusion of endosome and lysosome
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how does coxiella survive phagocytosis?
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thrives in low pH of lysosome
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what causes rash in rickettsia?
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damage to epithelial tissue, blood vessels dilate and RBCs escape
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