What part of the Cell wall on gram POSITIVE organisms will induce TNF and IL-1?
What part of the cell outer membrane gram NEGATIVE orgnisms induces TNF and IL-1?
Gram + cell wall makes Lipoteichoic acid--> induces IL-1 and TNF and is major surface antigen
Gram - outter membrane makes Lipid A--> inducses IL-1 and TNF and is major surface antigen
1. Location of B-lactamase enZ in bacteria
2. Provides rigid support and protects against osmotic gradient (has peptide side chains with x-link via transpeptidase)
3. Protects organims against phagocytosis
4. mediates adhereance to surfaces, especially foriegn surfaces
What is unique about Mycoplasm bacteria?
What about Mycobacteria?
Mycoplasma has sterols but no cell wall
mycobacteria have mycolic acid and high lipid content
What bugs don't Gram Stain well?
These Microbes May Lack Real Color.
Treponema (too thin to be visualized).
Mycobacteria (high lipid content; mycolic acids in cell wall detected by carbolfuchsin in acid- fast stain).
Mycoplasma (no cell wall).
Legionella pneumophila (primarilyintracellular).
Rickettsia (intracellular parasite).
Chlamydia (intracellular parasite; lacks classic peptidoglycan because of low muramic acid).
What bugs stain with Giemsa stain?
Certain Bugs Really Try my Patience.
Chlamydia, Borrelia, Rickettsia, Trypanosomes, Plasmodium.
What Stains with Ziehl-Neelson stain?
Ziehl =Acid-fast bacteria (Nocardia, Mycobacteria), protozoa (Cryptosporidium oocysts).
Indian ink = Cryptococcus Neoformans
Silver Stain= Legionella, H.pylori and Fungi (Pneumocystisis)
Cryptococcus neoformans will stain......
with India Ink
What organisms stains PAS+?
What disease pathology does it cause?
Stains glycogen, mucopolysaccharides; used to diagnose Whipple disease (Tropheryma whipplei)
Chocolate Agar with factors V (NAD+) and X (hematin)
H.influenza = gram - rod
What special culture can you use to detect N. Meningitis or N. Gonorrhea
Thayer-Martin (VPN) media: Vancomycin (inhibits gram-positive organisms), Trimethoprim, Colistin (inhibits gram- negative organisms except Neisseria), and Nystatin (inhibits fungi)
Very Typically Cultures Neisseria
What bug do we culture on a Potatoe agar = Bordet-Gengou agar
Bordet = Bordetlla
What cultures on Tellurite agar or Loffler medium?
What cultures on Lowenstein Jensen agar?
What cultures on Eaton Agar but requires cholesterol?
Tellurite and Loffler = Cornye Diptheria
Lowentein-Jensen agar = M.Tuberculosis
What is special about Nocardia, Pseudomonas aeruginosa and Mycobacterium TB?
All Obligate Aerobes and use an O2 dependent system to generate ATP
Nagging Pests Must Breath
(reactivated TB likes to go to Apices of lung d/t high O2 content)
P.aeruginoas is aerobe seenin burn wounds, comoplication of diabetes
What bacteria are Obligate Anaerobes?
Why are thye anaerobes?
What antibiotics are useless against them?
Anaerobes Frankly Can’t Breathe Air:
Fusobacterium, Clostridium, Bacteroides, and Actinomyces.
They lack catalase and/or superoxide dismutase and are thus susceptible to oxidative damage.
AmiO2lgycosides are worthless on these guys bc they need oxygen to enter bacterial cell
What bugs are Obligate intracellular organims?
Stay inside (cells) when it is Really CHilly and COld.
Rickettsia, CHlamydia, COxiella. Rely on host ATP.
What bugs are facultative intracellular bugs?
Some Nasty Bugs May Live FacultativeLY.
Salmonella, Neisseria, Brucella, Mycobacterium, Listeria, Francisella, Legionella, Yersinia pestis.
What are my Encapsulated Bacteria?
What doe the capsule do for them?
What pts are at risk for infections with these?
Streptococcus pneumoniae, Haemophilus influenzae type B, Neisseria meningitidis, Escherichia coli, Salmonella, Klebsiella pneumoniae, and group B Strep.
Their capsules serve as an antiphagocytic virulence factor. Capsule + protein conjugate serves as an antigen in vaccines.
Asplenics have decreased opsonizing ability and thus increased risk for severe infections. Give S. pneumoniae, H. influenzae, N. meningitidis vaccines
What are my Catalase + organisms?
What does it mean to be catalase +?
What Disease is susceptible to Catalase + organisms?
Cats Need PLACESS to hide.
Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E. coli, Staphylococci, Serratia.
Catalase degrades H2O2 into H2O and bubbles of O2 before it can be converted to microbicidal products by the enzyme myeloperoxidase. People with chronic granulomatous disease (NADPH oxidase deficiency) have recurrent infections with certain catalase ⊕ organisms.
What organsims are Urease +?
CHuck Norris hates PUNKSS.
Cryptococcus, H. pylori, Proteus, Ureaplasma, Nocardia, Klebsiella, S. epidermidis,
1. This bacteria produces yellow sulfur granules
2. This bacteria produces yellow pigments
3. This bacteria shows up as blue-green
4. This bacteria gives off a red pigment
Actinomyces israelii= yellow sulfur
Staph. Aureus = yellow pigment
Pseudomonas Aeruginosa = blue-green pigment
Serratia Marcescens = red pigment
What is the mechanism in which Protein A promotes evasion of host immune system?
Binds Fc region of IgG. Prevents opsonization and phagocytosis.
Expressed by S. aureus
What is the Mechanism of host evastion of IgA protease?
What bugs secreat this?
Enzyme that cleaves IgA in order to colonize respiratory mucosa.
Secreted by S. pneumoniae, H. influenzae type B, and Neisseria (SHiN)
What is the mechanism of host evasion by M protein
What bugs use this?
Helps prevent phagocytosis.
Expressed by group A streptococci. Shares similar epitopes to human cellular proteins (molecular mimicry); possibly underlies the autoimmune response seen in acute rheumatic fever.
What is the mechanims of Type III secreation system utilized by bacteria to evade host immune system?
Also known as “injectisome.” Needle-like protein appendage facilitating direct delivery of toxins from certain gram-negative bacteria (e.g., Pseudomonas, Salmonella, Shigella, E. coli) to eukaryotic host cell.
What is the Mechanism of action of the Diphtheria toxin?
Is it an endo or exotoxin?
What is it simular to?
EXOtoxin that inactivates elogation factor : EF-2
(see pharyngitis with grey pseudomemrane in back of throat + bulls neck from lymphadenopathy
Simular to Exotoxin A produced by Pseudomonas Aeruginosa
What is the mechanism of action of the Shiga toxin?
What disease symptoms does it cause?
What other organims produces a Shiga-like toxin?
Inactivate 60S ribosome by removing adenine from rRNA
Shigella: GI mucosal damage--> dysentery; ST also enhances cytokine release, causing hemolytic- uremic syndrome (HUS)
EHEC; 0157 releases Shiga-Like Toxin: see SLT enhances cytokine release, causing HUS but doesn't invade the host cells like Shigella
What is the MOA of the Heat Labile (LT) and Heat Stable (ST) released by
Heat Labile (LT) Overactivates adenylate cyclase (Increase cAMP)--> Increased Cl− secretion in gut and H2O efflux
Heat Stable (ST) Overactivates guanylate cyclase (Increases cGMP)--> DEcreased resorption of NaCl and H2O in gut
Watery diarrhea: “labile in the Air (Adenylate cyclase), stable on the Ground (Guanylate cyclase)”
Mechanism of Bacillius Antracis EDEMA factor EXOtoxin
Mimics the adenylate cyclase enzyme (Increase cAMP)
Likely responsible for characteristic edematous borders of black eschar in cutaneous anthrax
MOA of the Cholera Toxin (Exotoxin)
Overactivates adenylate cyclase (Increase cAMP) by permanently activating Gs-->
Cl− secretion in gut and H2O efflux with rice water diarrhea
MOA of Pertussis toxin (exotoxin)
Overactivates adenylate cyclase (Increasing cAMP) by disabling Gi, impairing phagocytosis to permit survival of microbe
How are the Tetanus and Botulinum toxin the same?
How are they different?
Both are proteases that cleave SNARE (soluble NSF attachment protein receptor), a set of proteins required for neurotransmitter release via vesicular fusion
Tetanus: Spasticity, risus sardonicus, and “lockjaw”; toxin prevents release of inhibitory (GABA and glycine) neurotransmitters from Renshaw cells in spinal cord
Botulinum: Flaccid paralysis, floppy baby; toxin prevents release of stimulatory (ACh) signals at neuromuscular junctionsflaccid paralysis
What is the Mechanism of Action of the toxin produced by Clostriduim Perfringens that results in necrosis?
How will this show up on agar?
Alpha toxin of Clostrium Perfringens
Phospholipase (lecithinase) that degrades tissue and cell membranes
Degradation of phospholipids -->myonecrosis (“gas gangrene”) and hemolysis (“double zone” of hemolysis on blood agar)
Mechanism of action of Steptolysin O and which bug carries it?
How does this manifest?
Strep O is a protein that degrades cell membranes (like RBCs)
Lyses RBCs; contributes to β-hemolysis; host antibodies against toxin (ASO) used to diagnose rheumatic fever (do not confuse with immune complexes of poststreptococcal glomerulonephritis)
What is the Mechanism of Action of Toxic Shock Syndrome Toxin relased by S. Aureus?
What other ogranism releases an exotoxin that has same mechanism?
Binds to MHC II and TCR outside of antigen binding site to cause overwhelming release of IL-1, IL-2, IFN-γ, and TNF-alpha ---> SHOCK
toxic shock syndrome: fever, rash, shock; other toxins cause scalded skin syndrome (exfoliative toxin) and food poisoning (enterotoxin)
*Strep Pyogenes releases Exotoxin A
What is the MOA of Exotoxin A?
What bug releases it?
It's a superantigen that binds to MHC II and TCR outside of antigen binding site to cause overwhelming release of IL-1, IL-2, IFN-γ, and TNF-α--> Shock
Released by Streptooccus Pyogenes
What is the result of an Endotoxin in the body?
What releases endotoxins?
LPS = endotoxin found on OUTer membrane of Gram - bacteria
Results spell out ENDOTOXIN
Edema Nitric oxide DIC/Death Outer membrane
TNF-α O-antigen eXtremely heat stable IL-1 Neutrophil chemotaxis
Describe the concept of Transformation
Ability to take up naked DNA (i.e., from cell lysis) from environment (also known as “competence”). A feature of many bacteria, especially S. pneumoniae, H. influenzae type B, and Neisseria (SHiN). Any DNA can be used. Adding deoxyribonuclease to environment will degrade naked DNA in mediumno transformation seen.
Explain the concept of Bacteria Conjugation: specifically F+ x F-
F+ plasmid contains genes required for sex pilus and conjugation. Bacteria without this plasmid are termed F–. Sex pilus on F+ bacterium contacts F− bacterium. A single strand of plasmid DNA is transferred across the conjugal bridge (also known as the “mating bridge”). No transfer of chromosomal DNA.
Explain the concept of Conjugation in bacteria in the: Hfr x F-
F+ plasmid can become incorporated into bacterial chromosomal DNA, termed high-frequency recombination (Hfr) cell. Replication of incorporated plasmid DNA may include some flanking chromosomal DNA. Transfer of plasmid and chromosomal genes.
What is Transposition?
Segment of DNA (e.g., transposon) that can “jump” (excision and reintegration) from one location to another, can transfer genes from plasmid to chromosome and vice versa. When excision occurs, may include some flanking chromosomal DNA, which can be incorporated into a plasmid and transferred to another bacterium (e.g., vanA gene from vancomycin-resistant Enterococcus to S. aureus).
A “packaging” event. Lytic phage infects bacterium, leading to cleavage of bacterial DNA. Parts of bacterial chromosomal DNA may become packaged in viral capsid. Phage infects another bacterium, transferring these genes.
What is Specialized Transuction?
What Genes are endoced in a specific lysogenic phage?
An “excision” event. Lysogenic phage infects bacterium; viral DNA incorporates into bacterial chromosome. When phage DNA is excised, flanking bacterial genes may be excised with it. DNA is packaged into phage viral capsid and can infect another bacterium.
Genes for the following 5 bacterial toxins are encoded in a lysogenic phage (ABCDE): ShigA-like toxin, Botulinum toxin (certain strains), Cholera toxin, Diphtheria toxin
Erythrogenic toxin of Streptococcus pyogenes
Prion diseases are caused by the conversion of a normal (predominantly α-helical) protein termed prion protein (PrPc) to a ______ which is transmissible via CNS-related tissue (iatrogenic CJD) or food contaminated by BSE-infected animal products (variant CJD).
Why is this so bad?
β-pleated form (PrPsc),
PrPsc resists protease degradation and facilitates the conversion of still more PrPc to PrPsc. Resistant to standard sterilizing procedures, including standard autoclaving.
Accumulation of PrPsc results in spongiform encephalopathy A and dementia, ataxia, and death.
—rapidly progressive dementia, typically sporadic (some familial forms). Bovine spongiform encephalopathy (BSE)—also known as “mad cow disease.”
—acquired prion disease noted in tribal populations practicing human cannibalism.
Increased opening pressure
Increased PMN (neutrophils)
Increased protein content
MEningitis d/t bacteria
Increased opening pressure
Fungal or TB meningits
Normal to elevated ICP
Increased to normal Protein
No Change to Glucose
Causes of Osteomyelitis if:
1. Sexually active
2. Diabetics or IV drug user
3. Sickle cell pt
1. Sexually active = N. Gonorrhea
2. Diabetics or IV drug user = Pseudomonase Aeurginoma or Serratia
3. Sickle cell pt= Salmonella
Cause of osteomyelits if
1. Joint replacement
2. Vertebral invovlement
3. Cat or dog bites
1. Joint replacement = S. Aureus or S. epidermidis
2. Vertebral invovlement= Mycobacterium TB
3. Cat or dog bites = Pasteruella multicoda
1. Comma- or S-shaped organisms; growth at 42°C
2. Protozoan; amebic dysentery; liver abscess
3. can cause HUS; makes Shiga-like toxin
4. Invades colonic mucosa
1. Comma- or S-shaped organisms; growth at 42°C: Campylobacter
2. Protozoan; amebic dysentery; liver abscess: E.histolytica
3. can cause HUS; makes Shiga-like toxin: EHEC or O157:H7
4. Invades colonic mucosa: Enteroinvasive E.Coli
1. Lactose ⊝; flagellar motility; has animal reservoir, especially poultry and eggs
2. Lactose ⊝; very low ID50; produces Shiga toxin (human reservoir only); bacillary dysentery
3. Day care outbreaks, pseudoappendicitis
1. Lactose ⊝; flagellar motility; has animal reservoir, especially poultry and eggs = Salmonella
2. Lactose ⊝; very low ID50; produces Shiga toxin (human reservoir only); bacillary dysentery = Shigella
3. Day care outbreaks, pseudoappendicitis = Y.enterocolitica