Exam 4 Flashcards
(402 cards)
1
Q
Gram + or - and Type - Staph Aureus
A
Gram + Cocci in clusters
2
Q
Characteristics of Staph Aureus
A
Beta-hemolytic, Catalase +, coagulase +, Faculative anaerobe
3
Q
Catalase + means?
A
organisms that can degrad hydrogen peroxide into H20 and O2 before it becomes harmful
4
Q
Catalase + organisms
A
Staph, E Coli, Pseudomonas Aeruginosa,
5
Q
O2 dependency for Staph Aureus
A
Faculative Anaerobe
6
Q
Virulence Factors of Staph Aureus
A
Protein A, Coagulase, hydorlinases
7
Q
What does Protein A do?
A
binds to Fc-IgG to inhibit complment activation and phagocytosis - characteristic of Staph Aureus
8
Q
What does Coagulase do?
A
promotes fibrin formation around the organism - Staph aureus
9
Q
Inflammatory Disease due to direct invasion of Staph Aureus
A
Cutaneous infection with abscesses, Pneumonia, septic arthritis, osteomyelitis, rapid onset bacterial endocarditis
10
Q
Exotoxin mediated manifestations of Staph Aureus
A
Scalded Skin Syndrome, Toxic Shock Syndrome, Staph Food poisoning
11
Q
Toxic Shock Syndrome
A
TSST-1 binds to MHC Class II to cause T-cell activation. Characteristic of Fever, diarrhea, rash, hypotension, desquamation of palms and soles, multiple organ failure
12
Q
Staph Aureus Food poisoning
A
due to enterotoxin - rapid onset for preformed toxin that is associated with V and non-bloody diarrhea
13
Q
Staph Epidermis - Gram Stain
A
Gram + cocci in clusters
14
Q
Staph Epidermis - characteristic in lab
A
Catalase +, Coagulate -, urease +, faculatative anaerobe
15
Q
Virulence Factor of Staph Epidermis
A
Protective polysacchatide intracellular adhesion that adheres to prosthetic devices.
16
Q
Clinical Manifestations of Staph Epidermis
A
Infections associated with foreign bodes - artificial joints, catheters, endocarditis of heart valves. Biofilms
17
Q
Staph Saprophyticus - gram
A
Gram + cocci in clusters
18
Q
Staph Saprophyticus - lab characteristics
A
Catalase +, coagulate -, urease +, faculative anaerboe, Gamma hemolytic
19
Q
Clinical manifestations of staph- saprophytic
A
UTIs in sexually active females (#2)
20
Q
how to distinguish Staph infections in the lab
A
1) Staph Aureus is beta hemolytic, coagulate +
2) Staph Epidermis is Coagulate -
3) Staph Saprophyticus is coagulate - and Gamma hemolytic
21
Q
Streptococcus pyrogens - gram
A
Gram + cocci in chains
22
Q
Strep Pyrogens - lab characteristics
A
Beta hemolytic, Streptolycin O, Streptolysin S, Catalase negative, microaerophilic, encapsulated, inhibited by bacitracin
23
Q
Encapsulated - Strep pyrogens
A
by hyaluronic acid (from CT in the body)
24
Q
Virulence factors in Strep pyrogens
A
M Protein, Streptolysin O, Capsule, Streptokinase, DNAse
25
M protein
Virulence factor for Strep Pyrogens
anti-oponization, anti-phagocytic, antigenic and illicuts a strong humoral response by host!
26
Pyrogenic Effects of Strep Pyrogens
Pharyngitis, Impetigo, Cellulitis, Erysipela
27
Toxogenic conditions with Strep Pyrogens
Scarlet Fever, Toxic-shock like syndrome, Necrotizing fassciitis
28
Scarlet Fever
associated with Strep Pyrogens - strawberry tongue, pharyngitis, diffuse rash that spares the face
29
Post-Strep Associations
Glomerulonephritis and Rheumatic Fever
30
Glomerulonephritis
Type III immune response to strep Pyrogens, results in dark brown urine, facial edema - 2 weeks after strep infection. Can be post pharyngitis OR impetigo
31
Rhematic Fever
Type II immune response to strep pyrogens, M Factor illicuts autoAb via molecular mimicry to myocin in heart valves (mitral). Due to pharyngitis, but not skin manifestations of strep
32
Signs of Rheumatic Fever
JONES
JONES
J: polyarthritis of joints
O -
33
does early treatment of Strep Pyrogens with penicillin prevent Rheumatic fever, Glomerulnephriis, or both?
Only Rheumatic Fever
34
Strep Pneumonia - Gram
Gram + diplococci
35
Strep Pneumonia - lab characteritics
Optochin and Bile senstive
Alpha hemolytic
Catalase -
Faculative anaerobe
36
Virulence Factor of Strep Pneumonia
- Polysaccharide capsule that prevent complement and phagocytosis
IgA protease - prevents colonization and invasion of mucosa
37
Clinical Manifestations of Strep Pneumonia
MOPS: meningitis, otitis media, pneumonia of lower lobe, sinusitis or sepsis
38
Vaccines for Strep Pneumonia
Pneumovax for adults and Prevnar for kids
39
Pneumovax vs. Prevnar
both for Strep Pneumonia. Pneumovax is 23 valent IgM; Prevnar is 7 talent conguate to make IgG. Adult version is against active disease, Kid version is to reduce carriage and disease.
40
Viridan Streptococci - gram
Gram + cocci in chains
41
Viridans Strep. Laboratory Characteristics
Optochin and bile resistant, alpha hemolytic, catalase negative, facultative anaerboe
42
Virulence factor of viridans strep.
Synthesis of dextran from glucose to adhere to fibrin.
43
Clinical Manifestation sof Viridans Streptococci
Dental caries —> access blood strem and effect previously damaged valvues to cause endocarditis in mitral values. Or can also cause liver and brain abcesses
44
Dextran
produced in Viridans Strep to creaste a sticky surface that can adhere to teeth, oral tissue, fibrin/platelet aggregate deposits on heart valves.
45
Enterococcus Faecalis/Enterococcus Faecium - gram
Strep Type D - gram + cocci in chains
46
Enterococcus Faecalis/Enterococcus Faecium - lab characteristics
Bile resistant, alpha, beta, and gamma hemolyti, grows well on NaCl (6.5%), catalase - and facultative anaerobe.
47
Virulence Factor fo enterococcus
extracellular dextran helps bind to heart valves
48
Clinical Manifestations of Enterococcus
UTI, surgical wound, biliary tract infections, subacute endocarditis following Gu/GI procedures
49
Resistance in Enterococcus
resistant to penicillin and Vanc
50
what lab findings help distinguish between strep types?
1) Strep Pyrogens - sensitive to bacitracin and encapsulated
2) Strep Pneumo - senstive to optochin and bile
3)Viridan - resistant to optochin and bile
4) Enterococcus - grow on sodium choloride.
51
Clostridium Difficile - gram
Gram + spore forming rods
52
C. Diff - laboratory characteristics
Obligate anaerobe. Must be measured by ELISA or PCR of TOXIN in stool (not bacteria)
53
C. Diff Virulence Factors
Exotoxin A and B
54
C. Diff Exotoxin A
binds to the brush border of the SI to cause inflammation, cell death, and water diarrhea
55
C. Diff Exotoxin B
Disrupts cytoskeleton integrity of depolymerizing actin, leading to enterocyte death and necrosis —> gray psuedomembrane colitis.
56
Treatment of C. Diff
oral vancomycin *NOT IV or metronidozole
57
Clostridium Tetani - gram
Gram + spore forming rods
58
Costridium Tentani - metabolsim
obligate anaerobe
59
Virulence Factors for C. Tetani
Tetanospasmin
60
Tetanospasmin
endotoxin for C. Tetani that when punctured into wound, travels retrograde to CNS to cleave SNARE to block the release of GABA and glycine from Renshaw cells of spinal cord
61
Renshaw Cells
inhibitory interneurons that normally release gaba and glycine in spinal cord - inhibited by tetanospasmin toxin in C. Tetani
62
Clinical manifestations of C. Tetani
Spastic paralysis - rigidity, respiratory paralysis with Risus sardonicus, Trismus, opsothotonus
63
Risus sardonicus
raised eyebrow and open grin
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Trismus
Lock jaw
65
Opsothotonus
exaggerated back arching
66
Prevention of Tetanus
Toxoid vaccine to generate ab to toxin not organism.
67
Treatment of tetanus
anti-toxin with or without vaccine booster and diazepam.
68
C. Botulinum - gram
Gram + spore forming rods
69
C. Botulinum - metabolism
obligate anaerobe
70
Where is C. Boltulinum found?
soil, smoked fish,, canned food, honey
71
Mechanism of C. Botulinum
Preformed heat labile toxin is absorbed into gut and travels to Peripheral Nervous system (only) to inhibits SNARE release of ACh at NMJ
72
C. Botulinum clinical manifestations - adults
Flaccid descending paralysis through ingestion of preformed toxin —> absent muscle contraction, diplosis, ptosis.
73
C. Botulinum clinical manifestations - children
Floppy baby due to lack of robust gut flora following ingestion of spores in Honey. (NOT preformed toxin).
74
Clostridium Perfringes - gram
Gram + spore forming rods
75
C. Perfringes - metabolism
obligate anaerobes
76
C. Perfringes - virulence
Lechincinase or Alpha toxin
77
Lechincinase
alpha toxin of C. Perfringes that damages cell membranes of lipoproteins and cause RBC hemolysis.
78
Where is C. Perfringes found?
mostly in soil - motocycle accidents and military combat
79
Clinical manifestations ofC. Perfringes
Gas Gangrene (Closridial myonecrosis) and Clostridial food poisoning
80
Gas Gangrene
C. Perfringes - gas is produced under skin to cause crepitace and crackling due to alpha toxin —> leads to crushing type injury, cellulitis, compromised blood flow and hypoxia
81
Clostridial Food Poisoning
enterotoxin as bacterial sporulate in gut (not preformed), slow onset of development of toxin that disrupts tight junctions in ilium —> dysreguation of fluid transport.
82
E. Coli - gram
Gram - rods
83
E. Coli - Lab characteristics
Catalase +, beta hemoytic, Oxidase -, lactose fermentor, faculative anaerobe
84
Virulence Factors for E. coli
K capsule, Fimbriae, LT, ST and shiga-Like Toxins
85
K capsule
a virulence factor in E. coli that causes pneumonia and neonatal meningitis
86
Fimbriae in E. coli
Pilli necessary to colonize in UTI (#1)
87
LT
Heat Labile Enterotoxin of E coli - increases cAMP
88
ST
Heat Stabile Enterotoxin of E. coli - increases cGMP
89
Shiga-Like Toxin
inhibits 60S ribosome
90
ETEC
Enterotoxigenic E coli - non-invasive LT and ST toxins from water lead to watery diarrhea
91
EHEC
Enterohemorrhagic E Coli - Shiga like toxin causes hemorrhagic collitis and hemolytic c uremic syndrome. Due to uncooked meats. Leads to bloody diarrhea - but not fever.
92
Hemolytic Uremic Syndrome
Anemia, Thrombocytopenia, acute renal failure due to damage to endothelial cells in glomerulus where platelets adhere and clump to lyse RBCs.
93
What strain of E. coli ferments sorbitol?
all except EHEC
94
EIEC
Enteroinvasive E coli: bloody diarrhea with fever and pus to to shiga like toxin
95
Main clinical manifestations of E. Coli infections
Diarrhea , LPS acquired sepsis, septic shock, neonatal meningitis, UTI (#1), abdominal infections, hosptial acquired pneumonia
96
Pseudomonas Aeruginosa - gram
Gram - rods
97
Pseudomonas - Lab characteristics
Oxidase +, catalse +, non-lactose fermenter, oglibate aerobe, encapsulated
98
Pseudomonas Aeruginosa - virulence
Exotoxin A
99
PA exotoxin a
blocks EF-2 by fibosylation to inhibit protein synthesis.
100
Clinical manifestations of Pseudomonas Aeruginosa
Nosocomial pneumonia (#1, also in CF), Osteomyelitis, BURNS, UTI, purpuric pustula folliculitid, ecthyma grangrenosum, PSEUDDO - pneumonia, sepsis, otitis externa, UTI, drug use, diabetes, osteomyelitis
101
Osteomyelitis in Psuedomonas A. infection
mostly with IV drug users, diabetics, children
102
Neisseria Gonorrhoeae - gram
Gram - diplococci
103
Neisseria Gonorrhea - lab characteristics
Ferments glucose, but not maltose. Facultative anaerobe and intracellular (invades PMNs),
104
N. Gonorrhea - virulence Factors
LPS, Pilus - adherence, IgA protease for mucosal membrane adherence
105
N. Gonorrhea - clinical manifestations
Urititis, prostatis, orchtis, cervical conorrhea, pelvic inflammaotry disease, Polyarthritis of knee (asymettric)
106
Charactericis dischange of gonorrhea compared to chlamydia
G: white, purulent
C: watery
107
Congenital Infection of Gonorrhea vs. Chlamydia
G: neonatal conjutivitis (early onset)
C: 1-2 weeks post birth (conjunctivitis)
108
Fitz Hue Curtis
when gonorrhea infection spreads to peritoneum and adheres to the liver.
109
Bacteroides Fragilis - gram
Gram - rods
110
Virulence Factor of Bacteroides Fagilis
Tissue destructive enzymes, anti-phagocytic capsule, superoxide dismutase, LPS
111
Bacteroides fragilis - clinical manifestations
Peritonal infections
112
Chlamydia Trachomatis - gram
Gram -, but difficultt o stain due to lacking peptidoglycan layer
113
Chlamydia - lab characteristics
Oblicate intracellular (cannot make own ATP), facultative anaerobe
114
Chlamydia - virulence factors
resistant to lysozyes, non motile, non pilli, no exotoxins released
115
Chlamydia cell cycle
Elementary bodies are small dense infectious bodies that enter the cell.
Reticular body - dividing elementary bodies via binary fission (only in cells with ATP), where it i extruded back out in elementary form. This exhibits tropism.
116
Chlamydia A-C
Causes Trachoma - blindness by corneal scarring. (C with your eyes).
117
Chlamydia D-K
STI, often associated with N. Gonorrhea. Can be asymptomatic of urethritis, cervitis, PID. Active infection can lead to secondary neonatal conjunctitis and pneumonia - staccato funds
118
L1-3 Chlamydia
leads to lymphogranuloma venerium - infection of inguinal nodes with genital ulcers
119
Reiter’s Syndrome
Uvitis, urethritis, reactive arthritis of SI and Knee joints - due to chlamydia
120
Mycoplasma Pneumoniae - Gram
No gram staining due to lack of cell wall
121
Mycoplasma - Lab Characteristics
Membrane with cholesterol/sterols for stabilization, rod-shaped with tip point,
122
Detection of Mycoplasma
1) cold aggultinin 2) PCR
123
Virulence Factor of Mycoplasma
1) H202 to damage respiratory tract, 2) pilli
124
Clincial Manifestations of Mycoplasma
walking pneumonia - generally insidious with nonproductive cough.
125
what types of antibiotics are bactericidal?
Cell wall/membrane, DNA function and synthesis
126
What types (more specific) of antibiotics are bactericidal?
Penicillins, vancomycin, Cephalosporin, Fluoroquinolones, Nitrofuratoin, metronidazole, and Amingoglycosides***
127
what types of antibiotics are bacteriostatic?
Inhibitors of protein synthesis and metabolic pathways
128
What types (specific) of antibiotics are bacteriostatic?
Macrolides, tetracyclines, clindamycin, sulfonamides (NOT amincoglycosides)
129
Cell wall Inhibitor Antibiotics
Penicillins, Vancomycin, Cephalosporins
130
Protein Synthesis inhibitors - antibiotics
Macrolides - Azithromycin, Clarithromycin, Erythromycin; Tetracycline - Doxycycline, tetracycline; Clindamycin; Aminoglycosides - tobramycin, gentamicin;
131
DNA Function inhibitors - antibiotics
Fluroquinolones - ciproflaxin, levofloxican, Moxifloxican; nitrofuranoin, metronidazole (flagyl), sulfonamides - sulfamethoxazole-trimethoprim(TMP-SMX)
132
Mechanism of Action - Penicillin
Stage 3 (cross linking) of cell wall synthesis inhibition - binds to PBP to inhibit transpeptidase enzymes of peptidoglycan and activates autolytic enzymes
133
Bacterio-cidal vs static - Penicillin
Bacteriocidal
134
Vancomycin Mechanism of Action
Inhibits Stage 2 of cell wall synthesis
135
Bacterio-cidal vs static Vancomycin
Bacteriocidal
136
Cephalosporin - Mechanism of Action
Inhibits stage 3 of cell wall synthesis
137
Bacterio-cidal vs static - Cephalosporin
Bacteriocidal
138
Pharmacokinetics - Penicillin
Most are acid liable - preventing good oral absorption except with altered R group, Poor tissue penetration except for inflamed tissues; Renel and breast milk excretion.
139
Adverse Reactions - Penicillin
Hypersensitivity - IgE mediated with possibility of anaphylaxis; most common is a maculopapular rash that is generally mild. (rare: encephalopathy, seizures)
140
Pencillin G vs V
G: poor oral absoprtion - limited to IV use in hosptial
V: Acid resistant prototype with better oral absorbance, however less efficacy.
Both are narrow spectrum only and penicillinase sensitive
141
Penicillinase Resistant Penicillins
Dicloxacillin (oral), naficillin (IM/IV)
NOT suseptible to Penicillinase (Beta-lactamase)
142
Extended Spectrum Pencillins
Extended spectrum due to hydrophilicity - albe to penetrate porins of Gram (-) organisms.
susceptible to penicillinase
Ampicillin, Amoxicillin, Piperacillin
143
Ampicillin vs. Amoxicillin
Both are extended Spectrum penicillins
both are acid resistant, with Amoxicillin has better oral bioavailability.
Both can be given when Beta-Lactamase Inhibitors (Clavulanic Acid)
Risk of rash, diarrhea, superinfection
144
Piperacillin
Extended Spectrum Penicillin
anti-psuedomonal given IV only - effective against B Fragilis and Pseudomonas
145
Beta-Lactamase Inhibitors
Clavulanic Acid and Tazobactam
Resembles Beta-Lactam with not antibiotic activity- irreversible inhibitor of Beta-lactamase
used in combination with ampicillinase sensitive penicillins
146
Augmentin
Clavulanic Acid + Amoxicillin (oral)
147
Timentin
Clavulanic Acid + amoxicillin (IV)
148
Unasyn
Sulbacam + ampicillin (parenteral)
149
Zosyn
Toxabactam + piperacillin (parenteral)
150
Vancomycin - Pharmokinetics
Poor oral absorption - IV usually (except for GI use), Renal Excretion
151
Adverse Reactions - Vancomycin
Infusion related - Red Man: Chills, fever, rash, ototoxicity, renal toxicity
152
Cephalosporin - Pharmacokinetics
All orally avaliabiliy, good tissue penetration (PLACENTA), except brain and CSF. Ceftriaxone (3rd gen) penetrates into CSF.
Renal Excretion
153
what Cephalosporin penetrates into CSF?
Ceftriaxone (3rd)
154
Adverse Rxns - Cephalosporins
Hypersensitivity - not severe like penicillin; but avoid for people with immediate sensitivity to penicillin
Superinfection Risks
nephrotoxicity
155
Macrolides - Mechanism of Action
inhibits elongation of protein synthesis by blocking 50S and translocation of tRNA.
156
Bacterio-cidal vs static Macrolides
Bacteristatic
157
Tetracyclines - mechanism of action
Inhibits initiation of protein sytenshsi, by binding to 30S on A site to prevent ammoniacal tRA into mRNA.
158
Bacterio-cidal vs static tetracycline
Bacteriostatic
159
Clindamycin - mechanism of action
prevents elongation of peptide chain by binding to 50S and preventing translocation
160
Clindamycin - Bacterio-cidal vs static
Bacteriostatic
161
Aminoglycosides - mechanism
Binds irreversibly to 30S and blocks initiation, distorts codong reading frame, blocks translocation (breaks up polysome). blocks initiation! Requires O2 to be transported into bacteria
162
Bacterio-cidal vs static Aminoglycosides
Bactericidal!!
163
Types of Aminoglycosides
Tobramycin and Gentamicin
164
Types of tetracyclines
deoxycline, tetracycline
165
phamacokinetics of macrolides
Most are absorbed in GI and widely distributed except in train and CSF. Does cross placent and reaches fetus. ALL are excreted in breast milk, but usually okay. Depending on type of macrolide - liver and renal metabolism and excretion.
166
Excretion of macrolide
Bile excretion and liver metabolism: Azithromycin and Erythromycin; Renal in clarithromycin.
167
Absorption of macrolides
All in stomach. Azithromycin must be in empty stomach, Clarithromycin without regard to meals - food may improve absorption; Erythromycin - varies depending on salt form.
168
Free base erythromycin
destroyed by stomach acid - must have enteric coating
169
Stearate, esoolate, ethyl succinate erythromycin
acid resistant and well absorbed.
170
Estolate erythromycin
more bioavaliable in kids.
171
Special distibution of macrolides
Az/and clarithromycin concentrate in skin, lung, tonsils, cervix, sputum (pulmonary) and in macrophages.
172
Which macrolide are excreted in bile/metabolized in liver?
Azithromycin and erythromycin
173
Which macrolide is renaly excreted?
clarithromycin
174
adverse reactions of macrolides
GI distrubances - N, V, D (Erythromycin)
Hepatotoxicity
Prolonged QT interval leading to ventricular arrhythmia.
Drug interactions
175
Drug interactions in macrolides
Erythromycin and Clarithromyin both inhibit P450 to increase plasma toxicity (not azithromycin) - warfarin, cyclosporin, benzodiazepines
176
Pharmacokinetics of Tetracyclines
Oral absorption of variable bioavailability. Absorption is impaired by milk, aluminum, calcium, magnesium, iron, salts. Variable degree of tissue penetration - does go into placenta/fetal. Selective accumulation in gingival fluid, subum, bone and teeth; elimination: Doxycline: non-renal, in liver and excreted in bile. Long half life or 16-18 hours. Tetracycline: really eliminated - short acting
177
Elimination of doxycycline vs. tetracycline
deoxycycline is concentrated in liver and excreted in bile, long acting 16-18 hours; Tetracycline is renal excretion short acting of 6-8 hours.
178
Adverse Reactions to Tetracyclines
Selective accumulation in teeth and bone - depression of growth and discoloration - avoid during pregnancy and children
179
Drug interactions with tetracyclines
Antacids/Fe: decrease bioavalibility
Phenytoin/barbituates/barbamezepine: increase metabolism
Oral anticoagulants: increased anticoagulation effect
180
What is the best treatment of community acquired pneumonia?
Doxycycline
181
Clinamycin - pharmacokinetics
90% bioavailable orally, penetrates into most tissue, especially bone!, not into CSF, metabolized in liver and excreted in bile and breast milk.
182
Adverse Reactions to Clindamycin
Psuedomembranous Colitis, N, D, skin rashes, liver dysfunction, neutropenia, C. DIFF infections
183
Aminoglycosides pharmacokinetics
No oral admin, only IV or IM, Limited distribution to extracellular fluid and accumulates in renal cortex and inner ear. Excluded from CNS and eye. Excretion: kidney with 2-3 hour half life; but once daily dosing due to post-antibiotic effect. AVOID in late pregnancy.
184
Adverse Reactions to Aminoglycosides
Very toxic! irreversible 8th cranial nerve damage - auditory, vestibular; renal toxicity; contact dermatits, rashes, BM depression, nuero-muscular block to cause respiratory arrest; Drug-Drug interactions
185
drug interaction with Aminoglycosides
Synergy: beta lactams and aminoglycosides to cause increased entry
Inhibitory: irreverible binding to penicillin can be inactivating
186
Fluorquinolones types
Ciproflaxin, levfloxican, Moxiflocian
187
Fluroquinolones - mechanism
Inhibition of bacterial DNA gyros and topoisomerase IV to inhibit DNA function.
188
Fluoroquinolones - Bacterio-cidal vs static
bacteriacidal!
189
Nitrofurantoin - mechanism
prodrug that is reduced by bacterial enzymes to intermediates that cause DNA Damage.
190
Bacterio-cidal vs static - nitrofuranotin
Bacteriacidal
191
Metronidazole - mechanism
Prodrug that is transformed into nitro radical anion in protozoa and anaerobic bacteria. Anion kills by inducing DNA ds breaks and inhibiting replication
192
Metronidazole - Bacterio-cidal vs static
bacteriocidal
193
Sulfonamides
folic acid is required for synthesis of thymidine and purines. These are analogs of PAPA that inhibit dihydropteroate synthase. Selectively toxic because humans can get folic acid from diet.
194
sulfonamides Bacterio-cidal vs static
bacteriostatic
195
pharmacokinetics - fluroquinolones
Good oral avaliabiliby, but also can be parenteral; good tissue penetration and high urinary levels. Large Vd; renal excretion
196
Fluroquinolones - adverse reactions
GI: N, V, D, C.Diff; CNS: dizzy, headache, insomnia. Black box warning - increased risk of tendon rupture and arthropathies. Avoid in pregnancy or kids under 18; QT prolongation. Drug interactions
197
Drug interactions of fluroquinolones
Theophylline and caffeine - increase toxicity; antacids: reduce oral absoprtion; Cipro is a P450 inhibitor
198
Pharmacokinetics - nitrofurantoin
rapid and complete GI absorption, concentrated in renal tubules - not systemic. Excreted in urine.
199
Adverse rxns in Nitrofurantoin
GI tract: N, V, D; hypersensitivity - HA, hepatocellular damage, neuropaties.
200
Metronidazole - pharmacokinetics
Oral, good distribution into CSF and bone; metabolized in liver; do not breast feed while on drug.
201
Metronidazole - adverse rxns
N, headache, dry mouth, metallic taste, exacerbates candida infections, Antabuse-Like effect with alcohol, Durg interactions
202
Antabuse like effect
due to metronidzaole with alcohol - causes GI upset and headache
203
Drug interactions of metronicazole
inhibits CYP450
204
Phamacokinetics of sulfonamides
Weak acid, absorbed in stomach, but best on empty stomach. Wide distribution into pleural, ocular, synovial fluid, CSF, crosses placental and fetus, but predisposes neonates to kernicterus. Metabolism: N-acetylation to inactive form and excreted in breast milk and urine.
205
Adverse rxns Sulfonamides
Sensitization - up to stevens johnsons; renal damage, HA, GI, Drug intreaction
206
Drug interaction of sulfonamides
displaces bilirubin form albumin to increase risk of kernicterus in brain - brain damage in neonates and infants.
207
what are bacteriacidal antibiotics favored?
Severe, quick infections in immunocompromised patients.
208
Penicillin vs. cephalosporin
ceph: broader spectrum with gram (-), less suseptible to penicillinase and cross-reactivity.
209
Hepatic Elimination drugs
DQ CRIME: Doxycycline, Quinolones (cipro is renal CYP450 inhibit), Clindamycin, Rifampin (induces CYP450 toxicity), Isoniazid, Metronidazole (with alcohol- antabuse rxn), erythrmoycin like (clar and frith) inhibit P450
210
Beneficial Selective accumulation of antibiotics
Clindamycin in bone - to treat osteomyelitis
Macrolides: pulmonary to treat URI and pneumonia
tatracycline in gingiva and sebum to treat periodontal and acne.
211
Toxic selective accumulation of antibiotics
Aminoglycosides - in inner ear and renal brush border
tetracyclines in bone and teeth to halt growth and cause discoloration.
212
LPS
lipopolysaccharides - gram negative endotoxin, a PAMP that recognized by innate immune system. at low doses activates macrophages, B-cells, and alternative complement —> fever, acute phase rxns, inflammation; with high doses leads to shock and DIC.
213
Types of toxins that facilitate spread of microbes through tissue by breaking down ECM, degrading debris…
Hyaluonidase, collagenase, elastase, deoxyribounclease, streptokinase.
214
Hemolysin
toxin that damages cellular membrane to kill target cells.
215
Cytolysins
toxin that inserts into cell membrane to assemble multimeric protein that forms pore to cause cell lysis.
216
Lecithinase
toxin that degrades membrane components
217
Pyrogenic endotoxins
stimulate the production of cytokines; Scarlatinal and TSST-1 are examples that are super antigens that are T-cell activators that bind to MHC II to activate cytokine cascade (IL2 and IFNgamma).
218
what toxins inhibit protein synthesis
Diptheria, Pseudomonas Aeruginosa endotoxin, Shiga Toxin,
219
Pseudomonas Aeruginosa Exotoxin A Inactivated elongation factor
ADP ribosyltrasnferase that transfers ADP ribose from NDA to diphthamide on EF-2 to inactive it into the cytoplasm of liver cells.
220
Diptheria toxin
an ADP riboxyltransferase toxin that inhibits protein synthesis in the heart, kidney and nuerons
221
Shiga Toxin
of Shigella and E coli, toxin that inhibits protein synthesis by RNA N-glycosides that remove adenosine from 28S RNA to make 60S ribosome inactive.
222
How do toxins inhibit protein synthesis?
1) ADP ribosyltrasnferase to make inactive Translation machinery 2) make ribosomes inactive
223
how do toxins modify intracellular signaling pathways?
Increase cAMP, cGMP, cleave MAPKK protiens, alter actin
224
Heat Labile enterotoxins
in V. Cholerae and E coli - AND ribosyltranferase to increase cAMP to cause increase chloride secretion (and water) (changes intracellular signaling)
225
heat Stable enterotoxin
in E coli, activate gaunylate cyclase to increase cGAMP and change intracellular signaling
226
Pertussis toxin
anADP Ribosyltransferase to increase cAMP
227
Anthrax Edema Factor
adenylate cyclase to increase cAMP
228
Anthrax lethal factor
endopeptides that cleaves MAPKK to inactive signaling
229
Clostridium Difficile Toxin B
glucosyl transferase that alters actin cytoskeleton by transferring glucose from UDP glue to Rho GTPase to inactivate - change intracellular patwhay
230
Botulinum toxin
toxin that inhibits release of NT by acting like a n endopeptidase that inactive SNARE proteins to inhibit ACh release
231
Tetanus Toxin
toxin that inhibits release of NT by acting like a n endopeptidase that inactive SNARE proteins to inhibit Glycine and Gaba release
232
how do toxins enter the cells?
those that cross PM must have two domains - Active and binding. They use receptors on normal membranes to confer specific in location. and they enter cells through endocytosis where toxin is translated in cytosol
233
Prophylaxis/treatment of toxin mediated diseases
1) Antitoxin, 2) toxoid 3) passive immunization 4) active immunization
234
Antitoxin
antibodies bind to toxin to neutralize. Does not prevent infection or reverse the effects
235
Toxoids
derivative of toxin that retain immunogenicity but lack toxicity.
236
Passive immunization
admin antibody to patient to provide immediate, but temporary protection from infectious agent.
237
Active immunization
admin toxoid to elicit anti-toxic antibodies - 1) primary series and period boosters are required to achieve and maintain protection 2) active immunity persists due to immunologic memory.
238
Immunotoxin
hybrid molecules, toxin fragments that lack rector binding domain and are linked to a ligand with a receptor binding domain that binds to a receptor on a different from the native toxin receptor;. These can be used to kill tumor cells or in autoimmune treatment
239
Intrinsic vs. Acquired Resistance
intrinsic is natural properties of bacteria that make them resistant to antibiotics; acquired are genetic mutations, acquisition of new gene spread by mobile genetic elements.
240
Mechanisms of resistance
inactivate/modify drug; alter drug target; reduce ability to get to target
241
Porins
are on the outer membrane of gram - bacteria that are hydrophilic channels that are used for selective uptake of nutrients and hydrophilic antibiotics.
242
Efflux Pumps
pumps that pump from the cytoplasm to the extracellular space on both Gram + and -; used to pump antibiotics out of the cells
243
Peptidoglycan linkage
GlNAc-MurNAc
244
Peptidoglycan
precursors assemble in cyto and are transported to cell surface, where PBP cross links by transpeptidase or gransglycosylatse. Crucial for cell growth, separation, and sporuation.
245
what is important for cross linking in peptidoglycan?
D-Ala-D-Ala terminal peptides.
246
Action of Beta Lactamase
split amide bond in beta-lactam rin to make inactive. Very specific beta lactam rings!
247
Narrow Spectrum Beta lactamases
hydrolyze penicillin antibiotices but not cephalosporins of carbapenems. Exist on Gram + and -, transferred via plasmid or transposon.
248
bla
narrow spectrum beta lactase for Staph
249
TEM-1
narrow spectrum beta-lactamase for H influenza and E. coli
250
SHV-1
narrow spectrum beta-lactamase for Kiebsiella
251
Extended Spectrum Beta-Lactamases
Hydrolyze penicillin and MOST cephalosporin antibiodies. Occur only on Gram - Rods. Derived from plasmids, with mutations that have occurred in the narrow spectrum region.
252
CTX-M
ES Beta-Lactamase for E. coli
253
SHV-Type
ES beta lactamase for Kiebsiella
254
Amp-C Encoded Beta Lactamase
hydrolyzes penicillin and 1-3 cephalosporin and is NOT inhibited by beta-lactamase inhbitors! transferred chromosomal and only occurs in Gram - rods like Eneterbaeteria and Pseudomonas. Can be induced or constitutive.
255
Induced vs constitutive AmpC
Induced is resistance that is only on some of the time - induced by ampicillin and cefazolin, but constitutive is always on due to mutations!
256
Carbapenemases
Beta-lactamases that are active against oxyimo-cephalopsorins, cephamycins and carbapenems. Carbapenems are resistant to ESBL and ampC, so these are very hardy. Plasmid mediated and gram - rods only.
257
KPC
hydrolyze carbapenems and all beta lactams
258
NDM-1
hydrozlyes all beta lactams except aztreonam
259
Types of Beta-Lactamases
1) narrow secptrum 2) extended spectrum 3) amp-C encoded 4) carbapenemases
260
Altered PBPs in B-Lactam resistance
Mutation of gene or acquisition of new PBP genes to make the blockage of cross linkage unsuccessful.
261
MecA
in Staphylococci encodes for a low affinity PBP2a that is resistant to all Beta-lactam antibiotics except 5th generation cephalosporin. Found on MRSA
262
Mosaic PBP
transformation into own genome from another bacteria a lower affinity PBP found in Streptococcus pneumonia and N. Gonorrhoeae. Infers a gradual resistance compared to staph
263
Resistance mechanisms of B-Lactam antibiotics
1) Beta lactamase 2) altered PBP
264
Vancomycin mechanism
targets peptidoglycan precursor D-Ala-D-Ala peptide chain to disrupt cell wall synthesis
265
Vancomycin resistance
1) Modification of target 2) preventing drug-target interaction
266
Modification of target - vancomycin
vanA and vanB are transferred via plasmid to substitute termal D-ala for D-lactate on peptidoglycan precursor. Unable to cross link cell wall. Occurs in enterococcus
267
Preventing drug-target int. in Vancomycin
the unable to cross link creates thickened layers of peptidoglycan and leaves free d-ala-D-ala. Vancomycin remains bound to cell wall instead of precursor, so it doesn’t have an effect. (staph)
268
VISA
vancomyin intermediate suseptibility S. Aureus - most due to prolonged vancomycin use.
269
Quinolone mechanisms
target gyrase (GyrA or B) and topoisomerase (ParC and E) to cause DS DNA breaks.
270
Resistance to Quinolones
1) modify drug (rare), 2) drug efflux (rare) 3) modifying target (most common)
271
Modifying target - quinolones
1-2 NT mutation in GyrA or ParC so it can no longer bind to quinolone to be inhibited.
272
Macrolides - mechanims
binds to 23S of 50S bacterial ribosome to prevent peptide elongation.
273
Macrolide resistance
rarely drug modification; 1) modifying target 2) increased efflux
274
Modifying target - macrolide
erm demethylates 23S so macrolide cannot bind. Transferred via plasmid or transposon and cause resistance to macrolide and clindamycin. Induced and constitutive.
275
Induced vs. constitutive macrolide resistance
Induced is resistant to macrolides and sensitive to clindamycin; constitutive is where term is always on so it is resistant to both macrolide and clindamycin
276
Increased Efflux - macrolide
passed via chromosomal or plasmids and causes resistance to macrolide and sensitivity to clindamycin. Must use D-test to determine whether due to modification of target or efflux pump
277
D-Test
to differentiate between term and efflux pump resistance in macrolides. 1) stream agar plate 2) plate disc with erythromycin near disk with clindamycin. if there is an ERM mutation, you will see an induced resistance to clindamycin and blunting clearing zone. If due to efflux, there will be no blunging zone.
278
Amincoglycosides - Resistance
1) modifying drug (classical) 2) modifying target 3) preventing drug-target interaction
279
Modifying drug - aminoglycosides
due to plasmic, transposon, chromosme in gram + and -, muletiple modifiers that cause N-acetylation, O nucleotidylation, O phosphorylation.
280
Modifying target - amincoglycosides
plasmid to cause methylation of 16s rRNA (site of binding)
281
Preventing drug-target interaction - ahminoglycosides
ETC creates electrochemcial gradient for uptake of aminoglycosides. Anaerobic do not have ETC, so they are resistant.
282
what antibiotics target most Gram + cocci?
Penicillin V and G, Amox/Amp, cephalosporins, vancomycin, Clindamycin, macroclides, Doxycycline (NOT dicloxcillin, tetracycline, aminglycosides, DNA affectors)
283
what target community acquired penumonia?
Doxycycline
284
What antibiotics are good for strep pyro and pneuma?
All penicillins, cephalosporins, vancomycin, protein synthesis inhibitors (except aminoglycosides, nitofurantoin, metraonidazole)
285
what antibiotics are good for MSSA?
Penicllins that are beta-lactamse resistance - dicloxacillin, Amox w. Calv, pip -taz, cephalosporins, vanc, all protein syntehsis inhibitors, NOT DNA effectors or aminoglycosides
286
what antibiotics are good for MRSA?
Doxycycline, TMP-SMX, Clindamycin, vancomycin
287
What antibiotics are good for Gram - cocci?
cephtriazone (3rd ceph), and some macrolides and tetracycline
288
what antibiotics are good for most E. coli?
Aminoglycosides, Amox, Amox with Clav, pip-tazo, Nitro, ceph, tmp-smx
289
what antibiotics are good for resistant e. coli?
aminoglycosides, Cip-levo (only for those with skeletal maturity)
290
what antibiotics are good for pseudomonas?
Aminoglycisdes, cip-levo, pip-tax, 3rd ceph
291
what antibiotics are good for most anaerobes?
Pip-Tax, Penicillins, Amox, Amox/clav, cephs, tetracycline, Clindamycin, moxifloxican, metronidazole, NOT dicloxacillin, vanc, macrolides, cip/levo, nitrofurantoin
292
what antibiotics are good for C-Diff?
metronidozole, vancomycin.
293
what is C-diff caused by?
Clindamycin, Fluroquinolones, 2 and 3 gen ceph, amox-clav
294
what antibiotcs are good for bacteroides fragilis?
Pip-tax, Amox/clav, clindamycin, metronidazole
295
what antibiotics are good for atypical bacteria?
Doxycycline (not in pregnancy or kids), macrolides, fluroquinolones
296
two different ways bacterial evolve?
slow incrementa changes to non-pathogenic progenitors by mutations that modify existing genes OR quantum changes by acquisition of NEW genetic material by lateral transfer
297
Regulation of Gene expression in bacteria 2 methods
Regulation of transcription by increasing or decreases BP to promoter region OR DNA rearrangement in phase variation
298
Mechanisms of Genetic Variation in bacteria
Spontaneous, Recombination, Acquisition of nes DNA segments
299
Spontaneous mutation - genetic variation
errors in BP changes, deletions, duplications; typically are deleterious or neutral. Rarely confers selective advantages.
300
Recombination methods
1) antigenic variation 2) genetic exchange between related organisms
301
Antigenic recombination
Inversion of promoter sites to create selective advantage
302
Acquisition of new DNA segments
occurs via lateral transfer from other bacteria or higher organisms - via transposable elements, bacteriophage, plasmids, and pathogenicity islands
303
Transposable Elements
segment of DNA contained within bacteria of phage chromosome or within a plasmid that is able to be enzymatically moved.
304
Examples of transposable elements
1) transposons, IS elements, composite transposons
305
Transposon
must be a part of a self replicating organisms, encodes transposes and becomes integrated into bacterial chromosone.
306
IS
insertion sequences that just encode for transpsase
307
Composite transposon
carries genes of antibiotic resistance, toxin, adhesion, as well as transposes
308
Bacteriophage
virulence genes not normally part of bacterial genome that are expressed in lysogenized strains
309
Acquisition of new plasmids
via conjugation and trasduction
310
Pathogenicity Islands
insertions of one or more genes that influence pathogenicity - often have been acquired from unrelated organism.
311
T3SS
and PI that triggers salmonella invasion and inflammatory response into epithelial cells and translocates 30 effector porteins to host cytoplasm
312
ETEC
plasmid encoded enterotoxin that causes travelors diarrhea
313
EPEC
plasmid mediated his pathology that causes infant diarrhea in developing countries
314
EIEC
plasmid mediated invasion and epithelial destruction
315
Ehec
bateriophage! encoded toxin and plasmid encoded virulencef actor that causes hemoragic colitis and hemolytic uremic syndrome
316
EAEC
plasmid mediated aherence and pathology
317
mechanisms of exchange between bacteria
transformation, transduction, conjugation
318
Transformation
genetic transfer of naked DNA (either Ch or plasmid) in gram + and - bacteria; cell must be competent for uptake of DNA; most often occurs between same speciies
319
Transduction
mediated transfer via bacteriophages where virus adsorbs bacteria and injects Nucleic acids into cells where it undergoes viral cycle to release virus progeny.
320
Temperate bacteriphage
bacteriophage that does not always kil the host - can be in lytic or lysognic
321
Lytic infection
entrance of viral chromosome where it is multiplied and viral chrosomes are packaged and released by cell lysis
322
Lysogen formation
host is maintained as noninfectious prophage where DNA is inserted into host genome and passively replicated and can either enter lytic state or maintain lysogenic.
323
How does it remain in lysogenic state?
repressor proteins, and stress favors lytic cycle
324
Bacterial conversion
lysogenic conversion - genes expressed in lysogenic state and transducer and new phenotypic trait is found only in phage genome.
325
Bacterial conjugation
genetic transfer dependent on physical contact and mediated by bacterial plasmids (plasmid F); carried selective resistance and virulence.
326
types of bacterial plasmids
1) conjugative and non-conjugative and non-mobilized
327
Conjugative plasmids
self transmissible that mediate own transfer
328
Non-conjugative plasmid
can be mobilized to be passibvly transferred during conjugation by another plasmid in the same cell.
329
Mechanism of conjugation
cell comes in contact, single stranded nick in OriT and BP at 5’ end to initiate rolling replication cycle, ssDNA is transfered via sex pili, intregrates into bacterial chormoones
330
OriT
origin of transfer, F-DNA plasmid is coupled to this
331
Conjugative transposons
transposable elements that mediate conjugation between pairs of cells that often encode antibiotic resistance against tetrcycline.
332
Interspecies conjugation
occurs between gram + and Gram -; Gram - to fungi and plants
333
ftsz
tubulin equivalent in bacteria - responsible for division
334
MreB/PerM
actin in bacteria - polarity and Ch separation
335
Cres
intermidate filmanet in bacteria - shape
336
Bond in peptidoglycan
GlcNAc-MurNac
337
lysozyme
cleaves GlcNAc-MurNac bond
338
Major differences between gram + and -
Gram + has high osmotic pressure, lots of cross links, thick cell wall; L-lys - gly(5) - D-ala
Gram - low osmotic pressure, not many crosslinks, think, DAP-D-ala
339
What is characteristic of gram - bacteria
Asymmetric lipid bilayer that is barrier to antibics and protective from detergents and toxins
340
Components of asymmetric lipid bilayer
1) LPS 2) porins 3) lipoproteins
341
LPS
lipopolysaccharids - covalent linkes outer membrane
342
Porin
transmembrane channels in gram - that allow
343
Lipoproteins
proteins in Gram - wall that anchors outer membrane to peptidoglycan
344
LPS endotoxin
Lipid A: toxic component with core polysaccharide; trigger innate immune system to lead to inflammation and endotoxic shock
345
Components of gram +
Teichoic acid and Lipoteichoic acid
346
Teichoic acid
Polyglycerol and polyribitol backbone that covalently links PG layer and extends outward
347
Lipoteichoic acid
FA substition that is embedded in gram + cytoplasmic membrane
348
Function of Gram + cell wall
ion homeostasis, adherence for colonization, use TLR to trigger innate immune response and inflammation
349
Capsule
polysaccharide coat of bacteria that is anti phaygocytic, a virulence factor. It is antigenic - used as vaccine component
350
Biofilm
adherent polysaccharid/glycoprotein that adhere to inert surfaces, host cells, and is protective of phagocytosis and host defence. Limits antibiotics
351
Flagellae
used for motility
352
Pertinichous
flagella on all sides
353
Flagella moving counterclockwise
tumbling
354
flagella moving counterclockwise
swimming
355
Pili
fine appendages that help adhere to surfacea nd tissues - sex pili are used for conjugation
356
Secretion system
delivers proteins to cell surface, assemble organelles, exports to ECM, injects proteins or DNA
357
Binary Fission
produces two cells of equal size
358
Phases of bacteria growth
lag phase, exp. growth, stationary phase,d eat
359
Lag phase
in oculum, induction of growth in new medium
360
Exponential phase
logarithmic, increase in cell # and mass
361
Stationary phase
essential nutrients are consumed and toxic products accumulate to cause cell death.
362
where does antibiotic resistance work?
only on fast growing cells
363
Energy sources of bacteria
ATP, PMF (from flagellar rotation), NADPH, ATPase converts ATP,
364
Fermentation vs. Respiration
Fermentation anaerobic where you have facultative organic electron donor and acceptor; Respiration uses ATP generation with O2
365
indifferent anaerobe
ferments in presence of O2
366
Faculative
Respires in O2, ferments in absence of O2
367
Microaerophilic
grow sets at low O2, but can grow without O2
368
Sporulation
response to advere nutritional conditions that forms spores which are highly resistance and require no metabolism. For prolonged survival in adverse conditions.
369
Germination
sporulation back to metabollically active cells when nutritional needs are met
370
Empiric therapy
early antibiotic initiation with critically ill patients - broad spectrum considering what organisms are likely and resistant based on clinical context.
371
Definitive therapy
narrow spectrum due to microbiology result
372
Antimicrobial suseptibility testing
1) broth dilution, Disc diffusion (Kirby Bauer), E test,
373
Broth dilution
serial dilution in liquid media to determin MIC
374
MIC.
Minimal inhibitory concntration - lowest concentration antibiotic prevents growth
375
Disk Diffusion
Kirby Bauer - isolate susension and plate with discs of antibiotics and measure diameter of clearing
376
E -test
like KB, but with strip of concentration gradient to determine MIC
377
MBC
minimal bactericial concentration - lowest conc ab kills 99.9% of inoculum
378
MIC and MBC - bactericidal
MBC = MIC
379
MIC and MBC basteriostatic
MBC >> MIC
380
Minimun determinant for suseptible oranisms
Max CP is greater than MIC
381
Caveats of interpretation of bacteria suseptibility
does not account for penetration into tisue, does not account for number of bugs in the infection, does not consider host conditions (pH), does not consider host defense
382
Local Factors of antibiotics
Distribution and environment
383
Tx of meningitis
must cross BBB, inflammation makes endothelial border leaky to increase CSF concentration; host defesnse mechanism in CNS, must use bactericidal
384
Tx of bone infections
has opsonphagocytic removal (bacterial protective) and requires prolonged antibiotic use. Fluroquinolones are good.
385
Endocarditis tx
platelets and fibrin create niche to protect bacteria - bactericidal
386
Intracellular niche
rifampin, tatrcyclines, erythrmoycin penetrate better than ahminoglycosides and B-lacatms
387
Daptomycin
pulmonary surfactant inactives drug - cant tx pneumonia
388
Host factors to Antibiotics
1) Hx of adverse rxns
2) renal/liver function
3) age
4) genetic
5) pregnancy
6) Drug interactions
7) immune status
389
Age and antibiotic factors
sulfonamides - compete with bilirubin for binding to albumin, increase bilirubin cause kernicterus; tetracycine binds to bone and developing teeth - not recommended for kids
390
Genetic factors for antibiotics
G6PD deficiency causes hemolysis with antibiotics ; DM increased risk with fluroquinolones
391
Immune status considerations with Ab
if immunocompormised usually affected by uncommon agents, depend only on Ab and require bacteriocidal
392
Selective media
permits growth of organisms we wish to recover, but supresses growth of underised. Ie. MacConkey agar with bile salts and dye crystal violet to inhibit all except gram -
393
Differential Media
provides selective advantage for growth of one organism over another in polymicrobic specimen. could be chemical *sodium seleniate or temperature
394
MacConkey Agar
differential and selective for det and isolation of Gram -; can further separate lactose fermentation - turn red; from those that done remain clear.
395
Lactose fermenters
pick on macconkey agar - E. Coli and Klebsiella
396
Lactose non-fermenters
stay clear on macConkey agar - salmonella, shigella, pseudomonas
397
Hektoen Eneteric Agar
diff and selective for isolation of salmonella and shigella. Contains bile salts to inhibit non-eneric and dytes to inhibit growth of gram +. (high conc of bile salts to kill E. coli)
398
Orange on HE agar
fermenters for sucrose, salicin, or lactose - NOT salmonella or Shigella
399
Green blue colonies on HE agar
salmonalla or shigella - non fermenters
400
Black coloration of HE agar
combination of H2S with ferric ions to isolate salmonellae from shigella.
401
Sheep blood agar
common differential, non-selective. supports growth of most bacteria. Good for visualizing hemolysis positive colonies
402
Psuedomonas Isolation Agar
selective, formation of blue or blue-green pyocyanin pigments of pseudomonas aeruginoas.
