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107 Cards in this Set
- Front
- Back
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Gram + Bacteria
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Gram + Cocci
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What are the 3 major genus of Gram + cocci?
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1. Staphylococcus Aureus
2. Streptococcus 3. Enterococcus |
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What are the 3 species of streptococcus of clinical interest?
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1. Group A Strep (GAS)
2. S. Viridans 3. S. Pneumonia |
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Reservoir/ Entry, Toxins (MoA), C.P
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Staphylococcus Aureus (5 toxins, 2 major CP classes?)
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Nasopharynx → trauma or IC
1. a-toxin -- disrupt sm of bv 2. b-toxin -- disrupt phospholipid membrane 3. Exfoliative toxins -- scalded skin syndrome 4. Toxic Shock toxin -- toxic shock (hypovolemia, multi-organ failure) 5. Entertoxin -- superantigen → food poisoning 1. Localized pyogenic 2. Disseminated |
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What are sx of localized pyogenic in Staphylococcus aureus? (4)
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1. Skin infection
2. Endocarditis 3. Osteomyelitis 4. Pneumonia |
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What are sx of disseminated in staphylococcus aureus? (3)
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1. Scalded skin syndrome
2. Toxic shock syndrome 3. Food poisoning |
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In what population is Toxic Shock Syndrome common?
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women undergoing menses b/c tampon
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What is the most dangerous form of Staphylococcus Aureus?
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MRSA (multi-drug resistant)
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How do they become multi-drug resistant?
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acquisition of mec A gene → encodes penicillin binding protein 2A (alternate form that has < affinity for B-lactam)
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Group A Streptococcus (GAS)/ S. Pyogenes (3 toxins, 3 major CP classes)
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upper respiratory tract
1. Streptococcal pyrogenic exotoxin -- superantigen → strep toxic syndrome (scarlet fever) 2. Streptolysin S & O -- lyse blood cells 3. Exotoxin B -- necrotizing fascitis 1. pyogenic (localized) 2. Exotoxin-mediated (systemic) 3. Immunologic (autoimmune) |
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What are the sx of pyogenic in GAS? (4)
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1. Pharyngitis! -- strept throat
2. Pyoderma -- pus skin infection 3. Cellulitis -- deep tissue infection 4. Necrotizing fascitis -- flesh eater |
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What the sx of exotoxin-mediated in GAS? (2)
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1. Scarlet fever
2. Strep toxin syndrome |
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What is the sx of immunologic in GAS? (2)
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1. Rheumatic fever → endocarditis
2. Glomerulonephritis |
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What virulence factor is unique in GAS that allows spread?
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streptokinase A & B -- lyse clots to facilitate bacteremia
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Streptococcus Viridians
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oropharynx → Dental carry!
Endocarditis! (main cause) |
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Streptococcus Pneumonia (2 toxins)
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Nasopharynx → spread to lower resp tract
1. Autolysin -- degrade own peptidoglycan cell wall 2. Pneumolysin -- released after autolysis → destroy epithelial cell → ↑ infection 1. Pneumonia 2. Meningitis 3. Arthritis 4. Sepsis |
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When does disease occur in S. pnemonia?
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when spread to lower resp tract
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What facilitates spread to lower resp. tract? (2)
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1. IC
2. Smoking |
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Enterococcus
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GI/vaginal
1. endocarditis 2. Meningitis 3. UTI 4. Sepsis |
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Gram + rods (bacilli)
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What are the 3 clinically significant genus of gram + rods?
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1. Clostridia
2. Corynebacterium Diptheria 3. Listeria |
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What are the 4 clinically significant species of clostridia?
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1. C. botulinum
2. C. Tetani 3. C. Perfringens 4. C. Dificile |
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Which gram + rods are spore-forming?
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only clostridia
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How do spores aid w/ infection?
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facilitate transmission b/c endospore form can survive adverse environment - i.e: contaminate food
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Reservoir/ Entry, Toxins (MoA), C.P
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C . Botulinum
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Soil → food
Botulism toxin -- ↓ ACh @ NMJ → flaccid paralysis |
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C. Tetani
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Soil → wound
Tetanus toxin -- ↓ GABA & glycine→ spastic paralysis Lock jaw (trismus) -- rigid arching of back & legs, folding of arm |
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C. Perfringens
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GI or Soil → wound or food
a-toxin -- phospholipase → disrupt muscle cell membrane → Gas gangrene |
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C. Difficile
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GI → fecal-oral
Toxin A → Antibiotic associated diarrhea Toxin B → enterocolitis (plaques in colon) |
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Corynebacterium Diptheria
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human → respiratory
Diptheria toxin (A-B) A-subunit → ADP-ribosyl transferase binds to EF2 → blocks protein synthesis B-subunit → entry into cardiac & neural tissue 1. Myocarditis 2. Laryngeal nerve palsy |
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Listeria
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GI of Cow → diary product
Listeriolysin = escape phagosome into cytoplasm of macrophage → use actin to escape to surface & infect other cells 1. Septic Shock 2. Meningitis |
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Gram - Bacteria & Atypical Bacteria
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Gram - Rods (bacilli): Enteric
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What are the enteric gram - rods? (9 genus) Divided by replication site
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In & Out GI (2) -- E-coli, salmonella
In Gi (4) -- Shigella, campylobacter, helicobacter, vibrio Out Gi (3) -- Klebsiella, Proteus, Pseudomonas |
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Which are enterobacteria (5)?
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E-coli, salmonella, shigella, klebsiella, proteus
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What are the 4 types of E-coli? Watery or bloody diarrhea?
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1. Enterotoxigenic (ETEC) = watery
2. Enteropathogenic (EPEC) = watery 3. Enterinvasive (EIEC) = bloody 4. Shiga-toxin producing (STEC) or enterhemmorhagic (EHEC) = bloody |
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What is clinical presentation of E-coli?
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1. Meningitis
2. Sepsis 3. UTI 4. Diarrhea - bloody or watery |
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What VF allows E- coli to bind to uroepithelium? 2 types? Each type leads to which type of UTI?
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Pilli
Type 1 -- bind to mannonse → cystitis P-pilli -- bind to digalactoside → pyelonephritis |
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Reservoir of E-coli?
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GI & GU
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Where does E-coli replicate?
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in & out GI
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ETEC
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traveler’s contaminated food
LT & ST → Watery diarrhea |
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EPEC
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<2 yrs developing country
Disruption of cellular cytoskeleton w/ actin accumulation underneath site of attachment → Watery diarrhea |
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EIEC
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contaminated food
invasion of epithelial cells → inflammation & ulceration → bloody diarrhea w/ systemic: fever |
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EHEC
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developed world contaminated food
shiga-like toxins (Stx) → bloody diarrhea |
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What are the 4 species of salmonella? how do they differ?
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clinical presentation differ
1. S. Enteriditis 2. S. Typhimurium 3. S. Typhi 4. S. paratyphi |
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Salmonella (spread?)
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poultry/ eggs → fecal -oral → in & out GI
No toxins - spread via macrophages (bacteremia) S. Enteriditis → gastroenteritis S. Typhimurium → vascular endothelium → organs S. typhi & s. paratyphi → typhoid fever -- rose spots |
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Which one only has human reservoir?
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S. Typhi
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Shigella
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humans → fecal-oral → In GI
Shiga → kills intestinal endothelial cells 1. Bloody diarrhea 2. GI ulcers |
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Klebsiella
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upper resp/GI → (opportunisitic) → Out GI
No toxins 1. Pneumonia 2. UTI |
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What 2 disorders ↑ risk of klebsiella infection?
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pulmonary disease, alcoholism
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Proteus (rep site?, VF?)
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Outside GI
VF: Urease → ↑ pH GU → Primary cause of UTI |
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Campylobacter
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GI animals → undercooked poultry → in GI
Invasive penetrating GI mucosa → Leading cause of Diarrhea! |
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Helicobacter
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in Gi
Vacuolating cytotoxin (VacA) = produce cytoplasmic vacuoles after inducing apoptosis Chronic gastritis Ulceration |
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Vibrio
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Shellfish → in GI
Cholera toxin → watery diarrhea |
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Pseudomonas
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Gi human →(opportunistic) → out gi
Exotoxin A= (-) host cell protein synthesis → necrosis Exotoxin B= induces apoptosis Ecthyma Gangrenosum Sepsis Diabetic osteomyleitis |
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Gram - Rods: respiratory
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Haemophilus influenza
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Respiratory → local OR systemic
Capsule - polyribitol phosphate (PRP) = (-) phagocytosis Encapsulated (systemic) = HiB Meningitis Acute epiglotttis Sepsis Non-encapsulated (localized) Otitis media Sinusitis |
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Haemophilus ducreyi
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STD
no exotoxins Chancroid - painful genital ulcer |
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Legionella Pneumophila
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Acquatic → contaminated water → alveolar macrophages (respiratory)
Legionnaires’disease - Pneumonia- fever & non-productive cough |
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Gram negative cocci
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What is the clinically significant genus of gram (-) cocci?
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Neisseriaceae
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What species of Neisseriaceae are clinically sign.?
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N. Meningitidis & N. Gonorhoeae
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What is unique about LPS of neisseriaceae?
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LipoOLIGOsaccharide not lipoPOLYsaccharide (shorter carb)
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Which species is more likely to cause bacteremia?
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N. Meningitidis b/c it is encapsulated
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N. Gonorrhoeae (VF for attachment?)
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Humans → STD → mucosal epithelial cells: throat, urethra, cervix, eye
Pili & Opa protein - attachment to mucosal epithelial cells Men: Purulent urethral discharge Women: Dysuria, Painful sex, pelvic inflammatory disease |
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N. Meningititidis
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human nasopharynx → respiratory
1. Meningitis 2. Septicemia- Meningococcemia (Waterhouse-friderichsen syndrome - most dangerous form) |
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Atypical Bacteria
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What are the atypical bacteria (5)? Distinguishing features of each?
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1. Chlamydiae & rickettsia -- obligate intracellular bacteria
2. Acid-fast bacteria -(MycoBacteria)-- mycolic acids (waxes interlaced w/ peptidoglycan); stain bright red 3. Actinmyocetes -- look similar to fungi 4. Mycoplasma-- wall-less 5. Spirochetes -- thin so do not take up dye |
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Obligate intracellular
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What are the 2 obligate intracellular bacteria?
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1. Chlamydia
2. Rickettsia |
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How do they survive inside a cell? (3)
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1. Inhibit lysosome fusion w/ phagosome
2. Inhibit acidification of phagosome 3. Escape from phagosome into cytoplasm |
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What is unique about chlamydiae (cell wall)? (2)
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1. No peptidoglycan
2. resemble gram - bacteria cell wall but no Muramic acid |
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B.c chlamydia lacks muramic acid in cell wall allows what?
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resistance to lysozyme
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Which of 3 strategies used by intracellular bacteria is unique to only chlamydia?
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inhibit lysosomal fusion
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What unique about chlamydia reproductive cycle?
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2 forms:
1. Elementary bodies (EB) 2. Reticulate bodies (RB) |
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Which form is infectious?
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EB
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Which form is metabolically active?
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RB
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What species of chlamydiae leads to disease (3)?
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1. C. Trachomatis
C. Psittaci 3. C. Pneumoniae |
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All chlamydiae induces damage how?
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granulomatous formation
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What are the 3 serotypes of C. Trachomatis? How do they differ?
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clinical presentation differ
1. A,B,C 2. D-K 3. L1-L3 |
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C. Trachomatis
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humans → STD or vertical (underdeveloped) → eyes, genitals, lungs
A, B, C→ reproductive tract infection + Chronic conjunctivitis (permanent) D-K → inclusion Conjunctivitis (temporary) L1-L3 → Lymphogranuloma venereum -- lymphoadenopathy in areas draining genital tract |
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C. Psittaci
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Birds → bird feces → lungs, liver, spleen
Psittacosis-- atypical pneumona w/ fever & non-productive cough |
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C.Pneumoniae
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Humans → respiratory
Pneumonia |
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Mycobacteria
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What is unique about mycobacteria? (2)
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1. Mycolic acids
2. Lipoarabinomannan |
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What is the hallmark of mycobacteria staining?
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Acid fastness
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How does damage occur by Mycobacterium?
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Granulomatous inflammation -- no exo or endotoxins
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What are the 3 clinically relevant species of mycobacterium?
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1. M. tb
2. MAC 3. M. Leprae |
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Which Mycobacteria cause TB? (2)
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1. M. Tuberculosis
2. MAC |
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Which mycobacterium is the most common co-infection in late AIDS?
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M. Avium
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Which is an obligate intracellular parasite?
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M. Leprae
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Where do mycobacterium Tuberculosis reside?
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intracellular - Macrophages
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M. Tuberculosis
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Humans only → respiratory → intracellular macrophages
Primary Tb -- localized to lungs -- asymptomatic Secondary Tb -- dormant state is reactivated → disseminates: pulmonary, lymph node, CNS |
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M. Avium-intracelluare complex (MAC)
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Soil & water → resp. (opportunistic: most common opport. bacterial infection in AIDS)
Pulmonary infections |
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Which form of pathogenesis in M. Leprae depends on what?
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if cell-mediated immunity is intact
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M. Leprae (leprosy)
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Armadillos only → exudate of skin lesions from leprosy patient → obligate intracellular parasites of macrophages → skin, nerves, eyes, testes
2 Forms: 1. Tuberculoid -- granulomatous (strong cell-mediated) → nerve & skin 2. Lepromatous -- infiltrative (weak cell-mediated) → blindness, infertility, neuropathy |
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Actinomyces
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What is unique about actinomyces?
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branching gram + rods → look like fungi
Actinomyces Israelli= Normal flora of oral cavity → local trauma (dental extraction) → mouth, lung, GI Eroding abscesses in mouth, lung, GI Sulfur granules -- Yellowish microcolonies |
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Mycoplasma
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What is unique about mycoplasma?
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lack cell wall
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Instead of cell wall, what do they have?
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triple-layered membrane w/ Sterols
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How did sterols get there?
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not synthesized by organism, but acquired from medium or tissue where organism is growing
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What 2 species of mycoplasma is associated w/ disease?
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1. M. Pneumoniae
2. M. Genitalium |
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M. Pneumoniae (pathogenesis)
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human → respiratory
Attach to cilia in bronchial epithelium → interfere w/ ciliary action → inflammatory rxn in lungs “Walking” Pneumonia (mild) |
