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101 Cards in this Set
- Front
- Back
- 3rd side (hint)
Bacterial Virulence Factors
Prot. A IgA protease M protein |
-help evade host immune response
Protein A: staph aureus -binds Fc region of Ig to prevent opsonization and phagocytosis IgA protease: SHiN (S. pneumoniae, H. influenza B, Neisseria) -cleaves IgA allowing colonization of respiratory mucosa M protein: group A strep -helps prevent phagocytosis |
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pseudomembranous colitis
-presentation -treatment |
-greenish, foul smelling watery diarrhea
-abdominal cramps, fever, leukocytosis, lethargy -follows clindamycin rx Treatment: metronidazole or vancomycin |
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cAMP inducers
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Vibrio + E.Coli (ETEC)= activates AC via Gs
Pertusus= inhibits Gi, causing AC to remain active Bacillus anthracis= toxin itself is an AC |
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which organisms do not take gram stain?
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"These Rascals May Microscopically Lack Color"
1. Treponema 2. Ricketsia 3. M. TB 4. Mycoplasma 5. Legionella 6. Chlamydia |
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SHiN bacteria
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Strep pneumonia
H. Influenza Neisseria 1. are ENCAPSULATED 2. acquire AB resistance via transformation (take up DNA from environment) 3. IgA protease: cleaves IgA allowing organisms to colonize mucosal surfaces (esp. respiratory surfaces) |
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Encapsulated Bacteria
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Kapsules Shield the SHiN
Klebsiella Salmonella S. pneumonia H. influenza Neisseria |
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Staphylococcus organisms
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-Catalase positive
-found in CLUSTERS Coagulase + = staph aureus Coagulase - : 1. S. epidermidis: novobiocin sn; endocarditis 2. S. saprophyticus: novobiocin rs; UTI's |
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Streptococcus
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-Gram Positive Cocci in CHAINS
-Catalase - 3 groups: alpha: partial hemolysis (green) beta: complete hemolysis (clear) gamma: no hemolysis (red) |
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alpha strep
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does not completely hemolyze hb so shows up as green
1. S. pneumonia: encapsulated, optochin sn, bile soluble 2. S. viridians: NOT encapsulated, optochin RS, NOT bile soluble |
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beta strep
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complete hemolysis of hb-->bili-->clear
1. S. pyogenes (Group A) : bacitracin sn 2. Group B: bacitracin RS |
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gamma strep
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NO HEMOLYSIS-->RED
1. enterococcus 2. peptostreptococcus (anaerobe) |
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Gram positive RODS
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1. clostridium (anaerobe)
2. corynebacterium 3. listeria 4. bacillus (aerobe) |
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Gram + branching filaments
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1. actinomyces
2. nocardia |
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Skin Infections caused by both Staph aureus and Strep pyogenes?
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1. Folliculitis
2. Cellulitis 3. Impetigo |
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Gram + infections that cause neonatal death
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1. group B
2. E. Coli 3. Listeria |
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Gram + Obligate Aneorobes
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anaerobes Cant Breath Air
1. Clostridium 2. Bacteroides 3. Actinomyces |
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Obligate Aerobes Gram +
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Nagging Pests Must Breathe
1. Nocardia 2. Pseudomonas aeruginosa 3. M. tb 4. bacillus |
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components of adaptive immunity
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1. B cells-->plasma cells
2. T cells 3. antibodies |
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components of innate immunity
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1. neutrophils
2. monocytes-->macrophages 3. dendritic cells 4. NK cells 5. mast cells 6. basophils 7. eosinophils 8. complement |
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antigen presenting cells
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1. macrophages
2. B cells 3. dendritic cells |
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neutrophil chemotaxis stimulated by:
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1. IL-8
2. Leukotriene B4 3. complement C5a |
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Uses of interferons
alpha, beta, gamma |
alpha, beta: inhibit viral protein synthesis by inducing ribonuclease production (degrades viral mRNA)
gamma: incr. expression of MHC I (all cells), MCH Il (APCs) |
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need to give preformed antibodies (passive immunity) after exposure to the following toxins in addition to vaccination
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To Be Healed Rapidly:
1. tetanus 2. botulinum 3. HBV 4. Rabies 5. RSV (for premature babies in winter months!) |
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Positive ANA
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SLE
Sjogren's scleroderma poly/dermatomyositis rheumatoid arthritis juvenile arthritis mixed connective tissue dz |
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Bruton's Agammaglobulinemia
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-X linked (BOYS)
-B cell def (def. tyrosine kinase gene: low levels of all Ig's) -recurrent Bacterial infections after 6mos (passive immunity gone) |
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Thymic aplasia (DiGeorge)
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-3rd/4th pouches fail to develop: no thymus (no T cell maturation); no PTH (hypoCa, tetany)
-congenital defects in heart/great vessels -recurrent viral, fungal, protozoal infxns -90% have 22.q11 deletion |
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SCID
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-defect of early stem cell differentiation
-most commonly d/t adenosine deaminase deficiency -last defense is cytotoxic NK cells -no thymic shadow on newborn CXR Presentation: 1. severe recurrent infxns w/ weird organisms 2. chronic diarrhea 3. failure to thrive |
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Chronic mucocutaneous candidiasis
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-T cell dysfunction against candida albicans
-treat w/ ketoconazole |
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X linked immunodeficiencies
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1. Wiskott-Aldrich
2. Bruton's agammaglobulinemia 3. Chronic Granulomatous dz 4. Hyper IgM syndrome (inc. IgM, dec. IgG): -->X linked (no CD ligand) -->AR (no CD40) -->NEMO deficiency |
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Wiskott-Aldrish
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-thrombocytopenia and purpura
-eczema (TRUNCAL) -recurrent pyogenic infections: no IgM against capsular polysaccharides of bacteria -low IgM, high IgA -X linked |
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Ataxia Telangiectasia
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-IgA def
-cerebellar Ataxia, poor smooth pursuit of moving target w/ eyes -telangiectasias of face (>5yo) -defective DNA repair gene: 1. inc.lymphoma/acute leukemia 2. radiation sn (avoid XRAYS) -usually inc AFP at >8 mos -avg. age of death = 25 yo |
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Selective Ig deficiencies
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-IgA most common
-most appear healthy except for frequent sinus and lung infections, atopy, asthma -1/600 european descent -Most impt feature is possible anaphylaxis to blood transfusions and blood products!! |
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IL-12 receptor deficiency
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increased mycobacterial infections!
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Phagocyte deficiencies
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1. Chronic granulomatous dz
2. Chediak-Higashi dz 3. Job's syndrome (hyperIgE syndrome) 4. leukocyte adhesion def. syndrome |
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Chronic Granulomatous Dz
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-X linked!
-lack NADPH oxidase: impotent phagocytes 1. can engulf things but cannot produce O2 radicals 2. dx w/ a negative NBT test (phagocyte cannot oxidize yellow dye to blue-black) -susceptible to organisms w/ catalase -prophylaxis: bactrim, INF-gamma |
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Chediak-Higashi dz
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-defective LYST gene (lysosomal transport)
-defective phagocyte lysosome resulting in GIANT cytoplasmic granules in PMNs Presentation: 1. partial albinism 2. recurrent respiratory tract and skin infxns 3. neuro d/o (seizures, periph. neuropathy, etc) |
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Job's syndrome (hyperIgE syndrome)
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-T cells don't produce IFN-gamma; therefore PMN's fail to respond to chemotactic stimuli
-hi levels of IgE and Eosinophils Presentation: 1. Eczema 2. Recurrent cold staph aureus abscesses (cold b/c fail to produce appropriate inflamm. responses) 3. course facial features: broad nose, frontal bossing, deep set eyes, doughy skin 4. commonly retains primary teeth (get 2 rows of teeth) |
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leukocyte adhesion defect syndrome
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-Abnormal integrins (cannot integrate into tissues): phagocytes cannot exit circulation
Presentation: 1. delayed separation of umbilicus 2. recurrent bacterial infxns |
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Deficient C5-C9
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Neisseria bacteremia (gonococcal and meningococcal)
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germ tube test
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-tests for pseudohyphae formation
-dxic of candida albicans |
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CAMP test
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distinguish between Group A and Group B strep
-Group B has + CAMP test (ids partial hemolytic agent produced by group B strep) |
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Diplococci
Gram -? gram +? |
gram negative diplococci: neisseria
gram positive diplococci: strep pneumo |
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causes of meningitis
1. most common 2. most severe 3. etc |
most common: strep pneumo
most severe: n. meningitis etc: h. influenza |
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Interstitial pneumonia (atypical)
1. organisms 2. treatment |
1. legionella, mycoplasma, chlamydia pneumonia (also chlamydia psittaci)
2. macrolides (erythromycin, azithromycin) |
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first and second most common cause of gram - sepsis
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1. E.coli
2. Klebsiella |
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urease + gram negatives
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1. h. pylori
2. proteus |
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infections associated w/ pseudomonas
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PSEUDOmonas:
1. pneumonia 2. sepsis 3. external otitis (swimmers) 4. UTI 5. diabetic and drug use osteomyelitis |
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bilateral bell's palsy
seen in? 1. 2. |
1. lyme disease
2. guillan barre |
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antibiotics for ANAEROBES
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1. metronidazole
2. clindamycin |
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Organisms that don't gram stain
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1. Spirochetes: Borrelia, Leptospira, Treponema (BLT)
2. Gardnerella vaginalis (gram variable) 3. Rickettsiae 4. Chlamydia 5. Mycoplasma pneumoniae |
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Resistance Mechanisms
PCN Aminoglycosides Vancomycin |
PCN: B-lactamase cleaves of B lactam ring; or altered PBP in MRSA and PCN resistant s. pneumo
Aminoglycosides: modification via acetylation, adenylation, phosphorylation Vancomycin: terminal D ala of cell wall component replaced w/ D-lac; dec. afficinity |
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Resistance Mechanisms
Chloramphenicol Macrolides Tetracyclines |
Chloramphenicol: modification via acetylation
Macrolides: methylation of rRNA near erythromycin's ribosome binding site Tetracycline: dec. uptake or inc. transport out of cell |
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Resistance Mechanisms
Sulfonamides Quinolones Cephalosporins |
Sulfonamides: altered EZ (bacterial dihydropteroate synthetase), dec. uptake or inc. PABA synthesis
Quinolones: altered gyrase or reduced uptake Cephalosporins: B-lactamase or altered PBP site (MRSA, pcn resistant s. pneumo) |
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What are the macrolides and what are they used for?
MOA? |
MACE causes "PUS"
Azithromycin, clarithromycin, erythromycin Pneumonia, URIs, STDs MOA: 50S protein inhibitor/blocks translocation |
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photosensitivity causing drugs
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SAT for Photo
Sulfonamides Amiodarone Tetracyclines |
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Legionella pneumophilia
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1. gram - rod; stain w/ SILVER
2. Legionnaire's dz= severe atypical pneumonia and fever 3. pontiac fever: mild flulike syndrome 4. grow on charcoal yeast extract w/ iron and cystein 5. detect ag in urine 6. no person to person transmission 7. treat w/ erythromycin |
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Haemophilus influenza :
diseases |
haEMOPhilus
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epiglottitis
meningitis otitis media pneumonia |
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Pseudomonas aeuriginosa :
diseases |
PSEUDOmonas
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pneumonia (esp. CF)
sepsis (black lesions on skin) External otitis media (swimmer's ear) UTIs Diabetic and Drug use Osteomyelitis |
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EF2 inactivation by which organisms
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1. Corynebacterium
2. Pseudomonas aeruginosa via EXOTOXIN |
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capsular K antigen
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virulence factor of enterobactericeae:
COFFEe E. coli, salmonella, shigella, klebsiella, enterobacter, serratia, proteus |
Capsular
O antigen Flagellar antigen Ferment glucose Enterobactericiae |
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Klebsiella
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gram - rod
intestinal flora red currant jelly sputum also causes UTIs 4 A's of klebsiella: |
1. Aspiration pneumonia
2. Abscess in lungs 3. Alcoholics 4. di-A-betics |
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Virulence of Shigella vs. Salmonella
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Shigella > Salmonella
(10 org vs. 100000 org) |
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Spirochetes
1. Members 2. Staining |
Borrelia (wright's or giemsa stain)
Leptospira Treponema (dark-field microscopy) |
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Organisms found in animal urine
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1. leptospira
2. hantavirus what does leptospira cause? |
-flulike sx
-fever -h/a -abdominal pain -JAUNDICE (weil's dz: severe form->icterohemorrhagic, liver and kidney dysfxn, fever, hemorrhage and anemia) -photophobia w/ conjunctivitis |
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Lyme Disease
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-borrelia, ixodes tick vector
-stain w/ giemsa or wright -treatment: doxy, ceftriaxone BAKE a key LYME pie |
B: bell's palsy (stage 2)
A: arthritis (Stage 3) K: kardiac block (stage 2) E: erythema migrans (stage 1) |
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VDRL positive but not an STD
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T. Pertenue
Causes? |
Yaws: infection of skin, bone and joints
heal with KELOIDS (excess collagen): limb and nasal deformities disease of the tropics |
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rash on palms and soles
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1. syphilis (maculopapular rash)
2. rickettsiae 3. coxsackie virus (migrates to wrist, ankles and then TRUNK) |
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argyll robertson pupil
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prostitute's pupil:
accomodates but does not react (to light) assoc. w/ tertiary syphilis other sx of tertiary syphilis? |
1. neurosyphilis (tabes dorsalis) : loss of proprioception; positive rombert
2. gummas (chronic granulomas) 3. aortitis (vasa vasorum destruction-->tree barking) |
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disease associated with clue cells
treated w? |
Gardnerella vaginalis
-gram variable ROD -causes vaginosis treated w/ METRONIDAZOLE Sx: |
1. gray vaginal discharge with fishy odor
2. not painful 3. polymicrobial infection (assoc. w/ other infections) |
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Rickettsial disease transmitted by:
1. tick 2. fleas 3. human body louse |
Tick: Rocky mountain fever (rickettsia rickettsii) and ehrlichiosis (ehrlichia)
Fleas: endemic typhus (r. typhi) Louse: epidemic typhus (r. prowazekii) difference between rickettsial rash and typhus rash |
Rickettsial rash: soles and palms--> trunk
typhus rash: trunk-->outward spread; does not involve palms and soles |
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agent that causes Q fever
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Rickettsiae: Coxiella burnetii
How is it diff. from the other rickettsia bacteria? |
1. does not have classic triad (fever, h/a, rash); instead causes FEVER and interstitial pneumonia
2. can form spores 3. has negative weil-felix reaction 4. has NO vector (aerosol transmission) |
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Weil-felix reaction
how does it work? what organism does it test for? |
px serum with rickettsia antibodies reacts with proteus antigens--> agglutination
which rickettsia agent does not have a positive weil-felix reaction? |
Coxiella burnetti
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why are rickettsia and chlamydia OBLIGATE intracellular organisms?
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Rickettsia: need CoA and NAD+
Chlamydia: cannot make their own ATP Treatment for either organism? |
Tetracycline (also erythromycin for chlamydia)
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what makes chlamydial cell wall unique?
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lacks muramic acid
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chlamydia trachomatis SEROTYPES
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A-C: africa, blindness, chronic infection
D-K: PID, urethritis, ectopic pregnancy, neonatal pneumonia or conjunctivitis L1-L3: lympogranuloma venereum (acute lymphadenitis): first present as ulcers then get inguinal lymphadenitis, and can cause rectal dz (may be confused w/ IBD!) |
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Upper limb, lateral breast lymph drainage
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axillary
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stomach lymph drainage
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celiac
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duodenum, jejunum lymph drainage
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super mesenteric
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sigmoid colon lymph drainage
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colic--> inf. mesenteric
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rectum, anal canal above pectinate line lymph drainage
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internal iliac
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anal canal below pectinate line lymph drainage
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superficial inguinal
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testes lymph drainage
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superficial and deep plexus-->para aortic
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scrotum lymph drainage
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superficial inguinal
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thigh (superficial) lymph drainage
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superficial inguinal
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lateral side of dorsum of foot lymph drainage
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popliteal
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right side of head and right arm lymph drainage
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right lymphatic duct
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thoracic duct
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drains entire body except right half of head and right arm
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acute phase reactants
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IL-1: pyogenic, activates endothelium to expression adhesion molecules
IL-6: stimulate acute phase reactants and immunoglobulins TNF-alpha: septic shock, leukocyte recruitment, vascular leake -secreted by what? |
macrophages
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C3a, C5a
what do they mediate? |
anaphylaxis
C3a: activates mast cells and basophils C5a: activates neutrophil chemotaxis what else activates neutrophil chemotaxis |
Neutrophil chemotaxis:
IL-8 C5a leukotriene B4 |
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C1 esterase deficiency
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hereditary angioedema
(inc. bradykinin) |
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C3 deficiency
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severe and recurrent pyogenic sinusy and resp. tract infections
inc. susceptibility to type III hyperSN reactions why incr. susceptibility to type III? |
C3 responsible for removing IC from bloodstream!
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C5-C9 deficiency
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Neisseria bacteremia
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DAF (GPI anchored ez) deficiency
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complement mediated lysis of RBCs and PNH
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To Be Healed Rapidly, give preformed ab following exposure to the following:
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Tetanus
Botulinum HBV Rabies |
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IL2
secreted by? stimulates what? |
secreted by Th1:
stimulates Th1 cells (+ FB) stimulates CD8 cells |
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CD18 deficiency
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causes leukocyte adhesion deficiency
-neutrophilia since the neutrophils cannot exit circulation -cannot get to site of infection either--> reuccrent bacterial infections, absent pus formation, delayed separation of umbilicus |
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Ig that activates complement
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IgG, IgM
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first antibody to be produced in any antigen reaction
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IgM
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sterols in cell membrane
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mycoplasma
what does mycoplasma cause? treatment? |
causes atypical pneumonia
treat with tetracycline or azithromycin (pcn resistant b/c no cell wall) |
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lack muramic acid in cell wall
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chlamydia
what are its two forms |
Elementary body: for Enfecting and Entering via Endocytosis
Reticulate body: replicates in cell by fission |
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cell wall contains mycolic acid
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Mycobacterium
what is the treatment for mycobacterium tb? MAC? Leprosy? |
tb:
RIPE for treatment: rifampin, isoniazid, pyranizamide, ethambutol, MAC: azythromycin, rifampin, ethambutol, streptomycin Leprosy: dapsone, rifampin, clofazimine |