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101 Cards in this Set

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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
pseudomembranous colitis

-presentation
-treatment
-greenish, foul smelling watery diarrhea
-abdominal cramps, fever, leukocytosis, lethargy
-follows clindamycin rx

Treatment:
metronidazole or vancomycin
cAMP inducers
Vibrio + E.Coli (ETEC)= activates AC via Gs

Pertusus= inhibits Gi, causing AC to remain active

Bacillus anthracis= toxin itself is an AC
which organisms do not take gram stain?
"These Rascals May Microscopically Lack Color"

1. Treponema
2. Ricketsia
3. M. TB
4. Mycoplasma
5. Legionella
6. Chlamydia
SHiN bacteria
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)
Encapsulated Bacteria
Kapsules Shield the SHiN

Klebsiella
Salmonella
S. pneumonia
H. influenza
Neisseria
Staphylococcus organisms
-Catalase positive
-found in CLUSTERS

Coagulase + = staph aureus
Coagulase - :
1. S. epidermidis: novobiocin sn; endocarditis
2. S. saprophyticus: novobiocin rs; UTI's
Streptococcus
-Gram Positive Cocci in CHAINS
-Catalase -

3 groups:
alpha: partial hemolysis (green)
beta: complete hemolysis (clear)
gamma: no hemolysis (red)
alpha strep
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
beta strep
complete hemolysis of hb-->bili-->clear

1. S. pyogenes (Group A) : bacitracin sn

2. Group B: bacitracin RS
gamma strep
NO HEMOLYSIS-->RED

1. enterococcus
2. peptostreptococcus (anaerobe)
Gram positive RODS
1. clostridium (anaerobe)
2. corynebacterium
3. listeria
4. bacillus (aerobe)
Gram + branching filaments
1. actinomyces
2. nocardia
Skin Infections caused by both Staph aureus and Strep pyogenes?
1. Folliculitis
2. Cellulitis
3. Impetigo
Gram + infections that cause neonatal death
1. group B
2. E. Coli
3. Listeria
Gram + Obligate Aneorobes
anaerobes Cant Breath Air

1. Clostridium
2. Bacteroides
3. Actinomyces
Obligate Aerobes Gram +
Nagging Pests Must Breathe

1. Nocardia
2. Pseudomonas aeruginosa
3. M. tb
4. bacillus
components of adaptive immunity
1. B cells-->plasma cells
2. T cells
3. antibodies
components of innate immunity
1. neutrophils
2. monocytes-->macrophages
3. dendritic cells
4. NK cells
5. mast cells
6. basophils
7. eosinophils
8. complement
antigen presenting cells
1. macrophages
2. B cells
3. dendritic cells
neutrophil chemotaxis stimulated by:
1. IL-8
2. Leukotriene B4
3. complement C5a
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)
need to give preformed antibodies (passive immunity) after exposure to the following toxins in addition to vaccination
To Be Healed Rapidly:

1. tetanus
2. botulinum
3. HBV
4. Rabies
5. RSV (for premature babies in winter months!)
Positive ANA
SLE
Sjogren's
scleroderma
poly/dermatomyositis
rheumatoid arthritis
juvenile arthritis
mixed connective tissue dz
Bruton's Agammaglobulinemia
-X linked (BOYS)
-B cell def (def. tyrosine kinase gene: low levels of all Ig's)
-recurrent Bacterial infections after 6mos (passive immunity gone)
Thymic aplasia (DiGeorge)
-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
SCID
-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
Chronic mucocutaneous candidiasis
-T cell dysfunction against candida albicans
-treat w/ ketoconazole
X linked immunodeficiencies
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
Wiskott-Aldrish
-thrombocytopenia and purpura
-eczema (TRUNCAL)
-recurrent pyogenic infections: no IgM against capsular polysaccharides of bacteria
-low IgM, high IgA
-X linked
Ataxia Telangiectasia
-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
Selective Ig deficiencies
-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!!
IL-12 receptor deficiency
increased mycobacterial infections!
Phagocyte deficiencies
1. Chronic granulomatous dz
2. Chediak-Higashi dz
3. Job's syndrome (hyperIgE syndrome)
4. leukocyte adhesion def. syndrome
Chronic Granulomatous Dz
-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
Chediak-Higashi dz
-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)
Job's syndrome (hyperIgE syndrome)
-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)
leukocyte adhesion defect syndrome
-Abnormal integrins (cannot integrate into tissues): phagocytes cannot exit circulation
Presentation:
1. delayed separation of umbilicus
2. recurrent bacterial infxns
Deficient C5-C9
Neisseria bacteremia (gonococcal and meningococcal)
germ tube test
-tests for pseudohyphae formation
-dxic of candida albicans
CAMP test
distinguish between Group A and Group B strep

-Group B has + CAMP test (ids partial hemolytic agent produced by group B strep)
Diplococci

Gram -?
gram +?
gram negative diplococci: neisseria

gram positive diplococci: strep pneumo
causes of meningitis

1. most common
2. most severe
3. etc
most common: strep pneumo
most severe: n. meningitis
etc: h. influenza
Interstitial pneumonia (atypical)

1. organisms
2. treatment
1. legionella, mycoplasma, chlamydia pneumonia (also chlamydia psittaci)

2. macrolides (erythromycin, azithromycin)
first and second most common cause of gram - sepsis
1. E.coli
2. Klebsiella
urease + gram negatives
1. h. pylori
2. proteus
infections associated w/ pseudomonas
PSEUDOmonas:
1. pneumonia
2. sepsis
3. external otitis (swimmers)
4. UTI
5. diabetic and drug use osteomyelitis
bilateral bell's palsy

seen in?
1.
2.
1. lyme disease
2. guillan barre
antibiotics for ANAEROBES
1. metronidazole
2. clindamycin
Organisms that don't gram stain
1. Spirochetes: Borrelia, Leptospira, Treponema (BLT)
2. Gardnerella vaginalis (gram variable)
3. Rickettsiae
4. Chlamydia
5. Mycoplasma pneumoniae
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
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
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)
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
photosensitivity causing drugs
SAT for Photo

Sulfonamides
Amiodarone
Tetracyclines
Legionella pneumophilia
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
Haemophilus influenza :

diseases
haEMOPhilus
epiglottitis

meningitis

otitis media

pneumonia
Pseudomonas aeuriginosa :

diseases
PSEUDOmonas
pneumonia (esp. CF)
sepsis (black lesions on skin)
External otitis media (swimmer's ear)
UTIs
Diabetic and Drug use Osteomyelitis

EF2 inactivation by which organisms
1. Corynebacterium
2. Pseudomonas aeruginosa

via EXOTOXIN
capsular K antigen
virulence factor of enterobactericeae:

COFFEe

E. coli, salmonella, shigella, klebsiella, enterobacter, serratia, proteus
Capsular
O antigen
Flagellar antigen
Ferment glucose
Enterobactericiae
Klebsiella
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
Virulence of Shigella vs. Salmonella
Shigella > Salmonella
(10 org vs. 100000 org)
Spirochetes

1. Members
2. Staining
Borrelia (wright's or giemsa stain)
Leptospira
Treponema (dark-field microscopy)
Organisms found in animal urine
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
Lyme Disease
-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)
VDRL positive but not an STD
T. Pertenue

Causes?
Yaws: infection of skin, bone and joints

heal with KELOIDS (excess collagen): limb and nasal deformities
disease of the tropics
rash on palms and soles
1. syphilis (maculopapular rash)
2. rickettsiae
3. coxsackie virus (migrates to wrist, ankles and then TRUNK)
argyll robertson pupil
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)
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)
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
agent that causes Q fever
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)
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
why are rickettsia and chlamydia OBLIGATE intracellular organisms?
Rickettsia: need CoA and NAD+

Chlamydia: cannot make their own ATP

Treatment for either organism?
Tetracycline (also erythromycin for chlamydia)
what makes chlamydial cell wall unique?
lacks muramic acid
chlamydia trachomatis SEROTYPES
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!)
Upper limb, lateral breast lymph drainage
axillary
stomach lymph drainage
celiac
duodenum, jejunum lymph drainage
super mesenteric
sigmoid colon lymph drainage
colic--> inf. mesenteric
rectum, anal canal above pectinate line lymph drainage
internal iliac
anal canal below pectinate line lymph drainage
superficial inguinal
testes lymph drainage
superficial and deep plexus-->para aortic
scrotum lymph drainage
superficial inguinal
thigh (superficial) lymph drainage
superficial inguinal
lateral side of dorsum of foot lymph drainage
popliteal
right side of head and right arm lymph drainage
right lymphatic duct
thoracic duct
drains entire body except right half of head and right arm
acute phase reactants
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
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
C1 esterase deficiency
hereditary angioedema
(inc. bradykinin)
C3 deficiency
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!
C5-C9 deficiency
Neisseria bacteremia
DAF (GPI anchored ez) deficiency
complement mediated lysis of RBCs and PNH
To Be Healed Rapidly, give preformed ab following exposure to the following:
Tetanus
Botulinum
HBV
Rabies
IL2

secreted by?
stimulates what?
secreted by Th1:

stimulates Th1 cells (+ FB)
stimulates CD8 cells
CD18 deficiency
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
Ig that activates complement
IgG, IgM
first antibody to be produced in any antigen reaction
IgM
sterols in cell membrane
mycoplasma

what does mycoplasma cause? treatment?
causes atypical pneumonia

treat with tetracycline or azithromycin (pcn resistant b/c no cell wall)
lack muramic acid in cell wall
chlamydia

what are its two forms
Elementary body: for Enfecting and Entering via Endocytosis

Reticulate body: replicates in cell by fission
cell wall contains mycolic acid
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