3/30 micro Flashcards
Lipoteichoic acid
- where is it found?
- induces what?
Gram (+) cell wall.
- teichoic acids only found in gram (+)s.
- induces TNF & IL-1.
Outer membrane
-whats the antigen?
O polysaccharide
Periplasm
- where is it?
- found in which bugs?
- space btwn cytoplasmic membrane & outer membrane in gram (-) bugs.
- this is the location of beta-lactamases.
dipicolinic acid
-where is this found?
In a spore.
Capsule
-gram (+) or (-)?
Both can have it.
Peptidoglycan
-gram (+) or (-)?
Both
Which bugs are pleomorphic?
Rickettsia & chlamydia.
Which bug has no cell wall?
mycoplasma
Chlamydia
-what does it lack in its cell wall?
muramic acid
Mucicarmine
-helps visualize what?
Capsule
India ink/mucicarmine stain shows bug
-think what?
Cryptococcus neoformans
Chocolate agar with factors V (NAD+) and X (hematin)
-which bug?
H. influenzae
Thayer-Martin
-whats in it?
VPN media
- Vancomycin (inhibits gram-positive organisms)
- Polymyxin (inhibits gram-negative organisms except Neisseria)
- Nystatin (inhibits fungi)
*“to connect to Neisseria, please use your VPN client”
Bordet-Gengou (potato) agar
-which bug?
Bordetella pertussis
Regan-Lowe medium
-which bug?
Bordetella pertussis
Tellurite agar, Löffler medium
-which bug?
C. diphtheriae
Löwenstein-Jensen agar
-which bug?
M. tuberculosis
Eaton agar, requires cholesterol
-which bug?
M. pneumoniae
Pink colonies on MacConkey agar
-which type of bugs?
Lactose-fermenting enterics
How does E. coli look on EMB agar?
-colonies with green metallic sheen
Charcoal yeast extract agar buffered with cysteine & iron
-which bug?
Legionella
Sabouraud agar
-which bug?
Fungi
*“Sab’s a fun guy!”
Obligate aerobes
- name them:
- mnemonic:
Nocardia, Pseudomonas, & MycoBacterium tuberculosis.
*Nagging Pests Must Breathe.
Obligate anaerobes
- name them:
- mnemonic:
Clostridium, Bacteroides, and Actinomyces
*Can’t Breathe Air.
Obligate anaerobes
- which enzymes do they lack?
- unique characteristics?
- catalase &/or superoxide dismutase
- Generally foul smelling (short-chain fatty acids), are difficult to culture, and produce gas in tissue (CO2 &H2).
Which type of ABx is useless against anaerobes bc it req O2 to enter bacterial cell?
aminoglycosides
Obligate intracellular
- which bugs?
- mnemonic:
Rickettsia, Chlamydia, Coxiella burnetti.
*Stay inside (cells) when it is Really Cold.
Encapsulated bacteria
- name them
- mnemonic
SHiNE SKiS.
- Strep pneumoniae
- H. influenzae type B
- N. meningitidis
- E. coli
- Salmonella
- Klebsiella pneumoniae
- group B Strep
Vaccine for encapsulated bugs
-must include what?
-Capsule + protein conjugate serves as an antigen in vaccines.
Aplenic pt
-give them which vaccines?
Give S. pneumoniae, H. influenzae, N. meningitidis vaccines.
Catalase-positive organisms
- name them
- mnemonic:
You need PLACESS for your cats.
Pseudomonas, Listeria, Aspergillus, Candida, E. coli, S. aureus, Serratia.
Why conjugate a capsular antigen w/a protein?
-A polysacc. Ag alone cannot be presented to T cells.
-Conjugating it w/a protein enhances immunogenicity by
promoting T-cell activation and subsequent class switching.
Pneumococcal vaccine
- which vaccine = conjugated to protein
- which vaccine is not?
-PCV (pneumococcal conjugate vaccine, i.e., Prevnar)
-PPSV (pneumococcal polysaccharide vaccine with
no conjugated protein, i.e., Pneumovax)
Name the conjugate vaccines:
- PCV (pneumococcal conjugate vaccine)
- H. influenzae type B (conjugate vaccine)
- Meningococcal vaccine (conjugate vaccine)
Urease-positive bugs
- name them
- mnemonic:
CHuck Norris hates PUNKSS.
- Cryptococcus
- H. pylori
- Proteus
- Ureaplasma
- Nocardia
- Klebsiella
- S. epidermidis
- S. saprophyticus.
Protein A
- whats it do?
- which bug is it found in?
- Binds Fc region of IgG. Prevents opsonization and phagocytosis.
- Expressed by S. aureus.
Which bugs secrete IgA protease?
-mnemonic?
SHiN
-S. pneumoniae, H. influenzae type B, and Neisseria
M protein
- whats it do?
- which bug is it found in?
- Helps prevent phagocytosis.
- Expressed by group A streptococci.
Exotoxin
-coded by?
Plasmid or bacteriophage
Endotoxin
-coded by?
Bacterial chromosome
Exotoxin vs endotoxin
-which one more toxic?
Exotoxin much more toxic.
Exotoxin vs endotoxin
-which one is antigenic?
- Exotoxin = antigenic, induces high-titer antibodies called antitoxins.
- Endotoxin = poorly antigenic
Exotoxin vs endotoxin
-vaccine available?
- Exotoxin: Toxoids used as vaccines.
- Endotoxin: No toxoids formed and no vaccine available
toxoid
-define:
Exotoxin thats been partially denatured by formalin, acid, or heat.
Exotoxin vs endotoxin
-heat stability:
- exotoxin: Destroyed rapidly at 60°C=140F (except staphylococcal enterotoxin).
- endotoxin: Stable at 100°C=212F(=BP of water) for 1 hr.
A-B exotoxin
- function of A subunit?
- function of B subunit?
- A subunit = active subunit w/toxin activity
- B subunit = binds to host, involved w/entry.
Which bugs’ toxin:
-Inactivate elongation factor (EF-2).
- C. diphtheriae = Diphtheria toxin
- Pseudomonas = Exotoxin A
*both = ADP ribosylating A-B toxins.
Which bugs’ toxin:
-Inactivate 60S ribosome by removing adenine from rRNA.
- Shigella = shigatoxin
- EHEC (including O157:H7) = shiga-like toxin
*both = ADP ribosylating A-B toxins.
Shiga toxin
-what can it cause?
-dysentery & HUS.
Shigella vs EHEC
-difference?
EHEC does not invade host cells.
Shiga-like toxin
-what can it cause?
HUS
EHEC: shiga like toxin
-targets which types of cells?
EHEC frequently causes HUS b/c the toxin targets
colonic mucosal cells AND renal endothelial cells
Which bugs make toxins that cause inc. fluid secretion?
ETEC, cholera, Bacillus anthracis.
ETEC:
-what are its 2 toxins & what do they do?
1) LT (heat-labile toxin) = inc. cAMP = Cl secretion into gut & water follows = diarrhea.
2) ST (heat-stabile toxin) = inc. cGMP = dec. NaCl & H2O resorption in gut = diarrhea.
ETEC: 2 toxins
-mnemonic:
Watery diarrhea:
-Labile in the Air (Adenylate cyclase), Stable on the Ground (Guanylate cyclase).
Bacillus anthracis
- whats its toxin that causes fluid secretion?
- hows it work?
Edema factor = mimics cAMP = Likely responsible for characteristic edematous borders of black eschar in cutaneous anthrax.
Vibrio cholerae
- toxin?
- mech?
Cholera toxin = permanently activates Gs = inc. cAMP = inc Cl secretion into the gut = diarrhea.
*Voluminous “rice-water” diarrhea.
Bordetella pertussis
- whats its toxin?
- whats it do?
Pertussis toxin = disabled Gi = inc. cAMP = impairs phagocytosis to permit survival of microbe.
-Whooping cough: the toxin may not be the cause of the cough.
Bordetella pertussis
- what are the 3 stages?
- in which one is pt most contagious?
- in which stage are the “whoops”.
1) Catarrhal = most contagious.
2) Paroxysmal = whooping cough
3) Convalescent stage
Bordetella pertussis
- where does it infect?
- does it cause productive or non-productive cough?
- Invades resp. tract & attaches (via filamentous hemagluttinin) to ciliated epithelium of trachea/bronchi.
- Evades immune response and destroys the ciliated cells causing whooping cough.
- non-productive cough bc cilia is destroyed.
Does bordetella pertussis invade the body?
No.
- It attaches to ciliated epithelial cells of the bronchi and then releases its exotoxins.
- The FHA, a pili rod extending from its surface, is involved in this binding. Antibodies directed against the FHA prevent binding and disease, and thus they are protective.
Bordetella pertussis
-how does it damage the ciliated cells?
Tracheal cytotoxin: This toxin destroys the ciliated epithelial cells, resulting in impaired clearance of bacteria, mucus, and inflammatory exudate. This toxin is probably responsible for the violent cough.
Which bugs have exotoxins that inhibit release of NTs?
C. tetani & C. botulinum.
C. tetani & C. botulinum
- which one causes flaccid paralysis?
- which one causes spastic paralysis?
- Tetani = spastic
- Botulinum = flaccid
*if botox was spastic, it would be against the point cuz then you’d get wrinkles. Whole point is to make the muscle remain flaccid.
Presentation of botulinum poisoning?
- Initially = diplopia & dysphagia.
- Followed by general muscle weakness, which rapidly leads to sudden respiratory paralysis and death.
Which bugs have exotoxins that lyse cell membranes?
-what are their toxins called?
- C. perfringens = Alpha toxin = Phospholipase(lecithinase)
- S. pyogenes = Streptolysin O = lyses RBCs
What will WBC count look like in pertussis infection?
It will look like a viral infection = more lymphocytes than neutros.
Which bugs have superantigens that can cause shock?
-name the toxins:
- S. aureus = Toxic shock syndrome toxin (TSST-1)
- S. pyogenes = Exotoxin A
How do superantigens work?
-what chemicals do they cause to be released?
-Bring MHC II and TCR in proximity to outside of antigen binding site to cause overwhelming release of IFN-γ and IL-2 => shock.
Toxic shock syndrome:
-Sxs:
Fever, rash, shock.
How does endotoxin lead to DIC?
-activates what mediator?
Activates tissue factor
Tissue factor
- aka?
- which coag. pathway does it activate?
- aka thromboplastin
- Extrinsic pathway.
Which bugs use transformation more than most?
- mnemonic:
- what else do these bugs have in common?
SHiN
- S. pneumoniae
- H. influenzae type B
- Neisseria
*these all have IgA protease.
Bacterial Conjugation: F+ × F–
- whats transferred?
- are chromosomal genes transferred?
- is plasmid transferred?
- plasmid is replicated and transferred.
- no chromosomal genes are transferred.
*key = plasmid is replicated first, so after conjugation, both bugs are F+.
If F+ plasmid is incorporated into bacterial chromosomal DNA, what do you call it?
-termed high-frequency recombination (Hfr) cell.
Bacterial Conjugation: Hfr × F–
- whats transferred?
- are chromosomal genes transferred?
- is plasmid transferred?
- Replication of incorporated plasmid DNA may include some flanking chromosomal DNA.
- Transfer of plasmid and chromosomal genes.
Transposition
-how can this lead to ABx resistance spread?
- Segment of DNA (transposon) that can “jump” (excision and reintegration) from one location to another, can transfer genes from plasmid to chromosome and vice versa.
- When excision occurs, may include some flanking chromosomal DNA, which can be incorporated into a plasmid and transferred to another bacterium.
- Examples include antibiotic resistance genes on R plasmid.
Genes for the following 5 bacterial toxins are encoded in a lysogenic phage:
-mnemonic:
ABCDE
- ShigA-like toxin
- Botulinum toxin (certain strains)
- Cholera toxin
- Diphtheria toxin
- Erythrogenic toxin of S. pyogenes (scarlet fever)
Gram (+) rods
- name them
- mnemonic:
from CC to MLB - Grant uses a rod (baseball bat).
- Clostridium (anaerobe)
- Corynebacterium
- Listeria
- Bacillus (aerobe)
- Mycobacterium
Bile soluble
-does it survive in bile?
No
-its lysed in bile.
Which bug grows in 6.5% NaCl?
Enterococcus
α-hemolytic bacteria
-what color ring in blood agar?
green
β-hemolytic bacteria
-what color ring in blood agar?
clear area
Coagulase
- how does it cause coagulation?
- what does coagulase allow the bug to do?
- Activates prothrombin.
- form a fibrin clot around itself => abscess.
S. Aureus
-commonly colonizes where?
Nose
Minor skin infections are usually caused by which bugs?
Almost exclusively caused by either S. pyogenes (GAS) or by S. aureus.
Scalded skin syndrome
- which bug?
- which toxin?
- mechanism?
- which disease has similar process going on?
- S. aureus = exfoliative toxin
- Toxin cleaves desmoglein in desmosomes of skin, which attach keratinocytes together in stratum spinosum.
*Pemphigus vulgaris = IgG against desmoglein.
S. aureus
- toxic shock: which toxin?
- why were women getting this disease more than men?
-tampons and TSST-1 from staph aureus.
MRSA
-how did it gain resistance to methicillin & nafcillin?
Altered penicillin-binding proteins (PBPs)
-transpeptidase = PBP
S. Aureus
-problems caused by exotoxin release:
- gastroenteritis
- toxic shock
- scalded skin syndrome
Endocarditis of artificial heart valves
- which bug?
- Tx:
S. epidermidis
-vanco
Strep Pneumo
- main disease it causes:
- mnemonic:
MOPS
- meningitis
- otitis media (in children)
- pneumonia
- sinusitis
Strep Pneumo
-whats it look like?
lancet-shaped, gram (+) diplococci.
- encapsulated
- IgA protease
Strep pneumo has no virulence w/o its _______.
Capsule
Strep viridans:
-which one causes dental caries?
Streptococcus mutans
Strep viridans:
- which one causes subacute bacterial endocarditis at damaged valves?
- what allows it to infect the cardiac valves?
S. sanguinis
- These bacteria produce an extracellular dextran which bind to fibrin-platelet aggregates on damaged heart valves.
- dextrans also allow binding to tooth enamel.
Which bug synthesizes dextrans from glucose?
-and what does it allow it to bind to?
Strep. viridans => S. sanguinis
- which bind to fibrin-platelet aggregates on damaged heart valves.
- also allows binding to tooth enamel.
*this is why it causes subacute endo, needs fibrin aggregates to attach to the valves. So need previous
damage.
Scalded skin syndrome = from which bug?
S. aureus
Scarlet fever = from which bug?
Strep. pyogenes.
M-protein
- seen in which bug?
- function?
- Abs to it: pros & cons?
- Strep. pyogenes
- prevents phagocytosis
- Abs against M-protein enhance host defense BUT can give rise to rheumatic fever bc they’re very similar to cardiac myocyte myosin chain = molecular mimicry.
ASO titers
-good for detecting what?
Recent S. pyogenes infection
-these Ab titers only high during during infection.
Strep. pyogenes: rheumatic fever
-what are criteria for Dx rheumatic fever?
J♥NES criteria for rheumatic fever
- Joints—polyarthritis
- ♥—carditis
- Nodules (subcutaneous)
- Erythema marginatum
- Sydenham chorea
PSGN
-preceded by what?
strep pyogenes pharyngitis OR impetigo.
*Impetigo more commonly precedes glomerulonephritis than pharyngitis.
rheumatic fever
-preceded by what?
strep pyogenes pharyngitis
Scarlet fever
- which bug?
- mechanism?
- Sxs:
- strep pyogenes
- Exotoxin (pyrogenic/erythrogenic) = produces fever (so it is pyrogenic) and causes a scarlet-red rash.
- The rash begins on the trunk and neck, and then spreads to the extremities, sparing the face. The skin may peel off in fine scales during healing.
- scarlet rash with sandpaper-like texture, strawberry tongue, circumoral pallor.
Scarlet fever
-how does the erythrogenic toxin cause the rash/desquamation?
Erythrogenic toxin is known to damage the plasma membranes of blood capillaries under the skin and produce a red skin rash.
Scarlet fever vs Kawasaki
-what does kawasakis have that scarlet fever doesnt?
Kawasakis has bilateral conjunctivitis.
Neonatal meningitis vs adult meningitis
-difference in presentation?
neonatal meningitis may not present w/stiff neck.
GBS
-what diseases can it cause?
Pneumonia, meningitis, strep.
Mucormycosis
-affects what type of pts?
DKA & immunosuppressed.
-ie. leukemic pts.
Aspergillus vs Mucor
-diff in appearance?
- Mucor = 90 degree angles, non-septate.
- Aspergillus = 45 degree angles, septate.
EHEC: verotoxin
-aka?
shiga-like toxin
Neonatal meningitis: 0-3 months
-#1 cause?
GBS
-followed by E.coli & Listeria.
Meningitis: > 3 months old (infants and adults)
-cause?
- Strep pneumo
- N. meningitidus
Rubeola
-aka?
Measles
Measles
- Sxs:
- mnemonic:
3 C’s
-Cough. coryza, conjunctivitis.
+ koplik spots.
Coccidio vs histo
-distinguishing the spherule vs macro.
- coccidio = spherule filled w/endospores = much LARGER than RBC.
- histo = macro filled w/histo = smaller than RBC.
Rotavirus
-which family of viruses?
Reovirus
Most common cause of acute gastroenteritis in industrialized countries:
campylobacter
Negative sense RNA viruses:
-what must they carry w/them in order to be infectious?
RNA-dependent RNA-polymerase.
recurrent C.dif colitis
-what drug = oral w/little systemic absorption?
fidaxomicin = bacteriocidal *vanc = bacteriostatic.
Which ones the pinworm?
-Tx:
Enterobius vermicularis
- scotch tape one.
- albendazole or pyrantel pamoate.
environmental influences permitting toxin synthesis
-which bugs?
gram (+) spore forming rods
- Bacillus & clostridium
- once spores germinate they can start making spores.
- Need proper environment to germinate.
Why is primaquine added to chloroquine tx of P.vivax/ovale?
To prevent recurrence by killing the dormant hypnozoites in the liver.
P. vivax & P. ovale
-how often does the fever occur?
every 48 hrs.
Prevention of neonatal tetanus:
vaccinating the pregnant mother.
-IgG will cross placenta.
Central catheters
-is the femoral vein a good place for them?
NO
-avoid femoral placement!
acute rheumatic fever
-can it occur after GAS impetigo?
No
-just pharyngitis.
Pyrrolidonyl arylamidase (PYR) test:
- replaced what other test?
- which bug is (+)?
- replaced bacitracin test.
- S. pyogenes = PYR (+).
Pseduohyphae
-think what?
candida
Kinesin
-direction:
anterograde (takes vesicles from neuron soma to axon terminal).
(-) => (+)
- (+) end of MT is at axon terminal.
- (-) end of MT is in neuron soma
Dynein
-direction
retrograde
+) => (-
2 most common causes of hematogenous osteomyelitis
#1 = s. aureus #2 = strep. pyogenes
What skin lesion can pseudomonas cause?
-in which type of pts?
-ecthyma gangrenosum in immunocompromised pts.
What is CAMP factor and who makes it?
- GBS makes CAMP factor.
- enlarges area of hemolysis formed by s. aureus.
What week of gestation do women get screened for GBS?
-if positive, when do they get which ABx?
- Screen pregnant women at 35–37 weeks.
- Patients with (+) culture receive intrapartum penicillin prophylaxis.
GBS strep
-main virulence factor
capsule
Enterococci
-which lancefield group?
D
Group D strep: non-enterococci
-name it:
strep. bovis
Subacute endocarditis in colon cancer patients
-which bug?
Group D strep
- strep bovis.
- or enterococcus s/p GU/GI operations.
Group D strep
-how to differentiate enterococci vs strep bovis?
Only enterococci can grow in 6.5% NaCl, bovis can not.
-both can grow in bile.
Corynebacterium diphtheriae
- how does it get its exotoxin?
- mechanism of exotoxin?
- β-prophage
- Potent exotoxin inhibits protein synthesis via ADP-ribosylation of EF-2.
Diphtheria
- if toxin gets into blood, what cells are preferentially damaged?
- what can this lead to?
Heart & neural cells.
-myocarditis, arrythmias,
Dx of diphtheria
- culture will show what?
- Is there a certain test that can help?
- Gram-positive rods with metachromatic (blue and red) granules.
- Black colonies on cystine-tellurite agar.
- Elek test for toxin.
Diphtheria
-prevention:
-Toxoid vaccine prevents diphtheria (against beta-subunit of toxin).
Diphtheria
-Tx:
1) Antitoxin
2) penicillin/macrolide
3) DPT vaccine.
Elek test
-what is it?
differentiates btwn toxic and
non-toxic strains.
How do you kill spores?
Autoclave: steaming at 121°C for 15 minutes.
Spore forming bugs: -what class are they?
- gram (+) rods
- Bacillus, clostridium.
- coxiella burnetti
Autoclave: why is pressure necessary?
-pressure necessary or all water will evaporate and it will be dry. water will germinate them and make them easier to kill.
Tetanus
-how is Dx made?
Clinically made: good Hx & physical.
Botulinum toxin
-heat labile or heat stabile?
- Labile
* only real heat labile exotoxin = staph aureus enterotoxin.
Botulism
-is there a difference in mechanism of adults getting it vs. babies?
- adults get sick from ingesting pre-formed toxin, not from ingesting the actual bug/spore b/c the bug is outcompeted by our normal flora.
- babies lack the robust intestinal flora to keep c. botulinum at bay = so they can get sick from the spores.
botulinum toxin commonly found in:
Honey & canned goods.
- canned goods = anaerobic environment.
- clostridium = anaerobes.
Hyphae
-only seen in which form of a fungus?
Mold
-Yeast are unicellular fungi that do not grow as hyphae.
Diphtheria toxin
-mech:
ADP-ribosylation of EF-2: inhibits protein synthesis.
Polar granules that stain deeply w/aniline dyes:
C. diphtheria
EF-2: what does it do?
Necessary for tRNA to insert new AAs into growing protein chain during translation.
Pseudomonas
- shape:
- gram stain:
- lactose fermenting?
- oxidase +/-?
- gram (-) rod
- non-lactose fermenting.
- oxidase +
E. coli
-lactose fermenter?
yes
Salmonella + Shigella
- lactose fermenters?
- oxidase +/-?
- None lactose fermenters
- oxidase (-)
H2S prod
- what color on TSI or Hektoen agar?
- shigella or salmonella?
- Black on TSI or Hektoen agar
- salmonella
Where are peyers patches located?
ileum
Shigella
-was makes it cause so much disease? invasion or toxin?
Invasion
*nontoxigenic strains have also been found that cause significant disease.
Secondary bacterial pneumonia after viral URI
-causative agent:
#1 = strep pneumo #2 = staph aureus
Normal CD4 count for healthy adults?
400-1400 cells/uL
Do protozoans incite an eosinophilic response?
No, only invasive helminths.
bacterial vaginosis
-caused by:
gardnerella vaginalis
Gas gangrene
-Tx:
-IV penicillin G
Double zone of hemolysis: beta & alpha
-seen in which bug?
C. perfringens
Anaerobic hemolytic bug:
C. perfringens
C. perfringens
-besides hemolysis & gas gangrene, what can it cause?
Late onset food poisoning.
-we are NOT ingesting preformed toxin here like c. botulinum for example. Here, we ingest the spore, wait for it to germinate, produce toxins, and then we get the diarrhea.
C. dif
- name the 2 toxins & what they cause:
- how do they cause cell death?
-exotoxin A => watery diarrhea
-exotoxin B => pseudomembranous colitis
*these exotoxins both induce APOPTOSIS of epithelial
cells of colonic mucosa.
C. dif
-How to Dx?
- Diagnosed by detection of one or both toxins in stool.
- lots of pts are colonized w/c. dif but not all of those are strains that produce the toxin. So you check for the toxin, not the bug.
What is unique about bacillus anthracis capsule?
-whats it made of?
The only bacterium with a polypeptide capsule.
-contains d-glutamate.
Bacillus anthracis
- what are the 2 toxins?
- can they cause pathology on their own?
- lethal factor (LF) and edema factor (EF).
- both toxins must be present to cause symptoms.
Bacillus anthracis
-edema factor: mechanism?
-acts as adenylate cyclase, inc. cAMP intracellularly.
Bacillus anthracis
-lethal factor: mechanism?
- exotoxin that acts as a protease and cleaves MAP KINASE.
- Map kinase = controls cell growth.
- So LF responsible for tissue necrosis. This causes tissue necrosis thats seen in the black eschar.
Bacillus anthracis
-Tx:
fluoroquinolones or doxycycline
Cutaneous anthrax
-black eschar: is it painful?
No - its painless.
Pulmonary anthrax
-what will CXR show?
Widened mediastinum on CXR in the 2nd phase.
Bacillus cereus
-whats the pre-formed toxin called that causes the N/V?
Cereulide
Bacillus cereus
- emetic type:
- diarrheal type:
- Emetic type = N/V w/in 1–5 hr.
- Diarrheal type = watery, nonbloody diarrhea and GI pain within 8–18 hr.
Actinomyces vs. Nocardia
-gram + or -?
gram (+)
- Where is actinomyces found?
- Where is nocardia found?
- actinomyces = normal flora of mouth.
- nocardia = soil.
Nocardia
-what does it cause in immunocompromised?
-Pulmonary infections in immunocompromised.
Nocardia
-what does it cause in immunocompetant?
-Cutaneous infections after trauma in immunocompetent.
PPD (+) if:
-current infection, past exposure, or BCG vaccinated.
PPD (-) if:
-no infection or anergic (steroids, malnutrition, immunocompromise) and in sarcoidosis.
What the most specific TB test?
-why is it more specific?
Interferon-γ release assay (IGRA) is a more specific test; has fewer false positives from BCG vaccination.
TB
-which virulence factor allows it intracellular bacterial prolif? AKA which ones allow it to survive the phagolysosome?
-sulfatide (surface glycolipids) inhibit phagolysosomal fusion.
reactivation TB
-seen in which part of lung?
apex
-b/c oxygen tension is highest at apex of lung due to dec. pulm circulation there, and TB = ob. aerobe
TB
-is it intracellular? if so, which cells does it invade?
yes. macros.
M. avium–intracellulare
-prophylaxis:
azithromycin
M. avium–intracellulare
-grows best in what condition?
grows best at 41 C.
Which agar grows TB best?
Löwenstein-Jensen agar
Cord factor
- what bug is it in?
- what does it do?
-Virulent strains of TB
-inhibits macrophage maturation and induces release of
TNF-α.
TB
-what is its main virulence factor?
Cord factor.
Why would cord factor want to induce release of TNF-alpha?
the cord factor induces the macro to release TNF-alpha which is pro-inflammatory. Why would the bug want to inc. inflammation/macrophage activation? Isn’t that bad for the bug? No, because although it wont be able to spread, the bug knows that we will form a granuloma around it, which it can survive and lay dormant in.
Mycobacterium leprae
- which tissues does it invade?
- why?
Likes cool temperatures (infects skin and superficial nerves—“glove and stocking” loss of sensation).
Mycobacterium leprae
-can it be grown in vitro?
Can NOT be grown in vitro.
Mycobacterium leprae
-whats its reservoir in the U.S.?
Reservoir in United States: armadillos.
Leprosy
-aka?
Hansen disease
Lepromatous leprosy:
- better or worse than tuberculoid?
- whats the primary immune defense?
- worse
- characterized by low cell-mediated immunity with a humoral Th2 response.
Tuberculoid leprosy
- better or worse than lepromatous?
- whats the primary immune defense?
- better
- characterized by high cell-mediated immunity with a largely Th1-type immune response.
Tuberculoid leprosy
-Sxs:
-limited to a few hypoesthetic, hairless skin plaques.
Lepromatous leprosy:
-Sxs:
-presents diffusely over the skin, with leonine (lion-like) facies, and is communicable.
Lepromatous leprosy:
-Tx:
Dapsone, rifampin, and clofazimine for 2–5 years for lepromatous form.
Tuberculoid leprosy
Dapsone and rifampin for 6 months for tuberculoid form.
clofazimine
-what is it?
Used to treat lepromatous leprosy.
Tuberculoid v Lepromatous
-Will their biopsies differ?
- If you biopsy Tuberculoid lesions = small amnts of bacteria, b/c its contained.
- If you biopsy Lepromatous lesions = lots of bacteria present
Lepromatous
-fertility issues?
-Internal testicular damage => infertility.
Leposy
-most commonly involved nerves?
The most frequently enlarged nerves are those closest to the skin-the greater auricular, the ulnar (above the elbow), the posterior tibial, and the peroneal (over the fibula head).
