FA - Micro - Clinical Bacteriology Flashcards
Gram(+) + Branching filaments + Aerobe,acid fast.
Nocardia
Gram(+) + Branching filaments + Anaerobe, not acid-fast.
Actinomyces
Gram(+) + Cocci + Catalase(+) + Coagulase (+).
S.aureus
Gram(+) + Cocci + Catalase(+) + Coagulase(-) + Novobiocin (S).
S.epidermidis
Gram(+) + Cocci + Catalase(+) + Coagulase(-) + Novobiocin (R).
S.saprophyticus
Gram(+) + Cocci + Catalase(-).
Streptococcus
Gram(+) + Rods + Anaerobe.
Clostridium
Gram(+) + Rods + Aerobe
Bacillus
Gram(+) + Rods + Acid-fast
Mycobacterium
Gram(+) + Rods.
Corynebacterium + Listeria.
Gram(+) + Cocci + Catalase(-) + Hemolysis(partial hemolysis - green).
α-hemolytic:
- S.pneumoniae
- Viridans streptococci (mutans)
S.pneumoniae features:
- Capsule
- Optochin sensitive
- Bile soluble (lysed by bile)
Viridans streptococci features:
- NO capsule
- Optochin resistant
- Bile insoluble
Gram(+) + Cocci + Catalase(-) + Hemolysis (complete hemolysis - clear).
β-hemolysis:
- Group A (S.pyogenes)
- Group B (S.agalactiae)
Feature of S.pyogenes to distinguish from S.agalactiae?
Bacitracin sensitive.
Gram(+) + Cocci + Catalase(-) + Hemolysis(no hemolysis)
γ-hemolytic:
- Group D (enterococcus)
- Non enterococcus
E.faecalis:
Growth in bile and 6.5% NaCl.
Nonenterococcus, growth in bile, not 6.5% NaCl.
S.bovis.
Either α- or γ- hemolytic:
Enterococcus
α-hemolytic bacteria:
Green ring around colonies on blood agar:
- S.pneumoniae
- Viridans streptococci
β-hemolytic bacteria:
Clear area of hemolysis on blood agar:
- S.aureus
- S.pyogenes
- S.agalactiae
- L.monocytogenes
What does S.aureus cause?
- Inflammatory disease
- Toxin-mediated disease
- MRSA infection
What inflammatory disease does S.aureus cause?
- Skin infections
- Organ abscesses
- Pneumonia (often after influenza virus infection)
- Endocarditis
- Osteomyelitis
- Septic arthritis.
What toxin-mediated disease does S.aureus cause?
- Toxic shock syndrome
- Scalded skin syndrome (exfoliative toxin)
- Rapid-onset food poisoning (enterotoxins)
What is the mechanism of MRSA staph resistance?
Altered penicillin-binding protein.
–> Resistant to METHICILLIN + NAFCILLIN.
What is basically the TSST?
A superantigen that binds to MHC II and TCR –> POLYCLONAL T-cell activation.
What predisposes to toxic shock syndrome?
Use of vaginal packing or nasal tampons.
What happens with S.aureus food poisoning?
Ingestion of preformed toxin –> Short incubation period (2-6hr).
Enterotoxin is heat STABLE –> Not destroyed by cooking.
What must be kept in mind about S.epidermidis?
Contaminates blood cultures.
Of which conditions is S.pneumoniae the MCC?
MCC of:
- Meningitis
- Otitis media
- Pneumonia
- Sinusitis
With what is Pneumococcus often associated?
- “Rusty” sputum
- Sepsis in SCA and splenectomy.
- NO virulence without capsule.
Which viridans strep causes subacute bacterial endocarditis at damaged valves?
S.sanguinis
Sanguis = Blood
What does S.sanguinis make?
Dextrans
Where do the dextrans of S.sanguinis bind to?
To fibrin-platelet aggregates on damaged heart valves.
What does S.pyogenes cause?
- Pyogenic –> Pharyngitis, cellulitis, impetigo erysipelas.
- Toxigenic –> Scarlet fever, toxic shock-like syndrome, necrotizing fasciitis.
- Immunologic –> RF, acute GN.
What is the role of ASO titer?
Detects recent S.pyogenes infection.
What are the main criteria for RF?
Jones criteria:
Joints - Polyarthritis O - carditis N - Nodules (subcutaneous) E - Erythema marginatum S - Sydenham chorea
Impetigo or pharyngitis more commonly precedes post-strep GN?
Impetigo.
What happens in Scarlet fever?
- Blanching, sandpaper-like body rash.
- Strawberry tongue.
- Circumoral pallor.
in the setting of group A strep pharyngitis (ERYTHROGENIC TOXIN (++)).
What does S.agalactiae cause?
- Pneumonia
- Meningitis
- Sepsis
mainly in Babies –> Group B for Babies.
What does S.agalactiae produce?
CAMP factor - which enlarges the area of hemolysis formed by S.aureus.
CAMP stands for the authors of the test, not cyclic AMP.
Which test is (+) for S.agalactiae?
Hippurate test
Whens should pregnant women be screened?
At 35-37wks.
What should be done if a positive culture is found?
Patients with (+) culture receive intrapartum penicillin prophylaxis.
To which drug are Enterococci resistant?
Penicillin G
What can the enterococci cause?
- UTI
- Biliary tract infections
- Subacute endocarditis - Following GI/GU procedures.
Lancefield grouping is based on what?
On differences in the C carbohydrate on the bacterial wall.
What hemolysis do Enterococci produce?
VARIABLE hemolysis (either α- or γ-).
What does S.bovis in the blood mean?
Cancer in the colon.
What encodes the diphtheria exotoxin?
A β-prophage.
How does diphtheria toxin inhibits protein synthesis?
Via ADP-ribosylation of EF-2.
What are the symptoms of diphtheria?
- Pseudomembranous pharyngitis (gray-white membrane).
- Lymphadenopathy
- Myocarditis
- Arrhythmias
What is the lab diagnosis of C.diphtheriae?
Based on Gram(+) rods with metachromatic (blue and red) granules and POSITIVE Elek test for toxin.
What colonies does C.diphtheriae produce and in which agar?
Black colonies on cystine-tellurite agar.
What do spores have at their core?
Dipicolinic acid.
How do we kill spores?
Must autoclave by steaming at 121C for 15mins - as is done to surgical equipment.
Spore-forming gram(+) bacteria found in soil:
- B.anthracis
- C.perfringens
- C.tetani
Is Coxiella burnetti spore former?
YES.
What does tetanospasmin block?
Glycine and GABA (both inhibitory) from Renshaw cells in spinal cord.
Is the botox heat labile or heat stable?
Heat labile.
What happens in floppy baby syndrome?
Ingestion of C.botulinum SPORES (not preformed toxin AS IN ADULTS) in honey causes disease.
What does the α-toxin of C.perfringens cause?
It is a lecithinase - a phospholipase - that cause myonecrosis (gas gangrene) and hemolysis.
How many toxins does C.difficile produce?
2 Toxins - A and B.
What is the role of toxin A?
Enterotoxin - Binds to the brush border of the gut.
What is the role of toxin B?
Cytotoxin, causes cytoskeletal disruption via actin depolymerization –> Pseudomembranous colitis –> Diarrhea.
Which 2 drugs are known to cause pseudomembranous colitis?
- Ampicillin
- Clindamycin
- -> Associated with PPI use.
How is C.difficile colitis diagnosed?
By detection of one or both toxins in stool BY PCR.
For recurrent cases of pseudomembranous colitis, what may prevent relapse?
Fecal transplant!!!
What happens in cutaneous anthrax?
PAINLESS PAPULE surrounded by vesicles –> Ulcer with black eschar (painless, necrotic) –> Uncommonly progresses to bacteremia and death.
What happens in pulmonary anthrax?
Inhalation of spores –> Flu-like symptoms that rapidly progress to:
- Fever.
- Pulmonary hemorrhage.
- Mediastinitis.
- Shock.
What is another name for pulmonary anthrax?
Woolsorter’s disease - Inhalation of spores from contaminated wool.
What is the cause of “reheated rice syndrome”?
B.cereus
What are the features of B.cereus poisoning?
- Emetic type –> usually seen with rice and pasta - Nausea and vomiting within 1-5hr.
- Diarrheal type –> Causes watery, non bloody diarrhea, GI pain within 8-18hrs.
What substance is the cause of B.cereus EMETIC TYPE food poisoning?
Cereulide - a preformed toxin.
How is L.monocytogenes acquired?
- Ingestion of unpasteurized dairy products and cold deli meats.
- Via transplacental transmission
- By vaginal transmission during birth.
What does L.monocytogenes form in order to avoid the immune system?
Form “rocket tails” (via actin polymerization) that allow intracellular movement and cell-to-cell spread across cell membranes –> Avoiding antibody.
What is characteristic about L.monocytogenes?
- Tumbling motility in broth.
2. ONLY Gram(+) to produce LPS.
What can L.monocytogenes cause?
- Amnionitis
- Septicemia
- Spontaneous abortion in pregnant women
- Granulomatosis infantiseptica
- Neonatal meningitis
- Meningitis in immunocompromised patients
- Mild gastroenteritis in healthy individuals
What is the treatment of L.monocytogenes?
- Gastroenteritis usually self-limited.
2. Ampicillin in infants, immunocompromised patients, and the elderly in empirical treatment of meningitis.
Where do we find Actinomyces?
- Normal oral flora.
- Reproductive.
- GI.
Where do we find Nocardia?
Found in soil.
What does actinomyces cause?
- Oral/facial abscesses
- Drain through sinus tracts
- Forms yellow “sulfur granules”
- -> CAN ALSO CAUSE PID WITH IUDs.
What does Nocardia cause?
- Pulmonary infections in immunocompromised (can mimic TB but with NEGATIVE PPD).
- Cutaneous infections after trauma in immunocompetent.
How do we treat Actinomyces?
With penicillin.
How do we treat Nocardia?
With sulfonamides (TMP-SMX).
Who usually gets primary TB?
Nonimmune host (usually child).
What happens usually in primary TB?
- Hilar nodes
- Ghon focus (usually in mid zone of lung)
Ghon complex.
What are the 4 possible outcomes of primary TB?
- Heals by fibrosis –> Immunity and hypersensitivity –> Tuberculin(+).
- Progressive lung disease (HIV, malnutrition) –> Death (rare).
- Severe bacteremia –> Miliary TB –> Death.
- Preallergic lymphatic or hematogenous dissemination –> Dormant tubercle bacilli in several organs –> Reactivation in adult life.
Who usually gets secondary TB?
Partially immune hypersensitized host (usually adult) - Reinfection.
What happens in secondary TB?
Fibrocaseous cavitary lesion (usually upper lobes).
What happens when TB gets reactivated?
Extrapulmonary TB:
- CNS –> Parenchymal tuberculoma or meningitis.
- Vertebral body (Pott disease)
- Lymphadenitis
- Renal
- GI + LIVER.
- Adrenals
When is the PPD (+)?
- Current infection
- Past exposure
- BCG vaccinated
When is PPD(-)?
- No infection or anergic (steroids, malnutrition, immunocompromise)
- Sarcoidosis
What is a more specific test for TB than BCG vaccination?
IFN-γ release assay (IGRA) - Has FEWER FALSE(+) from BCG vaccination.
Mention some Mycobacteria.
- M.tuberculosis –> TB, often resistant to drugs.
- M.kansasii –> Pulmonary TB-like symptoms.
- M.avium-intracellulare –> Causes disseminated, non-TB disease in AIDS - often resistant to multiple drugs.
- M. scrofulaceum (cervical lymphadenitis in children).
- M. marinum (hand infection in aquarium handlers).
What is the prophylactic treatment for M.avium-intracellulare?
Azithromycin, when CD4
What are the 5 main TB symptoms?
- Fever
- Night sweats
- Weight loss
- Cough = Productive + Non productive
- Hemoptysis
Cord factor creates …?
A “serpentine cord” appearance in virulent M.tuberculosis strains.
- Inhibits macrophage maturation.
- Induces release of TNF-alpha.
What do sulfatides (SURFACE GLYCOLIPIDS) inhibit?
Phagolysosomal fusion.
What temperature does M.leprae like?
COOL temperatures –> skin and superficial nerves.
–> “GLOVE AND STOCKING” loss of sensation.
Is it possible to grow M.leprae?
CANNOT be grown in vitro.
What is the reservoir of M.leprae in the US?
Armadillos.
What is another name for Leprosy?
Hansen disease.
What are the 2 forms of Hansen disease?
- Tuberculoid
2. Lepromatous
What happens in lepromatous leprosy?
- Presents diffusely over the skin, with leonine facies.
- It is communicable.
- Low cell-mediated immunity with a humoral Th2 response.
What happens in tuberculoid leprosy?
- Limited to a few hypoesthetic, hairless skin plaques.
2. High cell-mediated immunity with a largely Th1-type immune response.
What is the treatment for leprosy?
- Dapsone + rifampin for 6 months for tuberculoid form.
2. Dapsone + rifampin + clofazimine for 2-5yrs for lepromatous form.
Which type of leprosy can be lethal?
LEpromatous –> LEthal.
Gram(-) + Diplococcus + Maltose fermenter.
N.meningitis
Gram(-) + Diplococcus + Maltose NON fermenter.
N.gonorrhoeae
Gram(-) + “Coccoid” rods.
- H.influenza
- Pasteurella
- Brucella
- B.pertussis
- Francisella tularensis
Gram(-) + Oxidase(+) + Comma-shaped + Grows in 42C.
C.jejuni
Gram(-) + Oxidase(+) + Comma-shaped + Grows in alkaline media.
V.cholerae
Gram(-) + Oxidase(+) + Comma-shaped + Produces urease.
H.pylori