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Microbiology > FA - Micro - Clinical Bacteriology > Flashcards

FA - Micro - Clinical Bacteriology Flashcards

0
Q

Gram(+) + Branching filaments + Aerobe,acid fast.

A

Nocardia

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1
Q

Gram(+) + Branching filaments + Anaerobe, not acid-fast.

A

Actinomyces

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2
Q

Gram(+) + Cocci + Catalase(+) + Coagulase (+).

A

S.aureus

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3
Q

Gram(+) + Cocci + Catalase(+) + Coagulase(-) + Novobiocin (S).

A

S.epidermidis

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4
Q

Gram(+) + Cocci + Catalase(+) + Coagulase(-) + Novobiocin (R).

A

S.saprophyticus

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5
Q

Gram(+) + Cocci + Catalase(-).

A

Streptococcus

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6
Q

Gram(+) + Rods + Anaerobe.

A

Clostridium

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7
Q

Gram(+) + Rods + Aerobe

A

Bacillus

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8
Q

Gram(+) + Rods + Acid-fast

A

Mycobacterium

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9
Q

Gram(+) + Rods.

A

Corynebacterium + Listeria.

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10
Q

Gram(+) + Cocci + Catalase(-) + Hemolysis(partial hemolysis - green).

A

α-hemolytic:

  1. S.pneumoniae
  2. Viridans streptococci (mutans)
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11
Q

S.pneumoniae features:

A
  1. Capsule
  2. Optochin sensitive
  3. Bile soluble (lysed by bile)
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12
Q

Viridans streptococci features:

A
  1. NO capsule
  2. Optochin resistant
  3. Bile insoluble
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13
Q

Gram(+) + Cocci + Catalase(-) + Hemolysis (complete hemolysis - clear).

A

β-hemolysis:

  1. Group A (S.pyogenes)
  2. Group B (S.agalactiae)
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14
Q

Feature of S.pyogenes to distinguish from S.agalactiae?

A

Bacitracin sensitive.

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15
Q

Gram(+) + Cocci + Catalase(-) + Hemolysis(no hemolysis)

A

γ-hemolytic:

  1. Group D (enterococcus)
  2. Non enterococcus
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16
Q

E.faecalis:

A

Growth in bile and 6.5% NaCl.

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17
Q

Nonenterococcus, growth in bile, not 6.5% NaCl.

A

S.bovis.

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18
Q

Either α- or γ- hemolytic:

A

Enterococcus

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19
Q

α-hemolytic bacteria:

A

Green ring around colonies on blood agar:

  1. S.pneumoniae
  2. Viridans streptococci
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20
Q

β-hemolytic bacteria:

A

Clear area of hemolysis on blood agar:

  1. S.aureus
  2. S.pyogenes
  3. S.agalactiae
  4. L.monocytogenes
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21
Q

What does S.aureus cause?

A
  1. Inflammatory disease
  2. Toxin-mediated disease
  3. MRSA infection
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22
Q

What inflammatory disease does S.aureus cause?

A
  1. Skin infections
  2. Organ abscesses
  3. Pneumonia (often after influenza virus infection)
  4. Endocarditis
  5. Osteomyelitis
  6. Septic arthritis.
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23
Q

What toxin-mediated disease does S.aureus cause?

A
  1. Toxic shock syndrome
  2. Scalded skin syndrome (exfoliative toxin)
  3. Rapid-onset food poisoning (enterotoxins)
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24
Q

What is the mechanism of MRSA staph resistance?

A

Altered penicillin-binding protein.

–> Resistant to METHICILLIN + NAFCILLIN.

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25
Q

What is basically the TSST?

A

A superantigen that binds to MHC II and TCR –> POLYCLONAL T-cell activation.

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26
Q

What predisposes to toxic shock syndrome?

A

Use of vaginal packing or nasal tampons.

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27
Q

What happens with S.aureus food poisoning?

A

Ingestion of preformed toxin –> Short incubation period (2-6hr).
Enterotoxin is heat STABLE –> Not destroyed by cooking.

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28
Q

What must be kept in mind about S.epidermidis?

A

Contaminates blood cultures.

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29
Q

Of which conditions is S.pneumoniae the MCC?

A

MCC of:

  1. Meningitis
  2. Otitis media
  3. Pneumonia
  4. Sinusitis
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30
Q

With what is Pneumococcus often associated?

A
  1. “Rusty” sputum
  2. Sepsis in SCA and splenectomy.
  3. NO virulence without capsule.
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31
Q

Which viridans strep causes subacute bacterial endocarditis at damaged valves?

A

S.sanguinis

Sanguis = Blood

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32
Q

What does S.sanguinis make?

A

Dextrans

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33
Q

Where do the dextrans of S.sanguinis bind to?

A

To fibrin-platelet aggregates on damaged heart valves.

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34
Q

What does S.pyogenes cause?

A
  1. Pyogenic –> Pharyngitis, cellulitis, impetigo erysipelas.
  2. Toxigenic –> Scarlet fever, toxic shock-like syndrome, necrotizing fasciitis.
  3. Immunologic –> RF, acute GN.
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35
Q

What is the role of ASO titer?

A

Detects recent S.pyogenes infection.

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36
Q

What are the main criteria for RF?

A

Jones criteria:

Joints - Polyarthritis
O - carditis
N - Nodules (subcutaneous)
E - Erythema marginatum
S - Sydenham chorea
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37
Q

Impetigo or pharyngitis more commonly precedes post-strep GN?

A

Impetigo.

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38
Q

What happens in Scarlet fever?

A
  1. Blanching, sandpaper-like body rash.
  2. Strawberry tongue.
  3. Circumoral pallor.
    in the setting of group A strep pharyngitis (ERYTHROGENIC TOXIN (++)).
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39
Q

What does S.agalactiae cause?

A
  1. Pneumonia
  2. Meningitis
  3. Sepsis
    mainly in Babies –> Group B for Babies.
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40
Q

What does S.agalactiae produce?

A

CAMP factor - which enlarges the area of hemolysis formed by S.aureus.
CAMP stands for the authors of the test, not cyclic AMP.

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41
Q

Which test is (+) for S.agalactiae?

A

Hippurate test

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42
Q

Whens should pregnant women be screened?

A

At 35-37wks.

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43
Q

What should be done if a positive culture is found?

A

Patients with (+) culture receive intrapartum penicillin prophylaxis.

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44
Q

To which drug are Enterococci resistant?

A

Penicillin G

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45
Q

What can the enterococci cause?

A
  1. UTI
  2. Biliary tract infections
  3. Subacute endocarditis - Following GI/GU procedures.
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46
Q

Lancefield grouping is based on what?

A

On differences in the C carbohydrate on the bacterial wall.

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47
Q

What hemolysis do Enterococci produce?

A

VARIABLE hemolysis (either α- or γ-).

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48
Q

What does S.bovis in the blood mean?

A

Cancer in the colon.

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49
Q

What encodes the diphtheria exotoxin?

A

A β-prophage.

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50
Q

How does diphtheria toxin inhibits protein synthesis?

A

Via ADP-ribosylation of EF-2.

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51
Q

What are the symptoms of diphtheria?

A
  1. Pseudomembranous pharyngitis (gray-white membrane).
  2. Lymphadenopathy
  3. Myocarditis
  4. Arrhythmias
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52
Q

What is the lab diagnosis of C.diphtheriae?

A

Based on Gram(+) rods with metachromatic (blue and red) granules and POSITIVE Elek test for toxin.

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53
Q

What colonies does C.diphtheriae produce and in which agar?

A

Black colonies on cystine-tellurite agar.

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54
Q

What do spores have at their core?

A

Dipicolinic acid.

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55
Q

How do we kill spores?

A

Must autoclave by steaming at 121C for 15mins - as is done to surgical equipment.

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56
Q

Spore-forming gram(+) bacteria found in soil:

A
  1. B.anthracis
  2. C.perfringens
  3. C.tetani
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57
Q

Is Coxiella burnetti spore former?

A

YES.

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58
Q

What does tetanospasmin block?

A

Glycine and GABA (both inhibitory) from Renshaw cells in spinal cord.

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59
Q

Is the botox heat labile or heat stable?

A

Heat labile.

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60
Q

What happens in floppy baby syndrome?

A

Ingestion of C.botulinum SPORES (not preformed toxin AS IN ADULTS) in honey causes disease.

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61
Q

What does the α-toxin of C.perfringens cause?

A

It is a lecithinase - a phospholipase - that cause myonecrosis (gas gangrene) and hemolysis.

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62
Q

How many toxins does C.difficile produce?

A

2 Toxins - A and B.

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63
Q

What is the role of toxin A?

A

Enterotoxin - Binds to the brush border of the gut.

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64
Q

What is the role of toxin B?

A

Cytotoxin, causes cytoskeletal disruption via actin depolymerization –> Pseudomembranous colitis –> Diarrhea.

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65
Q

Which 2 drugs are known to cause pseudomembranous colitis?

A
  1. Ampicillin
  2. Clindamycin
    - -> Associated with PPI use.
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66
Q

How is C.difficile colitis diagnosed?

A

By detection of one or both toxins in stool BY PCR.

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67
Q

For recurrent cases of pseudomembranous colitis, what may prevent relapse?

A

Fecal transplant!!!

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68
Q

What happens in cutaneous anthrax?

A

PAINLESS PAPULE surrounded by vesicles –> Ulcer with black eschar (painless, necrotic) –> Uncommonly progresses to bacteremia and death.

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69
Q

What happens in pulmonary anthrax?

A

Inhalation of spores –> Flu-like symptoms that rapidly progress to:

  1. Fever.
  2. Pulmonary hemorrhage.
  3. Mediastinitis.
  4. Shock.
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70
Q

What is another name for pulmonary anthrax?

A

Woolsorter’s disease - Inhalation of spores from contaminated wool.

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71
Q

What is the cause of “reheated rice syndrome”?

A

B.cereus

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72
Q

What are the features of B.cereus poisoning?

A
  1. Emetic type –> usually seen with rice and pasta - Nausea and vomiting within 1-5hr.
  2. Diarrheal type –> Causes watery, non bloody diarrhea, GI pain within 8-18hrs.
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73
Q

What substance is the cause of B.cereus EMETIC TYPE food poisoning?

A

Cereulide - a preformed toxin.

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74
Q

How is L.monocytogenes acquired?

A
  1. Ingestion of unpasteurized dairy products and cold deli meats.
  2. Via transplacental transmission
  3. By vaginal transmission during birth.
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75
Q

What does L.monocytogenes form in order to avoid the immune system?

A

Form “rocket tails” (via actin polymerization) that allow intracellular movement and cell-to-cell spread across cell membranes –> Avoiding antibody.

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76
Q

What is characteristic about L.monocytogenes?

A
  1. Tumbling motility in broth.

2. ONLY Gram(+) to produce LPS.

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77
Q

What can L.monocytogenes cause?

A
  1. Amnionitis
  2. Septicemia
  3. Spontaneous abortion in pregnant women
  4. Granulomatosis infantiseptica
  5. Neonatal meningitis
  6. Meningitis in immunocompromised patients
  7. Mild gastroenteritis in healthy individuals
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78
Q

What is the treatment of L.monocytogenes?

A
  1. Gastroenteritis usually self-limited.

2. Ampicillin in infants, immunocompromised patients, and the elderly in empirical treatment of meningitis.

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79
Q

Where do we find Actinomyces?

A
  1. Normal oral flora.
  2. Reproductive.
  3. GI.
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80
Q

Where do we find Nocardia?

A

Found in soil.

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81
Q

What does actinomyces cause?

A
  1. Oral/facial abscesses
  2. Drain through sinus tracts
  3. Forms yellow “sulfur granules”
    - -> CAN ALSO CAUSE PID WITH IUDs.
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82
Q

What does Nocardia cause?

A
  1. Pulmonary infections in immunocompromised (can mimic TB but with NEGATIVE PPD).
  2. Cutaneous infections after trauma in immunocompetent.
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83
Q

How do we treat Actinomyces?

A

With penicillin.

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84
Q

How do we treat Nocardia?

A

With sulfonamides (TMP-SMX).

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85
Q

Who usually gets primary TB?

A

Nonimmune host (usually child).

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86
Q

What happens usually in primary TB?

A
  1. Hilar nodes
  2. Ghon focus (usually in mid zone of lung)
    Ghon complex.
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87
Q

What are the 4 possible outcomes of primary TB?

A
  1. Heals by fibrosis –> Immunity and hypersensitivity –> Tuberculin(+).
  2. Progressive lung disease (HIV, malnutrition) –> Death (rare).
  3. Severe bacteremia –> Miliary TB –> Death.
  4. Preallergic lymphatic or hematogenous dissemination –> Dormant tubercle bacilli in several organs –> Reactivation in adult life.
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88
Q

Who usually gets secondary TB?

A

Partially immune hypersensitized host (usually adult) - Reinfection.

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89
Q

What happens in secondary TB?

A

Fibrocaseous cavitary lesion (usually upper lobes).

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90
Q

What happens when TB gets reactivated?

A

Extrapulmonary TB:

  1. CNS –> Parenchymal tuberculoma or meningitis.
  2. Vertebral body (Pott disease)
  3. Lymphadenitis
  4. Renal
  5. GI + LIVER.
  6. Adrenals
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91
Q

When is the PPD (+)?

A
  1. Current infection
  2. Past exposure
  3. BCG vaccinated
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92
Q

When is PPD(-)?

A
  1. No infection or anergic (steroids, malnutrition, immunocompromise)
  2. Sarcoidosis
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93
Q

What is a more specific test for TB than BCG vaccination?

A

IFN-γ release assay (IGRA) - Has FEWER FALSE(+) from BCG vaccination.

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94
Q

Mention some Mycobacteria.

A
  1. M.tuberculosis –> TB, often resistant to drugs.
  2. M.kansasii –> Pulmonary TB-like symptoms.
  3. M.avium-intracellulare –> Causes disseminated, non-TB disease in AIDS - often resistant to multiple drugs.
  4. M. scrofulaceum (cervical lymphadenitis in children).
  5. M. marinum (hand infection in aquarium handlers).
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95
Q

What is the prophylactic treatment for M.avium-intracellulare?

A

Azithromycin, when CD4

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96
Q

What are the 5 main TB symptoms?

A
  1. Fever
  2. Night sweats
  3. Weight loss
  4. Cough = Productive + Non productive
  5. Hemoptysis
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97
Q

Cord factor creates …?

A

A “serpentine cord” appearance in virulent M.tuberculosis strains.

  1. Inhibits macrophage maturation.
  2. Induces release of TNF-alpha.
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98
Q

What do sulfatides (SURFACE GLYCOLIPIDS) inhibit?

A

Phagolysosomal fusion.

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99
Q

What temperature does M.leprae like?

A

COOL temperatures –> skin and superficial nerves.

–> “GLOVE AND STOCKING” loss of sensation.

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100
Q

Is it possible to grow M.leprae?

A

CANNOT be grown in vitro.

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101
Q

What is the reservoir of M.leprae in the US?

A

Armadillos.

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102
Q

What is another name for Leprosy?

A

Hansen disease.

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103
Q

What are the 2 forms of Hansen disease?

A
  1. Tuberculoid

2. Lepromatous

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104
Q

What happens in lepromatous leprosy?

A
  1. Presents diffusely over the skin, with leonine facies.
  2. It is communicable.
  3. Low cell-mediated immunity with a humoral Th2 response.
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105
Q

What happens in tuberculoid leprosy?

A
  1. Limited to a few hypoesthetic, hairless skin plaques.

2. High cell-mediated immunity with a largely Th1-type immune response.

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106
Q

What is the treatment for leprosy?

A
  1. Dapsone + rifampin for 6 months for tuberculoid form.

2. Dapsone + rifampin + clofazimine for 2-5yrs for lepromatous form.

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107
Q

Which type of leprosy can be lethal?

A

LEpromatous –> LEthal.

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108
Q

Gram(-) + Diplococcus + Maltose fermenter.

A

N.meningitis

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109
Q

Gram(-) + Diplococcus + Maltose NON fermenter.

A

N.gonorrhoeae

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110
Q

Gram(-) + “Coccoid” rods.

A
  1. H.influenza
  2. Pasteurella
  3. Brucella
  4. B.pertussis
  5. Francisella tularensis
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111
Q

Gram(-) + Oxidase(+) + Comma-shaped + Grows in 42C.

A

C.jejuni

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112
Q

Gram(-) + Oxidase(+) + Comma-shaped + Grows in alkaline media.

A

V.cholerae

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113
Q

Gram(-) + Oxidase(+) + Comma-shaped + Produces urease.

A

H.pylori

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114
Q

Gram(-) + Rods + Lactose fermenter + Fast fermenter.

A
  1. Klebsiella
  2. E.coli
  3. Enterobacter
115
Q

Gram(-) + Rods + Lactose fermenter + SLOW fermenter.

A
  1. Citrobacter

2. Serratia

116
Q

Gram(-) + Rods + Lactose NON fermenter + Oxidase(-).

A
  1. Shigella
  2. Salmonella
  3. Proteus
  4. Yersinia
117
Q

Gram(-) + Rods + Lactose NON fermenter + Oxidase(+).

A

Pseudomonas

118
Q

Lactose-fermenting enteric bacteria grow what colonies on MacConkey agar?

A

PINK colonies.

119
Q

Does E.coli produce β-galactosidase?

A

Yes - Breaks down lactose into glucose and galactose.

120
Q

Lactose fermenters in EMB agar produce what colonies?

A

PURPLE/BLACK colonies. (E.coli –> purple with a green sheen).

121
Q

What about penicillin and gram(-) bugs?

A

Penicillin G and Vancomycin CANNOT entry gram(-).

Gram(-) may be susceptible to penicillin derivatives such as ampicillin and amoxicillin.

122
Q

Which enzyme do BOTH Neisseria produce?

A

IgA protease.

123
Q

Meningococci or gonococci have polysaccharide capsule?

A

Meningococci.

124
Q

Is there a vaccine for gonorrhea?

A

NO - Due to rapid antigenic variation of pilus proteins.

125
Q

Is there a vaccine for meningitis?

A

Yes, but type B NOT WIDELY AVAILABLE.

126
Q

How is meningococci transmitted?

A

Respiratory and oral secretions.

127
Q

What do gonococci cause?

A
  1. Gonorrhea
  2. Septic arthritis
  3. Neonatal conjunctivitis
  4. PID
  5. F-H-C syndrome
128
Q

What should be given to neonates to prevent from neonatal conjunctivitis?

A

Erythromycin

129
Q

What do we give for meningitis PROPHYLAXIS?

A
  1. Rifampin
  2. Ciprofloxacin
  3. Ceftriaxone - prophylaxis in close contacts.
130
Q

How do we treat N.gonorrhoeae infection?

A
  1. Ceftriaxone

2. Azithromycin/doxycycline for possible Chlamydia coinfection.

131
Q

What is the treatment for meningitis?

A

Ceftriaxone or Penicillin G.

132
Q

What do nontypeable strains of H.influenza cause?

A

MCC of mucosal infections:

  1. Otitis media
  2. Conjunctivitis
  3. Bronchitis
    - -> As well as invasive infections since the vaccine for capsular type B was introduced.
133
Q

Does H.influenza produce IgA protease?

A

Yes

134
Q

What does Haemophilus cause?

A
  1. Epiglottitis
  2. Meningitis
  3. Otitis media
  4. Pneumonia
135
Q

Does H.influenza cause the flu?

A

NO - Influenza virus does.

136
Q

What vaccine do we have for H.influenza?

A

Contains type B capsular polysaccharide (polyribosylribitol phosphate) conjugated to diphtheria toxoid or other protein.
Given between 2 and 18 months of age.

137
Q

Does L.pneumophila gram stain good?

A

No, poor gram staining - Use silver stain.

138
Q

Where does L.pneumophila grow?

A

Grow on charcoal yeast extract culture with iron and cysteine.

139
Q

How is L.pneumophila detected clinically?

A

By the presence of antigen in urine.

140
Q

How is L.pneumophila transmitted?

A

Aerosol transmission from environmental water source habitat (e.g., air conditioning systems, hot water tanks).
NO person-to-person contact.

141
Q

What is the treatment for L.pneumophila?

A

Macrolide or quinolone.

142
Q

What does L.pneumophila cause?

A
  1. Legionnaire’s disease

2. Pontiac fever

143
Q

What happens in legionnaire’s disease?

A
  1. Severe pneumonia –> OFTEN UNILATERAL + LOBAR.
  2. Fever
  3. GI
  4. CNS symptoms
    - -> Common in SMOKERS + CHRONIC LUNG DISEASE.
144
Q

What happens in Pontiac fever?

A

Mild flu-like syndrome.

145
Q

What specific lab finding may L.pneumophila show?

A

HYPOnatremia.

146
Q

Mention some general features of P.aeruginosa.

A
  1. Aerobic + Motile
  2. Non-lactose fermenting
  3. Oxidase (+)
  4. Produces pyocyanin (blue-green pigment)
  5. Has grape-like odor.
147
Q

What is the source for P.aeruginosa?

A

Water

148
Q

What does P.aeruginosa produce?

A
  1. Endotoxin –> Fever, shock
  2. Exotoxin A (inactivates EF-2)
  3. Phospholipase C –> Degrades cell membranes.
  4. Pyocyanin –> Generate ROS.
149
Q

With what is P.aeruginosa associated?

A

PSEUDOMONAS

  1. Pneumonia, pyocyanin.
  2. Sepsis.
  3. Ecthyma gangrenosum.
  4. UTIs.
  5. Diabetes, drug use.
  6. Osteomyelitis (eg puncture wounds).
  7. Mucoid polysaccharide capsule.
  8. Otitis externa (swimmer’s ear).
  9. Nosocomial infections (catheters, equipment).
  10. A exotoxin.
  11. Skin infections (hot tub folliculitis).
150
Q

What is ecthyma gangrenosum?

A
  1. Rapidly progressive, necrotic cutaneous lesions caused by Pseudomonas bacteremia.
  2. Typically seen in immunocompomised patients.
151
Q

What is the treatment for P.aeruginosa?

A

CAMPFIRE

  1. Carbapenems.
  2. Aminoglycosides.
  3. Monobactams.
  4. Polymyxins (eg polymyxin B, colistin).
  5. Fluoroquinolones (eg ciprofloxacin, levofloxacin).
  6. ThIRd- and 4th gen cephalosporins (eg ceftazidime, cefepime).
  7. Extended-spectrum penicillins (eg piperacillin, ticarcillin).
152
Q

What key facts should ring a bell for P.aeruginosa?

A
  1. Water connection –> HOT TUB FOLLICULITIS.
  2. Burn victims
  3. Chronic pneumonia in CF patients associated with a biofilm.
153
Q

Mention the major virulence factors of E.coli.

A
  1. Fimbriae
  2. K capsule
  3. LPS endotoxin
154
Q

What does fimbriae of E.coli do?

A

Cystitis - Pyelonephritis.

155
Q

What does K capsule of E.coli do?

A
  1. Pneumonia

2. Neonatal meningitis

156
Q

What does LPS endotoxin of E.coli do?

A

Septic shock.

157
Q

What is the toxin and mechanism of EIEC?

A
  1. Microbe invades intestinal mucosa and causes necrosis and inflammation.
  2. Clinical manifestations similar to Shigella.
158
Q

What is the toxin and mechanism of ETEC?

A
  1. Produces heat-labile and heat-stable enterotoxins.
  2. NO inflammation or invasion.
    - -> Traveler’s diarrhea.
159
Q

What is the toxin and mechanism of EPEC?

A
  1. No toxin produced.
  2. Adheres to apical surface.
  3. Flattens villi.
  4. Prevents absorption.
160
Q

Who does EPEC usually hit?

A

Diarrhea, usually in children (Pediatrics).

161
Q

What is the toxin and mechanism of EHEC?

A
  1. O157:H7 is the most common serotype.
  2. Produces Shiga-like toxin that causes HUS = Triad of anemia, thrombocytopenia, and acute renal failure DUE TO MICROTHROMBI forming on DAMAGED ENDOTHELIUM –> MECHANICAL HEMOLYSIS (schistocytes) + Platelet consumption + Decr. renal blood flow.
162
Q

What is the mechanism of EHEC?

A
  1. Microthrombi form on endothelium damaged by toxin –> Mechanical hemolysis (schistocytes formed) and DOWN renal blood flow.
  2. Microthrombi consume platelets –> thrombocytopenia.
163
Q

How do we distinguish EHEC from other E.coli?

A

Does NOT ferment sorbitol.

164
Q

Mention some major features of K.pneumoniae?

A
  1. Intestinal flora –> lobar pneumonia in alcoholics and diabetics when ASPIRATED.
  2. Very mucoid colonies caused by abundant polysaccharide capsules.
  3. Dark red “currant jelly” sputum (blood/mucus).
  4. Also cause of nosocomial infection.
165
Q

What are the 4A’s of K.pneumoniae?

A
  1. Aspiration pneumonia
  2. Abscess in lungs and liver
  3. Di-A-betics
  4. Alcoholics.
166
Q

Salmonella vs Shigella - Flagella?

A

Shigella has NO flagella.

167
Q

Salmonella vs Shigella. Hematogenous spread?

A

Salmonella can spread hematogenously.

Shigella only cell-to-cell transmission - NO hematogenous spread.

168
Q

Salmonella vs Shigella. Reservoir?

A

Salmonella –> Many animals.

Shigella –> Only humans and primates.

169
Q

Salmonella vs Shigella. Hydrogen sulfide?

A

Salmonella –> Produces hydrogen sulfide (H2S).

Shigella –> Does not produce hydrogen sulfide.

170
Q

Salmonella vs Shigella. Antibiotics?

A

Salmonella –> May PROLONG fecal excretion.

Shigella –> SHORTEN duration of fecal excretion.

171
Q

Salmonella vs Shigella. PMNs or monocytes?

A

Salmonella –> Invades intestinal mucosa –> Monocytic response.
Shigella –> Invades intestinal mucosa –> PMN infiltration.

172
Q

Salmonella vs Shigella. GI manifestations?

A

Salmonella –> Constipation, followed by diarrhea.

Shigella –> Often causes bloody diarrhea (bacillary dysentery).

173
Q

Salmonella vs Shigella. Lactose fermentation?

A

Both do NOT ferment lactose.

174
Q

What does S.typhi cause?

A

Typhoid fever.

175
Q

Where is S.typhi found?

A

Only in humans.

176
Q

What characterizes S.typhi?

A
  1. Rose spots on the abdomen.
  2. Fever
  3. Headache
  4. Constipation –> Diarrhea
177
Q

Where can S.typhi remain and cause a carrier state?

A

In the gallbladder.

178
Q

What is a major cause of bloody diarrhea especially in children?

A

C.jejuni

179
Q

How is C.jejuni transmitted?

A
  1. Fecal-Oral through PERSON-TO-PERSON contact.
  2. Via ingestion of undercooked, contaminated poultry or meat + unpasteurized milk.
  3. Contact with INFECTED ANIMALS is also a risk factor.
180
Q

What are the features of C.jejuni?

A
  1. Comma or S-shaped WITH POLAR FLAGELLA.
  2. 42C growth
  3. Oxidase (+)
181
Q

To what neurological condition is C.jejuni a common antecedent?

A

To Guillain-Barre syndrome and reactive arthritis.

182
Q

What does V.cholera produce?

A

Rice-water diarrhea via enterotoxin that permanently activates Gs, incr. cAMP –> Sensitive to STOMACH ACID (acid labile).
==> Requires LARGE INOCULUM (high ID50) unless host has DECR. GASTRIC ACIDITY.

183
Q

Mention some features of V.cholera?

A
  1. Comma-shaped
  2. Oxidase(+)
  3. Grows in alkaline media
184
Q

How is Y.enterocolitica transmitted?

A

Usually from:

  1. Pet feces (e.g., puppies)
  2. Contaminated milk
  3. Pork
185
Q

What can Y.enterocolitica cause?

A

Acute diarrhea or PSEUDOAPPENDICITIS –> RLQ pain due to MESENTERIC ADENITIS +/- TERMINAL ILEITIS.

186
Q

What does Y.enterocolitica mimic?

A

Crohn disease or appendicitis.

187
Q

Mention some features of H.pylori.

A

Curved, TERMINALLY FLAGELLATED, gram(-) rod that is:

  1. Catalase (+).
  2. Oxidase (+).
  3. Urease (+).
188
Q

Mention 2 ways to diagnose H.pylori.

A
  1. Urea breath test

2. Fecal antigen test for diagnosis

189
Q

Acidic or alkaline environment does H.pylori cause?

A

Alkaline –> Helps survive in acidic mucosa.

190
Q

What is the MC initial therapy?

A

Triple therapy:

  1. PPI
  2. Clarithromycin
  3. Either amoxicillin or metronidazole (Amoxi if ALCOHOLIC/ Metro if penicillin-allergy)
191
Q

Mention the 3 spirochetes.

A
  1. Borrelia
  2. Leptospira
  3. Treponema
    ==> Spiral-shaped bacteria with AXIAL FILAMENTS.
192
Q

Of the 3 spirochetes, which one can be visualised?

A

Only Borrelia using aniline dyes (Wright or Giemsa stain) in light microscopy DUE TO SIZE.

193
Q

How is Treponema visualized?

A

By

  1. Dark-field microscopy.
  2. Direct fluorescent antibody (DFA) microscopy.
194
Q

Where is Leptospira interrogans found?

A

In water contaminated with animal urine.

195
Q

Mention some features of leptospirosis.

A
  1. Flu-like symptoms
  2. Jaundice
  3. Photophobia with CONJUNCTIVAL SUFFUSION (erythema without exudate).
  4. MYALGIA, CLASSICALLY OF CALVES.
    ==> Prevalent among surfers and in tropics (Hawaii).
196
Q

What is another name for Weil’s disease?

A

Icterohemorrhagic leptospirosis.

197
Q

What happens in Weil’s disease?

A

Severe form with JAUNDICE + AZOTEMIA from liver and kidney dysfunction:

  1. Fever.
  2. Hemorrhage.
  3. Anemia.
198
Q

Ixodes tick carries which 3 microorganisms?

A
  1. Borrelia burgdorferi
  2. Babesia
  3. Anaplasma spp.
199
Q

What is the natural reservoir for B.burgdorferi?

A

The mouse.

200
Q

Where is B.burgdurferi infection common?

A

In northeastern US.

201
Q

Mention some initial symptoms of Lyme disease.

A
  1. Erythema chronicum mirgans
  2. Flu-like symptoms
  3. +/- facial nerve palsy
202
Q

Mention some later symptoms of Lyme disease.

A
  1. Monoarthritis (large joints)
  2. Migratory polyarthritis
  3. Cardiac –> AV block
  4. Neurologic –> Encephalopathy, facial nerve palsy, polyneuropathy.
203
Q

What is the treatment for Lyme disease?

A
  1. Doxycycline

2. Ceftriaxone

204
Q

What is the treatment for Syphilis?

A

Penicillin G.

205
Q

What is the presentation of 1o syphilis?

A

Localized disease presenting with painless chancre.

206
Q

Can we visualize treponemes in fluid from chancre?

A

If available, use dark-field microscopy to visualize treponemes in fluid from chancre.

207
Q

What is the serologic testing in 1o syphilis?

A
  1. VDRL/RPR (non specific) (+) in 80%.

2. Confirm diagnosis with FTA-ABS (specific test).

208
Q

What happens in 2o syphilis?

A

Disseminated disease with constitutional symptoms.
1. Maculopapular rash (palms and soles).
2. Condylomata lata = Smooth, moist, painless, wart-like white lesions on genitals.
3. Lymphadenopathy.
4. PATCHY HAIR LOSS.
==> Confirmable with dark-field microscopy.

209
Q

What is the serologic testing during secondary syphilis?

A

VDRL/RPR (non specific)

FTA-ABS is specific to confirm diagnosis.

210
Q

Mention the main features of 3o syphilis.

A
  1. Gummas (chronic granulomas)
  2. Aortitis (vasa vasorum destruction)
  3. Neurosyphilis (tabes dorsalis, “general paresis”)
  4. Argyll-Robertson pupil
211
Q

Mention some signs of 3o syphilis.

A
  1. Broad-based ataxia
  2. (+) Romberg
  3. Charcot joint
  4. STROKE WITHOUT HTN
212
Q

What should be tested for neurosyphilis?

A

Test CSF with VDRL + FTA-ABS + PCR.

213
Q

Mention some features of congenital syphilis.

A
  1. Saber shins
  2. Saddle nose
  3. CN VIII deafness
  4. Hutchinson teeth
  5. Mulberry molars
  6. RHAGADES (linear scars at angle of mouth).
  7. Snuffles (nasal discharge).
  8. Short maxilla.
214
Q

When does placental transmission of syphilis occur?

A

Typically after 1st trimester, so mother should be treated early in pregnancy.

215
Q

What is the Argyll-Robertson pupil?

A

Constricts with accomodation but is not reactive to light.

Associated with 3o syphilis.

216
Q

How else do we call Argyll-Robertson pupil?

A

“Prostitute pupil” - accomodates but does not react.

217
Q

Discuss the features of VDRL.

A
  1. Detects nonspecific antibody that reacts with BEEF CARDIOLIPIN.
  2. Inexpensive, widely available test for syphilis, quantitative, sensitive but not specific.
  3. Many false positives.
218
Q

False positives of VDRL include what?

A
  1. Viral infection (mono, hep)
  2. Some drugs
  3. SLE
  4. Leprosy.
  5. Rheumatic fever.
219
Q

What is the Jarisch-Herxheimer reaction?

A

Flu-like syndrome (fever, chills, headache, myalgia) after antibiotics are started - due to killed bacteria after releasing toxins.

220
Q

Mention some main zoonotic bacteria.

A
  1. Anaplasma spp
  2. Bartonella spp
  3. Borrelia burgdorferi
  4. Borrelia recurrentis
  5. Brucella spp
  6. Campylobacter
  7. Chlamydophila psittaci
  8. Coxiella burnetti
  9. Ehrlichia chaffeensis
  10. Francisella tularensis
  11. Leptospira spp
  12. Mycobacterium leprae
  13. Pasteurella multocida
  14. Rickettsia prowazekii
  15. Rickettsia rickettsii
  16. Rickettsia typhi
  17. Salmonella spp. (except S.typhi)
  18. Yersinia pestis
221
Q

What disease does Anaplasma spp cause?

A

Anaplasmosis

222
Q

What is the transmission and source of Anaplasma?

A

Ixodes ticks (live on deer and mice).

223
Q

What does Bartonella spp. cause?

A
  1. Cat scratch disease

2. Bacillary angiomatosis

224
Q

What disease does Borrelia recurrentis cause?

A

Relapsing fever.

225
Q

How is relapsing fever transmitted?

A

Louse (recurrent due to variable surface antigens).

226
Q

How is brucellosis transmitted?

A

Via unpasteurized dairy.

227
Q

Mention what does Coxiella burnetti cause?

A

Q fever.

228
Q

How is C.burnetti transmitted?

A
  1. Aerosols of cattle

2. Sheep amniotic fluid

229
Q

How is leprosy transmitted?

A

Humans with lepromatous leprosy - or armadillo (rare).

230
Q

What does P.multocida cause?

A
  1. Cellulitis

2. Osteomyelitis

231
Q

What does R.prowazekii cause?

A

Epidemic typhus.

232
Q

How is R.prowazekii transmitted?

A

HUMAN-TO-HUMAN via human body louse.

233
Q

What does R.rickettsii cause?

A

Rocky mountain spotted fever.

234
Q

How is R.rickettsii transmitted?

A

Dermacentor (DOG) ticks.

235
Q

What does R.typhi cause?

A

Endemic typhus (NOT epidemic typhus).

236
Q

How is R.typhi transmitted?

A

Via fleas.

237
Q

Mention some features of G.vaginalis.

A

A pleomorphic, gram-VARIABLE rod involved in vaginosis.

238
Q

What is the presentation of G.vaginalis infection?

A

Gray vaginal discharge with a FISHY smell - NON painful (vs. vaginitis).

239
Q

Is G.vaginalis associated with sexual activity?

A

Yes - but NOT sexually transmitted.

240
Q

What characterizes bacterial vaginosis?

A

Overgrowth of certain anaerobic bacteria in vagina.

241
Q

What are the clue cells?

A

Seen in vaginosis:

Vaginal epithelial cells covered with Gardnerella bacteria ==> Have STIPPLED appearance along OUTER MARGIN.

242
Q

What is the treatment for G.vaginalis?

A

Metronidazole - or clindamycin.

243
Q

Treatment for ALL Rickettsial diseases and vector-borne illness?

A

Doxycycline

244
Q

Where is Rickettsia rickettsii endemic?

A

In the South Atlantic states, especially North Carolina ==> Despite its name, NOT IN THE ROCKY MOUNTAINS.

245
Q

What characterizes the rash of R.rickettsii?

A

Typically starts at the wrists and ankles and then spreads to trunk, palms, and soles.

246
Q

What does R.rickettsii cause?

A

Rocky Mountain spotted fever.

247
Q

Classic triad of RM spotted fever?

A
  1. Headache
  2. Fever
  3. Rash (vasculitis)
248
Q

Palms and soles rash?

A
  1. Coxsackievirus A infection (hand, foot, mouth disease)
  2. RM spotted fever
  3. 2o syphilis.
249
Q

Cause and vector of endemic typhus?

A

R.typhi (fleas).

250
Q

Cause and vector of epidemic typhus?

A

R.prowazekii (human body louse).

251
Q

Feature of rash in typhus?

A

Starts centrally and spreads out, sparing palms and soles.

252
Q

Cause and vector of Ehrlichiosis?

A

Ehrlichia (vector is tick).

253
Q

Feature of Ehrlichiosis?

A

Monocytes with morulae (mulberry-like inclusions) in cytoplasm.

254
Q

Cause and vector of anaplasmosis?

A

Anaplasma (tick).

255
Q

Feature of anaplasma?

A

Granulocyte with morulae in cytoplasm.

256
Q

Cause and vector of Q fever?

A

Coxiella burnetti (NO ARTHROPOD VECTOR).

257
Q

Q fever transmission?

A

SPORES inhaled as aerosols from cattle/sheep amniotic fluid.

258
Q

Q fever presentation?

A

As PNEUMONIA.

259
Q

2 forms of Chlamydia?

A
  1. Elementary body (small, dense) is “Enfectious” and Enters cell via Endocytosis –> Transforms into reticulate body.
  2. Reticulate body Replicates in cell by fission –> Reorganizes into elementary bodies.
260
Q

C.trachomatis causes what?

A
  1. Reactive arthritis (Reiter syndrome)
  2. Follicular conjunctivitis
  3. Non gonococcal urethritis
  4. PID
261
Q

C.pneumoniae and C.psittaci cause what?

A

Atypical pneumonia - transmitted by aerosol.

262
Q

What is the treatment for Chlamydiae?

A
  1. Azithromycin (favored because one treatment).

2. Doxycycline

263
Q

Special feature of C.psittaci?

A

Notable for an avian reservoir (PARROTS).

264
Q

Lab diagnosis of Chlamydiae?

A

Cytoplasmic inclusions seen on Giemsa or fluorescent antibody - stained smear.

265
Q

Unusual about the Chlamydial cell wall?

A

It lacks classic peptidoglycan (DUE TO REDUCED MURAMIC ACID) ==> Beta-lactam antibiotics LESS EFFECTIVE.

266
Q

C.trachomatis types A, B, and C cause what?

A

Chronic infection - cause blindness due to follicular conjunctivitis in Africa.
ABC = Africa/Blindness/Chronic infection.

267
Q

C.trachomatis types D-K cause what?

A
  1. Urethritis
  2. PID
  3. Ectopic pregnancy
  4. Neonatal pneumonia (staccato cough) WITH EOSINOPHILIA
  5. Neonatal conjunctivitis
268
Q

Chlamydia trachomatis types L1, L2, L3 cause what?

A

Lymphogranuloma venereum - small painless ulcers on genitals –> swollen, painful inguinal lymph nodes that ulcerate (“buboes”).

269
Q

Treatment for Lymphogranuloma venereum?

A

Doxycycline.

270
Q

Classic cause of atypical pneumonia?

A

Mycoplasma pneumoniae.

271
Q

Features of atypical pneumonia?

A
  1. Insidious onset
  2. Headache
  3. Non productive cough
  4. Patchy or diffuse interstitial infiltrate
  5. X-ray looks WORSE than patient
  6. High titer of cold agglutinins (IgM), which can agglutinate or lyse RBCs.
272
Q

M.pneumoniae grows on?

A

Eaton agar - Contains sterols.

273
Q

M.pneumoniae treatment?

A
  1. Macrolide
  2. Doxycycline
  3. Fluoroquinolone
    Penicillin INEFFECTIVE since Mycoplasma have no cell wall.
274
Q

M.pneumoniae can be seen on Gram?

A

NO

275
Q

Frequent outbreaks of M.pneumoniae?

A

Military recruits and prisons.

276
Q

S.aureus - Protein A:

A

Virulence factor –> Binds Fc-IgG –> Inhibiting complement activation + Phagocytosis.

277
Q

S.aureus - Commonly colonizes the?

A

NARES.

278
Q

TSST presents as?

A
  1. Fever.
  2. Vomiting.
  3. Rash.
  4. Desquamation.
  5. Shock.
  6. End-organ failure.
    ==> Results in incr. AST + ALT + BILIRUBIN.
279
Q

S.aureus has coagulase. Which means?

A

Forms fibrin clot around self –> Abscess.

280
Q

Does S.pneumoniae have IgA protease?

A

YES.

281
Q

Ehrlichiosis is transmitted via?

A

AMBLYOMMA - Lone Star ticks.

282
Q

F.tularensis is transmitted via?

A
  1. Ticks.
  2. Rabbits.
  3. Deer fly.
283
Q

Yersinia pestis is transmitted via?

A

Fleas - Rats and prairie dogs are reservoirs.

284
Q

Q fever is …?

A

Queer - It has no rash or vector and its causative organism can survive outside its endospore form.
NOT in rickettsia genus, but closely related.

Microbiology (46 decks)

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