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Step 1 2019 First Aid Flashcards > Micro FA Clinical bacteriology pg 134-150 > Flashcards

Micro FA Clinical bacteriology pg 134-150 Flashcards

1
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4
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Staphylococci novobiocin test

A

Novobiocin—Saprophyticus is Resistant; Epidermidis is Sensitive.
On the office’s “staph” retreat, there was no stress.

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5
Q

Streptococci optochin/bacitracin test

A

Optochin—Viridans is Resistant; Pneumoniae is Sensitive.
OVRPS (overpass).

Bacitracin—group B strep are Resistant; group A strep are Sensitive.
B-BRAS.

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6
Q

α-hemolytic bacteria

A

Partial reduction of hemoglobin causes greenish or brownish color without clearing around growth on blood agar A. Include the following organisms:

Streptococcus pneumoniae (catalase ⊝ and optochin sensitive)

Viridans streptococci (catalase ⊝ and optochin resistant)

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7
Q

β-hemolytic bacteria

A

Complete lysis of RBCs –> pale/clear area surrounding colony on blood agar A.

Include the following organisms:

ƒ Staphylococcus aureus (catalase and coagulase ⊕)

  • Listeria & E. Coli

ƒ Streptococcus pyogenes—group A strep (catalase ⊝ and bacitracin sensitive)

ƒ Streptococcus agalactiae—group B strep (catalase ⊝ and bacitracin resistant)

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8
Q

Virulence factor of S. aureus, fxn?

A

Protein A (virulence factor) binds Fc-IgG, inhibiting complement activation and phagocytosis.

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9
Q

Where does S. aureus colonize?

A

Commonly colonizes the nares, ears, axilla, and groin.

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10
Q

Inflammatory disease manifestations of S. aureus?

A

skin infections, organ abscesses, pneumonia (often after influenza virus infection), endocarditis, septic arthritis, and osteomyelitis.

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11
Q

How does MRSA resistance occur?

A

resistance due to altered penicillin-binding protein. mecA gene from staphylococcal chromosomal cassette involved in penicillin resistance

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12
Q

Staphylococcal toxic shock syndrome (TSS)

A

fever, vomiting, rash, desquamation, shock, end-organ failure. TSS results in INC AST, INC ALT, Inc bilirubin. Associated with prolonged use of vaginal tampons or nasal packing.

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13
Q

S. aureus food poisoning - how does it happen? sx?

A

S aureus food poisoning due to ingestion of preformed toxin –> short incubation period (2–6 hr) followed by nonbloody diarrhea and emesis. Enterotoxin is heat stable –> not destroyed by cooking.

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14
Q

How does s. aureus lead to abscess formation?

A

S aureus makes coagulase and toxins. Forms fibrin clot around itself –> abscess

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15
Q

S. epidermidis - colonizes what?

A

Normal flora of skin; contaminates blood cultures.

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16
Q

How does S. epidermidis lead to infections of prosthetic devices and IV catheters?

A

by producing adherent biofilms

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17
Q

Characteristics of S.epidermidis

A

Gram ⊕, catalase ⊕, coagulase ⊝, urease ⊕ cocci in clusters. Novobiocin sensitive. Does not ferment mannitol (vs S aureus).

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18
Q

Characterics of S. aureus?

A

Gram ⊕, β-hemolytic, catalase ⊕, coagulase ⊕ cocci in clusters

ferments mannitol on salt agar (halophilic)

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19
Q

S. saprophyticus characteristics

A

Gram ⊕, catalase ⊕, coagulase ⊝, urease ⊕ cocci in clusters. Novobiocin resistant.

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20
Q

Characteristics of S. pneumo?

A

Gram ⊕, α-hemolytic, lancet-shaped diplococci A. Encapsulated. IgA protease. Optochin sensitive

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21
Q

S. pneumo most commonly causes?

A

ƒ Meningitis ƒ Otitis media (in children) ƒ Pneumonia ƒ Sinusitis

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22
Q

What provides the virulence for S. pneumo?

A

capsule

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23
Q

Pneumococcus is associated with:

A

“rusty” sputum, sepsis in patients with sickle cell disease, and asplenic patients

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24
Q

Characteristics of viridans group

A

Gram ⊕, α-hemolytic cocci. Resistant to optochin, differentiating them from S pneumoniae which is α-hemolytic but optochin sensitive. Normal flora of the oropharynx

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25
Q

Streptococcus mutans and S mitis cause ____ _____

A

Streptococcus mutans and S mitis cause dental caries.

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26
Q

S sanguinis makes ____ that bind to ______ ______ on damaged heart valves, causing _______ ________ _________

A

S sanguinis makes dextrans that bind to fibrin platelet aggregates on damaged heart valves, causing subacute bacterial endocarditis.

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27
Q

S. pyogenes characteristics

A

Bacitracin sensitive, β-hemolytic, pyrrolidonyl arylamidase (PYR) ⊕.

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28
Q

Diseases causes by S. pyogenes?

A

ƒ Pyogenic—pharyngitis, cellulitis, impetigo (“honey-crusted” lesions), erysipelas

ƒ Toxigenic—scarlet fever, toxic shock–like syndrome, necrotizing fasciitis

ƒ Immunologic—rheumatic fever, glomerulonephritis

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29
Q

virulence factor of S. pyogenes

A

Hyaluronic acid capsule and M protein of s.pyogenes inhibit phagocytosis.

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30
Q

How to test for recent S pyogenes infection?

A

ASO titer or anti-DNase B antibodies

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31
Q

Which strains of S. pyogenes cause rheu fever/ GN?

A

Strains causing impetigo can induce glomerulonephritis.

“Ph”yogenes pharyngitis can result in rheumatic “phever” and glomerulonephritis.

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32
Q

Sx of Scarlet fever?

A

blanching, sandpaper-like body rash, strawberry tongue, and circumoral pallor in the setting of group A streptococcal pharyngitis (erythrogenic toxin ⊕).

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33
Q

S. agalacticae characteristics?

A

Gram ⊕ cocci, bacitracin resistant, β-hemolytic, colonizes vagina;

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34
Q

What does S. agalactiae cause?

A

causes pneumonia, meningitis, and sepsis

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35
Q

Tests for S. agalactiae?

A

Hippurate test ⊕. PYR ⊝ CAMP (+)

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36
Q

When do we screen pregnant women for S. agal?

A

Screen pregnant women at 35–37 weeks of gestation with rectal and vaginal swabs. Patients with ⊕ culture receive intrapartum penicillin prophylaxis.

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37
Q

Streptococcus bovis - characteristics and diseases?

A

Gram ⊕ cocci, colonizes the gut. S gallolyticus (S bovis biotype 1) can cause bacteremia and subacute endocarditis and is associated with colon cancer.

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38
Q

Characteristics of Enterococci?

A

Catalase ⊝, PYR ⊕, variable hemolysis. G + cocci

grows in 6.5% NaCl

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39
Q

Enterococci - NF of? Diseases caused by?

A

Enterococci (E faecalis and E faecium) are normal colonic flora that are penicillin G resistant and cause UTI, biliary tract infections, and subacute endocarditis (following GI/GU procedures).

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40
Q

Do enterococci or streptococci bovis grow in Nacl/bile?

A

Enterococci are more resilient than streptococci, can grow in 6.5% NaCl and bile (lab test).

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41
Q

B. anthracis characteristics?

A

Gram ⊕, spore-forming rod, Has a polypeptide capsule (poly d-glutamate)

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42
Q

How do anthrax colonies look?

A

Colonies show a halo of projections, sometimes referred to as “medusa head” appearance.

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43
Q

3 parts of anthrax toxin?

A

(an exotoxin consisting of protective antigen, lethal factor, and edema factor

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44
Q

Sx of pulm anthrax?

A

most commonly from contaminated animals or animal products, although also a potential bioweapon –> flu-like symptoms that rapidly progress to fever, pulmonary hemorrhage, mediastinitis, and shock.

CXR may show widened mediastinum.

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45
Q

B. cereus - what type of food? why?

A

Spores survive cooking rice (reheated rice syndrome). Keeping rice warm results in germination of spores and enterotoxin formation

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46
Q

sx of B. cereus

A

Emetic type usually seen with rice and pasta. Nausea and vomiting within 1–5 hr. Caused by cereulide, a preformed toxin.

Diarrheal type causes watery, nonbloody diarrhea and GI pain within 8–18 hr.

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47
Q

Characteristics of Clostridia?

A

Gram ⊕, spore-forming, obligate anaerobic rods.

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48
Q

C. tetani - what toxin? moa?

A

Produces tetanospasmin, an exotoxin causing tetanus. Tetanospasmin blocks release of GABA and glycine from Renshaw cells in spinal cord.

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49
Q

Sx of C. tetani?

A

spastic paralysis, trismus (lockjaw), risus sardonicus (raised eyebrows and open grin), opisthotonos (spasms of spinal extensors).

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50
Q

Prevention and treatment for Tetanus?

A

Prevent with tetanus vaccine. Treat with antitoxin +/− vaccine booster, antibiotics, diazepam (for muscle spasms), and wound debridement.

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51
Q

C. botulinum - toxin? mech?

A

Produces a heat-labile toxin that inhibits ACh release at the neuromuscular junction, causing botulism.

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52
Q

What leads to botulism in adults and children?

A

. In adults, disease is caused by ingestion of preformed toxin. In babies, ingestion of spores (eg, in honey) leads to disease (floppy baby syndrome).

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53
Q

Sx of botulism and Tx?

A

Symptoms of botulism (the 4 D’s): Diplopia, Dysarthria, Dysphagia, Dyspnea

Treat with human botulinum immunoglobulin.

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54
Q

Where is botulism found?

A

Botulinum is from bad bottles of food, juice, and honey (causes a descending flaccid paralysis).

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55
Q

Local botox injections is used for?

A

Local botox injections used to treat focal dystonia, achalasia, and muscle spasms. Also used for cosmetic reduction of facial wrinkles.

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56
Q

C. perfringens - toxin? MoA?

A

Produces α-toxin (lecithinase, a phospholipase) that can cause myonecrosis (gas gangrene A; presents as soft tissue crepitus) and hemolysis

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57
Q

How can C. perfringens lead to food poisoning?

A

If heavily spore-contaminated food is cooked but left standing too long at < 60°C, spores germinate –> vegetative bacteria –> produce heat-labile enterotoxin –> food poisoning symptoms in 10-12 hours, resolution in 24 hours.

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58
Q

C. diff - toxin? MoA?

A

Produces 2 toxins. Toxin A, an enterotoxin, binds to brush border of gut and alters fluid secretion. Toxin B, a cytotoxin, disrupts cytoskeleton via actin depolymerization. Both toxins lead to diarrhea –> pseudomembranous colitis

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59
Q

C. Diff infection usually follows admin of meds?

A

Often 2° to antibiotic use, especially clindamycin or ampicillin; associated with PPIs.

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60
Q

Complication of C. diff?

A

toxic megacolon

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61
Q

Tx of C. diff?

A

oral vancomycin, metronidazole, or fidaxomicin

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62
Q

C. diphtheriae characteristics

A

Gram ⊕ rods occurring in angular arrangements

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63
Q

Exotoxin of C. diphteriae

A

Causes diphtheria via exotoxin encoded by β-prophage. Potent exotoxin inhibits protein synthesis via ADP-ribosylation of EF-2, leading to possible necrosis in pharynx, cardiac, and CNS tissue.

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64
Q

Sx of C. diphtheriae

A

pseudomembranous pharyngitis (grayish-white membrane A) with lymphadenopathy, myocarditis, and arrhythmias.

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65
Q

Dx of C. diphtheriae

A

gram ⊕ rods with metachromatic (blue and red) granules and ⊕ Elek test for toxin.

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66
Q

What does C. diptheriae look like? which stain?

A

Cornye = club shaped (metachromatic granules on Löffler media). Black colonies on cystine-tellurite agar.

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67
Q

L. monocytogenes characteristics

A

Gram ⊕, facultative intracellular rod

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68
Q

Where do we acquire Listeria from?

A

acquired by ingestion of unpasteurized dairy products and cold deli meats, transplacental transmission, by vaginal transmission during birth

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69
Q

Why does refrigeration of meats not stop Listeria infection?

A

Listeria grows well at refrigeration temperatures (4°–10°C; “cold enrichment”).

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70
Q

How does Listeria avoid antibodies?

A

Forms “rocket tails” (red in A) via actin polymerization that allow intracellular movement and cell to cell spread across cell membranes, thereby avoiding antibody. Characteristic tumbling motility in broth.

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71
Q

Diseases caused by Listeria?

A

amnionitis, septicemia, and spontaneous abortion in pregnant women;

granulomatosis infantiseptica;

neonatal meningitis;

meningitis in immunocompromised patients;

mild, selflimited gastroenteritis in healthy individuals.

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72
Q

Tx of Listeria?

A

Ampicillin

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73
Q

Where is Nocardia and Actinomyces found normally?

A

Nocardia - Found in soil

Actinomyces - Normal oral, reproductive, and GI flora

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74
Q

Sx of Nocardia?

A

Causes pulmonary infections in immunocompromised (can mimic TB but with a neg PPD)

cutaneous infections after trauma in immunocompetent, can spread to CNS

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75
Q

Sx of Actinomyces

A

Causes oral/facial abscesses that drain through sinus tracts; often associated with dental caries/ extraction and other maxillofacial trauma; forms yellow “sulfur granules”; can also cause PID with IUDs

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76
Q

Rx for Nocardia/Actinomyces?

A

Treatment is a SNAP: Sulfonamides—Nocardia; Actinomyces—Penicillin

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77
Q

Mycobacteria - causes what?

A

Mycobacterium tuberculosis (TB, often resistant to multiple drugs).

M avium–intracellulare (causes disseminated, non-TB disease in AIDS; often resistant to multiple drugs). Prophylaxis with azithromycin when CD4+ count < 50 cells/ mm3.

M scrofulaceum (cervical lymphadenitis in children).

M marinum (hand infection in aquarium handlers).

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78
Q

Virulence factors of mycobacteria

A

Cord factor creates a “serpentine cord” appearance in virulent M tuberculosis strains; activates macrophages (promoting granuloma formation) and i_nduces release of TNF-α._

Sulfatides (surface glycolipids) inhibit phagolysosomal fusion.

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79
Q

TB sx?

A

fever, night sweats, weight loss, cough (nonproductive or productive), hemoptysis.

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80
Q

PPD test of TB?

A

PPD ⊕ if current infection or past exposure. PPD ⊝ if no infection and in sarcoidosis or HIV infection (especially with low CD4+ cell count).

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81
Q

Sign of secondary TB?

A

Caseating granulomas with central necrosis and Langhans giant cell

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82
Q

How to Dx Leprosy?

A

via skin biopsy or tissue PCR

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83
Q

Reservoir of leprosy in US?

A

armadillos

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84
Q

T or F Mycobacterium leprae cannot be grown in vitro?

A

True.

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85
Q

Sx of mycobacteria leprae - 2 forms?

A

ƒ Lepromatous—presents diffusely over the skin, with Leonine (Lion-like) facies B, and is communicable (high bacterial load); characterized by low cell-mediated immunity with a largely Th2 response. Lepromatous form can be Lethal.

ƒ Tuberculoid—limited to a few hypoesthetic, hairless skin plaques; characterized by high cellmediated immunity with a largely Th1-type immune response and low bacterial load.

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86
Q

Tx of Leprosy?

A

dapsone and rifampin for tuberculoid form; clofazimine is added for lepromatous form

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87
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89
Q
A
90
Q

In what cells is N. gon commonly found

A

IC in neutrophils

91
Q

Neisseria Metabolize _____ and produce ___ _______

A

Metabolize glucose and produce IgA proteases

92
Q

Why is there no N. gon vaccine?

A

No vaccine due to antigenic variation of pilus protein

93
Q

N gonn v N meningiditis - capsule, maltose acid.

A
94
Q

N gonn causes?

A

Causes gonorrhea, septic arthritis, neonatal conjunctivitis (2–5 days after birth), pelvic inflammatory disease (PID), and Fitz-Hugh– Curtis syndrome

95
Q

N meningiditis causes?

A

Causes meningococcemia with petechial hemorrhages and gangrene of toes, meningitis, Waterhouse-Friderichsen syndrome (adrenal insufficiency, fever, DIC, shock)

96
Q

Prophylaxis or Tx for N meningitidis?

A

Rifampin, ciprofloxacin, or ceftriaxone prophylaxis in close contacts

Tx/ Ceftriaxone or Penicillin

97
Q

What other G- bact prod IgA protease?

A

H. influenza

98
Q

What does nontypeable H. influ strains cause?

A

Nontypeable (unencapsulated) strains are the most common cause of mucosal infections (otitis media, conjunctivitis, bronchitis) as well as invasive infections since the vaccine for capsular type b was introduced

99
Q

Culture medium for H. influ?

A

Culture on chocolate agar, which contains factors V (NAD+) and X (hematin) for growth; can also be grown with S aureus, which provides factor V via RBC hemolysis

100
Q

H. influ causes?

A

HaEMOPhilus causes Epiglottitis (endoscopic appearance in , can be “cherry red” in children; “thumb sign” on lateral neck x-ray), Meningitis, Otitis media, and Pneumonia.

101
Q

What does H. influ vaccine contain? when given?

A

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

102
Q

Virulence factors of B. pertussis?

A

Virulence factors include pertussis toxin (disables Gi), adenylate cyclase toxin (Inc cAMP), and tracheal cytotoxin

103
Q

3 stages of pertussis?

A

Three clinical stages:

ƒ Catarrhal—low-grade fevers, Coryza.

ƒ Paroxysmal—paroxysms of intense cough followed by inspiratory “whooP” (“whooping cough”), posttussive vomiting.

ƒ Convalescent—gradual recovery of chronic cough.

104
Q

Tx of pertussis?

A

Treatment: macrolides; if allergic use TMP-SMX.

105
Q

Brucella - transmitted thru?

A

Transmitted via ingestion of contaminated animal products (eg, unpasteurized milk).

106
Q

Where does brucella live in the body?

A

Survives in macrophages in the reticuloendothelial system.

107
Q

Sx of Brucella

A

Typically presents with undulant fever, night sweats, and arthralgia.

108
Q

Tx of Brucella

A

doxycycline + rifampin or streptomycin.

109
Q

What stain used for Legionella? why? what growth medium?

A

Gram stains poorly—use silver stain. Grow on charcoal yeast extract medium with iron and cysteine.

110
Q

Sx of Legionella

A

Legionnaires’ disease—severe pneumonia (often unilateral and lobar A), fever, GI and CNS symptoms. Common in smokers and in chronic lung disease. Pontiac fever—mild flu-like syndrome.

Labs - hyponatremia

111
Q

Tx of Legionella

A

macrolide or quinolone

112
Q

Characteristics of Pseudomonas aeruginosa

A

Aeruginosa—aerobic; motile, catalase ⊕, gram ⊝ rod. Non-lactose fermenting. Oxidase ⊕. Frequently found in water. Has a grape-like odor

113
Q

Dx assoc with Pseudomonas

A

PSEUDOMONAS is associated with:

Pneumonia,
Sepsis,
Ecthyma gangrenosum,
UTIs,
Diabetes,
Osteomyelitis,
Mucoid polysaccharide capsule,
Otitis externa (swimmer’s ear),
Nosocomial infections (eg, catheters, equipment), Addicts (drug abusers),
Skin infections (eg, hot tub folliculitis, wound infection in burn victims).

114
Q

How does P. aeruginosa lead to chronic pneumonia in CF pt?

A

Mucoid polysaccharide capsule may contribute to chronic pneumonia in cystic fibrosis patients due to biofilm formation

115
Q

What is seen in immunocompromised pt if infected with Pseudomonas

A

Ecthyma gangrenosum—rapidly progressive, necrotic cutaneous lesion B caused by Pseudomonas bacteremia.

116
Q

What does Pseudomonas produce?

A

Produces PEEP:

Phospholipase C (degrades cell membranes); Endotoxin (fever, shock);
Exotoxin A (inactivates EF-2);
Pigments: pyoverdine and pyocyanin (blue-green pigment A; also generates reactive oxygen species)
117
Q

Tx Pseudomonas

A

Treatments include “CAMPFIRE” drugs:

ƒ Carbapenems

ƒ Aminoglycosides
ƒ Monobactams
ƒ Polymyxins (eg, polymyxin B, colistin)
ƒ Fluoroquinolones (eg, ciprofloxacin, levofloxacin)
ƒ ThIRd- and fourth-generation cephalosporins (eg, ceftazidime, cefepime)
ƒ Extended-spectrum penicillins (eg, piperacillin, ticarcillin)

118
Q

Similarities between Salmonella and Shigella

A

Both Salmonella and Shigella are gram ⊝ rods, non-lactose fermenters, oxidase ⊝, and can invade the GI tract via M cells of Peyer patches.

119
Q

How do Salmonella vs Shigella spread?

A

Salmonella spread hematogenously (move w/ flagella)

Shigella spread cell to cell - no flagella

120
Q

Does Salmonella or Shigella produce H2S?

A

Salmonella

121
Q

How does antibiotics affect the fecal excretion in Salmonella/Shigella?

A

Prolongs duration in Salmonella, shortens duration in Shigella

122
Q

Sx and Immune response of Salmonella & Shigella?

A

S. typhi - primarily monocytes

constipation, followed by diarrhea

Salmonella spp. (except S typhi)- possibly bloody diarrhea, immune response is PMNs in disseminated disease.

Shigella - primarily PMN infiltration,
Fever, crampy abdominal pain
–> tenesmus, bloody mucoid stools (bacillary dysentery)

123
Q

Vaccines of Salmonella typhi

A

Oral vaccine contains live attenuated S typhi

IM vaccine contains Vi capsular polysaccharide

124
Q

Sx/ of S. typhi & Tx/

How does it have a carrier state?

A

ƒ Causes typhoid fever (rose spots on abdomen, constipation, abdominal pain, fever; later GI ulceration and hemorrhage); treat with ceftriaxone or fluoroquinolone

ƒ Carrier state with gallbladder colonization

125
Q

Common sources of Salmonella gastroenteritis

A

poultry, eggs, pets, turtles

126
Q

Which species of Shigella produce the most toxin?

A

ƒ In order of decreasing severity (less toxin produced): S dysenteriae, S flexneri, S boydii, S sonnei

127
Q

What cells does Shigella invade?

A

M cells

128
Q

Yersenia transmitted from?

A

pet feces (puppies)

contaminated milk

pork

129
Q

Yersenia enterocolitica leads to what infection?

A

acute diarrhea

pseudo appendicitis ( RLQ pain due to mesenteric adenitis/ terminal ileitis)

130
Q

Which bacteria ferment lactose? How does it grow on agar?

A

Fermentation of lactose –> pink colonies on MacConkey agar.

purple/black colonies on EMB agar

Examples include Citrobacter, Klebsiella, E coli, Enterobacter, and Serratia (weak fermenter).

Lactose is key. Test with MacConKEE’S agar.

131
Q

How does E. coli ferment lactose? how do its colonies look on agar?

A

E coli produces β-galactosidase, which breaks down lactose into glucose and galactose.
E coli grows colonies with a green sheen.

132
Q

E. coli virulence factors?

A

E coli virulence factors:

fimbriae—cystitis and pyelonephritis (P pili);

K capsule—pneumonia, neonatal meningitis;

LPS endotoxin—septic shock.

133
Q

MoA of EIEC? looks like what other bact?

A

Microbe invades intestinal mucosa and causes necrosis and inflammation. Sx similar to Shigella

134
Q

MoA of ETEC?

A

Produces heat-labile and heat-stable enteroToxins. No inflammation or invasion.

135
Q

MoA of EPEC? patient pop?

A

No toxin produced. Adheres to apical surface, flattens villi, prevents absorption.

Diarrrhea, usually only in children

136
Q

MoA of EHEC?

A

Dysentery (toxin alone causes necrosis and inflammation).

137
Q

EHEC - what do you get it from?

A

Often transmitted via undercooked meat, raw leafy vegetables.

138
Q

Shiga like toxin cause what triad?

A

triad of anemia, thrombocytopenia, and acute kidney injury

139
Q

pathogenesis of HUS?

A

due to microthrombi forming on damaged endothelium –> mechanical hemolysis (with schistocytes on peripheral blood smear), platelet consumption, and dec renal blood flow.

140
Q

Diff of EHEC from other E. Coli?

A

Does not ferment sorbitol (vs other E coli).

141
Q

Klebsiella causes?

A

lobar pneumonia in alcoholics and diabetics when aspirated.

142
Q

Mucoid colonies of Klebsiella caused by?

A

lots of polysacc capsules

143
Q

5 A’s of KlebsiellA:

A

Aspiration pneumonia

Abscess in lungs and liver

Alcoholics

DiAbetics

“CurrAnt jelly” sputum

144
Q

Characteristics of C. jejuni

A

Gram ⊝,

comma or S shaped (with polar flagella) A,

oxidase ⊕,

grows at 42°C (“Campylobacter likes the hot campfire”).

145
Q

C. jejuni infections is related to what other diseases?

A

Common antecedent to Guillain-Barré syndrome and reactive arthritis.

146
Q

Transmission of C. jejuni

A

Fecal-oral transmission through personto-person contact or via ingestion of undercooked contaminated poultry or meat, unpasteurized milk. Contact with infected animals (dogs, cats, pigs) is also a risk factor.

147
Q

C. jejuni causes? patient pop?

A

Major cause of bloody diarrhea, especially in children.

148
Q

V. cholerae characteristics?

A

Gram ⊝, flagellated, comma shaped A, oxidase ⊕, grows in alkaline media

149
Q

Endotoxin of Cholera does what?

A

Produces profuse rice-water diarrhea via enterotoxin that permanently activates Gs, Inc cAMP

150
Q

Why does V. cholerae have a high infectious dose?

A

Sensitive to stomach acid (acid labile); requires large inoculum (high ID50) unless host has Dec gastric acidity

151
Q

What is the source of transmission of V. cholerae?

A

Transmitted via ingestion of contaminated water or uncooked food (eg, raw shellfish).

152
Q

Characteristics of H. pylori

A

A
Curved, flagellated (motile), gram ⊝ rod A that is triple ⊕: catalase ⊕, oxidase ⊕, and urease ⊕

153
Q

Dx of H. pylori?

A

(can use urea breath test or fecal antigen test for diagnosis).

154
Q

How does h. pylori survive in acidic mucosa?

A

Urease produces ammonia, creating an alkaline environment, which helps H pylori survive in acidic mucosa

155
Q

What part of the stomach does H. pylori colonize?

A

antrum

156
Q

Diseases caused by H. pylori? Inc risk of what diseases?

A

causes gastritis and peptic ulcers (especially duodenal).

Risk factor for peptic ulcer disease, gastric adenocarcinoma, and MALT lymphoma.

157
Q

Tx of H. Pylori?

A

Most common initial treatment is triple therapy: Amoxicillin (metronidazole if penicillin allergy) + Clarithromycin + Proton pump inhibitor;

Antibiotics Cure Pylori.

Bismuth-based quadruple therapy if concerned about macrolide resistance.

158
Q

Ex of Spirochetes?

A

Includes Borrelia (big size), Leptospira, and Treponema

159
Q

Which spirochete can be visualized?

A

Only Borrelia can be visualized using aniline dyes (Wright or Giemsa stain) in light microscopy due to size.

160
Q

How do we visualize Treponema?

A

Treponema is visualized by dark-field microscopy or direct fluorescent antibody (DFA) microscopy.

161
Q

vector of Lyme disease also spreads what other diseases?

A

transmitted by the Ixodes deer tick A (also vector for Anaplasma spp. and protozoa Babesia)

162
Q

Lyme disease is most common in what part of the US?

A

NE US

163
Q

Stage 1 of Lyme disease?

A

Stage 1—early localized: erythema migrans (typical “bulls-eye” configuration B is pathognomonic but not always present), flu-like symptoms.

164
Q

Stage 2 of Lyme disease?

A

Stage 2—early disseminated: secondary lesions, carditis, AV block, facial nerve (Bell) palsy, migratory myalgias/transient arthritis.

165
Q

Late stage of Lyme disease?

A

Stage 3—late disseminated: encephalopathy, chronic arthritis.

166
Q

A Key Lyme pie to the FACE:

A

Facial nerve palsy (typically bilateral)

Arthritis

Cardiac block - all those are secondary

Erythema migrans (primary) & encephalopathy (tertiary)

167
Q

Tx of Lyme disease

A

doxycycline (1st line); amoxicillin and, if severe illness, CNS signs, or heart block, ceftriaxone

168
Q

A pt who has had a H. influ vaccine can still get ?

A

Non typeable strains - can still get otitis media, conjunctivitis, bronchitis

169
Q

Getting the H. influ vaccine stops getting which diseases?

A

meningitis
cellulitis
epiglotitis
arthritis

170
Q

Why can pertussis be mistaken for a viral infection?

A

Bc of huge lymphocytic infiltrate due to immune response

171
Q

Why is there a dec in gluc/K+ in pertussis?

A

Pertussis toxin disables Gi –> will stimulate islet of Langerhans –> (+) insulin –> dec glucose

Inc insulin will also shift K+ into cells = hypokalemia

172
Q

Legionella on xray

A

unilobar infiltrate with consolidation

173
Q

Renal issues with Legionella?

A

may prod tubulointerstitial disease w/ destruction of JGA –> hyporeninemic hypoaldosteronism

= type IV renal tubular acidosis

174
Q

Sx/ of Leptospirosis?

A

Leptospirosis—flu-like symptoms, myalgias (classically of calves), jaundice, photophobia with conjunctival suffusion (erythema without exudate

175
Q

patient pop of Leptospirosis

A

Hawaii (tropical) surfer!

176
Q

Weil disease Sx? causative organism?

A

Weil disease (icterohemorrhagic leptospirosis)—severe form with jaundice and azotemia from liver and kidney dysfunction, fever, hemorrhage, and anemia.

Leptospira Interrogans

177
Q

Primary syphillis - sx? dx?

A

Localized disease presenting with painless chancre.

Use fluorescent or dark-field microscopy to visualize treponemes in fluid from chancre .

VDRL ⊕ in ~ 80%.

178
Q

Secondary syphilis sx?

A

Disseminated disease with constitutional symptoms,

  • maculopapular rash (including palms D and soles),
  • condylomata lata (smooth, painless, wart-like white lesions on genitals),
  • lymphadenopathy,
  • patchy hair loss
179
Q

Dx of secondary syphilis?

A

VDRL/RPR (nonspecific), confirm diagnosis with specific test (eg, FTA-ABS).

180
Q

Tertiary syphilis sx?

A 
Gummas F (chronic granulomas),
aortitis (vasa vasorum destruction),
neurosyphilis (tabes dorsalis, “general paresis”), Argyll Robertson pupil (constricts with accommodation but is not reactive to light; also called “prostitute’s pupil” since it accommodates but does not react).
181
Q

Signs of tertiary syphilis?

A

broad-based ataxia, ⊕ Romberg, Charcot joint, stroke without hypertension.

182
Q

When does placental transmission of syphilis occur? when to treat?

A

, treat mother early in pregnancy, as placental transmission typically occurs after first trimester.

183
Q

Sx of Congenital syphilis

A

facial abnormalities such as rhagades (linear scars at angle of mouth), snuffles (nasal discharge), saddle nose, notched (Hutchinson) teeth , mulberry molars, and short maxilla; saber shins; CN VIII deafness

184
Q

Causes a False positive on VDRL test

A

False-Positive results on VDRL with:

  • *P**regnancy
  • *V**iral infection (eg, EBV, hepatitis)
  • *D**rugs
  • *R**heumatic fever
  • *L**upus and leprosy

(anti phospholipid syndrome)

185
Q

what type of bacteria can lead to a flu like syndrome after antibiotics are started?

A

Spirochetes

Jarisch-Herxheimer reaction
Flu-like syndrome (fever, chills, headache, myalgia) after antibiotics are started; due to killed bacteria (usually spirochetes) releasing toxin

186
Q

Presents as a gray vaginal discharge with a fishy smell; nonpainful (vs vaginitis).

A

Garnerella vaginalis

187
Q

characteristics of gardnerella?

A

A pleomorphic, gram-variable rod involved in bacterial vaginosis

188
Q

Clue cells (_______ ______ ______ covered with ________) have stippled appearance along outer margin

A

Clue cells (vaginal epithelial cells covered with Gardnerella) have stippled appearance along outer margin

189
Q

Test for Gardnerella

A

Amine whiff test—mixing discharge with 10% KOH enhances fishy odor

190
Q

Tx of Gardnerella

A

metronidazole or clindamycin

191
Q

Caused by Chlamydia trachomatis?

A

neonatal and follicular adult conjunctivitis , nongonococcal urethritis, PID, and reactive arthritis.

192
Q

Chlamydiae cannot make their own ___ so they are ______ _______ organisms

A

Chlamydiae cannot make their own ATP, so they are obligate intracellular organisms

193
Q

2 forms of Chlamydia?

A

2 forms: ƒ Elementary body (small, dense) is “Enfectious” and Enters cell via Endocytosis; transforms into reticulate body. ƒ Reticulate body Replicates in cell by fission; Reorganizes into elementary bodies.

194
Q

Why are B lactams antibiotics ineffective with chlamydia?

A

The chlamydial cell wall lacks classic peptidoglycan (due to reduced muramic acid), rendering β-lactam antibiotics ineffective.

195
Q

Tx of Chlamydia?

A

Treatment: azithromycin (favored because one-time treatment) or doxycycline.

Add ceftriaxone for possible concomitant gonorrhea.

196
Q

Which species of chlamydia cause of atypical pneumonia?

A

Chlamydophila pneumoniae and Chlamydophila psittaci cause atypical pneumonia; transmitted by aerosol.

197
Q

How to Dx Chlamydia? what stain/smear?

A

Lab diagnosis: PCR, nucleic acid amplification test. Cytoplasmic inclusions (reticulate bodies) seen on Giemsa or fluorescent antibody– stained smear.

198
Q

causes small painless ulcers on genital –> leading to swollen painful inguinal lymph nodes that ulcerate (buboes)

A

Chlamydia trachomatis serotype Types L1, L2, and L3

199
Q

How to treat Lymphogranuloma venereum?

A

Doxycyclin (no in pregnancy) and erythromycin

200
Q

Serotypes C. trachomatis D-K cause?

A

Urethritis/PID, ectopic pregnancy, neonatal pneumonia (staccato cough) with eosinophilia, neonatal conjunctivitis (1–2 weeks after birth).

201
Q

C. trachomatis serotypes A-C cause?

A

Chronic infection, cause blindness due to follicular conjunctivitis in Africa

ABC = Africa, Blindness, Chronic infection

202
Q

Rocky mountain spotted fever - causal agent, vector

A

Rickettsia rickettsii, vector is tick

203
Q

Geographic distribution of Rocky mountain spotted fever

A

disease occurs primarily in the South Atlantic states, especially North Carolina.

204
Q

3 diseases seen with palms and soles rash?

A

Palms and soles rash is seen in Coxsackievirus A infection (hand, foot, and mouth disease), Rocky Mountain spotted fever, and 2° Syphilis (you drive CARS using your palms and soles).

205
Q

Rash progression of Rocky mountain spotted fever v Typhus?

A

Rash typically starts at wrists and ankles and then spreads to trunk, palms, and soles.

Typhus rash starts centrally and spreads out, sparing palms and soles.
Rickettsii on the wRists, Typhus on the Trunk.

206
Q

Typhus causal agents? vector?

A

Endemic (fleas)—R typhi.

Epidemic (human body louse)—R prowazekii

207
Q

Vector for both Ehrlichia and Anaplasma?

A

Erlichlia - Amblyomma

Anaplasma - Ixodes

tick

208
Q

Difference in presentation of Ehrlichiosis and Anaplasmosis?

A

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

Anaplasma - Granulocytes with morulae C in cytoplasm.

MEGA berry— Monocytes = Ehrlichiosis Granulocytes = Anaplasmosis

209
Q

Common cause of culture neg endocarditis? other causes? Affects which valve most often?

A

Coxiella Burnetti

Coxiella burnetti, Bartonella spp, HACEK (Haemophilus, Aggregatibacter [formerly Actinobacillus], Cardiobacterium, Eikenella, Kingella).

affects mitral valve most often

210
Q

Sx of Coxiella?

A

Presents with headache, cough, influenza-like symptoms, pneumonia, possibly in combination with hepatitis.

211
Q

Which vector for Q fever?

A

no vector for Coxiella burnetti - spores inhaled aerosols from cattle/sheep amniotic fluid

212
Q

What’s diff about Q fever?

A

Q fever is Queer because it has no rash or vector and its causative organism can survive outside in its endospore form.

213
Q

Most common cause of atypical pneumonia?

A

Mycoplasma pneumoniae

214
Q

Sx of atypical pneumonia?

A

(insidious onset, headache, nonproductive cough, patchy or diffuse interstitial infiltrate

215
Q

Mycoplasma outbreak freq in what pt pop?

A

frequently in patients <30 years old; outbreaks in military recruits and prisons.

216
Q

Dx of Mycoplasma?

A

X-ray looks worse than patient. High titer of cold agglutinins (IgM), which can agglutinate RBCs. Grown on Eaton agar.

217
Q

membrane of mycoplasma has?

A

sterols - for stability

218
Q

Tx of Mycoplasma?

A

macrolides, doxycycline, or fluoroquinolone (penicillin ineffective since Mycoplasma has no cell wall).

219
Q

Mycoplasma can cause what in children, normally seen as an allergic rxn?

A

Steven Johnson syndrome variant

220
Q
A

Step 1 2019 First Aid Flashcards (63 decks)

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