Bacterial Infections Flashcards

(70 cards)

1
Q

What makes Listeria monocytogenes unique among foodborne pathogens?

A

Gram+, grows in cold (fridge risk)

Targets: Pregnant (amnionitis/stillbirth), neonates (granulomatosis infantiseptica), immunocompromised (meningitis)

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2
Q

How does Listeria present in neonates?

A

Granulomatosis infantiseptica: Rash + sepsis

Meningitis (exudative)

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3
Q

What type of inflammation does Listeria cause?

A

Suppurative inflammation (neutrophil-dominated)

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4
Q

What are the CSF findings in Listeria meningitis?

A

Acute pyogenic pattern with Gram(+) bacilli

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5
Q

What are the 3 key neonatal manifestations of Listeria?

A

Papular red rash (extremities)

Placental abscesses

Meconium with Gram(+) bacilli

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6
Q

Which populations are most vulnerable to severe Listeria?

A

Pregnant women (amnionitis/stillbirth)

Neonates (granulomatosis infantiseptica)

Immunocompromised (meningitis)

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7
Q

What is the mechanism of diphtheria toxin?

A

ADP-ribosylation of EF-2 → inhibits protein synthesis → cell death

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8
Q

What characterizes the respiratory form of diphtheria?

A

Gray-black pseudomembrane (fibrinosuppurative exudate) that can obstruct airways

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9
Q

What are the 5 main organs affected in systemic diphtheria?

A

Heart (fatty change/myofiber necrosis)

Nerves (demyelination)

Liver (fatty change)

Kidneys (necrosis)

Adrenals (necrosis)

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10
Q

How does cutaneous diphtheria present?

A

Chronic ulcers with dirty gray membrane

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11
Q

What bacterium causes whooping cough?

A

Bordetella pertussis

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12
Q

What are the 3 clinical stages of pertussis?

A

Catarrhal (mild cold symptoms)

Paroxysmal (severe coughing fits with “whoop”)

Convalescent (gradual recovery)

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13
Q

What pathological change occurs in the airways?

A

Laryngotracheobronchitis with mucosal erosion and inflammation

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14
Q

What are 5 key infections caused by P. aeruginosa?

A

CF pulmonary infections

Burn wound sepsis

Contact lens keratitis

Swimmer’s ear (otitis externa)

Ecthyma gangrenosum

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15
Q

What is the characteristic lung pathology?

A

“Fleur-de-lis” necrotizing pneumonia (pale necrotic centers + hemorrhagic rims)

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16
Q

What skin lesion suggests pseudomonal sepsis?

A

Ecthyma gangrenosum (oval necrotic-hemorrhagic lesions)

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17
Q

What immune cells are crucial for TB defense?

A

CD4+ T cells (Th1 response)

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18
Q

What’s the difference between TB pathology in immunocompetent vs immunocompromised?

A

Normal immunity: Caseating granulomas

Weak immunity: No granulomas, unchecked bacterial growth

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19
Q

What characterizes Primary TB lesions?

A

Ghon focus: Consolidation (lower part of upper lobe or upper part of lower lobe)

Ghon complex: Ghon focus + pulmonary hilar node involvement

Ranke complex: Healed, calcified Ghon complex

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20
Q

What are Primary TB sequelae?

A

Healing by fibrosis (in immunocompetent individuals with anti-TB therapy)

Latency → reactivation (with immune compromise)

Progressive primary TB

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21
Q

Describe Progressive Primary TB lesions

A

Resembles acute bacterial pneumonia

Lobar consolidation

Hilar adenopathy

Pleural effusion

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22
Q

Progressive Primary TB sequelae?

A

Miliary pulmonary TB

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23
Q

Secondary TB lesion?

A

Simon focus: Apical consolidation

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24
Q

Secondary TB sequelae?

A

Healing by fibrosis

Localized cascating destructive lesions

Progressive secondary TB

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25
Progressive Secondary TB lesions?
Spread into adjacent lung → erosion into bronchi/vessels → cavitation Pleural involvement: effusions, empyema, obliterative fibrous pleuritis
26
Progressive Secondary TB sequelae?
Healing by fibrosis Miliary pulmonary TB
27
Miliary pulmonary TB lesions?
Scattered small foci of consolidation throughout lungs
28
Miliary pulmonary TB sequelae?
Systemic Miliary TB
29
What is the most common extrapulmonary TB manifestation?
Lymphadenitis (Scrofula)
30
What is TB osteomyelitis called when it affects vertebrae?
Pott disease
31
Which part of the GI tract is most commonly affected by TB?
Ileum
32
What are the two forms of hematogenously spread TB?
Disseminated TB (multiple organs) Miliary TB (specific pattern)
33
How is miliary TB pathologically identified?
Multiple small, yellow-white foci scattered throughout organ parenchyma
34
What patient population gets disseminated MAI infection?
Profoundly immunocompromised patients
35
Histologic hallmark of MAI infection?
Macrophages filled with acid-fast bacilli
36
What organism causes leprosy?
Mycobacterium leprae
37
Compare tuberculoid vs lepromatous leprosy immunity
Tuberculoid: Intact cell-mediated immunity Lepromatous: Depressed cell-mediated immunity
38
Nerve involvement in both leprosy forms
Tuberculoid: Asymmetric Lepromatous: Symmetric
39
Lepromin skin test results
Tuberculoid: Positive Lepromatous: Negative
40
Histology of tuberculoid leprosy
Granulomatous inflammation around nerves
41
Histology of lepromatous leprosy
Macrophages (Lepra cells) filled with acid-fast bacilli (Globi)
42
Causative organism of syphilis
Treponema pallidum
43
Two key histologic features of syphilis
Plasma cell-rich inflammation Obliterative endarteritis
44
What is the hallmark lesion of primary syphilis?
Painless anogenital chancre (heals spontaneously)
45
Name 3 features of secondary syphilis
Mucocutaneous lesions Condyloma lata (broad-based plaques) Systemic symptoms (fever, malaise, lymphadenopathy)
46
What is condyloma lata?
Broad-based, painless plaques in secondary syphilis
47
What organs are affected in tertiary syphilis?
Aorta, CNS, Liver, Bones, Testes
48
What is a gumma?
Granuloma with central coagulative necrosis surrounded by plasma cells
49
When does congenital syphilis occur?
During maternal primary/secondary syphilis (high organism burden)
50
Name 3 classic congenital syphilis stigmata
Saddle nose deformity Hutchinson teeth Saber shin
51
What triad makes up Hutchinson's syndrome?
Interstitial keratitis + Hutchinson teeth + 8th nerve deafness
52
What are the screening tests for syphilis?
Non-treponemal tests (RPR, VDRL)
53
When are false-positive RPR/VDRL results seen?
Pregnancy, autoimmune disorders, other infections
54
What causes false-negative RPR/VDRL?
Prozone phenomenon (antibody excess prevents flocculation)
55
What are the confirmatory tests for syphilis?
Treponemal tests (FTA-ABS, MHA-TP)
56
What organisms are included in Rickettsial diseases?
Rickettsia, Orientia, Ehrlichia, Anaplasma
57
Match the disease to its vector: Epidemic typhus Scrub typhus RMSF Ehrlichiosis Anaplasmosis
Lice Chigger mites Dog tick Lone star tick Deer tick
58
What is the main pathogenic mechanism of Rickettsial infections?
Endothelial cell infection → vasculitis → endothelial injury
59
What are the histologic findings in Rickettsial infections?
Vasculitis with mononuclear inflammation ± necrosis, thrombosis, hemorrhage
60
What is the major fatal complication of RMSF?
ARDS from pulmonary vasculitis
61
What causes Lemierre syndrome?
Fusobacterium necrophorum → thrombophlebitis of jugular vein
62
What anaerobes commonly cause: Head/neck infections Abdominal infections Female genital infections
Prevotella/Porphyromonas Bacteroides + E. coli Prevotella + E. coli/GBS
63
What does C. perfringens cause?
Gas gangrene (wounds/uterus), food poisoning, bowel sepsis
64
Why is C. septicum gangrene concerning?
Associated with underlying malignancy
65
How does tetanus present?
Spastic paralysis from toxin in wounds/neonatal stumps
66
What disease does C. botulinum cause and what type of paralysis?
Botulism - flaccid paralysis
67
How does C. botulinum typically grow to cause disease?
In inadequately cooked/preserved foods (anaerobic conditions)
68
What condition does C. difficile cause?
Pseudomembranous colitis
69
When does C. difficile proliferate to cause disease?
When normal gut bacteria are reduced by antibiotics
70
Compare C. botulinum vs C. difficile:
Botulinum: Foodborne, neurotoxin → flaccid paralysis Difficile: Antibiotic-associated, colon toxin → pseudomembranous colitis