⬅ Home
2# Bacterial Infections
1. Which laboratory test is most specific for identifying Streptococcus agalactiae?
Optochin sensitivity
Positive hippurate hydrolysis test
Bile solubility
Oxidase positivity
Explanation:
Group B Streptococcus is characteristically hippurate hydrolysis positive, which helps differentiate it from other streptococci.
2. The MOST important reservoir contributing to late-onset neonatal GBS disease is:
Maternal vagina during delivery
Neonatal respiratory tract
Contaminated medical equipment
Breast milk or placenta capsules
Explanation:
Late-onset neonatal GBS disease has been linked to contaminated placenta capsules and breast milk.
3. Which virulence factor is the MAIN determinant of pathogenicity in Streptococcus agalactiae?
Polysaccharide capsule
CAMP factor
Hyaluronidase
IgA-binding proteins
Explanation:
The polysaccharide capsule is the main virulence factor and provides resistance to phagocytosis.
4. Late-onset neonatal GBS infection is MOST commonly associated with:
Pneumonia
Granulomatosis infantiseptica
Purulent meningitis
Necrotizing enterocolitis
Explanation:
Purulent meningitis is the most common manifestation of late-onset GBS disease.
5. Which characteristic best differentiates Listeria monocytogenes from Group B Streptococcus?
β-hemolysis on blood agar
Tumbling motility at 25°C
CAMP test positivity
Hippurate hydrolysis
Explanation:
Listeria shows characteristic tumbling motility at 25°C and umbrella growth in semi-solid media.
6. Cephalosporins are ineffective against Listeria monocytogenes because:
The organism is intracellular
Listeria lacks penicillin-binding proteins
β-lactamase production
Intrinsic resistance despite in-vitro susceptibility
Explanation:
Listeria is clinically resistant to cephalosporins despite laboratory sensitivity.
7. Which virulence factor allows Listeria monocytogenes to spread from cell to cell?
ActA protein
Internalin A
Listeriolysin O
Phospholipase C
Explanation:
ActA promotes actin polymerization, enabling intracellular motility and cell-to-cell spread.
8. Granulomatosis infantiseptica is classically associated with:
Early-onset GBS infection
Late-onset neonatal sepsis
Early-onset listeriosis
Congenital toxoplasmosis
Explanation:
Early-onset neonatal listeriosis may present with granulomatosis infantiseptica.
9. The neurotoxin responsible for spastic paralysis in tetanus acts by inhibiting:
Acetylcholine release
Dopamine synthesis
Glycine receptors
GABA release
Explanation:
Tetanospasmin inhibits release of inhibitory neurotransmitters, especially GABA, causing spastic paralysis.
10. The characteristic “drumstick” appearance of Clostridium tetani is due to:
Central spore
Large terminal spore
Capsule formation
Swarming motility
Explanation:
A large round terminal spore gives C. tetani its classic drumstick appearance.
11. Neonatal tetanus most commonly results from:
Application of animal dung to umbilical stump
Transplacental transmission
Breast milk contamination
Hospital-acquired infection
Explanation:
Poor umbilical cord hygiene is the classic cause of neonatal tetanus.
12. Botulinum toxin causes paralysis by inhibiting release of:
GABA
Glycine
Acetylcholine
Norepinephrine
Explanation:
Botulinum toxin blocks acetylcholine release, resulting in flaccid paralysis.
13. Which food is MOST strongly associated with infant botulism?
Canned vegetables
Smoked fish
Fermented dairy
Honey
Explanation:
Infant botulism results from ingestion of spores, classically from honey.
14. Which feature helps differentiate botulism from Guillain-Barré syndrome?
Descending paralysis
Preserved sensation and consciousness
Respiratory failure
Autonomic dysfunction
Explanation:
Botulism presents with flaccid paralysis without sensory loss or altered consciousness.
15. Mycobacterium leprae primarily infects which cell type?
Schwann cells
Keratinocytes
Macrophages only
Endothelial cells
Explanation:
Schwann cell involvement explains the prominent peripheral neuropathy in leprosy.
16. Lepromatous leprosy is characterized by:
Strong cell-mediated immunity
Pauci-bacillary lesions
Multi-bacillary disease
Localized skin lesions
Explanation:
Lepromatous leprosy shows poor immunity and heavy bacillary load.
17. The “pack of cigars” appearance on slit-skin smear is seen in:
Tuberculoid leprosy
Borderline leprosy
Indeterminate leprosy
Lepromatous leprosy
Explanation:
Dense clumps of bacilli inside macrophages are typical of lepromatous leprosy.
18. Which drug combination is correct for treating tuberculoid leprosy?
Rifampicin + dapsone + clofazimine
Rifampicin + dapsone
Dapsone alone
Isoniazid + rifampicin
Explanation:
Tuberculoid leprosy is treated with rifampicin and dapsone for 6 months.
19. Which feature is typical of tuberculoid leprosy?
Visible nerve enlargement
Diffuse skin lesions
High infectivity
Foamy macrophages
Explanation:
Tuberculoid leprosy shows strong immunity with localized disease and enlarged nerves.
20. Mycobacterium leprae cannot be cultivated in vitro primarily because it is:
Acid-fast negative
Spore forming
An obligate intracellular slow grower
Anaerobic
Explanation:
M. leprae is an obligate intracellular organism and cannot grow in cell-free media.