Question 1. Anaerobic bacteria are intrinsically resistant to:
- Beta lactams
- Metronidazole
- Aminoglycoside
- Meropenem
Answer. (3) (Aminoglycoside)
Read And Learn More: Micro Biology And Immunology Multiple Choice Question And Answers
All anaerobic bacteria are intrinsically resistant to Aminoglycoside, quinolones, fosfomycin, trimethoprim, aztreonam
Species-dependant intrinsically resistance in anaerobes :
- Metronidazole : Propionibacterium and Actinomyces
- Rifampicin: F. necrophorum, F. mortiferum
- Cephalosporins: difficile
- Cefotetan & vancomycin: innocuum
- Bacteroides fragilis group: Aminoglycosides, aminopenicillins
- Fusobacterium: Macrolides
Question 2. True about obligate anaerobes:
- In absence of oxygen it grows well
- In absence of oxygen, it does not grow
- In presence of oxygen, it grows but does not utilize the oxygen
Answer. (1) (In absence of oxygen it grows well)
- Obligate anaerobes grow only in absence of oxygen as oxygen is lethal to them.
- Aerotolerant anaerobes tolerate oxygen for some time and grow in presence of oxygen,but do not utilize.
Question 3. Gas gangrene and Tetanus caused by which group of bacteria:
- Campylobacter
- Clostridium
- Citrobacter
- Cardiobacterium
Answer. (2) (Clostridium)
- Gas gangrene is caused by Clostridium perfringens and Tetanus is caused by Clostridium tetani.
Question 4. Nonmotile clostridia is:
- Cl. perfringens
- Cl. novyi
- Cl. botulinum
- Cl. difficult
Answer. (1) (Cl. perfringens)
- All Clostridia are motile except Cl. perfringens and Cl. tetani type VI.
- Clostridia show stately type of motility.
- All Clostridia are noncapsulated except Cl. perfringens and Cl. butyricum.
Question 5. Oval bulging terminal spores seen in:
- Cl. tertium
- Cl. welchii
- Cl. perfringens
- Cl. histolyticum
Answer. (1) (Cl. tertium)
All clostridia produce bulging spore (spore are wider than the bacilli) except
- Cl.bifermentans and Cl. sordelli tertium produces Oval and terminal spore (tennis racket shaped)
Question 6. True statement about Clostridium perfringens are all except:
- Gas gangrene—alpha toxin is produced by type A strains and responsible for profound toxemia
- Clostridium perfringens is not the major cause of gas gangrene
- Present in normal feces
- C.perfringens types C strains are responsible for necrotizing enteritis
Answer. (2) (Clostridium perfringens is not..)
- Clostridium perfringens is the most common cause of gas gangrene (60% of the total cases) followed by novyi and septicum (20–40%)
Question 7. A male is presented with left mid thigh crushed injury. Which is the most essential step to prevent gas gangrene in this patient?
- Wound debridement
- Anti-gas gangrene serum
- Anti tetanus
- Hyperbaric oxygen
Answer. (1) (Wound debridement)
Early surgical debridement is the most crucial step in the management of gas gangrene to remove all devitalised tissues so as to remove conditions that produce anaerobiosis.
Question 8. True about gas gangrene:
- a-toxin is main cause of the toxaemia associated with gas gangrene
- Caused by mainly Clostridium intestinale
- Low oxygen tension in tissue is important precondition
- Devitalized tissue predisposes to gas gangrene
- Not occur if dead tissue is not present
Answer. (1, 3, 4, 5) (a-toxin is main cause of the toxaemia associated with gas gangrene, Lowoxygen tension in tissue is important precondition, Devitalized tissue predisposes to gas gangrene, Not occur if dead tissue is not present)
- a-toxin is the principle virulence factor of gas gangrene
- Gas gangrene is mainly caused Clostridium perfringens
- The development of gas gangrene requires an anaerobic environment and contamination of a wound with perfringens.
- Devitalized tissue, foreign bodies, and ischemia reduce locally available oxygen levels and favor outgrowth of perfringens.
- In the absence of devitalized tissue, the presence of clostridia does not necessarily lead to infection.
Question 9. Best treatment for contaminated wound with necrotic material is:
- Anti-gas gangrene serum
- Debridement
- Antibiotics
- Tetanus toxoid
Answer. (2) (Debridement)
- Contaminated wound with necrotic material is suggestive of higher risk of clostridial infection and gas gangrene.
Question 10. Regarding Clostridium perfringens gas gangrene, false is:
- Common cause of gas gangrene
- Nagler reaction positive
- Most common toxin is Hyaluronidase
- Food poisoning strain of Cl. perfringens produces heat resistant spores
Answer. (3) (Most common toxin is Hyaluronidase)
- Most common toxin is ‘α toxin’ not ‘Hyaluronidase’
- Cl. perfringens produces 4 Major (Lethal) Toxins alfa, beta, iota, epsilon
- Commonest cause of gas gangrene is Clostridium perfringens type A (60%)
About Other Options
Option b: Nagler reaction positive for Cl. perfringens and Cl. bifermentans
For detail of Nagler’s reaction: Refer Chapter review
Option d: Food poisoning strain of Cl. perfringens (mostly Type A) characterized by their marked heat-resistant spores but feeble production of α and theta toxin.
Instead they produce heat-labile enterotoxin (similar to LT of coli)
Also remember
‘Gas gangrene-producing Cl. perfringens strains do not produce Spores in tissue/media.
Question 11. Gastrointestinal enteritis necroticans is caused by:
- Clostridium difficile
- Clostridium perfringens
- Botulinum
- Campylobacter jejuni
- Pseudomonas
Answer. (2) (Cl. perfringens)
Enteritis necroticans (Pigbel in New Guinea):
- Caused by Cl. Perfringens type-C strains with heat resistant spores
- Spores germinates in intestine producing beta toxin
- Usually following a pig meat diet along with a trypsin inhibitors like sweet potato
Question 12. True about gas gangrene:
- Underlying skin and muscles are normal
- Caused by tetanospasmin toxin
- Muscle rigidity and spasms are characteristic
- Most common organism implicated is perfringens
- Passive immunization does not help
Answer. (4) (Most common organism implicated is perfringens)
- Most common organism implicated in Gas gangrene is Clostridium perfringens followed by novyi and septicum
- Underlying skin and muscles are gangrenous
- Gas gangrene is caused by α-toxin
- Pain and crepitus in muscle are characteristic of Gas gangrene
- Passive immunization Anti α-toxin (anti gas gangrene serum) is of great value for the treatment of Gas gangrene.
Question 13. A 32-year-old male has got clean wound without laceration. He had booster does of TT 6 years back. What is next line of management
- Wound care with single dose of tetanus toxoid
- Wound care with Juman Tet Ig with tetanus toxoid single dose
- Wound care with complete course of tetanus toxoid
- Wound care with no immunization
Answer. (1) (Wound care with single dose of tetanus toxoid)
- Clean wound, TT 6 years back (category B)- One dose of TT is sufficient to prevent transmission.
Question 14. A patient is presented with trismus with opisthotonus position. The probable causative agent is:
- Clostridium tetani
- Clostridium perfringens
- Clostridium difficile
Answer. (1) (Clostridium tetani)
Question 15. Mechanism of action of tetanospasmin:
- Inhibition of GABA release
- Inhibition cAMP
- Inactivation of Ach receptors
- Inhibition of cGMP
Answer. (1) (Inhibition of GABA release)
- Mechanism of action of tetanospasmin is: Acts presynaptically and inhibits of glycine and GABA release that leads to spastic contraction of muscles.
Question 16. Which of the following is false for tetanus?
- Produces heat-resistant spores
- Person-to-person transmission does not occur
- Incubation period is 6–10 days
- Three doses of primary vaccination is protective
Answer. (4) (Three doses of primary…)
According to National immunisation schedule:
- Primary course of immunisation includes:
- ‘3 doses of DPT at 4–8 week apart followed by booster of DPT at 16–24 month followed by booster of DPT at 5–6 year followed by booster of TT at 10 and 16 year.’
About Other options: - C.tetani produces heat-resistant spores
- Person-to-person transmission does not occur in tetanus
- Incubation period of tetanus is 6–10 days.
Question 17. Site of action of tetanus toxin:
- Presynaptic terminal of spinal cord
- Postsynaptic terminal of spinal cord
- Neuromuscular junction
- Muscle fibers
Answer. (1) (Presynaptic…)
- Tetanospasmin: Blocks release of inhibitory transmitters glycine and GABA at CNS and
Pre synaptic terminal of spinal cord → leads to spastic paralysis - The manifestations of Tetanus and strychnine poisoning are similar except
Tetanospasmin acts at Presynaptic terminal whereas strychnine acts at postsynaptic terminal.
Question 18. True about tetanus:
- Gram –ve spore forming organism
- Produces Telanolysin and Tetanospasmin
- Trismus and neck stiffness are early sign
- Generalized tonic-clonic seizure occurs on hyperstimulation
- Wound debridement is necessary
Answer. (2, 3, 4, 5) (Produces Telanolysin and Tetanospasmin, Trismus and neck stiffness are early sign, Generalized tonic tonic-clonic seizure occurs on hyperstimulation, Wound debridement is necessary)
- Option a: Cl. tetani is Gram +ve spore forming organism
- Option b: Tetanolysin and Tetanospasmin are the principle toxin produced by Cl. tetani
- Option c: 1st symptom-↑ masseter tone (trismus/lock jaw) then → descending tetanus
- Option d: ‘Tetanus patient should be isolated to protect them from noise and light which may provoke convulsion’
- Option e: Prophylactic measures include- Wound toilet, antibiotic and most importantly immunization.
Question 19. A 25-year boy is presented with deep injury and abrasions on the left shoulder, thigh and leg with immunization status unknown. What is to be given now?
- DTaP only
- DTaP + Ig
- dTonly
- dT + Ig
Answer. (2) (DTaP + Ig)
DTaP (complete immunization) + Human Tetanus Ig is recommend for this condition.
- Human Tetanus Ig- because it’s a deep injury
- DTaP (complete immunization)- because no h/o immunization. Acellular pertussis (aP) is given instead of killed pertussis vaccine after 5 year of age.
Question 20. A 10-year-old boy following a road traffic accident presents to the casualty with contaminated wound over the left leg. He has received his complete primary immunization before preschool age and received a booster of DT at school entry age. All of the following can be done except:
- Injection of TT
- Injection of human antiserum
- Broad spectrum antibiotics
- Wound debridement and cleaning
Answer. (2) (Injection of human antiserum)
- Treatment of tetanus consists of (Wound debridement + Antibiotic + immunization)
- For treatment of wound injury, we have to know the type of wound and the immune category that the patient belongs to.
- This history is suggestive of:
- 10-year-old child Taken complete immunization with booster of DT at school entry age—indicates taken complete immunization > 5 to < 10 year back So belongs to Immunity category B
- Type of wound- contaminated (other wound categories)
- Treatment required for Category B with contaminated (other wound) Toxoid 1 dose
- Antibiotic has role to eradicate the source of toxin (No role after 6 hour when the toxin is already formed)
- HT Ig has role in category C and D persons, i.when the complete immunization taken > 10 year or the immunization is not complete/unknown.
- Treatment: All type of wounds need surgical toilet followed by: Immunization.
Question 21. A person has received complete immunization against tetanus 10 years ago. Now he presents with a clean wound without any lacerations from an injury sustained 2.5 hours ago. He should now be given:
- Full course of tetanus toxoid
- Single dose of tetanus toxoid
- Human Tet globulin
- Human Tet globulin and single dose of toxoid
Answer. (2) (Single dose of tetanus toxoid)
- Type of wound: Clean wound without any lacerations from an injury sustained 2.5 hours ago
- Patient belongs to Immunity category C complete immunization taken 10 years ago
- So, Treatment required for Category C with simple wound is: Toxoid 1 dose
Question 22. Wrong about Cl. tetani:
- Main reservoir- Soil, human and animal intestine
- MC mode of transmission- Trauma and contaminated wound
- Herd immunity- not useful
- MC season –winter and dry
Answer. (4) (MC season –winter and dry)
- Tetanus shoes seasonal variation, in India, > 50% of cases occur in- July to September
- Main reservoir: Soil, human and animal intestine
- MC mode of transmission: Trauma and contaminated wound
- Herd immunity not useful for tetanus
Question 23. For neontatal tetanus elimination, the incidence should be….:
- Less than 0.5/1000 live birth
- Less than 1/1000 live birth
- Less than 0.1/1000 live birth
- Less than 10/1000 live birth
Answer. (3) (Less than 0.1/1000 live birth)
Question 24. Period of communicability for tetanus:
- 7 days
- 14 days
- 21 days
- None
Answer. (4) (None)
- Tetanus is NOT infectious from man to man.
Question 25. An adult with no immunization history presents with a clean non-penetrating wound 2 hrs back. What measure has to be taken?
- Full course of tetanus toxoid
- Single dose of tetanus toxoid
- Nothing required
- Human Tet globulin and single dose of toxoid
- Clostridium botulinum
Answer. (1) (Full course…)
- It’s a case of simple wound (clean and non penetrating) and category-D (unimmunized)
- The recommendation for simple wound and category D is Full dose of tetanus toxoid
- Clostridium Botulinum
Question 26. True about food botulism:
- Symptoms resembles strychnine poisoning
- Most common botulinum toxin serotype is type C and D
- The bacteria invades the intestine
- Botulinum toxin acts by blocking A.ch release
Answer. (4) (Botulinum toxin acts by blocking A.ch release)
- MC botulinum toxin is serotype A, B, and Most severe is type A
- Tetanus resembles strychnine poisoning
- C. botulinum is non invasive. Disease is toxin mediated.
Question 27. True about Botulinum toxin:
- Interfere with adrenergic transmission
- Interfere with Cholinergic transmission
- Increase release of synaptic vesicles
- Inhibit release from synaptic vesicles
- Act also on CNS
Answer. (2, 4) (Interfere with Cholinergic transmission, Inhibit release from synaptic vesicles)
Botulinum toxin blocks the release of Acetylcholine at synapses of NM junction (MC site), peripheral ganglia and parasympathetic nerve ending; however it has no action on CNS.
Question 28. Botulism is most commonly due to:
- Egg
- Milk
- Meat
- Canned vegetables
Answer. (4) (Canned vegetables)
- The most common food associated with botulism are home-preserved foods such as home-canned vegetables, smoked or pickled fish, homemade cheese and similar low acid food.
Question 29. Botulism causes:
- Descending flaccid paralysis
- Descending spastic paralysis
- Ascending paralysis
- Ascending spastic paralysis
Answer. (1) (Descending flaccid paralysis)
- Botulism blocks acetylcholine release, hence causes Descending flaccid paralysis.
Question 30. Botulinum affects all except:
- Neuromuscular junction
- Preganglionic junction
- Postganglionic nerves
- CNS
Answer. (4) (CNS)
- ‘Botulinum neurotoxin, acts on peripheral cholinergic nerve terminals, but not on CNS:
Question 31. An 18-year-old male presented with acute onset descending paralysis of 3 days duration. There is also history of blurring of vision for the same duration. On examination, the patient has quadriparesis with areflexiBoth the pupils are nonreactive The most probably diagnosis is:
- Poliomyelitis
- Botulism
- Diphtheria
- Porphyria
Answer. (2) (Botulism)
Points in favor:
Descending paralysis, blurring of vision, quadriparesis (flaccid paralysis), areflexia and nonreactive pupils
Also know:
- Causes of Descending paralysis: Tetanus, botulism, polio, diphtheria
- Tetanus causes spastic paralysis whereas botulism causes flaccid paralysis
Question 32. The following statements are true regarding botulism except:
- Infant botulism is caused by ingestion of preformed toxin
- Clostridium botulinum A, B, C and F cause human disease
- The gene for botulinum toxin is encoded by a bacteriophage
- Clostridium baratti may cause botulism
Answer. (1) (Infant botulism is caused by ingestion of preformed toxin)
- ‘Infant botulism occurs due to ingestion of Clostridium botulinum and toxin is released inside.
Whereas foodborne botulism occurs due to preformed toxin mixed with canned food’
Question 33. Among the toxin produced by Clostridium botulinum, the non-neurotoxic one is:
- A
- B
- C1
- C2
- D
Answer. (4) (C2)
All subtypes (A–G) of Botulinum toxin are pharmacologically similar (neurotoxin), except C2 (enterotoxin)
Question 34. Most sensitive test to detect Clostridium difficile diarrhea:
- PCR to detect toxin gene
- Culture
- Histopathology of intestinal biopsy
- Rapid test to detect toxin antigen
Answer. (1) (PCR to detect toxin gene)
- PCR to detect toxin B gene is the highly sensitive and specific for diagnosis of C.difficile infection.
Question 35. A 47-year-old hospitalized man who has received multiple antibiotics in the last 10 days develops diarrheA fecal sample is sent to the laboratory. Which of the following test is used to establish Clostridium difficile as a causative agent of diarrhea?
- Immunofluorescence
- ELISA for toxins
- PCR for toxin genes
- Culture
Answer. (2) (ELISA for toxins)
- Clostridium difficile is commensal in human gut; it can cause antibiotic-associated diarrhea only when it expresses the toxin genes to produce toxins such as Toxin A and B.
- Hence, mere isolation by culture cannot differentiate between a commensal C.difficile with a pathogenic C.difficil Detection of toxin gene by PCR can tell you that it’s a toxigenic strain, but cannot confirm the expression of those genes to produce the toxin.
- Hence, though it is a controversial MCQ, the best answer in this case would be direct detection of toxin antigens by ELISA which reveals its pathogenic association with a diarrhea casHowever, the final answer depends upon the mind setup of question paper setter.
Question 36. Cause of Clostridium difficile-associated diarrhea:
- Trauma
- Dairy products
- Fried rice
- Antibiotic use
Answer. (4) (Antibiotic use)
- Prolonged broad-spectrum antibiotic therapy is the most important risk factor for
Clostridium difficile-associated diarrhea.
Question 37. Pseudomembranous colitis is caused by:
- Clostridium perfringens
- Clostridium difficile
- Clostridium tetani
- Clostridium botulinum
Answer. (2) (Clostridium difficile)
- Pseudomembranous colitis is caused by Clostridium difficile
Question 38. Clostridium difficile infection occurs after:
- After prolong antibiotic therapy
- Pantoprazole increases the risk
- Associated with use of rectal thermometer
- Increased with proportion of hospital stay
Answer. (1, 2, 3, 4) (After prolong antibiotic therapy, Pantoprazole increases the risk, Associated with use of rectal thermometer, Increased with proportion of hospital stay)
Question 39. Pseudomembranous colitis, all are true except:
- Toxin A is responsible for clinical manifestation
- Toxin B is responsible for clinical manifestation
- Blood in stools is a common feature
- Summit lesions is an early histopathological finding
Answer. (3) (Blood in stools is a common feature)
Says: Stools are almost never Grossly bloody and range from unformed to watery or mucoid in consistency, with a characteristic odor.
About Other option:
- Cl. difficile Toxins: A → Enterotoxin and B → Cytotoxin
- Both are required for manifestation.
- In the earliest stage, Summit lesion, i.tiny superficial intercryptal erosions may be founTopley 10/e p1120
Question 40. A patient of acute lymphocytic leukemia with fever and neutropenia develops diarrhea after administration of amoxycillin therapy, which of the following organism is most likely to be the causative agent:
- Salmonella typhi
- Clostridium difficile
- Clostridium perfringens
- Shigella flexneri
Answer. (2) (Clostridium difficile)
Points favoring diarrhea after administration of amoxicillin therapy
Question 41. DOC for pseudomembranous enterocolitis:
- Oral vancomycin
- Penicillin
- Oral ampicillin
- Clindamycin
Answer. (1) (Oral vancomycin)
Etiological agent for pseudomembranous enterocolitis is Clostridium difficile.
Treatment of Clostridium difficile infection: Refer chapter review
Question 42. With reference to Bacteroides fragilis the following statements are true, except:
- B.fragilis is the most frequent anaerobe isolated from clinical samples
- B.fragilis is not uniformly sensitive to metronidazole
- The lipopolysaccharide formed by fragilis is structurally and functionally different from the conventional endotoxin
- Shock and disseminated intravascular coagulation are common in Bacteroides bacteremia
Answer. (4) (Shock and disseminated intravascular coagulation are common in Bacteroides bacteremia) B.‘fragilis LPS are 100–1000 times less biologically potent than endotoxin associated with aerobic gram-negative bacteria.
This accounts for the lower frequency of DIC and purpura in Bacteroides bacteremia than in facultative aerobic gram-negative bacillary bacteremia.’
About Other options:
Option a: ‘Bacteroides are the most common anaerobes isolated in clinical specimen.’
Option b: ‘Metronidazole is active against gram-negative anaerobes, including the B. fragilis group; resistance is rare but has been reported’ Harrison
Question 43. A patient presents with frontal abscess. Foul smelling pus is aspiratePus shows red fluorescence on ultraviolet examination. The most likely organism causing the frontal abscess is:
- Bacteroides
- Peptostreptococcus
- Pseudomonas
- Acanthamoeba
Answer. (1) (Bacteroides)
- Frontal abscess with foul smelling pus: Points towards anaerobic infection
- Fluorescence on ultraviolet examination: Indicates Prevotella melaninogenica which was previously classified under Bacteroides infection.
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