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USMLE STEP 1, 2, 3 > Internal Medicine_Infectious Diseases_4 > Flashcards

Internal Medicine_Infectious Diseases_4 Flashcards

Bacteria_Clostridium, Clostridioides (D. diff), and Bacteroides.

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USMLE® Step 1 flashcards
1
Q

What is the Gram-stain and morphology of Clostridium spp.?

A

Gram-positive, spore-forming, obligate anaerobic rod.

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2
Q

What toxin does Clostridium tetani produce?

A

Tetanospasmin, an exotoxin.

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3
Q

What is the mechanism of action of tetanospasmin?

A

Cleaves SNARE proteins involved in neurotransmitter release and blocks release of GABA and glycine from Renshaw cells in the spinal cord via retrograde axonal transport.

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4
Q

What are the clinical manifestations of Clostridium tetani infection?

A

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

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5
Q

What is the pathogenesis of Clostridium tetani?

A

Pathogen remains localized to wound site; toxin spreads.

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6
Q

How can Clostridium tetani be prevented?

A

Tetanus vaccine.

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7
Q

What is the treatment for Clostridium tetani infection?

A

Antitoxin (tetanus immune globulin), ± vaccine booster, antibiotics, diazepam (for muscle spasms), wound debridement.

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8
Q

What is the Gram-stain and morphology of Clostridium botulinum?

A

Gram-positive, spore-forming, obligate anaerobic rod.

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9
Q

What toxin does Clostridium botulinum produce?

A

Botulinum toxin (heat-labile).

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10
Q

What is the mechanism of action of botulinum toxin?

A

Cleaves SNARE proteins and blocks ACh release at the neuromuscular junction → flaccid paralysis.

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11
Q

What are the clinical manifestations of Clostridium botulinum infection?

A

Flaccid paralysis, floppy baby syndrome in infants (caused by ingestion of spores in honey), ingestion of preformed toxin in adults (e.g., canned food), key symptoms (5 Ds): diplopia, dysarthria, dysphagia, dyspnea, descending flaccid paralysis.

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12
Q

What are the key features of Clostridium botulinum infection?

A

No sensory deficits.

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13
Q

What is the source of Clostridium botulinum?

A

Contaminated food (e.g., canned goods, honey, or bad bottles of food/juice).

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14
Q

What is the treatment for Clostridium botulinum infection?

A

Human botulinum immunoglobulin and local Botox injections (used for focal dystonia, hyperhidrosis, muscle spasms, cosmetic purposes).

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15
Q

What is the Gram-stain and morphology of Clostridium perfringens?

A

Gram-positive, spore-forming, obligate anaerobic rod.

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16
Q

What toxin does Clostridium perfringens produce?

A

α-Toxin (lecithinase, a phospholipase).

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17
Q

What is the mechanism of action of α-Toxin?

A

Degrades cell membranes → myonecrosis (gas gangrene) and hemolysis.

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18
Q

What are the clinical manifestations of Clostridium perfringens infection?

A

Gas gangrene (presents as soft tissue crepitus) and food poisoning: late-onset (10–12 hours) watery diarrhea and abdominal cramping; resolves within 24 hours.

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19
Q

What is the pathogenesis of Clostridium perfringens?

A

Spore-contaminated food cooked at low temperatures and left standing allows spores to germinate.

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20
Q

What are the associated features of Clostridium perfringens?

A

Spontaneous gas gangrene can occur via hematogenous seeding; most commonly caused by Clostridium septicum in colonic malignancy.

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21
Q

What type of bacteria is Clostridium tetani?

A

A gram-positive bacillus, obligate anaerobe, and spore-former.

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22
Q

Where is Clostridium tetani commonly found in the environment?

A

In soil.

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23
Q

What features of Clostridium tetani enable its survival in harsh conditions?

A

The ability to form metabolically inactive spores resistant to heat, radiation, and chemicals.

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24
Q

How does Clostridium tetani typically infect humans?

A

Through puncture wounds from rusty nails or barbed wire.

Animal feces.

Infants could have an infected umbilical stump.

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25
Q

What is the main toxin produced by Clostridium tetani?

A

Tetanospasmin, a protease that targets SNARE proteins.

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26
Q

How does tetanospasmin affect neurons?

A

It is transported retrogradely along axons to the spinal cord.
It cleaves SNARE proteins in Renshaw cells, inhibiting the release of GABA and glycine (inhibitory neurotransmitters).

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27
Q

What is the result of the toxin’s action on the nervous system?

A

Spastic paralysis.
Classic symptoms include risus sardonicus (an “evil grin”) and lockjaw (trismus).
Severe cases involve opisthotonos (arched back due to neck and spine muscle contraction).
Failure to thrive in infants.

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28
Q

What are the hallmark signs of tetanus?

A

Lockjaw (trismus).
Risus sardonicus (evil grin).
Opisthotonos (backward arching of the head, neck, and spine).
Hyperreflexia.

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29
Q

What is the primary method for preventing tetanus?

A

Tetanus vaccine (DTaP or Tdap), a toxoid vaccine that induces an antibody response to the inactivated toxin. Co-administered with diphtheria and pertussis vaccines as DTaP for children or Tdap for older children and adults. The tetanus vaccine is a toxoid vaccine, which means it is derived from a toxin that has been made harmless, but still provokes an immune response. This produces an antibody response to the toxin, not to the organism itself.

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30
Q

How are active tetanus infections managed?

A
  • Metronidazole
  • Benzodiazepine
  • For clean, minor wounds: Administer the vaccine if the patient has had fewer than three doses or if the last dose was given over 10 years ago.
  • For dirty or severe wounds: Administer the vaccine if the last dose was given more than 5 years ago. Add tetanus immunoglobulin (Ig) if the patient has received fewer than three doses.
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31
Q

What type of bacteria is Clostridium botulinum?

A

A gram-positive, spore-forming, obligate anaerobe.

32
Q

How is Clostridium botulinum typically transmitted?

A

Through improperly canned foods, which create anaerobic conditions that allow spores to germinate and produce botulinum toxin.

33
Q

Why should honey be avoided in infants under 12 months?

A

Honey may contain Clostridium botulinum spores, which can germinate in the underdeveloped GI tract of infants and cause floppy baby syndrome, a condition caused by Clostridium botulinum spores colonizing the intestines of infants, leading to toxin production and resulting in hypotonia and weakness.

34
Q

What environmental feature makes C. botulinum spores resilient?

A

he ability to form metabolically inactive spores resistant to heat, radiation, and chemicals.

35
Q

What is the primary toxin produced by Clostridium botulinum?

A

Botulinum toxin, a protease that cleaves SNARE proteins.

36
Q

How does botulinum toxin affect neurons?

A

It inhibits the release of acetylcholine at the neuromuscular junction, leading to flaccid paralysis. The toxin prevents vesicle fusion with the presynaptic membrane by cleaving SNARE proteins.

37
Q

What is the progression of paralysis in botulism?

A

Begins with cranial nerve dysfunction (e.g., ptosis and diplopia).
Progresses to descending flaccid paralysis involving the trunk and limbs.
Finally the associated symptoms are constipation, poor feeding, repiratory failure.

38
Q

What are the initial symptoms of botulism?

A

First: Bulbar symptoms: Diplopia (double vision), ptosis (drooping eyelids).
Second: Descending flaccid paralysis (symmetrical weakness).

39
Q

How is botulism diagnosed?

A

Stool antigen.

Clinical suspicion of botulism may be confirmed by quickly identifying the toxin in bodily fluids (e.g., serum, vomit, gastric acid, stool) and/or food.

Supportive: repetitive nerve stimulation study.

40
Q

What are the two main types of Botulism?

A

Foodborne botulism
most commonly in adults and due to ingestion of pre-formed toxin

Infant botulism
most commonly in infants and due to ingestion of spores

41
Q

What is the best measure for the prevention of Foodborne botulism?

A

Sterilization of food in a pressure cooker (autoclave) should be done at 121°C (249°F) for a minimum of 15 minutes, or at 134°C (273°F) for a minimum of 3 minutes.

Food should be boiled twice before being canned to kill spores that may have germinated after the first round of boiling. The temperature should be at 100°C (212°F). In contrast to the spores, the toxin can be destroyed by being boiled once at 100°C (212°F) for 15 minutes.

42
Q

How is food botulism managed?

A

In adults, and patients older than 1-years-old, the administration of equine botulinum antitoxin may improve the outcome and the course of the disease and is less costly than the human-derived form that is given to patients less than 1 years old.

Eradication of toxin through bowel emptying (induced by medication).

43
Q

What type of bacterium is Clostridium perfringens?

A

Clostridium perfringens is a gram-positive, spore-forming bacillus that can grow in dirt and soil.

44
Q

What type of infections is Clostridium perfringens associated with?

A

Gas gangrene (clostridial myonecrosis):
A soft tissue infection leading to gas production and tissue necrosis.

Food poisoning:
Due to ingestion of a large number of spores producing toxins in the gut.

45
Q

What environmental conditions favor the growth of Clostridium perfringens spores?

A

Spores are metabolically inactive but resistant to:
Heat, Radiation, and Chemical exposure

46
Q

How is Clostridium perfringens classified in terms of oxygen requirements?

A

It is classified as an obligate anaerobe or an aerotolerant anaerobe (can live in conditions with very low oxygen).

47
Q

What is the characteristic appearance of Clostridium perfringens on blood agar?

A

It forms a double zone of hemolysis:

Complete (beta-hemolysis) inner hemolysis (theta toxin).
Partial (alpha-hemolysis) outer hemolysis (alpha toxin).
48
Q

What is the primary toxin produced by Clostridium perfringens responsible for gas gangrene?

A

The alpha toxin:

It cleaves lecithin in cell membranes.
Causes red blood cell hemolysis and tissue necrosis.
49
Q

What are the clinical features of food poisoning caused by Clostridium perfringens?

A

Watery diarrhea

Symptoms typically begin 2–12 hours after ingestion of improperly stored or reheated food.

50
Q

What is the preferred first-line treatment for Clostridium perfringens gas gangrene?

A

Clostridial myonecrosis, also known as gas gangrene, is characterized by gas production under the infected tissue. This gas is produced as the organism consumes carbohydrates and can be detected as crepitus, or a crackling sensation on palpation.

IV Penicillin G

May require surgical debridement.

51
Q

What historical context is associated with Clostridium perfringens infections?

A

Historically associated with wounds sustained in military combat settings, particularly those contaminated with soil or fecal matter.

52
Q

What unique environmental feature allows Clostridium perfringens to persist in soil?

A

Its ability to form metabolically inactive spores allows it to survive harsh environmental conditions.

53
Q

What type of bacterium is Clostridioides difficile?

A

Gram-positive, spore-forming, obligate anaerobe.

54
Q

What is the primary transmission route for C. diff?

A

Fecal-oral route through ingestion of bacterial spores.

55
Q

What percentage of people have C. diff as part of their normal gut flora?

A

Around 5% of the population have both the toxigenic and non-toxigenic strains.

56
Q

What are common risk factors for C. diff infections?

A

Increased age, recent antibiotic use (e.g., clindamycin, fluoroquinolones, cephalosporins, penicillins), and chronic PPI therapy.

57
Q

What are the toxins produced by C. diff?

A

Toxin A (TcdA) and Toxin B (TcdB).

58
Q

What is the mechanism of action for C. diff toxins?

A

Disrupt cytoskeletons and tight junctions of colonic mucosal cells, increasing permeability and causing inflammation.

Clostridioides difficile toxins A & B primarily disrupt intercellular tight junctions. These toxins inactivate Rho proteins, which are essential for maintaining the integrity of tight junctions. As a result, paracellular permeability increases, allowing toxins and other harmful substances to pass between the cells and cause damage to the gut epithelium.

59
Q

What severe complication can arise from C. diff infection?

A

Toxic megacolon.

60
Q

What tests are used to diagnose C. diff infections?

A

NAAT (nucleic acid amplification test)

PCR for GDH

EIA (enzyme immunoassay).

61
Q

What does a stool test for glutamate dehydrogenase (GDH) indicate?

A

It detects all strains of C. diff but does not distinguish between toxigenic and nontoxigenic strains.

62
Q

What are hallmark symptoms of C. diff infection?

A

High-volume watery diarrhea, often with leukocytosis and fever.

63
Q

What type of colitis is characteristic of C. diff?

A

Pseudomembranous colitis, marked by yellow-white exudates on colonic mucosa. Patients will commonly present with 3 or more watery stools a day, LLQ abdominal pain, fever, and leukocytosis.

64
Q

What indicates a fulminant C. diff infection?

A

3 or more watery stools a day, LLQ abdominal pain, fever, and leukocytosis.

Potentially blood in stool.

Severe pain, Hypotension, Hypovolemia, Shock, paralytic ileus (distention, or megacolon.

65
Q

What is the first-line treatment for non-severe C. diff?

A

Oral vancomycin or fidaxomicin.

66
Q

What indicated severe C. diff?

A

WBC > 15 k
Cr > 1.5 x baseline

67
Q

What is the treatment for severe C. diff?

A

Oral vancomycin or fidaxomicin, sometimes combined with IV metronidazole.

68
Q

How is refractory or recurrent C. diff treated?

A

Prolonged taper of vancomycin or fidaxomicin.

Bezlotoxumab (toxin B monoclonal antibody).

Fecal microbiota transplant (FMT).

69
Q

What is the treatment for fulminant C. diff infection?

A

vancomycin (PO) + metronidazole (IV)

Colectomy

70
Q

Why are C. diff spores resistant to alcohol-based hand sanitizers?

A

They are metabolically dormant and require handwashing with soap and water for removal.

71
Q

What precautions should be taken to prevent C. diff transmission in hospitals?

A

Contact precautions, including gown and gloves, for infected patients.

Handwashing with soap and water.

72
Q

What non-motile, anaerobic, gram-negative rod, found in the human gastrointestinal (GI) tract, particularly the colon, is known to cause endogenous infections (Dental abscesses, pulmonary abscesses, abdominal abscesses, diverticulitis, appendicitis, and gynecological infections)?

A

Bacteroides fragilis

This occurs when there is a breach of Mucosal Barrier from trauma, surgery, or perforation, releasing B. fragilis from the colon into sterile areas (peritoneum, bloodstream, etc.). They can evade the immune system with their capsule (preventing phagocytosis and destroy tissue through proteases and hydrolytic enzymes. They also have Fimbriae/Pili, LPS, and Beta-Lactamases which contribute to their pathogenicity.

73
Q

Bacteroides fragilis most commonly causes _____-microbial intra-abdominal infections leading to abscess formation.

A

Most commonly causes of polymicrobial intra-abdominal infections leading to abscess formation.

Often following bowel perforation (e.g., diverticulitis, appendicitis, trauma, surgery)

74
Q

An intra-abdominal abscess should be treated with … ?

A

Metronidazole (gold standard for anaerobes) due to the high likelihood of B. fragilis (along with others; poly-microbial).

Treatment usually includes:
Beta-Lactam/Beta-Lactamase Inhibitors
(e.g., piperacillin-tazobactam, ampicillin-sulbactam)
Carbapenems
(e.g., imipenem, meropenem)

Surgical Management:
Drainage of abscesses is critical for treatment success

75
Q

When a patient with a history of abdominal surgery, trauma, or perforation presents with fever, abdominal pain, and leukocytosis, think … ?

A

Bacteroides fragilis as part of a polymicrobial infection.

Clostridium spp., E. coli, and Peptostreptococcus are often involved.

76
Q

What is the hallmark virulence factor and a driver of abscess formation with intra-abdominal infections?

A

capsule

77
Q

Question: A 55-year-old male presents with fever, abdominal pain, and tenderness in the right lower quadrant 5 days after undergoing emergency surgery for a perforated appendix. CT scan shows a fluid-filled collection in the right lower quadrant. Which of the following organisms is most likely responsible for the abscess?

(A) Escherichia coli
(B) Bacteroides fragilis
(C) Enterococcus faecalis
(D) Clostridium perfringens
(E) Pseudomonas aeruginosa
A

Answer:
(B) Bacteroides fragilis

While E. coli is a major player in intra-abdominal infections, B. fragilis is the most common anaerobic organism involved in abscess formation. The polysaccharide capsule of B. fragilis promotes abscess formation, distinguishing it from E. coli.

USMLE STEP 1, 2, 3 (45 decks)

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