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USMLE STEP 2 and 3 > Internal Medicine_Infectious Diseases_11 > Flashcards

Internal Medicine_Infectious Diseases_11 Flashcards

Bacteria_e.coli, kleb, Serratia, Salm., Yersinia, Campy, Vibrio, Proteus, Pseudom, Burkholderia

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USMLE® Step 1 flashcards
1
Q
A
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2
Q

What are the common infections caused by Klebsiella pneumoniae, Enterobacter spp., and Serratia marcescens?

A

Enterobacter family of bacteria that play a significant role as nosocomial infections and share the notable trait of multidrug resistance.

Patients tend to get pneumonia and urinary tract infections.

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3
Q

What is a shared feature of Klebsiella pneumoniae, Enterobacter spp., and Serratia marcescens?

A

Multidrug resistance and fermentation of lactose.

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4
Q

What agar do lactose fermenters like Klebsiella pneumoniae form pink colonies on?

A

MacConkey agar.

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5
Q

What is unique about Serratia marcescens’ lactose fermentation?

A

It ferments lactose slowly and can appear non-lactose fermenting initially.

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6
Q

What is a distinguishing feature of Enterobacter spp. in terms of motility?

A

Enterobacter spp. are motile.

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7
Q

Is Serratia marcescens motile?

A

yes

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8
Q

Is Klebsiella pneumoniae motile?

A

No.

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9
Q

What pigment does Serratia marcescens produce?

A

Prodigiosin, which gives a red pigment.

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10
Q

What type of patients are particularly at risk for Klebsiella pneumoniae infections?

A

Alcoholics, and those with aspiration pneumonia or abscess formation.

Other infections: GU infections, bacteremia, and intrabdominal infection.

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11
Q

What enzyme does Klebsiella pneumoniae produce, aiding its pathogenesis?

A

Urease, which hydrolyzes urea into carbon dioxide and ammonia.

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12
Q

What is the consistency and appearance of sputum in Klebsiella pneumoniae infections?

A

Currant jelly-like (viscous, resembling currant jelly).

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13
Q

What radiological findings might you see in a patient with Klebsiella pneumoniae?

A

Cavitation and pulmonary necrosis.

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14
Q

What is the treatment for Klebsiella?

A

Cephalosporins or fluoroquinolne

Consider multi-drug resistance due to ESBL.

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15
Q

What type of bacteria is Salmonella?

A

Salmonella is a gram-negative rod with peritrichous flagella for motility.

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16
Q

what reservoirs usually house Salmonella?

A

poultry, milk, eggs, or pets like turtles.

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17
Q

What protects Salmonella from host defenses?

A

A polysaccharide capsule (O-antigen) helps Salmonella resist host defenses.

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18
Q

How does Salmonella survive within hosts?

A

It is facultative intracellular, able to live inside macrophages.

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19
Q

What is a unique growth trait of Salmonella?

A

It produces hydrogen sulfide (H2S), forming black colonies on certain media.

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20
Q

What serious complications can NTS cause?

A

Gastroenteritis (diarrhea, emesis, abdominal pain, fever).

Bacteremia, meningitis, and osteomyelitis.

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21
Q

How is Salmonella diagnosed?

A

Stool culture.

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22
Q

How is NTS treated?

A

supportive care.

high risk/severe: fluoroquinolones or ceftriaxone

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23
Q

How is typhoidal Salmonella (TS) spread?

A

Through the fecal-oral route, typically via contaminated food or water.

Colonizes the gallbladder (usually asymptomatic patients).

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24
Q

What clinical symptoms are associated with typhoidal Salmonella?

A

Fever (usually step-wise) is the first clinical sign with a high plateau.

Relative bradycardia where HR is lower than anticipated given temp.

Rose spots (macules on chest and abdomen).

Abdominal pain (intestinal bleeding and sepsis due to crossing the intestinal barrier through M cells) by the third week of infection.

Hepatosplenomegaly.

Osteomyelitis.

Meningitis.

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25
Q

What antigen is unique to TS and resists host immunity?

A

Vi polysaccharide capsule antigen.

Allows proliferation in macrophages.

Prevents neutrophilic response
(lack of chemotaxis, opsonization, and oxidative burst)

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26
Q

Where is typhoidal Salmonella (TS) most prevalent?

A

TS infections predominantly occur in developing countries, which may be affected by poor sanitation (i.e., endemic regions are found within South-Central and East Asia as well as Southern Africa).

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27
Q

How is typhoidal Salmonella treated and prevented?

A

Treated with fluoroquinolones or azithromycin and prevented with vaccines (live attenuated or conjugate). A live attenuated vaccine is taken orally to protect against enteric fever. The conjugate vaccine (Vi capsular polysaccharide vaccine linked to Tetanus toxoid protein) is administered as an injection to provide robust protection against enteric fever

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28
Q

Salmonella is _____ labile

A

acid

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29
Q

Which patient population commonly get osteomyelitis from NTS?

A

osteomyelitis commonly occur in patients with sickle cell disease.

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30
Q

Which bacteria are the most common Non-typhoidal Salmonella (NTS)?

A

Salmonella Enteritidis and Salmonella Typhimurium

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31
Q

What is the gram staining and morphology of Shigella spp.?

A

Shigella spp. are gram-negative bacilli.

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32
Q

What type of colonies does Shigella form on Hektoen enteric agar?

A

Blue-green colonies due to the lack of hydrogen sulfide (H2S) production.

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33
Q

What distinguishes Shigella from Salmonella on Hektoen agar?

A

Shigella forms blue-green colonies (no H2S production)

Salmonella forms black colonies

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34
Q

Is Shigella motile or non-motile?

A

Shigella is non-motile.

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35
Q

How does Shigella resist acidic environments?

A

It is acid-stable, requiring fewer microorganisms to cause infection.

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36
Q

What structure does Shigella manipulate for intracellular movement?

A

Actin filaments of the host’s cytoskeleton.

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37
Q

Where in the gastrointestinal tract does Shigella invade?

A

M cells in the Peyer’s patches of the mucosa.

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38
Q

What type of diarrhea is caused by Shigella?

A

Bloody diarrhea with inflammatory cells (leukocytes).

Other symptoms are abdominal cramps and fever.

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39
Q

What severe syndrome can Shigella dysenteriae lead to?

A

Hemolytic Uremic Syndrome (HUS).

Shiga toxin damages endothelial cells in glomeruli, creating schistocytes and causing platelet aggregation, thrombocytopenia, microangiopathic hemolytic anemia (MAHA), with acute kidney injury.

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40
Q

What is the target of Shiga toxin in protein synthesis?

A

The 60S ribosomal subunit.

Shiga toxin produced by Shigella dysenteriae, which is structurally and functionally similar to Shiga-like toxin of enterohemorrhagic E. coli, acts by inactivating the 60S ribosomal subunit, leading to inhibition of protein synthesis.

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41
Q

In which population is HUS most commonly seen?

A

Children under 5 years of age.

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42
Q

What specialized system does Shigella use to inject effector proteins into host cells?

A

Type III secretion system.

Shigella spp. possess a type Ill secretion system, a needle-like apparatus used to inject effector proteins into host cells; these proteins help the bacteria evade host immune responses and promote their invasion and intracellular survival.

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43
Q

How is Shigella spread?

A

Person-to-person.

Food.

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44
Q

How is Shigella diagnosed?

A

stool culture.

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45
Q

How is Shigella treated?

A

fluroquinolone or macrolide.

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46
Q

What is the gram stain and morphology of E. coli?

A

E. coli is a gram-negative rod.

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47
Q

What are the significant subtypes of E. coli, and what diseases are they associated with?

A

ETEC –> most common cause of travelers diarrhea

STEC or ETEC –> invasive bloody diarrhea in children and causes HUS

EPEC –> most common cause of watery diarrhea in developing countries

EIEC –> similar to Shigella causing watery or bloody diarrhea

All are self-limited and require just supportive care with the exception of ETEC which is normally self limited but in severe cases is treated with a macrolide of fluoroquinolone.

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48
Q

How can E. coli be identified on EMB (eosin-methylene blue) agar?

A

It produces a metallic green sheen.

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49
Q

What are the key microbiologic traits of E. coli?

A
  • Ferments lactose
  • Has the K antigen on its capsule (neonatal meningitis)
  • Is catalase-positive
  • Has fimbriae for attachment
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50
Q

What are the common infections caused by E. coli?

A

Urinary tract infections (UTIs)
Neonatal meningitis (k1 capsular antigen)
Gram-negative sepsis

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51
Q

What is the primary transmission method for Enterohemorrhagic E. coli (EHEC)?

A

Consuming undercooked meat.

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52
Q

What distinguishes EHEC from other E. coli types biochemically?

A

EHEC does not ferment sorbitol.

53
Q

What is one of the most significant EHEC strains?

A

O157:H7

The specific serotype of EHEC commonly associated with outbreaks

54
Q

What toxin does EHEC produce, and what is its mechanism of action?

A

Shiga-like toxin, which inhibits the 60S ribosomal subunit and prevents protein synthesis.

55
Q

What syndrome is associated with EHEC in children under 10?

A

Hemolytic-uremic syndrome (HUS).

56
Q

What are the toxins produced by Enterotoxigenic E. coli (ETEC), and what do they do?

A

Heat-labile toxin:
Increases cAMP and inhibits absorption of Na and Cl.

Heat-stable toxin:
Increases cGMP and increases Cl secretion and reduces Na absorption.

Both lead to watery diarrhea.

57
Q

What is the transmission route for ETEC?

A

Contaminated water sources.

58
Q

How do the diarrheal symptoms differ between EHEC and ETEC?

A

EHEC causes bloody diarrhea, whereas ETEC causes watery diarrhea.

59
Q

What is the primary virulence factor for neonatal meningitis caused by E. coli?

A

The K antigen on the capsule.

60
Q

What gram stain and morphology characterize Yersinia bacteria?

A

Gram-negative bacilli.

61
Q

What unique microscopic appearance does Yersinia exhibit?

A

Bipolar staining resembling a safety pin.

62
Q

What is the reservoir and transmission route for Yersinia enterocolitica?

A

Found in dog feces, transmitted via contaminated milk, dairy products, and unpasteurized milk.

63
Q

What are the typical symptoms of Yersinia enterocolitica infection?

A

Fever, abdominal pain, and bloody diarrhea.

64
Q

How does Yersinia enterocolitica infection mimic appendicitis?

A

Causes acute right lower quadrant abdominal pain (pseudoappendicitis).

65
Q

What are the zoonotic reservoirs for Yersinia pestis?

A

Rodents, including rats and prairie dogs.

66
Q

What role do fleas play in Yersinia pestis transmission?

A

Fleas act as vectors, transmitting the bacteria from animals to humans.

67
Q

What is the hallmark clinical sign of bubonic plague caused by Yersinia pestis?

A

Painful, swollen lymph nodes called buboes.

Also presents with fever, chills, malaise, myalgias.

Disseminated disease leads to sepsis and pneumonia.

68
Q

What are severe manifestations of disseminated Yersinia pestis infection?

A

Tissue necrosis, disseminated intravascular coagulation (DIC), septic shock, and multi-organ dysfunction.

69
Q

What secretion system is utilized by Yersinia spp. for virulence?

A

Type III secretion system to translocate Yops (Yersinia-associated outer proteins).

70
Q

What antibiotics are effective against Yersinia spp.?

A

Aminoglycosides (e.g., streptomycin) and tetracyclines.

Fluoroquinolones can also be used.

However treatment is usually supportive.

71
Q

Is there a vaccine available for Yersinia pestis, and who is it recommended for?

A

Yes, an inactivated (killed) vaccine is available, typically for high-risk groups like laboratory personnel and field workers in endemic areas.

72
Q

What is Guillain-Barré syndrome, and how is it related to Campylobacter jejuni?

A

Guillain-Barré syndrome is a neurological disorder characterized by bilateral ascending weakness and loss of reflexes. It is an autoimmune response triggered by Campylobacter jejuni infection.

73
Q

What is the Gram stain and shape of Campylobacter jejuni?

A

Campylobacter jejuni is a gram-negative, curved rod.

Campylobacter jejuni appears as “seagull wing” shaped rods.

74
Q

At what temperature does Campylobacter jejuni optimally grow?

A

Campylobacter jejuni grows optimally at 42°C, making it thermophilic.

75
Q

What are the common reservoirs for Campylobacter jejuni?

A

Poultry, cattle, sheep, and dogs are common reservoirs for Campylobacter jejuni.

76
Q

What is the primary mode of transmission for Campylobacter jejuni?

A

Campylobacter jejuni is transmitted via the fecal-oral route, often through contaminated food, especially poultry.

77
Q

What are the common symptoms of Campylobacter jejuni infection?

A

Cramping, abdominal pain, fever, and sometimes bloody diarrhea.

Campylobacter jejuni invades epithelial cells of the gastrointestinal tract, leading to inflammation and diarrhea.

78
Q

Which enzyme produced by Campylobacter jejuni is vital for aerobic respiration?

A

Campylobacter jejuni produces oxidase.

79
Q

Beside GBS, what other autoimmune issue is triggered by Campylobacter jejuni infection?

A

reactive arthritis (Reiter’s syndrome).

Can’t see: Conjunctivitis or uveitis (eye inflammation)
Can’t pee: Urethritis (urinary symptoms)
Can’t climb a tree: Arthritis (joint pain and swelling)

80
Q

How is Campylobacter jejuni infection treated?

A

Usually supportive with or without antibiotics (fluoroquinolone or macrolide)

81
Q

What shape and staining characteristics do Vibrio cholerae, Vibrio vulnificus, and Vibrio parahaemolyticus share?

A

They are comma-shaped, gram-negative, oxidase-positive bacilli.

82
Q

What is the primary transmission route for Vibrio cholerae?

A

Fecal-oral route.

83
Q

What is a characteristic feature of Vibrio cholerae growth?

A

It grows optimally in alkaline media

84
Q

What toxin mechanism does Vibrio cholerae use to cause diarrhea?

A

The cholera toxin permanently activates Gs protein, leading to overactivation of adenylate cyclase → increased cAMP → sodium and chloride efflux → profuse watery (rice water) diarrhea.

85
Q

What is the classic symptom of Vibrio cholerae infection?

A

“Rice-water” diarrhea.

86
Q

Why are Vibrio bacteria considered acid-labile?

A

They require a high number of ingested organisms to survive the acidic environment of the stomach and cause infection.

87
Q

Where is vibrio endemic?

A

3rd world countries with poor water treatment

88
Q

How are Vibrio parahaemolyticus and Vibrio vulnificus commonly transmitted?

A

Through consumption of raw oysters or other contaminated seafood.

89
Q

What is the primary treatment for cholera?

A

Aggressive oral rehydration.

can add fluoroquinolone, macrolide, or tetracycline.

90
Q

What serious complication can Vibrio vulnificus cause?

A

Severe wound infections.

Vibrio vulnificus lives in marine environments and can be ingested from seafood such as oysters. Infection can be from a wound or walking along a beach. Infection is associated with high iron levels in blood from conditions like hemochromatosis. Can present rapidly with progressive cellulitis, necrotizing infection, bullous rash, and sepsis.

91
Q

Vibrio vulnificus is treated in what manner?

A

tetracycline and ceftriaxone

92
Q

What is the prognosis of Vibrio vulnificus?

A

this infection has a high mortality rate.

93
Q

In terms of epidemelogy, what is important about Yersinia pestis?

A

must report!

94
Q

How is Yersinia pestis diagnosed?

A

culture and serology

95
Q

What type of bacterium is Proteus mirabilis?

A

Proteus mirabilis is a gram-negative, facultative anaerobe.

96
Q

What is a key feature of Proteus mirabilis on agar culture plates?

A

Proteus mirabilis demonstrates swarming motility.

97
Q

What type of stones are associated with Proteus mirabilis infection?

A

Proteus mirabilis is associated with struvite stones (staghorn calculi).

98
Q

How does Proteus mirabilis contribute to the formation of struvite stones?

A

The urease activity of Proteus mirabilis raises urine pH, creating an alkaline environment that promotes the precipitation of struvite stones.

99
Q

What is the characteristic odor of Proteus mirabilis infections?

A

Proteus mirabilis infections are characterized by a distinct fishy odor.

100
Q

What common infections are caused by Proteus mirabilis?

A

Proteus mirabilis is a common cause of urinary tract infections, especially complicated UTIs. Can also lead to abdominal infections.

101
Q

What are the effective treatment options for Proteus mirabilis?

A

Treatment options include ampicillin and sulfonamides (e.g., TMP-SMX)

Can also use:
fluoroquinolones, cephalosporins, carbapenems, and aminoglycosides.

102
Q

What type of bacterium is Pseudomonas aeruginosa?

A

Pseudomonas aeruginosa is an aerobic, oxidase-positive, catalase-positive, gram-negative bacillus that thrives in aquatic environments.

103
Q

What is a unique feature of Pseudomonas aeruginosa in terms of appearance and smell?

A

Pseudomonas aeruginosa produces characteristic pigments, such as pyocyanin (blue), pyoveridin (yellow-green), pyomelanin (brown), and pyorubin (red).

Pseudomonas aeruginosa emits a distinctive grape-like odor.

104
Q

What nosocomial infections is Pseudomonas aeruginosa a major cause of?

A

It causes nosocomial pneumonia and pulmonary infections, especially in cystic fibrosis patients.

Hospitalized patients and those intubated have an increased chance of developing a nosocomial infection.

Pseudomonas aeruginosa is also frequently associated with urinary tract infections, particularly in the presence of indwelling urinary catheters.

105
Q

Which populations are at higher risk of osteomyelitis caused by Pseudomonas aeruginosa?

A

IV drug users and diabetics are at increased risk.

106
Q

What increases Pseudomonas aeruginosa’s pathogenicity?

A

Pseudomonas aeruginosa produces a capsule-like polysaccharide called alginate.

107
Q

The risk of what specific type of infection is increased due to Pseudomonas aeruginosa in burn patients?

A

The risk of having a wound infected by Pseudomonas aeruginosa is increased after suffering from a burn.

108
Q

What skin infections are associated with Pseudomonas aeruginosa?

A

It can cause hot tub folliculitis and ecthyma gangrenosum.

Hot tub folliculitis is characterized by itchy red bumps around hair follicles after using a hot tub.

Ecthyma gangrenosum, characterized by black, necrotic skin lesions that is usually a manifestation of sepsis where Pseudomonas aeruginosa is the culprit.

109
Q

What is the primary mechanism of action of exotoxin A produced by Pseudomonas aeruginosa?

A

It inactivates elongation factor-2 (EF-2) through ADP ribosylation, halting protein synthesis.

110
Q

What outer ear infection can be caused by Pseudomonas aeruginosa?

A

Otitis externa, commonly known as swimmer’s ear.

111
Q

What type of motility does Pseudomonas aeruginosa exhibit?

A

It demonstrates swarming motility on semisolid surfaces.

112
Q

Which antibiotics are effective against Pseudomonas aeruginosa?

A

Cefepime
Carbapenem
Piperacillin-tazobactam
Aminoglycosides (e.g., tobramycin, gentamicin, amikacin)
Ticarcillin

fluoroquinolones can be used but Pseudomonas frequently becomes resistant.

113
Q

What type of bacteria is Burkholderia spp. classified as?

A

Gram-negative, catalase-positive, oxidase-positive, obligate aerobic bacilli.

114
Q

Where are Burkholderia spp. commonly transmitted from?

A

Direct contact with contaminated soil or water.

115
Q

What condition is caused by Burkholderia pseudomallei?

A

Melioidosis.

Melioidosis is seen mostly in tropical areas (e.g. Southeast Asia,
South Asia, Australia).

Symptoms may include high fever, chest pain, headache, anorexia, and myalgias. Lesions on chest X-ray that might appear similar to those seen in pulmonary tuberculosis with or without cavitary lesions.

116
Q

Which patient population is critically impacted by infections caused by the Burkholderia cepacia complex (BCC)?

A

Immunocompromised individuals, particularly cystic fibrosis patients.

117
Q

What severe complications are associated with Burkholderia cepacia complex (BCC)?

A

Encephalomyelitis and abscess formation in the skin or organs.

118
Q

Why is Burkholderia spp. particularly challenging to treat?

A

Due to its multidrug resistance.

119
Q

How is Burkholderia cepacia treated?

A

Bactrim (TMP/SMX)

fluoroquinolones

cephalosporins

120
Q

What are the two forms of otitis externa?

A

Otitis Externa (Swimmers Ear) and Malignant Otitis Externa

121
Q

How is Otitis Externa (Swimmers Ear) treated?

A

Clean out ear canal and apply topical drops with antibiotics, steroids, and antiseptics

Ciprofloxacin, oxfloxacin, gentamycin

Hydrocortisone

122
Q

Malignant Otitis Externa is almost always caused by ______ .

A

Pseudomonas

123
Q

What are the risk factors for Otitis Externa (Swimmers Ear) and how does this condition present itself?

A

Swimming, ear canal trauma, intra-ear devices, all increase exposure and innoculation of Psuedomonas. Patients will complain of ear pain, itching and experience otorrhea.

124
Q

How can Otitis Externa (Swimmers Ear) be prevented with someone who routinely is exposed to water?

A

alcoholic acetic acid drops

125
Q

How is Otitis Externa (Swimmers Ear) diagnosed?

A

The diagnosis is clinical with use of otoscopy where the external ear canal is is erythematous and edematous.

126
Q

What characterizes Malignant Otitis Externa?

A

Invasive necrotizing infection of the ear canal and skull base

Severe ear pain with the patient’s ear (pinna) up and outwardly displaced

Otoscope shows granulation tissue, erythema, as well as otorrhea.

127
Q

What increases the risk for developing Malignant Otitis Externa ?

A

Diabetes

Immunocompromised

128
Q

What are the complications of Malignant Otitis Externa ?

A

Spreading to the bone, osteomyelitis

Cranial nerve lesions (facial nerve palsy)

129
Q

What is the treatment/management for Malignant Otitis Externa ?

A

CT/MRI

IV fluoroquinolone

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