Gram Negative Bacteria Flashcards Preview

FDN3 By Nathan and Minnie > Gram Negative Bacteria > Flashcards

Flashcards in Gram Negative Bacteria Deck (201)
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1
Q

What are some of the distinctive characteristics of the Enterobacteriaceae family?

A
  • Gram negative
  • Facultative anaerobes
  • Form Bacilli and Cocobacilli
  • Many are commensals of the human colon that cause disease under certain circumstances
  • Most can ferment glucose
  • Oxidase (-)
2
Q

Which members of the enterobacteriaceae family cannot ferment glucose?

A

Salmonella

Shigella

Proteus

3
Q

Escherichia coli are… [Gram stain, metabolism, shape distinctive morphology]

A

Escherichia coli are gram negative, facultative aneroibic bacilli that are typically part of the normal flora of the human colon.

They are catalase (+) and ferment lactose

4
Q

List the 5 subtypes of E. coli

A

ETEC = Enterotoxigenic

EHEC = Enterohermorrhagic

EPEC = Enteropathogenic

EIEC = Enteroinvasive

EAEC = Enteroaggregative

5
Q

What is significant about an organism that turns MacConkey agar pink?

A

The organism ferments lactose

6
Q

List the determinants of pathogenicity that apply to all E. coli subtypes

A
  • Alpha-heymolysin: Pore-forming
  • Aerobactin: Iron siderophore
  • Polysaccharide capsulse: Inhibits phagocytosis
  • Pili/fimbriae: Forms attachments
7
Q

What dieseases are commonly associated with E. coli infection?

A

Meningitis

UTI

Septic Shock

Nosocomial infections

Diarrhea (5 types)

8
Q

How is an E. coli infection diagnosed?

A

Culturable on routine media

EMB agar: appears metallic green

MacConkey agar: turns the agar pink due to ability to ferment lactose

9
Q

How are UTI and kidney infections caused by E. coli treated?

A

Trimethoprim/sulfamethoxazol

nitrofuratoin

fosfomycin

10
Q

What are the determinants of pathogenicity of ETEC?

A

2 toxins that are plasmid encoded and act on gut epithelial cells

  • Heat labile (LT): An A-B Toxin, increases cAMP
    • Similar to cholera toxin
  • Heat stable (ST): Increases cGMP
11
Q

Describe an ETEC infection

A

Enterotoxigenic diarrhea

  • “traveller’s diarrhea”
  • Watery stools
  • 24-72 hr incubation period
  • Spread through food and water contaminated with human wasta
12
Q

How is ETEC infection diagnosed?

A

ETEC grows cultures from stools

ELISA PCR available for ST and LT, but is not commonly used

13
Q

An E. coli strain positive for ST and LT is most likely..

A

ETEC

  • Causes enterotoxigenic diarrhea
  • “Traveler’s diarrhea”
  • Watery stools
14
Q

How is ETEC infection treated?

A

Rehydration

Ciprofloxacin or other fluroquinolone

15
Q

How can ETEC infection be prevented?

A

Avoid raw veggies, pre-peeled fruit, unpasturized dairy, lukewarm cooked foods

16
Q

Describe the Type III Secretion System

A

Type III secretion systems…

  • Form attachment and effacement lesions
  • Replace normal microvilli with pedastals at the point of attachment
  • Inject bacterial proteins into the cytoplasm of host cells by…
  1. Secretion apparatus is embedded into the host cell membrane
    - > Secretes toxins to the exterior of the bacterium
  2. Several secreted proteins insert into the host cell membrane and form a translocation complex
    - > Translocates toxins into the host cytoplasm
  3. Toxins have enzymatic activity, act as effector proteins
17
Q

What are the determinants of pathogenicity of EHEC?

A
  • Type III Secretion Systems
    • Injects toxin into host cell
  • Shiga-like toxin
    • Inhibits 60s unit of the human ribosome
  • Fimbriae
    • Forms attachment and effacement lesions
18
Q

Describe an EHEC infection

A

Enterohemorrhagic diarrhea E. coli

  • Bloody diarrhea
  • Crampy
  • Absent or low-grade fever
  • May lead to hemolytic-uremic syndrome (10% of case)
19
Q

What is hemolytic-uremic syndrome?

A

Accompanies ~10% of cases of EHEC; a result of shiga-like toxin

  • Decrease in platelets
  • Renal failure
    • Toxin damages endothelial cells in glomerulus -> Clumps of platelets form -> Causes lysis of RBCs
  • CNS dysfunction
20
Q

What distinguises EHEC from other E. coli strains?

A
  • Cannot ferment sorbitol
  • Immunoassay for shiga-like toxin in stool
  • O157:H7 serotype causes massive outbreaks
21
Q

How is EHEC infection treated?

A

Rehydration

(do NOT use antibiotics)

22
Q

How can EHEC infection be prevented?

A

Avoid undercooked meat and unpasteurized diary or juice

23
Q

Infection with which E. coli subfamily is associated with consumption of raw meat?

A

EHEC (enterohemorrhagic)

24
Q

Where is the reservoir for EHEC?

A

Cattle

Avoid infection by avoiding consumption of raw meat, unpasteurized dairy/juice

25
Q

Describe an EPEC infection

A

Enteropathogenic E. coli

  • Associated wtih childhood diarrhea in developing countries
  • Fever, bloody diarrhea
26
Q

What are the determinants of pathogenicity of EPEC?

A

Enteropathogenic E. coli

  • Bundle-forming pili
    • Responsible for initial attachment to intestinal epithelium
  • Type III secretion system
    • Injects Tir into cell membrane
    • Acts as a receptor for intimin (an adhesin)
27
Q

Describe the mechanism of action of EPEC infection

A
  • Bacteria bind to intestinal epithelial cells using bundle-forming pili
    • Disruption of the overlying mucosa
      • Fever, bloody diarrhea
28
Q

Where are EPEC and EIEC most commonly found?

A

Outside of the United states

Causative agents of diarrhea in developing countries

29
Q

Describe EAEC infection

A

Diarrhea in developing countries

(Rarely seen in the USA)

30
Q

Which E. coli determinant of pathogenicity is associated with sepsis?

A

LPS

31
Q

Salmonella enterica is a [Gram stain, metabolism, shape distinctive morphology]

A
  • Salmonella enterica* is a gram negative, facultative intracellular, facultative aerobic, bacillus.
  • Cannot ferment glucose or lactose
  • Motile (has flagella)
  • H2S (+)
  • Acid labile (usually killed by stomach acid)
32
Q

Which E. coli determinant of pathogenicity is associated with UTIs (bladder infections/lower UTI)

A

Type 1 fimbriae

33
Q

Which E. coli determinant of pathogenicity is required to cause meningitis?

A

K capsule

Commonly causes meningitis in neonates

34
Q

Which E. coli determinant of pathogenicity is associated with upper UTI/kidney infection?

A

P pili

35
Q

What is the reservoir for Salmonella enterica serovar typhi?

A

Gallbladder of human carriers

36
Q

What is the reservoir for Salmonella enterica serovar enteritidis?

A

Farm animals/uncooked chicken

Turtles and other reptiles

37
Q

What are the determinants of pathogenicity of Salmonella enterica serovar enteritidis?

A

Unique to S. enteritidis:

  • Type III Secretion systems
    • SPI1 (Salmonella pathogenicity island 1)
      • Causes ruffling on the surface of enterocytes
      • Induces internalization of S. enteritidis
    • SPI2
      • involved in dissemination of the bacteria

Common to S. enterica serovars:

  • Large inoculum causes disease
  • Bacteria survive and multiply in phagosomes of macrophages
  • Causes bacteremia when disseminated in bloodstream
38
Q

Which cells are most often inhabited by a Salmonella enterica infection?

A

Macrophages

39
Q

What is the clinical presentation of a Salmonella enterica sevofar enteritidis infection?

A

24-48 hours after ingestion…

  • Inflammatory diarrhea (food poisoning)
  • Nausea, vomiting
  • Fever in 50% of individuals
  • Bacteremia in 8% of healthy individuals
40
Q

What is unique about the diarrhea caused by Salmonella enteria serovar enteritidis, as compared to that caused by ETEC or EPEC?

A

Salmonella enteriditis is a bacteria of developed countries that causes ~15% of food-bourne illness in the USA

ETEC and EPEC are common in developing countries, and are often seen in the US in individals who have traveled to these countries

41
Q

How is Salmonella enteritidis infection treated?

A

The infection is self-limiting but…

  • Treat in immunocompromised patients or severe infections (bacteremia)
    • Fluroquinolones or ampicillin
  • Otherwise, antibiotics is not typically recommended because it may induce a carrier state
42
Q

MacConkey agar culture: which enterobacteriaceae organisms might be growing on the left in this picture?

A

Any lactose fermentor

  • E. coli
  • Klebsiella
  • Enterobacter
43
Q

How is a Salmonella enterica infection diagnosed?

A

Routine stool culture (for S. enteritidis or S. typhi)

  • Appears black on hektoen agar
  • Motile
  • H2S positive
  • Acid labile (killed by acid)

Can also do blood culture for S. typhi

44
Q

Which individuals are most susceptible to infection by Salmonella enterica?

A

Individuals with less stomach acid than normal

  • Pts taking -prazole drugs (protone pump inhibitors)
  • Pts. with H. pylori infection
  • Elderly people

(Also pts who are immunocompromised)

(higher pH than normal)

45
Q

In the United States, Salmonella typhi infection is most commonly seen in which individuals?

A

Travellers returning from Mexico, Latin America, Asia, India

46
Q

What is the clinical presentation of an individual infected wtih Salmonella typhi?

A

Typhoid Fever

  • Prolonged fever
  • Persistent bacteremia
  • Constipation or diarrhea
    • if diarrhea, “pea soup”
  • Abdominal pain
  • Occasional rash (pale, pink macules)
  • Occasional carrier state
    • Reservoir in galstones, shed in feces
47
Q

How is typhoid fever treated?

A

Always treat typhoid fever

  • Antibiotics
    • Fluroquinolone, ampicillin, chloramphenicol
  • Note: Resistance is becoming more common
48
Q

How are Salmonella enterica infections prevented?

A

S. enteritidis

  • Don’t eat raw/undercooked chicken
  • Hand hygiene if playing with farm animals

S. typhi

  • Parenteral capsular vaccine
  • Live attenuated oral vaccine
  • Administerd in the United States for travelers to Central/South America, Asia, Africa
49
Q

What are the determinants of pathogenicity of Salmonella typhi?

A

Unique to S. typhi serovars:

  • Can induce a carrier state in human (Typhoid Mary)
    • Reservoir in gallbladder; gallstones become infected
    • Shed in feces

Common to S. enterica serovars:

  • Large inoculum causes disease
  • Bacteria survive and multiply in phagosomes of macrophages
  • Causes bacteremia when disseminated in bloodstream
50
Q

Yersinia pestis is [Gram stain, metabolism, shape, distinctive morphology]

A

Yersinia pestis is a gram negative, facultatively anaerobic, bacillus.

It is encapsulated and has a bipolar appearance on a gram stain (“closed safety pin)

51
Q

What are the 3 medically relevant Yersinia species?

A
  • Yersinia pestis - Bubonic plague
  • Yersinia enterocolitica - Infectious diarrhea
  • Yersinia pseudotuberculosis - Infectious diarrhea
52
Q

Where is the environmental reservoir for Yersinia pestis?

What is the vector for human transmission?

A

Reservoir = rodents (prarie dogs in USA, rats historically)

Vector = fleas

53
Q

What are the 3 infections that may be caused by Yersinia pestis?

A

Bubonic plague

Pneumonic plague

Primary septicemic plague

54
Q

Describe the mechanism of Yersinia pestis infection from rodents to humans

A

Hms locus required for colonization in the flea foregut

  • Flea bites rodent reservoir
  • Y. pestis colonizes the foregut, inhibits swallowing
  • Causes flea to regurgitate last blood meal (containing Y. pestis) into new prey

-> New prey has been inoculated with Y. pestis

55
Q

What are the determinants of pathogenicity of Yersinia pestis?

A
  • Adhesins Ail
    • Chromosomally encoded adhesin
  • Type III secretion system
    • Secretes YOPS
  • YOPS (effector proteins)
    • Intoxicate host
    • Disable macrophages and neutrophils
      • Inhibition of phagocytosis and cytokind production
    • Allows bacteria to multiply to large numbers very quickly
  • Capsule: Fra1 (aka F1)
    • Antiphagocytic
  • Pla: Plasminogen activator
    • Cleaves fibrin to prevent clot formation
    • Allows for dissemination in the body
56
Q

Which Yersinia pestis determinant of pathogenicity allows the bacteria to multiply in large numbers in the human body?

A

YOPS: The effector proteins secreted by the Type III Secretion system

  • YOPS disable macrophages and neutrophils -> inhibits phagocytosis and cytokine produciton
57
Q

Describe the clinical presentation of bubonic plague

A

After 2-6 day incubation period (following flea bite)

  • Bubo forms (painful, swollen lymph node)
  • Fever, chills, myalgias, arthralgias, headache
  • Bubo enlarges; dry, erythematous
  • If no treatment
    • LPS release
    • Septic shock (secondary septicemic plague)
    • Necrosis of appendages
  • Bacteria may invade macrophages of lungs
    • Allows spread of disease via aerosols
58
Q

Which Yersinia pestis-associated disease is caused by a flea bite?

A

Bubonic plague

(no bubo in pneumonic plague or primary septicemic plague)

59
Q

Describe the clinical presentation of pneumonic plague

A

1-4 day incubation period after inhalation of Y. pestis aerosols

  • Fever, chills, headache, myalgia, weakness
  • Productive cough, may be bloody
  • Dyspnea
  • Very severe
  • Contagious via aerosols
60
Q

Describe the clnical presentation of primary septicemic plague

A

Follows direct inoculation of Y. pestis into bloodstream

  • Gastroenteritis
    • Nausea, vomiting, diarrhea, abdominal pain
  • No bubo = late diagnosis
61
Q

How is primary vs. secondary septicemic plague contracted?

A

Primary = direct inoculation of Y. pestis into bloodstream

Secondary = septic shock following bubonic plague

62
Q

Which Y. pestis infection is most associated with gastroenteritis?

A

Primary septicemic plague

63
Q

How is a Yersinia pestis infection diagnosed?

A

Blood cultures; Yersinia grows on normal lab media

If bubonic: culture bubo samples

If pneumonic: culture sputum samples

Giesma stain: Yersinia pestis has a bipolar appearance, like a closed safety pin

64
Q

How is Yersinia pestis infection treated?

A

Choice: Streptomycin or gentamicin

Alternative: Doxycycline or chloraphenicol

65
Q

How can Yersinia pestis infection be prevented?

A

There is a killed whole-cell vaccine, but it is not well tested and has unclear efficacy

It is not available in the USA

66
Q

A patient with an inflammed dry, painful, erythmatous lymph node was hiking in Arizona last week.

What is your leading diagnosis?

How would you confirm your hypothesis?

A

Leading diagnosis: Bubonic plague caused by Yersinia pestis infection

Confirm with blood and bubo culture; look for bipolar/closed safety pin-shaped bacteria on a giemsa stain

67
Q

What organism causes dysentery?

A

Shigella dysenteriae

68
Q

What kind of bacteria appear in this image?

A

Yersinia pestis;

Bipolar/closed safety pin appearance

This is a Giemsa stain

69
Q

Klebsilla pneumoniae is a [Gram stain, metabolism, shape, distinctive morphology]

A

Klebsilla pneumoniae is a gram negative, facultatively anaerobic bacillus.

Ferments lactose, immotile, urease positive

70
Q

What diseases are caused by Klebsiella pneumoniae?

A

Nosocomial infections

  • Hospital-acquired pneumonia
  • UTIs (esp. catheterized patients)
  • Blood infections
  • Wound infections/sepsis

Community acquired infections in immunocompromised individuals

  • Alcoholics
  • Diabetics
  • Patients with chronic respiratory disease
71
Q

What are the determinants of pathogenicity of Klebsiella pneumoniae?

A
  • Polysaccharide capsule
    • Prevents phagocytosis
    • Prevents complement deposition
  • Makes siderophores
    • Can scavenge iron
  • Very resistant to antibiotics
72
Q

What is the clinical presentation of a Klebsiella pneumoniae infection?

A

May cause pneumonia, UTI, or wound infection

Forms abscesses

Typically affect HADRs:

  • Hospitalized patients
  • Alcoholics
  • Diabetics
  • Indivdiuals with chronic Respiratory disesae
73
Q

Haemophilus are [size, Gram stain, shape, metabolic]

A

Haemophilus are small Gram-negative coccibacilli that grow both aerobically and anaerobically

74
Q

What symptoms does Haemophilius influenzae cause?

A

Otitis media, sinusitis, bronchitis, epiglottitis, pneumonia, and meningitis

75
Q

Bortedella are [Gram stain, shape]

A

Bordetella are Gram-negative coccobacilli

76
Q

Bordetella pertusis is [size, Gram stain, shape, metabolic]

A

Bordetella pertusis are tiny Gram-negative coccobacilli that are strict aerobes

77
Q

What are the determinants of pathogenicity of Bordetella pertusis?

A
  • Adhesins (pili, filamentous hemagglutinin, and pertactin)
  • Endotoxin
  • Exotoxins (4: pertussis toxin, adenylate cyclase toxin, dermonecrotic toxin, tracheal cytotoxin)
78
Q

What are three adhesins used by Bordetella pertusis?

What do they do?

A
  • Pili
  • Filamentous hemagglutinin
  • Pertactin

Allow adherence to ciliated epithelial cells in the upper airway

79
Q

In addition to allowing adherence to ciliated epithelial cells in the upper airway, what does filamentous hemagglutinin (FHA) of Bordetella pertusis do?

A

Mediates adherence to PMNs

(BInding of pertussis toxin increases number of FHA receptors on the cell surface of PMNs, increasing FHA binding and bacterial internalization, which allows them to survive inside phagocytes)

80
Q

What two types of toxins does Bordetella pertussis have?

A
  • Endotoxin
  • Exotoxins (4)
81
Q

What is pertussis toxin of Bordetella pertusis?

A

A-B toxin that exists as hexamer with subunits S1-S5

S2-S4 mediate toxin adherence to host

S1 ADP-ribosylates host cell G protein which increases cAMP levels

S5 acts as scaffold to position other subunits

Increases FHA receptors on PMN cell surface and inhibits recruitment of neutrophils to site of infection

82
Q

What does adenylate cyclase toxin of Bordetella pertussis do?

A

Inhibits leukocyte function by producing cAMP in the presence of host cell calmodulin

83
Q

What does dermonecrotic toxin of Bordetella pertusis do?

A

Localized tissue destruction in infection

84
Q

What is tracheal cytotoxin of Bordetella pertussis?

A

Peptidoglycan fragment that inhibits/kills ciliated cells and is pro-inflammatory

85
Q

How communicable is Bordetella pertussis?

How is it transmitted?

A

Highly communicable

Via droplets

Most contagious during the catarrhal stage

86
Q

What portion of the airway does Bordetella pertussis infect?

A

Upper airway

87
Q

What are the three stages of Bordetella pertusis infection?

A
  1. Incubation (2 weeks)
  2. Catarrhal stage: mild coughing and sneezing, patient is very infectious
  3. Paroxysmal stage: explosive cough followed by whoop during inhalation, may lead to exhaustion/cyanosis/vomiting/convusions, resolution is very slow
88
Q

During which disease stage is Bordetella pertusis most infectious?

A

Catarrhal stage

89
Q

Which diagnostic lab test finding is Bordetella pertussis infection associated with?

A

Atypical lymphocytosis

90
Q

How are samples of Bordetella pertussis collected and grown?

A

Collected from nasopharynx

Grown on Bordet-Gengou medium or charcoal-containing medium

91
Q

What is significant about Bordetella pertussis cultures after 4 weeks of symptoms?

A

Cultures are rarely positive after 4 weeks of symptoms

92
Q

When is antibiotic treatment for Bordetella pertussis infection most effective?

What happens after this window?

What is true about antibiotic treatment after the onset of the paroxysmal stage of Bordetella pertussis infection?

A

Antibiotic treatment for Bordetella pertussis infection is most effective in the catarrhal stage, before the “whooping” symptoms begin

After the onset of the paroxysmal stage, antibiotic treatment is not as effective at altering the course of disease

93
Q

What antibiotics are used to treat Bordetella pertussis infection?

A

Macrolides

(TMP/SMX may also be effective)

94
Q

What was the old vaccination strategy for pertussis?

Why was it discontinued?

A

Whole-cell killed vaccine combined with toxoid vaccines against tetanus and diphtheria

Poor long-term efficacy of pertussis component; seizures and hyporesponsive episodes; frequent side effects in kids

95
Q

What is the modern vaccination strategy for pertussis?

What is the booster?

Which group of people is recommended to receive Tdap and when?

A

DTap: uses acellular components of Bordatella pertussis (detoxified pertussis toxin, FHA, pertactin, fimbriae) to generate immunity

Tdap booster (reduced amounts of diphtheria and pertussis components)

Pregnant women should receive Tdap with each pregnancy

96
Q

Brucella spp. are [size, metabolic, Gram stan, shape]

A

Brucella are small aerobic Gram-negative coccibacilli

97
Q

What do Brucella spp. cause?

A

Brucellosis in humans as well as cattle, goats, and hogs

98
Q

How do humans acquire brucellosis?

Who is particularly at risk?

A

Exposure to infected animalks (contact with mucous membranes, cuts in skin, inhalation) or consumption of unpasteurized milk or other dairy products

Veterinatians, meat inspectors, others who work with meat/animals

99
Q

What cells can Brucella spp. survive in?

A

Macrophages

100
Q

What is the clinical presentation of brucellosis?

A

Fever*, chills, malaise, and drenching sweats

Infection can be chronic and last for weeks or months

(Fever may be undulant; rise and fall)

101
Q

What does diagnosis of brucellosis require?

A

Isolation of organism from blood or biopsy specimens, though Brucella spp. may take from 2-4 weeks to grow

Serological tests are also available

102
Q

What is the treatment for brucellosis?

A
  • Doxycycline + rifampin/gentamicin/streptomycin
  • Vaccine for animals not humans
103
Q

Francisella tularensis are [size, metabolic, Grains stain, shape]

A

Francisella tularensis are small, metabolically facultative, Gram-negative coccibacilli

(similar in morphology to Brucella)

104
Q

How do humans become infected with Francisella tularensis?

A

Contact with rabbits, squirrels, muskrats, beavers, and deeper through tiny breaks in skin, exposure of mucous membranes, ingestion, or inhalation (also via ticks)

105
Q

What is the classic case for infection with Francisella tularensis?

A

Skinning rabbits on a hunting trip

106
Q

In which cells does Francisella tularensis multiply?

A

Macrophages

107
Q

What is the clinical presentation of tularemia?

A

Site of innoculation is ulcerated

Regional lymphadenopathy

Fevers and chills

Possible pneumonia and dissemination to multiple organs

108
Q

What is notable about diagnostic testing for tularemia?

A
  • Francisella tularensis is difficult to grow in the lab and requires media
  • Serological assay available
109
Q

How is Francisella tularensis treated?

A
  • Streptomycin or gentamicin
  • Vaccine recommended for laboratory workers and others who have frequent contact with infected animals
110
Q

How is Klebsiella pneumoniae infection diagnosed?

A

Culture specimen from infection on routine lab media

  • Plump, gram (-) rods
  • Hypermucoviscous strains overproduce capsule and have a hypermucoid appearance

On MacConkey agar

  • Turns the agar pink (can ferment lactose)
111
Q

Pasteurella multocida are [size, Gram stain, shape, location where normally found]

A

Pasteurella multocida are small Gram-negative coccobacili that are part of the normal respiratory flora of some animals (especially cats and dogs)

112
Q

How is Klebsiella pneumoniae infection treated?

A

Very resistant to antibiotics!

If positive for extended-spectrum beta-lactamase (ESBL)

  • Use carbapenem

If positive for kelbsiella pneumoniae carbapenemase (KPC) or New Delhi Metalocarbapenemase (NDMC)

  • Use aminoglycoside, colistin, ceftazidime, avibactam, meropenem-vabobactam
113
Q

How do humans become infected by Pasteurella multocida?

A

Cat or dog bite

114
Q

Can zoonotic infections be acquired directly/indirectly/both from animals?

A

Zoonotic infections can be acquired both directly and indirectly from animals

115
Q

Neisseria are [Gram-stain, shape]

A

Neisseria are Gram-negative diplococci

116
Q

What antibiotics is Klebsiella pneumoniae resistant to?

A

All encode SHV Beta-lactamase on chromosome

  • Resistant to ampicillin, amoxicillin

Some encode Extended-spectrum beta-lacatamase (ESBL)

  • Resistant to all beta-lactams except carbapenem

Some encode Klebsiella pneumonia carbapenemase (KPC) or New Delhi Metalocarbapenemase (NDMC)

  • Resistant to almost all beta-lactams inclucding carbapenem
117
Q

Why is carbapenem used to treat Klebsiella pneumoniae?

A

Klebsiella pneumoniae is typically resistant to most early-line beta-lactam antibiotics

118
Q

What are the two medically relevant Neisseria bacteria?

A

Neisseria menigitidis and Neisseria gonorrhoeae

119
Q

What is Neisseria menigitidis a common cause of?

Who is at particular risk?

A

Meningitis and bloodstream infections

People living in crowded conditions (e.g. students in college dorms) are at particular risk

120
Q

What is notable about the polysaccharide capsule of Neisseria meningitidis?

A

Antiphagocytic and resists complement-mediated killing

Basis for serogrouping and target of vaccines

121
Q

Why is tetanus still a prevalent disease, given that there is an effective vaccination?

A

Tetanus spores have a reservoir in soil

122
Q

Which serogroup of Neisseria meningitidis causes large outbreaks in Africa?

A

Serogroup A

123
Q

How is Neisseria gonorrhoeae transmitted?

What is the clinical presentation?

A

Sexually transmitted (gonorrhea)

Local infections such as urethritis and cervicits but can spread regionally to cause epididymitis and pelvic inflammatory disease or systemically to cause disseminated gonorrhea

124
Q

What are the characterisitcs that define Enterobacteriaceae?

A

Gram negative rods that colonize or infect the GI tract

125
Q

Which members of Enterobacteriaceae commonly cause diarrhea?

A

Diarrhea is mESSYY

Minnie’s pneumonic:

  • E. coli
  • Salmonella enterica (Serovars enteritidis and typhi)
  • Shigella
  • Yersinia enterocolitica
  • Yersinia pseudotuberculosis
126
Q

How does Neisseria gonorrheoae avoid immune clearance?

A

Produces pili that change their antigenic make-up during the course of infection (antigenic variation)

127
Q

Moraxella catarrhalis are [size, Gram stain, shape, clinical presentation]

A

Moraxella catarrhalis are small Gram-negative cocci or coccobacilli that cause otitis media, sinusitis, bronchitis, and pneumonia

(morphologically and metabolically resemble Neisseria spp.)

128
Q

What virulence factor is linked to Traveler’s diarrhea?

A

LT

Heat Labile Toxin secreted by ETEC

129
Q

Where are Gram-negative anaerobes usually found?

What sort of infections do they cause?

What are they prone to form?

What are some examples of Gram-negative anaerobic bacteria?

A

Normal flora of upper and lower GI tract, respiratory tract, and female genital tract

Opportunistic pathogens (affect compromised host, such as when intestines ruptures or mouth contents aspirate into the lungs)

Prone to form polymicrobial abscesses that also include facultative anaerobic organisms such as E. coli

Bacteroides spp., Prevotella spp., Fusobacterium spp.

130
Q

What kind of bacteria exhibit “swarming motility?”

A

Proteus spp

  • Proteus mirabilis*
  • Proteus vulgaris*

131
Q

What diseases are associated with Proteus spp?

A

UTIs (Hospital Acquired and Community Associated)

Also associated with nosocomial infections

132
Q

Why do Proteus spp. exhibit swarming motility?

A

Each cell has hundreds of flagella

133
Q

Which bacteria is associated with the formation of “struvite” kidney stones?

Why?

A
  • Proteus* spp.
  • Proteus* is urease positive
  • Urease splits urea into ammonium hydroxide + CO2
  • This raises urine pH (makes it more alkaline)
  • This promotes the formation of struvite kidney stones
134
Q

Why do patients with multiple UTIs often develop kidney stones?

A

UTIs caused by Proteus are associated with “struvite” kidney stones

  • Proteus* is urease positive;
  • Urease -> splits urea into ammonium hydroxide -> raises pH -> Kidney stone formation
135
Q

What diseases are associated with Cerratia marcescens?

A

Often antibiotic resistant…

  • Nosocomial respiratory infections
  • UTIs
  • Bloodstream infections
136
Q

What diseases are associated with Citrobacter spp?

A

Often antibiotic resistant…

  • Nosocomial respiratory infections
  • UTIs
  • Bloodstream infections
137
Q

What diseases are associated with Enterobacter spp?

A

Often antibiotic resistant…

  • Nosocomial respiratory infections
  • UTIs
  • Bloodstream infections
138
Q

Which 3 members of Enterobacteraceae are associated with antibiotic resistant nosocomial respiratory infections, UTIs, and bloodstream infections?

A
  • Enterobacter spp.
  • Citrobacter spp.
  • Serratia marcescens
139
Q

Which bacteria is associated with the “red ring” around your shower?

A

Serratia marcescens

140
Q

Which bacteria is this likely to be?

A

Proteus spp.

Grows in this pattern due to swarming motility

141
Q

What are the 6 medically-important gram-negative rods?

A

PAL-VCH

  • Pseudomonas aeruginosa
  • Acinetobacter baumanni
  • Legionella pneumophila
  • Vibrio cholerae
  • Campylobacter jejuni
  • Helicobacter pylori
142
Q

A patient undergoing chemotherapy develops the following skin legion:

What is it called?

Which bacteria is causign the legion?

A

Ecthyma gangrenosum: A black eschar indicating cutaneous necrosis caused by Pseudomonas aeruginosa

143
Q

A patient presents with this rash after spending a week at a ski lodge. He his typical day on this vacation included skiing, drinking beers, and sitting in the hot tub.

What do you think is causing this rash?

A

Pseudomonas aeruginosa

He likely acquired the bacteria from the hot tub

144
Q

The pre-med undergrad working in your lab forgot to label the bacterial cultures; your PI assigns you to determine which bacteria is growing in which plates.

What bacteria is this?

A

Pseudomonas Aeruginosa

Colors are due to pyocanain and pyoverdin (a siderophore)

May also have a grape-like odor

145
Q

This is a picture of “coiling phagocytosis,” exhibited by which bacteria?

A

Legionella pneumophilia

146
Q

This is a bacterial culture growing on BCYE agar

What bacteria is this?

What is in the agar helping the bactera grow?

A

Legionella pneumophilia

  • Not visualized on gram stain, overgrown by other respiratory flora on normal agar

BCYE agar = buffered charcoal-yeast extract agar

  • Contains L-cysteine, agar, and antibiotics to prevent the growth of other bacteria
  • Both an enrichment agar and a selective agar
147
Q

This bacteria of the stomach is most likely…

A

Helicobacter pylori

Look for flagella and curved shape

148
Q

This is a picture of stomach epithellium:

What bacteria are also present?

What is allowing this bacteria to live in the acidic environment of the stomach?

A

Helicobacter pylori

Urease positive = cleaves ammonium hydroxide from urea. This creates a less acidic microenvironment in the mucus overlying the epithelium in which H. pylori grows, reproduces, and invades the stomach epithelium.

149
Q

Pseudomonadas aeruginosa is a [Gram stain, metabolism, shape distinctive morphology]

A

Pseudomonas aeruginosa is a gram negative, obligate aerobic rod.

It is found in faucets, drains of hospitals and often has fluorescent pigments

It does not ferment; Catalase (+), oxidase (+)

150
Q

List the determinants of pathogenicity of Pseudomonas aeruginosa

A

CASCQET - E (Like casket-y… kind of a stretch)

  • Can survive at high temperatures (42 C)
  • Adhesions
  • Siderophore-producing
  • Capsule
  • Quorum Sensing
  • Exotoxin A
  • Type III Secretion System
  • Endotoxin
151
Q

What is exotoxin A?

Which bacteria secrets it?

A

Exotoxin A is secreted by Pseudomonas aeruginosa

It ADP-ribosylates EF-2 of the host ribosome. This inhibits protein synthesis and leads to cell death

(Functions similarly to diphtheria toxin)

152
Q

What is quorum sensing?

Which bacteria have quorum-sensing abilities?

A

Quorum sensing allows bacteria to sense how many of them there are. Each bacteria secretes an autoinducer signal, and can sense the concentration of that signal.

Higher concentration => more bacteria are around => they secrete more toxins since there are enough of them to overpower host defenses

Pseudomonas aeruginosa has quorum-sensing abilities

153
Q

Patient with which genetic disorder are likely to be infected with Pseudomonas aeruginosa?

A

Cystic Fibrosis

P. aeruginosa colonizes the lungs of CF patients; it causes repeat infections and is the most common cause of respiratory failure in this population

154
Q

Which bacteria often causes skin infections in burn patients?

A

Pseudomonas aeruginosa

155
Q

What is the most common disease caused by Pseudomonas aeruginosa?

A

Pneumonia in hospitalized patients

  • Usually acute, may be necrotizing
  • Also causes other nosocomial infections
156
Q

What is the most common non-nosocomial infections caused by Pseudomonas aeruginosa?

A
  • Folliculitis: associated with under-chlorinated hot tubs
    • (The bacteria can survive and grow in hot temperatures)
  • Swimmer’s ear
  • Osteomyelitis: IV drug users and diabetics
157
Q

List the groups of patients and associated diseases that are likely caused by Pseudomonas aeruginosa

A
  • Cystic Fibrosis patients -> Pneumonia
  • Ventilated patients -> Pneumonia
  • Burn patients -> Skin infection
  • Catheterized patients -> UTI
  • Neutropenic patients (undergoing chemo) -> Bacteremia
  • IV drug users -> Osetomyelitis
  • Diabetics -> Osteomyelitis
  • Hot tub users -> Folliculitis
158
Q

How might Pseudomonas aeruginosa infection affect patients undergoing chemotherapy?

A

May cause bacteremia and cutaneous necrosis

  • Look for an ecthyma gangrenosum (black eschar)
159
Q

How can a Pseudomonas aeruginosa infection be diagnosed?

A
  • Grows on many types of lab media
  • Gram (-), Catalase (+), oxidase (+)
  • Grape-liek odor
  • Fluorescent pigments
160
Q

What causes Pseudomonas aeruginosa to appear fluorescent in cultures?

A

Siderophores

Pyocyanin and pyoverdin

161
Q

How is Pseudomonas aeruginosa treated?

A

Very reisistant to antibiotics; use 2 drugs until susceptibility is known

  • Choice: Aminoglycoside + beta-lactamase
    • Piperacillin, ceftazidime, cefepime, ceftolozane-tazobactam, imipenem/peropenem, aztreonam
  • Alternative: Quinolone + piperacillin

Note: Cefalosporins are not active against P. aeruginosa

162
Q

How can Pseudomonas aeruginosa infection be prevented?

A

Don’t use tap water to wash respiratory equipment (P. aeruginosa may be living in hospital faucets)

Be aware that P. aeruginosa may contaminate hospital disinfectants

163
Q

Acinetobacter baumannii is a [Gram stain, metabolism, shape distinctive morphology]

A

Acinetobacter baumannii is a gram negative, non-fermenting, bacillus or coccobacillus

164
Q

What diseases are caused by Acinetobacter baumannii?

A

Hospital-acquired infections

  • Pneumonia
  • Bloodstream infections
  • Wound infections
165
Q

How is Acinetobacter baumannii infection treated?

A

Very resistant to antibiotics!

Choice: carbapenem, amikacin, colistin

Note: Sublactams (beta-lactamase inhibitors) work against some strains

166
Q

Legionella pneumophilia is a [Gram stain, metabolism, shape distinctive morphology]

A

Legionella pneumophilia is a gram negative, obligate anaerobic, facultative intracellular, thin bacillus.

Oxidase (+)

Serogroup 1 causes 80% of disease

Infects amoebae

167
Q

Where is Pseudomonas aeruginosaI found?

A

Hospitals; faucets and drains

Under-chlorinated hot tubs

168
Q

Where is Legionella pneumophilia found?

A

Natural bodies of water

Cooling towers of air-conditioning units

Water distribution systems

169
Q

List the determinants of pathogenicity of Legionella pneumophilia

A
  • Infects macrophages
  • Dot - “Defect of Organelle Trafficking” genetic locus
  • Type IV secretion system
  • Phospholipase C
170
Q

How does Legionella pneumopilia infect macrophages?

A

Legionella pneumophilia promotes coiling phagocytosis

  • Promotes the formation of a long, thin, pseudopod by the macrophage
  • The macrophage wraps around the bacterium, engulfs it in a coiled vesicle to create a phagosome
  • This prevents the fusion of the phagosome with the lysosome
  • Legionella pneumophilia ​recruits ribosomes to the phagosome and basically lives in the nice, new remodeled phagosome it has created
171
Q

What is Dot?

Which bacteria posesses it?

Why is it important?

A

Dot stands for “defect of organelle trafficking”

It is a genetic locus posessed by Legionella pneumophilia

It carries the genes necessary to block phagosome/lysosome fusion, promote ribosome recruitment, and express a Type IV Secretion system

172
Q

What diseases are caused by Legionella pneumophilia?

A

Legionnarie’s Disease: Most common and most severe

Pontiac fever: less severe, self-limiting

173
Q

Which bacteria express phospholipase C?

What does it do?

A

Legionella pneumophilia

Phospholipase C is an exotoxin that hydrolyzes phosphatidyl choline in eukaryotic membranes

174
Q

Describe the clinical presentation of Legionnaire’s disease

A

Nosocomial or community acquired pneumonia

Usually severe

  • Fever >40.5 C (104 F)
  • Respiratory symptoms
  • Headahe
  • Change in neuro symptoms (headache and confusion_
  • Nausea, vomiting, diarrhea
  • Hyponatremia (low Na+ in blood)
  • Patchy infiltrate in 1 lobe of lung (sometimes)
175
Q

Pneumonia with respiratory symptoms, high fever >40.5 C, neurological symptoms, and GI symptoms is most likely caused by…

A

Legionella pneumophilia

176
Q

Which groups are more likley to be infected by Legionella pneumophilia?

A
  • Smokers
  • Alcoholics
  • Elderly
  • COPD patients
  • Immunocompromised patients
177
Q

How is Legionella pneumophilia transmitted?

A
  • Aspiration of water w/ Legionella pneumophilia from faucets or fountains
  • Inhallation of aerosol from air conditioning systems

Note: No person-person transmission

178
Q

Describe the clinical presentation of pontiac fever

Which bacteria is it caused by?

A

Fever and malaise

Usually self-limiting and not severe

Caused by Legionella pneumophilia

179
Q

How is a Legionella pneumophilia infection diagnosed?

A
  • Visualize with dieterle silver stain (Poorly visualized with gram stain)
  • Grows on BYCE agar (but grows slowly)
  • Direct fluorescent antibody
  • Urinary antigen test
    • Only detects serogroup 1
180
Q

How is Legionella pneumophilia infection treated?

A

Choice/first line: Macrolide or ciprofloxacin

If severe: Rifampin + macrolide or quinolone

181
Q

How can Legionella pneumophilia infection be treated?

A

Disinfect hospital water systems

182
Q

Describe the clinical presentation of a Vibrio vulnificus infection

A

Severe gastroenteritis and/or wound infection following cuts exposed to sea water

Life-threatening bacteremia in anyone with iron overload (liver disease)

183
Q

Why are patients with liver disease more sucesptible to life-threatening bacteremia due to Vibrio vulnificus infection?

A

Liver disease = iron overload

The bacteria grow really well when there is a lot of iron around

184
Q

Vibrio spp. is a family of [Gram stain, shape distinctive morphology]

A

Vibrio spp. are gram negative, curved rods that are “comma shaped”

185
Q

What are the 3 medically important species of Vibrio?

A
  • Vibrio cholerae*
  • Vibrio parahemolyticus*
  • Vibrio vulnificus*
186
Q

Where do Vibrio live?

A

Sea water, fresh water

187
Q

Describ the clinical presentation of a Vibrio parahemolyticus infection

A

Gastroenteritis due to the ingestion of raw/undercooked seafood

188
Q

Helicobacter pylori is a [Gram stain, metabolism, shape distinctive morphology]

A

Helicobacter pylori is a gram negative, slender, curved rod that grows best in microaerophilic environments (obligate aerobe that cannot survive in full oxygen)

Urease (+), Oxidase (+), Motile

189
Q

List the determinants of pathogenicity of Helicobacter pylori

A

VU-FAT (You view fat in people’s stomachs, where H. pylori lives)

  • VacA
  • Urease (+)
  • Flagella + Curved shape
  • Adherence
  • Type IV Secretion System
190
Q

What is VacA?

Which bacteria secrete it?

A

VacA is an exotoxin that causes the vacuolation of cultured epithelial cells

It is secreted by H. pylori

  • VacA (+) H. pylori causes peptic ulcer disease
191
Q

Describe the clinical presentation of an Helicobacter pylori infection

A

Peptic ulcer disease: Increased gastric acid production in the duodenum

Adenocarcinoma, non-Hodgkin lymphoma, MALT lymphoma: H. pylori is a risk factor. MALT lymphoma regresses in 50% of cases with antibiotic treatment

30% of people in the USA are infected with Helicobacter pylori

- Usually asymptomatic with GI inflammation

192
Q

How is a Helicobacter pylori infection diagnosed?

A

Poorly visualized with gram stain, does not grow well in culture

  • Endoscopy w/tissue biopsy
    • Stain with giesma or silver stain
    • Check urease activity using assay or breath test
  • Serologic tests for specific IgG
    • But IgG levels do not fall until 6 months after infection is cleared by abx
  • Antibody test to detect H. pylori in stool
193
Q

Describe a urease breath test

A
  • Ingest radiolabeled urea
  • If urease is present, it will cleave urea into ammonium hydroxide and CO2
  • Pt. will exhale radiolabled CO2
194
Q

How is a Helicobacter pylori infection treated?

A

Multi-drug protocol (3-4 drugs)

  • Proton pump inhibitor + Clarithromycin + amoxicillin
  • OR-
  • Proton pump inhibitor + Clarithromycin + metronidazole
195
Q

Campylobater jejuni is a [gram stain, metabolism, shape]

A

Campylobater jejuni is a gram negative, obligate aerobe, that is a curved rod with a little twist

196
Q

Describe the clinical presentation of a Campylobater jejuni infection

A

Gastroenteritis, diarrhea

197
Q

How can a Campylobater jejuni infection be prevented?

A

Proper food handling

198
Q

Why did it take so long for Helicobacter to be recognized as a pathogen?

A

It is poorly visualized by gram stain and difficult to grow in culture

199
Q

Which toxins ADP ribosylate EF-2?

A

Diphtheria toxin (Corynebacterium diphtheriae)

Exotoxin A (Pseudomonas aeruginosa)

200
Q

What are some of the key differences that distinguish infection caused by Francisella tularensis and infection caused by Brucella spp.?

A

Type of fever

  • F. tularensis = constant
  • Brucella = undulant (rises and falls)

Type of animal that carries it

  • F. tularensis = Wild animals
    • Rabbits, beavers, squirrels, muskrats
  • Brucella = Farm animals
    • Cattle, goats, hogs

Distinguishing symptoms

  • F. tularensis = painful ulceration
    • May lead to granuloma with caseating necrosis
  • Brucella = anorexia, arthralgia
    • May lead to osteomyelitis, arthritis (esp. in sacroilliac joint)
201
Q

A patient presents with this skin legion on her right hand that has lasted 1 week, a fever, and lymphadenopathy in the right cervical lymph nodes.

Using OLDCARTS, you determine that she noticed that the sore started to form ~1 day after a successful squirrel hunting trip with her friends

What is your leading diagnosis? Why?

How should it be treated?

A

Infection by Francisella tularensis

Contact with wild animal, fever, ulceration, regional lymphadenopathy

Treat with streptomycin or gentamicin to prevent systemic spread (pneumonia, dissemination to multiple organs, granuloma formation)