Gram Negative Bacteria Flashcards
(201 cards)
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…
- Secretion apparatus is embedded into the host cell membrane
- > Secretes toxins to the exterior of the bacterium - Several secreted proteins insert into the host cell membrane and form a translocation complex
- > Translocates toxins into the host cytoplasm - 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
Describe an EPEC infection
Enteropathogenic *E. coli*
* Associated wtih childhood diarrhea in developing countries
* Fever, bloody diarrhea
26
What are the determinants of pathogenicity of EPEC?
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
Describe the mechanism of action of EPEC infection
* Bacteria bind to intestinal epithelial cells using bundle-forming pili
* Disruption of the overlying mucosa
* Fever, bloody diarrhea
28
Where are EPEC and EIEC most commonly found?
Outside of the United states
Causative agents of diarrhea in developing countries
29
Describe EAEC infection
Diarrhea in developing countries
| (Rarely seen in the USA)
30
Which *E. coli* determinant of pathogenicity is associated with sepsis?
LPS
31
*Salmonella enterica* is a [Gram stain, metabolism, shape distinctive morphology]
* 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
Which *E. coli* determinant of pathogenicity is associated with UTIs (bladder infections/lower UTI)
Type 1 fimbriae
33
Which *E. coli* determinant of pathogenicity is required to cause meningitis?
K capsule
Commonly causes meningitis in neonates
34
Which *E. coli* determinant of pathogenicity is associated with upper UTI/kidney infection?
P pili
35
What is the reservoir for *Salmonella enterica* serovar typhi*?*
Gallbladder of human carriers
36
What is the reservoir for S*almonella enterica* serovar enteritidis*?*
Farm animals/uncooked chicken
Turtles and other reptiles
37
What are the determinants of pathogenicity of *Salmonella enterica* serovar enteritidis?
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
Which cells are most often inhabited by a *Salmonella enterica* infection?
Macrophages
39
What is the clinical presentation of a *Salmonella enterica* sevofar enteritidis infection?
24-48 hours after ingestion...
* Inflammatory diarrhea (food poisoning)
* Nausea, vomiting
* Fever in 50% of individuals
* Bacteremia in 8% of healthy individuals
40
What is unique about the diarrhea caused by *Salmonella enteria* serovar enteritidis*,* as compared to that caused by ETEC or EPEC?
*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
How is *Salmonella enteritidis* infection treated?
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
MacConkey agar culture: which enterobacteriaceae organisms might be growing on the left in this picture?
Any lactose fermentor
* *E. coli*
* *Klebsiella*
* *Enterobacter*
43
How is a *Salmonella enterica* infection diagnosed?
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
Which individuals are most susceptible to infection by *Salmonella enterica*?
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
In the United States, *Salmonella typhi* infection is most commonly seen in which individuals?
Travellers returning from Mexico, Latin America, Asia, India
46
What is the clinical presentation of an individual infected wtih *Salmonella typhi?*
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
How is typhoid fever treated?
Always treat typhoid fever
* Antibiotics
* Fluroquinolone, ampicillin, chloramphenicol
* Note: Resistance is becoming more common
48
How are *Salmonella enterica* infections prevented?
*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
What are the determinants of pathogenicity of *Salmonella typhi*?
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
*Yersinia pestis* is [Gram stain, metabolism, shape, distinctive morphology]
*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
What are the 3 medically relevant *Yersinia* species?
* *Yersinia pestis* - Bubonic plague
* *Yersinia enterocolitica* - Infectious diarrhea
* *Yersinia pseudotuberculosis* - Infectious diarrhea
52
Where is the environmental reservoir for *Yersinia pestis*?
What is the vector for human transmission?
Reservoir = rodents (prarie dogs in USA, rats historically)
Vector = fleas
53
What are the 3 infections that may be caused by *Yersinia pestis*?
Bubonic plague
Pneumonic plague
Primary septicemic plague
54
Describe the mechanism of *Yersinia pestis* infection from rodents to humans
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
What are the determinants of pathogenicity of *Yersinia pestis*?
* 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
Which *Yersinia pestis* determinant of pathogenicity allows the bacteria to multiply in large numbers in the human body?
YOPS: The effector proteins secreted by the Type III Secretion system
- YOPS disable macrophages and neutrophils -\> inhibits phagocytosis and cytokine produciton
57
Describe the clinical presentation of bubonic plague
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
Which *Yersinia pestis-*associated disease is caused by a flea bite?
Bubonic plague
(no bubo in pneumonic plague or primary septicemic plague)
59
Describe the clinical presentation of pneumonic plague
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
Describe the clnical presentation of primary septicemic plague
Follows direct inoculation of *Y. pestis* into bloodstream
* Gastroenteritis
* Nausea, vomiting, diarrhea, abdominal pain
* No bubo = late diagnosis
61
How is primary vs. secondary septicemic plague contracted?
Primary = direct inoculation of *Y. pestis* into bloodstream
Secondary = septic shock following bubonic plague
62
Which *Y. pestis* infection is most associated with gastroenteritis?
Primary septicemic plague
63
How is a *Yersinia pestis* infection diagnosed?
**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
How is *Yersinia pestis* infection treated?
Choice: Streptomycin or gentamicin
Alternative: Doxycycline or chloraphenicol
65
How can *Yersinia pestis* infection be prevented?
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
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?
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
What organism causes dysentery?
*Shigella dysenteriae*
68
What kind of bacteria appear in this image?
*Yersinia pestis;*
Bipolar/closed safety pin appearance
This is a Giemsa stain
69
*Klebsilla pneumoniae* is a [Gram stain, metabolism, shape, distinctive morphology]
*Klebsilla pneumoniae* is a gram negative, facultatively anaerobic bacillus.
Ferments lactose, immotile, urease positive
70
What diseases are caused by *Klebsiella pneumoniae?*
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
What are the determinants of pathogenicity of *Klebsiella pneumoniae?*
* Polysaccharide capsule
* Prevents phagocytosis
* Prevents complement deposition
* Makes siderophores
* Can scavenge iron
* **Very resistant to antibiotics**
72
What is the clinical presentation of a *Klebsiella pneumoniae* infection?
May cause pneumonia, UTI, or wound infection
**Forms abscesses**
Typically affect **HADRs:**
* **H**ospitalized patients
* **A**lcoholics
* **D**iabetics
* Indivdiuals with chronic **R**espiratory disesae
73
Haemophilus are [size, Gram stain, shape, metabolic]
Haemophilus are small Gram-negative coccibacilli that grow both aerobically and anaerobically
74
What symptoms does Haemophilius influenzae cause?
Otitis media, sinusitis, bronchitis, epiglottitis, pneumonia, and meningitis
75
Bortedella are [Gram stain, shape]
Bordetella are Gram-negative coccobacilli
76
Bordetella pertusis is [size, Gram stain, shape, metabolic]
Bordetella pertusis are tiny Gram-negative coccobacilli that are strict aerobes
77
What are the determinants of pathogenicity of Bordetella pertusis?
* Adhesins (pili, filamentous hemagglutinin, and pertactin)
* Endotoxin
* Exotoxins (4: pertussis toxin, adenylate cyclase toxin, dermonecrotic toxin, tracheal cytotoxin)
78
What are three adhesins used by Bordetella pertusis?
What do they do?
* Pili
* Filamentous hemagglutinin
* Pertactin
Allow adherence to ciliated epithelial cells in the upper airway
79
In addition to allowing adherence to ciliated epithelial cells in the upper airway, what does filamentous hemagglutinin (FHA) of Bordetella pertusis do?
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
What two types of toxins does Bordetella pertussis have?
* Endotoxin
* Exotoxins (4)
81
What is pertussis toxin of Bordetella pertusis?
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
What does adenylate cyclase toxin of Bordetella pertussis do?
Inhibits leukocyte function by producing cAMP in the presence of host cell calmodulin
83
What does dermonecrotic toxin of Bordetella pertusis do?
Localized tissue destruction in infection
84
What is tracheal cytotoxin of Bordetella pertussis?
Peptidoglycan fragment that inhibits/kills ciliated cells and is pro-inflammatory
85
How communicable is Bordetella pertussis?
How is it transmitted?
Highly communicable
Via droplets
Most contagious during the catarrhal stage
86
What portion of the airway does Bordetella pertussis infect?
Upper airway
87
What are the three stages of Bordetella pertusis infection?
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
During which disease stage is Bordetella pertusis most infectious?
Catarrhal stage
89
Which diagnostic lab test finding is Bordetella pertussis infection associated with?
Atypical lymphocytosis
90
How are samples of Bordetella pertussis collected and grown?
Collected from nasopharynx
Grown on Bordet-Gengou medium or charcoal-containing medium
91
What is significant about Bordetella pertussis cultures after 4 weeks of symptoms?
Cultures are rarely positive after 4 weeks of symptoms
92
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?
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
What antibiotics are used to treat Bordetella pertussis infection?
Macrolides
| (TMP/SMX may also be effective)
94
What was the old vaccination strategy for pertussis?
Why was it discontinued?
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
What is the modern vaccination strategy for pertussis?
What is the booster?
Which group of people is recommended to receive Tdap and when?
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
Brucella spp. are [size, metabolic, Gram stan, shape]
Brucella are small aerobic Gram-negative coccibacilli
97
What do Brucella spp. cause?
Brucellosis in humans as well as cattle, goats, and hogs
98
How do humans acquire brucellosis?
Who is particularly at risk?
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
What cells can Brucella spp. survive in?
Macrophages
100
What is the clinical presentation of brucellosis?
Fever\*, chills, malaise, and drenching sweats
Infection can be chronic and last for weeks or months
(Fever may be undulant; rise and fall)
101
What does diagnosis of brucellosis require?
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
What is the treatment for brucellosis?
* Doxycycline + rifampin/gentamicin/streptomycin
* Vaccine for animals not humans
103
Francisella tularensis are [size, metabolic, Grains stain, shape]
Francisella tularensis are small, metabolically facultative, Gram-negative coccibacilli
(similar in morphology to Brucella)
104
How do humans become infected with Francisella tularensis?
Contact with rabbits, squirrels, muskrats, beavers, and deeper through tiny breaks in skin, exposure of mucous membranes, ingestion, or inhalation (also via ticks)
105
What is the classic case for infection with Francisella tularensis?
Skinning rabbits on a hunting trip
106
In which cells does Francisella tularensis multiply?
Macrophages
107
What is the clinical presentation of tularemia?
Site of innoculation is ulcerated
Regional lymphadenopathy
Fevers and chills
Possible pneumonia and dissemination to multiple organs
108
What is notable about diagnostic testing for tularemia?
* Francisella tularensis is difficult to grow in the lab and requires media
* Serological assay available
109
How is Francisella tularensis treated?
* Streptomycin or gentamicin
* Vaccine recommended for laboratory workers and others who have frequent contact with infected animals
110
How is *Klebsiella pneumoniae* infection diagnosed?
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
Pasteurella multocida are [size, Gram stain, shape, location where normally found]
Pasteurella multocida are small Gram-negative coccobacili that are part of the normal respiratory flora of some animals (especially cats and dogs)
112
How is *Klebsiella pneumoniae* infection treated?
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
How do humans become infected by Pasteurella multocida?
Cat or dog bite
114
Can zoonotic infections be acquired directly/indirectly/both from animals?
Zoonotic infections can be acquired both directly and indirectly from animals
115
Neisseria are [Gram-stain, shape]
Neisseria are Gram-negative diplococci
116
What antibiotics is *Klebsiella pneumoniae* resistant to?
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
Why is carbapenem used to treat *Klebsiella pneumoniae?*
*Klebsiella pneumoniae* is typically resistant to most early-line beta-lactam antibiotics
118
What are the two medically relevant Neisseria bacteria?
Neisseria menigitidis and Neisseria gonorrhoeae
119
What is Neisseria menigitidis a common cause of?
Who is at particular risk?
Meningitis and bloodstream infections
People living in crowded conditions (e.g. students in college dorms) are at particular risk
120
What is notable about the polysaccharide capsule of Neisseria meningitidis?
Antiphagocytic and resists complement-mediated killing
Basis for serogrouping and target of vaccines
121
Why is tetanus still a prevalent disease, given that there is an effective vaccination?
Tetanus spores have a reservoir in soil
122
Which serogroup of Neisseria meningitidis causes large outbreaks in Africa?
Serogroup A
123
How is Neisseria gonorrhoeae transmitted?
What is the clinical presentation?
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
What are the characterisitcs that define *Enterobacteriaceae?*
Gram negative rods that colonize or infect the GI tract
125
Which members of *Enterobacteriaceae* commonly cause diarrhea?
Diarrhea is m**ESSYY**
**M**innie's pneumonic:
* **E**. coli
* **S**almonella enterica (Serovars enteritidis and typhi)
* **S**higella
* **Y**ersinia enterocolitica
* **Y**ersinia pseudotuberculosis
126
How does Neisseria gonorrheoae avoid immune clearance?
Produces pili that change their antigenic make-up during the course of infection (antigenic variation)
127
Moraxella catarrhalis are [size, Gram stain, shape, clinical presentation]
Moraxella catarrhalis are small Gram-negative cocci or coccobacilli that cause otitis media, sinusitis, bronchitis, and pneumonia
(morphologically and metabolically resemble Neisseria spp.)
128
What virulence factor is linked to Traveler's diarrhea?
LT
Heat Labile Toxin secreted by ETEC
129
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?
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
What kind of bacteria exhibit "swarming motility?"
Proteus spp
## Footnote
* Proteus mirabilis*
* Proteus vulgaris*
131
What diseases are associated with *Proteus* spp?
UTIs (Hospital Acquired and Community Associated)
Also associated with nosocomial infections
132
Why do *Proteus* spp. exhibit swarming motility?
Each cell has hundreds of flagella
133
Which bacteria is associated with the formation of "struvite" kidney stones?
Why?
* 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
Why do patients with multiple UTIs often develop kidney stones?
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
What diseases are associated with *Cerratia marcescens*?
Often antibiotic resistant...
* Nosocomial respiratory infections
* UTIs
* Bloodstream infections
136
What diseases are associated with *Citrobacter* spp?
Often antibiotic resistant...
* Nosocomial respiratory infections
* UTIs
* Bloodstream infections
137
What diseases are associated with *Enterobacter* spp?
Often antibiotic resistant...
* Nosocomial respiratory infections
* UTIs
* Bloodstream infections
138
Which 3 members of Enterobacteraceae are associated with antibiotic resistant nosocomial respiratory infections, UTIs, and bloodstream infections?
* *Enterobacter* spp.
* *Citrobacter* spp.
* *Serratia marcescens*
139
Which bacteria is associated with the "red ring" around your shower?
*Serratia marcescens*
140
Which bacteria is this likely to be?
*Proteus* spp.
Grows in this pattern due to swarming motility
141
What are the 6 medically-important gram-negative rods?
**PAL-VCH**
* *Pseudomonas aeruginosa*
* *Acinetobacter baumanni*
* *Legionella pneumophila*
* *Vibrio cholerae*
* *Campylobacter jejuni*
* *Helicobacter pylori*
142
A patient undergoing chemotherapy develops the following skin legion:
What is it called?
Which bacteria is causign the legion?
**Ecthyma gangrenosum**: A black eschar indicating cutaneous necrosis caused by ***Pseudomonas aeruginosa***
143
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?
*Pseudomonas aeruginosa*
He likely acquired the bacteria from the hot tub
144
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?
*Pseudomonas Aeruginosa*
Colors are due to pyocanain and pyoverdin (a siderophore)
May also have a grape-like odor
145
This is a picture of "coiling phagocytosis," exhibited by which bacteria?
*Legionella pneumophilia*
146
This is a bacterial culture growing on BCYE agar
What bacteria is this?
What is in the agar helping the bactera grow?
***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
This bacteria of the stomach is most likely...
*Helicobacter pylori*
Look for flagella and curved shape
148
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?
***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
*Pseudomonadas aeruginosa* is a [Gram stain, metabolism, shape distinctive morphology]
*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
List the determinants of pathogenicity of *Pseudomonas aeruginosa*
**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
What is exotoxin A?
Which bacteria secrets it?
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
What is quorum sensing?
Which bacteria have quorum-sensing abilities?
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
Patient with which genetic disorder are likely to be infected with *Pseudomonas aeruginosa*?
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
Which bacteria often causes skin infections in burn patients?
*Pseudomonas aeruginosa*
155
What is the most common disease caused by *Pseudomonas aeruginosa*?
Pneumonia in hospitalized patients
- Usually acute, may be necrotizing
- Also causes other nosocomial infections
156
What is the most common non-nosocomial infections caused by *Pseudomonas aeruginosa?*
* **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
List the groups of patients and associated diseases that are likely caused by *Pseudomonas aeruginosa*
* 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
How might *Pseudomonas aeruginosa* infection affect patients undergoing chemotherapy?
May cause bacteremia and cutaneous necrosis
- Look for an **ecthyma gangrenosum** (black eschar)
159
How can a *Pseudomonas aeruginosa* infection be diagnosed?
* Grows on many types of lab media
* Gram (-), Catalase (+), oxidase (+)
* Grape-liek odor
* Fluorescent pigments
160
What causes *Pseudomonas aeruginosa* to appear fluorescent in cultures?
Siderophores
Pyocyanin and pyoverdin
161
How is *Pseudomonas aeruginosa* treated?
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
How can *Pseudomonas aeruginosa* infection be prevented?
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
*Acinetobacter baumannii* is a [Gram stain, metabolism, shape distinctive morphology]
*Acinetobacter baumannii* is a gram negative, non-fermenting, bacillus or coccobacillus
164
What diseases are caused by *Acinetobacter baumannii?*
Hospital-acquired infections
* Pneumonia
* Bloodstream infections
* Wound infections
165
How is *Acinetobacter baumannii* infection treated?
Very resistant to antibiotics!
**Choice**: carbapenem, amikacin, colistin
**Note:** Sublactams (beta-lactamase inhibitors) work against some strains
166
*Legionella pneumophilia* is a [Gram stain, metabolism, shape distinctive morphology]
*Legionella pneumophilia* is a gram negative, obligate anaerobic, facultative intracellular, thin bacillus.
Oxidase (+)
Serogroup 1 causes 80% of disease
Infects amoebae
167
Where is *Pseudomonas aeruginosaI* found?
Hospitals; faucets and drains
Under-chlorinated hot tubs
168
Where is *Legionella pneumophilia* found?
Natural bodies of water
Cooling towers of air-conditioning units
Water distribution systems
169
List the determinants of pathogenicity of *Legionella pneumophilia*
* Infects macrophages
* Dot - "Defect of Organelle Trafficking" genetic locus
* Type IV secretion system
* Phospholipase C
170
How does *Legionella pneumopilia* infect macrophages?
*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
What is Dot?
Which bacteria posesses it?
Why is it important?
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
What diseases are caused by *Legionella pneumophilia?*
**Legionnarie's Disease**: Most common and most severe
**Pontiac fever**: less severe, self-limiting
173
Which bacteria express phospholipase C?
What does it do?
*Legionella pneumophilia*
Phospholipase C is an exotoxin that **hydrolyzes phosphatidyl choline** in eukaryotic membranes
174
Describe the clinical presentation of Legionnaire's disease
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
Pneumonia with respiratory symptoms, high fever \>40.5 C, neurological symptoms, and GI symptoms is most likely caused by...
*Legionella pneumophilia*
176
Which groups are more likley to be infected by *Legionella pneumophilia?*
* Smokers
* Alcoholics
* Elderly
* COPD patients
* Immunocompromised patients
177
How is *Legionella pneumophilia* transmitted?
* Aspiration of water w/ *Legionella pneumophilia* from faucets or fountains
* Inhallation of aerosol from air conditioning systems
Note: No person-person transmission
178
Describe the clinical presentation of pontiac fever
Which bacteria is it caused by?
Fever and malaise
Usually self-limiting and not severe
Caused by *Legionella pneumophilia*
179
How is a *Legionella pneumophilia* infection diagnosed?
* 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
How is *Legionella pneumophilia* infection treated?
**Choice/first line:** Macrolide or ciprofloxacin
**If severe:** Rifampin + macrolide or quinolone
181
How can *Legionella pneumophilia* infection be treated?
Disinfect hospital water systems
182
Describe the clinical presentation of a *Vibrio vulnificus* infection
Severe gastroenteritis and/or wound infection following cuts exposed to sea water
Life-threatening bacteremia in anyone with **iron overload** (liver disease)
183
Why are patients with liver disease more sucesptible to life-threatening bacteremia due to *Vibrio vulnificus* infection?
Liver disease = iron overload
The bacteria grow really well when there is a lot of iron around
184
*Vibrio* spp. is a family of [Gram stain, shape distinctive morphology]
*Vibrio* spp. are gram negative, curved rods that are "comma shaped"
185
What are the 3 medically important species of *Vibrio*?
* Vibrio cholerae*
* Vibrio parahemolyticus*
* Vibrio vulnificus*
186
Where do *Vibrio* live?
Sea water, fresh water
187
Describ the clinical presentation of a *Vibrio parahemolyticus* infection
Gastroenteritis due to the ingestion of raw/undercooked seafood
188
*Helicobacter pylori* is a [Gram stain, metabolism, shape distinctive morphology]
*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
List the determinants of pathogenicity of *Helicobacter pylori*
**VU-FAT** (You *view fat* in people's stomachs, where *H. pylori* lives)
* **V**acA
* **U**rease (+)
* **F**lagella + Curved shape
* **A**dherence
* **T**ype IV Secretion System
190
What is VacA?
Which bacteria secrete it?
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
Describe the clinical presentation of an *Helicobacter pylori* infection
**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
How is a *Helicobacter pylori* infection diagnosed?
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
Describe a urease breath test
* Ingest radiolabeled urea
* If urease is present, it will cleave urea into ammonium hydroxide and CO2
* Pt. will exhale radiolabled CO2
194
How is a *Helicobacter pylori* infection treated?
Multi-drug protocol (3-4 drugs)
* Proton pump inhibitor + Clarithromycin + amoxicillin
- OR-
* Proton pump inhibitor + Clarithromycin + metronidazole
195
*Campylobater jejuni* is a [gram stain, metabolism, shape]
*Campylobater jejuni* is a gram negative, obligate aerobe, that is a curved rod with a little twist
196
Describe the clinical presentation of a *Campylobater jejuni* infection
Gastroenteritis, diarrhea
197
How can a *Campylobater jejuni* infection be prevented?
Proper food handling
198
Why did it take so long for *Helicobacter* to be recognized as a pathogen?
It is poorly visualized by gram stain and difficult to grow in culture
199
Which toxins ADP ribosylate EF-2?
Diphtheria toxin *(Corynebacterium diphtheriae)*
Exotoxin A *(Pseudomonas aeruginosa)*
200
What are some of the key differences that distinguish infection caused by *Francisella tularensis* and infection caused by *Brucella* spp.?
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
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?
**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)
