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Gram (-) Bacilli - Enteric Tract Flashcards

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1
Q

List the gram (-) bacilli that often infect the enteric tract (12).

A 
Enterobacter 
Serratia
Klebsiella 
Salmonella (typhi and enteritidis)
Shigella (sonnei and dysenteriae)
E Coli (E coli + EHEC and ETEC)
Yersinia (enterocolitica and pestis)
Campylobacter 
Vibrio (cholerae, parahaemolyticus, and vulnificus)
Helicobacter pylori
Pseudomonas
Proteus
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2
Q

Enterobacter, Serratia, and Klebsiella motility

A

Enterobacter and Serratia = Yes (All enterobacteria that are motile are H2S positive - Black colonies on Hektoen Agar)
Klebsiella = No

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3
Q

What are some shared features between Enterobacter, Serratia, and Klebsiella?

A

Cause pneumonia and UTI most commonly

Nosocomial infections - all have multi-drug resistance since many hospital patients are on antibiotics

Ferment lactose - causes pink colonies on MacConkey Agar (only E Coli does this too)

Serratia does ferment lactose, but it’s slow so it might show up negative at times.

Treat all these guys with a carbapenem (resistance not normally seen)

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4
Q

Which bacteria are able to turn pink on MacConkey Agar?

A

Must be able to ferment lactose.

Enterobacter, Serratia, Klebsiella, E Coli

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5
Q

When cultured, what is special about Serratia?

A

Produces a red pigment (same pigment around sink and shower)

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6
Q

What are the 3 A’s of Klebsiella?

A

Alcoholics, Abscesses, Aspiration

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7
Q

Klebsiella defining features (vs enterobacter and serratia)

A

It is encapsulated (High risk for sickle cell and asplenia)

Urease Positive

Not motile

Patient coughs up red currant jelly sputum

Cavitary lesions on CXR (looks like TB a bit so look for TB distractors in questions)

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8
Q

Salmonella common features (both kinds)

A

Motile (H2S positive - All enterobacteria that are motile are H2S positive - Black colonies on Hektoen Agar)

Encapsulated

ACID LABILE - gets easily degraded in stomach. YOU NEED A REALLY HIGH DOSE TO CAUSE INFLAMMATION

If you are taking omeprazole or had pernicious anemia or any other conditions that lower stomach acidity you’d be more susceptible

Type 3 secretion system - protein that detects eukaryotic cells and secretes a protein that helps with infectivity

If we take in enough, it will reach colon and invade the lymphocytes there. It is facultative intracellular in macrophages.

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9
Q

Salmonella enteritidis

A

From eating undercooked chicken

Causes inflammatory diarrhea

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10
Q

What is the #1 cause of osteomyelitis in patients with sickle cell disease?

A

Salmonella typhi

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11
Q

Where do chronic carriers of salmonella typhi carry it?

A

Gall bladder

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12
Q

Typhoid Fever (Enteric Fever)

A

From Salmonella typhi

normally associated with constipation, but it can cause diarrhea that is like pea soup

Rose-colored macules on abdomen

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13
Q

Tx for salmonella typhi infection

A

Fluoroquinoline (Cipro)

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14
Q

Vaccine for salmonella typhi

A

Live attenuated

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15
Q

How can you differentiate Shigella from Salmonella on an agar?

A

Use Hektoin Agar

Salmonella: Black colonies
Shigella: Green colonies

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16
Q

How does the amount needed for infection differ between Shigella and Salmonella?

A

Shigella: Acid Stable - do not need much (10-100 organisms)

Salmonella: Acid Labile - need a ton (10,000+ organisms)

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17
Q

Shigella motility

A

Immotile

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18
Q

Which cells can Shigella live in?

A

It is facultative intracellular in M cells of Peyer’s Patches (salmonella was macrophages)

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19
Q

Characterize the diarrhea of Shigella

A

Bloody, inflammatory

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20
Q

Which species of Shigella is most common in USA?

A

Sonnei

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21
Q

Shigella mechanism

A

It is acid stable.

When it gets to intestine, it targets M cells (in Peyer’s Patches - organized lymphatics in epithelium).

M cells are scouts that sample things in lumen and bring back antigens. Shigella induces M cells to phagocytose it and then it escapes from the phagolysosome before it is degraded.

In the cytoplasm of the M cell now, Shigella uses the host cell’s actin cytoskeleton to create a tail that it uses to propel itself from one cell to another (similar to Listeria’s actin rocket)

Once it has invaded lymphoid tissue and enterocytes surrounding M cells it damages the tissues, releasing cytokines that trigger massive immune response

We will see fecal blood AND leukocytes (inflammatory diarrhea)

Note: Shigella also uses Type 3 secretion system to secrete inflammatory cytokines.

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22
Q

Special considerations in a child infected with Shigella dysenteriae

A

If a child has shigellosis from S. dysenteriae, there is a chance that the infection can precipitate Hemolytic Uremic Syndrome (HUS) - more common in E Coli, but possible here.

Young pt with prodromal diarrhea and a week or so later as things are starting to look up, they present with signs of acute renal failure - Think HUS

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23
Q

How does Shigella cause HUS?

A

Once it invades it releases Shiga Toxin.

When it gets into blood, the toxin can induce endothelial damage, including within glomerulus of kidney.

Damaged endothelium activates platelets and causes their aggregration. This lowers the amount of circulating platelets (low platelet count). Aggregates of platelets protruding from endothelium end up lysing RBCs as they pass by (RBC hemolysis).

HUS usually happens in kids

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24
Q

How does Shiga Toxin damage tissues?

A

Binds to 60S subunit of ribosomes and inhibits translation

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25
What is the #1 cause of UTIs?
``` E Coli (80% of cases) From Pili/Fimbrae ```
26
E Coli (all) on MacConkey Agar
Ferments lactose - turns pink
27
The E Coli (all) Capsule
Contains K antigen - used for serotyping
28
E Coli (all) stains green on...
Metallic green sheen on Eosin Methylene Blue (EMB) Agar
29
E Coli virulence factors (all species)
Capsule Pili/Fimbrae - needed for causing UTI LPS - causes sepsis. Located on outer cell membrane of ALL gram(-) bacteria.
30
What is the leading cause of gram (-) sepsis?
E Coli - from LPS endotoxin
31
When does E Coli cause neonatal meningitis?
When it is positive for K antigen
32
Enterohemorrhagic E Coli (EHEC) transmission
Eating undercooked meat (hamburgers)
33
What serotype of EHEC is known to cause massive outbreaks?
O157H7
34
EHEC differences from other E Coli's
Only E Coli that does not ferment sorbitol Bloody diarrhea
35
EHEC
Bloody diarrhea Doesn't ferment sorbitol Has a toxin called Shiga-like Toxin that acts at 60S subunit of ribosomes (like Shiga Toxin - same mechanism) Can cause HUS in children under 10
36
How is Enterotoxigenic E Coli (ETEC) transmitted?
"Traveler's Diarrhea" - Water sources
37
ETEC
Classic Hx of recent travel to Mexico where they drank the water (Montezuma's Revenge) Watery diarrhea (not bloody) 2 toxins: 1) Heat labile toxin that raises cAMP (like cholera toxin) 2) Heat stable toxin that raises cGMP
38
How is Yersinia enterocolitica transmitted?
puppy poop (mainly) Contaminated milk products Also resistant to cold temps (like listeria)
39
Who does Y. enterocolitica usually infect?
Typically toddlers since they're likely to get into the puppy poop and stank milk. Since it's encapsulated, look out for Sickle Cell and asplenic patients too.
40
What does Y. enterocolitica look like?
Bipolar staining - stains most heavily on each end. Looks like a safety pin.
41
Symptoms of Y. enterocolitica infection
Bloody diarrhea (bc it can be invasive) Invasiveness can lead to systemic effects like: Fever, leukocytosis, abscesses In abdomen, infection can lead to intestinal perforation, intussusception, necrotic small bowell, perilytic illness, etc Can mimic appendicitis - fever, elevated white count, RLQ pain in toddler Look out for other sick kids in day care or playing with puppies.
42
What bacterial infection can mimic appendicitis?
Y. enterocolitica
43
What bacteria caused the Bubonic Plague
Y. pestis
44
What is the main reservoir of Y. pestis?
Rodents (esp rats) In USA, it is prairie dogs
45
What is the main vector for Y. pestis infection?
Fleas that bite the rats/prairie dogs and then bite humans
46
Y. pestis presentation
When people become infected they have buboes (swollen, tender lymph nodes) Once it gets into the blood it can cause abscesses in organs, DIC, and cutaneous hemorrhage DIC is caused by endotoxin and can lead to necrosis of digits and other appendages.
47
What are some virulence factors for Y. pestis?
Exotoxins Yersina-associated outer proteins (YOPs) These factors cause dysfunction in macrophages and neutrophils by inhibiting phagocytosis and cytokine production (allows fast replication and spreading) Type 3 secretion system secretes the YOPs
48
Tx for Yersenia infections (both)
Aminoglycosides (Streptomycin) + doxycycline combo
49
Prevention for Yersinia infections (both)
Killed vaccine
50
What is an important, rare complication of Campylobacter infection?
Guillen Barre Syndrome Also, Reactive Arthritis
51
What kind of environment does Campylobacter prefer?
Thermophilic - likes to grow in heat > 42C
52
What does Campylobacter look like?
It is 1 of the 3 curved gram (-) rods (H Pylori, Vibrio, Campy)
53
What is the main reservoir for Campylobacter?
Intestinal tracts of other animals, like POULTRY
54
Campylobacter transmission
Fecal-oral During slaughtering process, gut perforation can cause bacteria to contaminate meat.
55
Characterize the diarrhea from a Campylobacter infection
lots of bloody diarrhea
56
Guillen Barre Syndrome
Occurs after being infected by some bacterial/viral entity such as Campylobacter (usual presentation) Autoimmune response causes demyelination of peripheral nerves Causes an ascending paralysis (opposite of Botulism) Starts at lower extremities
57
What region is endemic for Vibrio Cholerae
Cholera is endemic to developing countries like SE Asia
58
What does Vibrio look like?
Comma-shaped - 1 of the 3 curved gram (-) rods (H pylori, Vibrio, Campy)
59
Describe the stool associated with Cholera infection?
Profuse (10L - 20L per day) watery diarrhea (not bloody) Consistency is like rice water
60
How is Cholera transmitted?
Fecal-oral transmission via poor sanitation leading to contamination of food/water sources with HUMAN feces.
61
Cholera infection mechanism
It is toxin-mediated Cholera does NOT invade mucosa. It uses fimbrae to attach to ganglioside receptors in intestinal wall. Then, it secretes cholera toxin which causes the symptoms. Cholera toxin increases cAMP like so: It binds to and activates adenylyl cyclase (part of Gs pathway). Thus, it activates Gs pathway. This causes an increase in cAMP which increases secretion of water into intestinal lumen, hence watery diarrhea.
62
What kind of environment does Cholera prefer?
Alkaline - it grows on alkaline media and prefers a basic environment It is ACID LABILE and hates our stomach.
63
What can Vibrio parahaemolyticus and Vibrio vulnificus cause?
They can contaminate seafood, ESP oysters
64
Tx for Cholera
Oral rehydration with electrolytes Antibiotics may lessen duration of symptoms
65
What does H Pylori look like?
It is helical! 1 of the 3 curved gram (-) rods (H pylori, Vibrio, Campy)
66
How common is H Pylori infection?
Over 80% of adults in developing countries have been infected at some point ~50% of adults in US have been carriers
67
How does H Pylori move around
It is motile! It spins its flagella around to propel through stomach
68
Where in the body is H Pylori found?
near pyloris in antrum of stomach
69
What is one mechanism that helps H Pylori survive the stomach?
It is Urease (+) Urease splits urea into NH3 and CO2 which helps reduce the acidity of the environment and is necessary for helping it survive the stomach.
70
How is H Pylori infection diagnosed?
Urea Breath Test - Pt swallows urea labeled with radioactive carbon. The CO2 is exhaled as urea is split. If radionucleotides are detected on exhalation then we have a urease (+) organism in the stomach. OR Biopsy during endoscopy - directly test urease (+) with rapid test
71
Relationship between ulcers and H Pylori
95% of all duodenal ulcers are caused by H Pylori It is possible that chronic infection may increase acid production through the reduction of somatostatin or the elevation of gastrin. We don't know.
72
What happens if you do not receive treatment for H Pylori?
More severe symptoms can develop Adenocarcinoma of the stomach (~50% of all adenocarcinomas of the stomach may be due to H Pylori) Lymphoma of mucous-associated lymphoid tissue (MALT) MALToma - if you treat the infection the MALToma will go away.
73
Tx for H Pylori infection
Often requires triple or quadruple therapy Triple: 1) PPI - counters the increased acid production caused by chronic H Pylori 2) Amoxicillin 3) A Macrolide like Clarithromycin
74
People with Chronic Granulomatous Disease are especially susceptible to these infections
Infections from Catalase (+) organisms ESP pseudomonas
75
Pseudomonas respiration
Obligate aerobe - This helps distinguish pseudomonas from the rest of the enterobacteriaceae (they're mostly facultative anaerobes)
76
What kind of environment does pseudomonas prefer?
Thrives in aquatic environments - Hot Tub Folliculitis
77
What does pseudomonas look like on plating?
Produces a Blue-green pigment from production of pyocyanin (blue) and pyoverdin (green) May even turn wounds blue bc they make so much of it
78
The odor of pseudomonas
Fruity, grape-like odor
79
What is the #1 cause of gram (-) nosocomial pneumonia?
Pseudomonas!
80
What is the most common cause of respiratory failure in patients with cystic fibrosis?
Pseudomonas!
81
Who is at risk for developing pseudomonal osteomyelitis?
IV drug users - may directly introduce the microbe into blood Diabetics - more likely to develop traumatic injury that pseudomonas can enter
82
What types of patients should make you suspect pseudomonas?
Burn patients - often fatal and unresponsive to antibiotics in these patients It's encapsulated so... IV drug users Diabetics People with indwelling catheters - nosocomial UTIs
83
Pseudomonas symptoms
Causes 2 types of skin lesions: 1) pruritic, papular, pustular folliculitis - associated with people using under-chlorinated hot-tubs 2) If pseudomonas gets into circulation and causes sepsis, it can release toxin that damages tissues and causes cutaneous necrosis. - Black, necrotic lesions are called ecthyma granulosum Pseudomonas can also cause Swimmer's Ear - Otitis Externa
84
Pseudomonas toxin
Exotoxin A - very similar to diphtheria toxin (same mechanism/targets). It ribosylates elongation factor 2 which inhibits protein synthesis and causes cell death
85
Tx for pseudomonas
Antipseudomonal penicillins - Piperacillin + Tazobactam combo OR Aminoglycosides (can be used in combo with B-lactams) Fluoroquinolones (ESP for UTIs from pseudomonas)
86
Proteus respiration
Facultative anaerobe
87
Describe the motility of Proteus
When plated, it demonstrates swarming motility
88
Proteus presentation
May form Staghorn calculi in kidneys - This is due to the fact that it is Urease (+) - When urease breaks up urea to NH3 and CO2 it creates an alkaline environment. This is the perfect environment for precipitation of struvite stones (made of NH3, Mg, PO4). The stones cause pain/kidney damage but also act as way it can cause repeat infections. May cause UTIs Fishy odor
89
Tx for Proteus
Sulfonamides

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