Gram (-) Bacilli - Enteric Tract Flashcards
List the gram (-) bacilli that often infect the enteric tract (12).
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
Enterobacter, Serratia, and Klebsiella motility
Enterobacter and Serratia = Yes (All enterobacteria that are motile are H2S positive - Black colonies on Hektoen Agar)
Klebsiella = No
What are some shared features between Enterobacter, Serratia, and Klebsiella?
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)
Which bacteria are able to turn pink on MacConkey Agar?
Must be able to ferment lactose.
Enterobacter, Serratia, Klebsiella, E Coli
When cultured, what is special about Serratia?
Produces a red pigment (same pigment around sink and shower)
What are the 3 A’s of Klebsiella?
Alcoholics, Abscesses, Aspiration
Klebsiella defining features (vs enterobacter and serratia)
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)
Salmonella common features (both kinds)
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.
Salmonella enteritidis
From eating undercooked chicken
Causes inflammatory diarrhea
What is the #1 cause of osteomyelitis in patients with sickle cell disease?
Salmonella typhi
Where do chronic carriers of salmonella typhi carry it?
Gall bladder
Typhoid Fever (Enteric Fever)
From Salmonella typhi
normally associated with constipation, but it can cause diarrhea that is like pea soup
Rose-colored macules on abdomen
Tx for salmonella typhi infection
Fluoroquinoline (Cipro)
Vaccine for salmonella typhi
Live attenuated
How can you differentiate Shigella from Salmonella on an agar?
Use Hektoin Agar
Salmonella: Black colonies
Shigella: Green colonies
How does the amount needed for infection differ between Shigella and Salmonella?
Shigella: Acid Stable - do not need much (10-100 organisms)
Salmonella: Acid Labile - need a ton (10,000+ organisms)
Shigella motility
Immotile
Which cells can Shigella live in?
It is facultative intracellular in M cells of Peyer’s Patches (salmonella was macrophages)
Characterize the diarrhea of Shigella
Bloody, inflammatory
Which species of Shigella is most common in USA?
Sonnei
Shigella mechanism
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.
Special considerations in a child infected with Shigella dysenteriae
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
How does Shigella cause HUS?
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
How does Shiga Toxin damage tissues?
Binds to 60S subunit of ribosomes and inhibits translation
What is the #1 cause of UTIs?
E Coli (80% of cases) From Pili/Fimbrae
E Coli (all) on MacConkey Agar
Ferments lactose - turns pink
The E Coli (all) Capsule
Contains K antigen - used for serotyping
E Coli (all) stains green on…
Metallic green sheen on Eosin Methylene Blue (EMB) Agar
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.
What is the leading cause of gram (-) sepsis?
E Coli - from LPS endotoxin
When does E Coli cause neonatal meningitis?
When it is positive for K antigen
Enterohemorrhagic E Coli (EHEC) transmission
Eating undercooked meat (hamburgers)
What serotype of EHEC is known to cause massive outbreaks?
O157H7
EHEC differences from other E Coli’s
Only E Coli that does not ferment sorbitol
Bloody diarrhea
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
How is Enterotoxigenic E Coli (ETEC) transmitted?
“Traveler’s Diarrhea” - Water sources
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
How is Yersinia enterocolitica transmitted?
puppy poop (mainly)
Contaminated milk products
Also resistant to cold temps (like listeria)
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.
What does Y. enterocolitica look like?
Bipolar staining - stains most heavily on each end.
Looks like a safety pin.
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.
What bacterial infection can mimic appendicitis?
Y. enterocolitica
What bacteria caused the Bubonic Plague
Y. pestis
What is the main reservoir of Y. pestis?
Rodents (esp rats)
In USA, it is prairie dogs
What is the main vector for Y. pestis infection?
Fleas that bite the rats/prairie dogs and then bite humans
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.
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
Tx for Yersenia infections (both)
Aminoglycosides (Streptomycin) + doxycycline combo
Prevention for Yersinia infections (both)
Killed vaccine
What is an important, rare complication of Campylobacter infection?
Guillen Barre Syndrome
Also, Reactive Arthritis
What kind of environment does Campylobacter prefer?
Thermophilic - likes to grow in heat > 42C
What does Campylobacter look like?
It is 1 of the 3 curved gram (-) rods (H Pylori, Vibrio, Campy)
What is the main reservoir for Campylobacter?
Intestinal tracts of other animals, like POULTRY
Campylobacter transmission
Fecal-oral
During slaughtering process, gut perforation can cause bacteria to contaminate meat.
Characterize the diarrhea from a Campylobacter infection
lots of bloody diarrhea
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
What region is endemic for Vibrio Cholerae
Cholera is endemic to developing countries like SE Asia
What does Vibrio look like?
Comma-shaped - 1 of the 3 curved gram (-) rods (H pylori, Vibrio, Campy)
Describe the stool associated with Cholera infection?
Profuse (10L - 20L per day) watery diarrhea (not bloody)
Consistency is like rice water
How is Cholera transmitted?
Fecal-oral transmission via poor sanitation leading to contamination of food/water sources with HUMAN feces.
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.
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.
What can Vibrio parahaemolyticus and Vibrio vulnificus cause?
They can contaminate seafood, ESP oysters
Tx for Cholera
Oral rehydration with electrolytes
Antibiotics may lessen duration of symptoms
What does H Pylori look like?
It is helical!
1 of the 3 curved gram (-) rods (H pylori, Vibrio, Campy)
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
How does H Pylori move around
It is motile!
It spins its flagella around to propel through stomach
Where in the body is H Pylori found?
near pyloris in antrum of stomach
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.
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
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.
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.
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
People with Chronic Granulomatous Disease are especially susceptible to these infections
Infections from Catalase (+) organisms
ESP pseudomonas
Pseudomonas respiration
Obligate aerobe - This helps distinguish pseudomonas from the rest of the enterobacteriaceae (they’re mostly facultative anaerobes)
What kind of environment does pseudomonas prefer?
Thrives in aquatic environments - Hot Tub Folliculitis
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
The odor of pseudomonas
Fruity, grape-like odor
What is the #1 cause of gram (-) nosocomial pneumonia?
Pseudomonas!
What is the most common cause of respiratory failure in patients with cystic fibrosis?
Pseudomonas!
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
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
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
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
Tx for pseudomonas
Antipseudomonal penicillins - Piperacillin + Tazobactam combo
OR
Aminoglycosides (can be used in combo with B-lactams)
Fluoroquinolones (ESP for UTIs from pseudomonas)
Proteus respiration
Facultative anaerobe
Describe the motility of Proteus
When plated, it demonstrates swarming motility
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
Tx for Proteus
Sulfonamides
