Enterobacteriaceae Flashcards
1
Q
What are the general physiologic and structural properties of Enterobacteriaceae?
A
- Moderate in size
- Non–spore-forming, Gram-negative rods
- All share a common antigen (enterobacterial common antigen)
- All members can grow rapidly, aerobically or anaerobically (facultative anaerobes) on a variety of nonselective and selective media
- Members can be distinguished by their growth on MacConkey’s agar
- Resistance to bile salts is found in some members (e.g. Salmonella, Shigella)
2
Q
What are the contents of MacConkey’s agar?
A
- Bile salts
- Crystal violet (inhibits Gram-positives)
- Neutral red (responsible for the pink color of lactose fermenters)
3
Q
What are the virulence factors of Enterobacteriaceae?
A
- Endotoxin, whose toxic activity is dependent on the release of lipid A from LPS at cell lysis
- A hydrophilic capsule that repels the hydrophobic cell surface of phagocytes
- Antigenic phase variation, preventing antibody-mediated cell death
- Type III secretion systems
- Siderophores or iron-chelating compounds (e.g. enterobactin, aerobactin) to increase access to iron
- Resistance to serum killing
- Increasing antimicrobial resistance and a shift from natural resistance to mobile, transferrable gene pools of resistance
4
Q
What are the antigens of Enterobacteriaceae that are used in antigenic phase variation?
A
- O antigens: somatic
- K antigens: capsular
- H antigens: flagellar
5
Q
What are the clinically significant members of Enterobacteriaceae?
A
- Escherichia coli
- Salmonella
- Shigella
- Klebsiella
- Proteus
- Yersinia (for historic reasons)
6
Q
What are the strains of E. coli?
A
- Diarrheagenic strains that cause diarrhea, with symptoms that vary by the particular strain’s virulence factors
- Extraintestinal strains that can cause disease only if they leave the gut
- Commensal strains present in the colon that only cause disease in the presence of a large inoculum (e.g. penetrating abdominal trauma) or host compromise
7
Q
What are the two prominent strains of E. coli that cause gastroenteritis?
A
- Enterotoxigenic E. coli (ETEC)
- Shiga toxin–producing E. coli (STEC)
8
Q
What are the features of infection with enterotoxigenic E. coli (ETEC)?
A
- One of the most common causes of bacterial diarrhea in the developing world
- Accounts for 30% of traveler’s diarrhea cases
- The inoculum for the disease is high, so infections are primarily acquired through consumption of fecally contaminated food or water
- Secretory diarrhea caused by ETEC develops after a 1- to 2-day incubation period and persists for 3–5 days
- Symptoms include watery nonbloody diarrhea and abdominal cramps
9
Q
What are the enterotoxins produced by enterotoxigenic E. coli (ETEC)?
A
- Heat-stable toxins (STa and STb)—increases cGMP levels in the intestinal epithelium, leading to hypersecretion of fluids and inhibition of fluid absorption
- Heat-labile toxins (LT-I, LT-II)—increases cAMP levels, leading to enhanced secretion of chloride and decreased absorption of sodium and chloride, drawing out water by osmosis
10
Q
What are the features of infection with Shiga toxin–producing E. coli (STEC)?
A
- Infections are attributed to consumption of undercooked ground beef, water, unpasteurized milk, or fruit juices; or person-to-person spread
- A small inoculum (fewer than 100 bacteria) is needed
- Disease ranges from mild uncomplicated diarrhea to hemorrhagic colitis with severe abdominal pain and bloody diarrhea. Vomiting is observed in approximately half of patients, but fever is generally absent
- Within 2 days of onset, disease progresses to a bloody diarrhea with severe abdominal pain. Complete resolution of symptoms typically occurs after 4–10 days without treatment
- Hemolytic uremic syndrome (HUS) is characterized by acute renal failure, thrombocytopenia, and microangiopathic hemolytic anemia and is seen in 5–10% of infected children under 10 years of age
11
Q
What are the extraintestinal infections caused by E. coli?
A
- UTIs from colonic bacteria that contaminate the urethra, ascend into the bladder, and migrate to the kidneys or prostate. This is mediated by adhesins and P pili. More common in women due to their shorter urethras
- Neonatal meningitis, alongside S. agalactiae, in infants younger than 1 month
- Septicemia originating from infections of the urinary or GI tract. Has high mortality in immunocompromised patients
12
Q
What is the epidemiology of Salmonella?
A
- Salmonella colonizes virtually all animals, including poultry, reptiles, livestock, rodents, domestic animals, birds, and humans
- Animal-to-animal spread maintains the animal reservoir
- Serotypes such as Salmonella Typhi and Salmonella Paratyphi are highly adapted to humans and do not cause disease in nonhuman hosts
- Most infections result from ingestion of contaminated food products (e.g. poultry, eggs, dairy products) and, in children, from direct fecal–oral spread
13
Q
What is the pathogenesis of Salmonella infections?
A
- After ingestion and passage through the stomach, salmonellae attach to the mucosa of the small intestine and invade into the M (microfold) cells as well as into enterocytes
- The bacteria remain in endocytic vauoles, in which they replicate. The bacteria can also be transported across the cytoplasm and released into the blood or lymphatic circulation
- Regulation of attachment, engulfment, and replication is controlled primarily by pathogenicity islands
- The inflammatory response confines the infection to the GI tract, mediates the release of prostaglandins, and stimulates cAMP and active fluid secretion
14
Q
What are the diseases caused by Salmonella?
A
- Gastroenteritis
- Septicemia
- Typhoid fever
15
Q
What are the features of gastroenteritis caused by salmonellosis?
A
- Nausea, vomiting, and nonbloody diarrhea
- Can persist for 2–7 days before spontaneous resolution
