Deja Review Chapter 9 - Gram-Negative Rods (Enterics)

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CHAPTER 9 - Gram-Negative Rods (Enterics)

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CHAPTER 9 - Gram-Negative Rods (Enterics)

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ESCHERICHIA COLI

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ESCHERICHIA COLI

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Name the common diseases caused by Escherichia coli:

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Escherichia coli can cause diarrhea (bloody and nonbloody), urinary tract infections (UTIs) (most common cause), neonatal meningitis (second most common after group B streptococci), gram-negative sepsis (most common cause), and nosocomial pneumonia.

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Where does E. coli normally colonize and how is it transmitted?

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Escherichia coli is considered normal flora of the colon that is transmitted via fecal-oral route.

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How is an E. coli infection diagnosed?

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Laboratory culture. Escherichia coli is gram negative, oxidase negative, lactose fermenting, and β-hemolytic (although not all strains are lactose fermenting or β-hemolytic).

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Escherichia coli is classically associated with what three antigens? Which two are commonly used for serology?

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1. O antigen (somatic antigen)
2. K antigen (capsular antigen)
3. H antigen (flagellar antigen)

O and H are used for serology.

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What larger structure is the O antigen a part of?

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O antigen is part of lipopolysaccharide (LPS) (endotoxin).

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What does the lack of H antigen signify?

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H antigen is part of the flagellae. Strains without it lack flagellae and are nonmotile.

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Why would E. coli with the K1 antigen be troubling to physicians?

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K1 strains cause neonatal meningitis, bacteremia, and urinary tract infection.

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What are five strains of virulent enteric E. coli?

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1. Enterotoxigenic E. coli (ETEC)
2. Enterohemorrhagic E. coli (EHEC)
3. Enteroinvasive E. coli (EIEC)
4. Enteropathogenic E. coli (EPEC)
5. Enteroaggregative E. coli (EAEC)

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What two toxins does ETEC traveler's diarrhea produce?

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1. Heat-labile toxin (LT)
2. Heat-stable toxin (ST)

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What is the mechanism of heat LT?

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Constitutively activates Gs via adenosine diphosphate (ADP) ribosylation leading to constant activation of adenylate cyclase and high levels of cyclic adenosine mono-phosphate (cAMP). This causes increased secretion of Cl- ions from intestinal cells into the gastrointestinal (GI) lumen. Negative Cl- ions cause positively charged Na+ ions to follow. Water follows Na+ into the lumen leading to diarrhea.

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What is the mechanism of action for ST?

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Constitutively activates guanylate cyclase leading to increased cyclic guanosine monophosphate (cGMP) and ultimately decreased water absorption from the GI lumen

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Which other bacterial toxin is similar to LT toxin?

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Cholera toxin

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What toxin mediates EHEC diarrhea? What is the mechanism of action?

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Shiga-like toxin (verocytotoxin) inhibits 28S component of the 60S ribosome subunit, inhibiting protein synthesis leading to cell necrosis of the intestinal epithelium and hemorrhagic colitis.

Mnemonic: Shiga-like it's the 1960s

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How do patients with EHEC present?

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Afebrile and bloody diarrhea without inflammatory white blood cells. EHEC strain O157:H7 is associated with hemolytic uremic syndrome (HUS)

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What is the mechanism that causes hemolytic uremic syndrome (HUS)? What are the features of HUS?

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HUS occurs when Shiga-like toxin (verocytotoxin) enters the blood stream and damages the vascular endothelium. Cardinal features include thrombocytopenia, anemia, and acute renal failure.

Mnemonic: You can get HUS from a RAT (Renal failure, Anemia, Thrombocytopenia)

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How are patients typically exposed to EHEC O157:H7?

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Undercooked hamburger meat and direct contact with animals (child presents following a petting zoo visit)

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How is EHEC treated?

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Fluids and supportive therapy. Antibiotics are not useful and may predispose to HUS.

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The main virulence factors of EIEC are encoded by a plasmid shared by what other diarrhea causing bacteria?

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Shigella

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How do these plasmid-encoded proteins act?

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These plasmid-encoded proteins allow for adherence and direct invasion of epithelial cells in the gut.

Note that this is not toxin-mediated like ETEC and EHEC.

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How do patients with EIEC present?

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Fever and bloody diarrhea with inflammatory white blood cells (compare to EHEC)

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EPEC adheres to but does not invade intestinal cells and results in flattening of the intestinal villi. What is the consequence of this and how does it present?

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Flattening of the villi leads to malabsorp-tion. Patients present with fever and bloody diarrhea.

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Who does EPEC commonly affect?

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Children, associated with nursery breakouts

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Escherichia coli is the most common cause of UTIs, what is the key virulence factor?

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P-pili that mediate adhesion to urinary epithelium

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SALMONELLA AND SHIGELLA

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SALMONELLA AND SHIGELLA

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Salmonella and Shigella are the two important gram-negative bacteria that do not ferment lactose and cause enterocolitis. How are they differentiated?

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Salmonella produces gas from glucose fermentation, produces H2S, and is motile (can disseminate hematogenously)

Mnemonic: Salmon require energy (glucose) to swim (motile) and smell bad (H2S)

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Which is more virulent, Salmonella or Shigella?

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Shigella. Less than 10 organisms are required for Shigella to cause infection because it is very resistant to stomach acid. Salmonella is not as resistant and requires 106 to 109 organisms to cause disease.

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What other bacteria besides Shigella contain the Shiga toxin?

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The hemorrhagic and invasive strains of E. coli

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What are the mechanisms of the two subunits of Shiga toxin?

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Subunit A: Inhibits 60S ribosome, stopping protein synthesis, killing the intestinal cell

Subunit B: Helps subunit A enter cells by binding to the microvillus membrane in the large intestine

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What are the reservoirs for Shigella?

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Only humans, there are no animal carriers

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Why does Shigella only cause superficial ulcers and not invade blood vessels?

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Once Shigella enters M cells in the intestine, it uses actin tails to travel among cells without entering the extracellular matrix and remains contained only within the epithelial intestinal cells.

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Why is Shigella nonmotile?

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It lacks the H antigen that codes for motility.

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What symptoms are often seen with shigellosis?

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Dysentery, bloody diarrhea, fever, and lower abdominal cramps

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How is Shigella transmitted?

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Four Fs: fingers, food, flies, feces

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What populations are most often affected by Shigella?

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Nursing home residents and very young children (ages 2-4 years), especially those in developing countries

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What is the treatment of Shigella and what medications should be avoided?

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Treatment includes fluid/electrolyte replacement and antibiotics such as trimethoprim-sulfamethoxazole (TMP-SMX) and ciprofloxacin. Antidiarrhea medications such as loperamide can prolong illness or worsen the severity and should be avoided.

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Salmonella species are divided into typhoidal or nontyphoidal types?

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Typhoidal: Salmonella typhi and Salmonella paratyphi cause typhoid fever.

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Describe the diseases caused by each and the species included in each:

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Nontyphoidal: Salmonella enteritidis and Salmonella choleraesuis cause enterocolitis, osteomyelitis, and septicemia.

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How do typhoidal strains differ from nontyphoidal strains of Salmonella in terms of reservoirs?

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Salmonella typhi and S. paratyphi have only human reservoirs, while nontyphoidal strains have both human and animal reservoirs (chickens and turtles).

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What makes S. typhi resistant to macrophage killing?

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Inhibits phagolysosome fusion and defensins resist O2-dependent and independent killing.

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Where does infection with S. typhi begin and where does it spread to?

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Salmonella typhi begins in the ileocecal intestine and spreads hematogenously and through the lymphatic system to the liver, bone marrow, gallbladder, and spleen.

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What organ harbors S. typhi in a chronic carrier state?

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Gallbladder (remember Typhoid Mary)

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What cells in particular harbor S. typhi and facilitate its dissemination?

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Monocytes, those in Peyer patches in the ileocecal intestines are the initial target

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Typhoid fever is a protracted disease of about 3 weeks. Describe the pathogenesis and symptoms seen in each week:

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Week 1: Bacteremia with fever/chills

Week 2: Monocyte involvement with organ inflammation, abdominal pain, and rash

Week 3: Ulceration of Peyer patches, intestinal bleeding, and shock

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Describe the location and appearance of the rash seen in week 2:

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Rose spots, small, transient, pink rash located on the abdomen (seen in 30% of patients)

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What is the appropriate therapy for S. typhi infection?

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Ciprofloxacin, ceftriaxone, or azithromycin

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What disease is typhoid fever often mistaken for? Why?

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Appendicitis, patients present with right lower quadrant abdominal pain without rash.

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What are some sources of Salmonella?

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Undercooked poultry, meat, eggs, greens

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How does nontyphoidal Salmonella cause enterocolitis and describe the type of diarrhea?

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Salmonella directly invades epithelial cells of the small and large intestines. Presents with fever and bloody diarrhea with inflammatory white blood cells (similar to EIEC).

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How do you treat Salmonella enterocolitis?

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Fluid/electrolyte replacement as the disease resolves within a week

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What patients are at increased risk for Salmonella osteomyelitis and sepsis?

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Sickle cells disease patients due to functional asplenia

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VIBRIO

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VIBRIO

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Describe the characteristic appearance of Vibrio cholerae:

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Gram-negative rod with a single polar flagellum, giving it a comma shape

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What does V. cholerae require in order to cause the clinical disease cholera?

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Infection of V. cholerae with the CTX phage that encodes the cholera toxin

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What is the mechanism of action of cholera toxin?

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Constitutively activates Gs via ADP ribosylation leading to constant activation of adenylate cyclase and high levels of cAMP. This causes increased secretion of Cl~ ions from intestinal cells into the GI lumen followed by positively charged Na+ ions. Water follows Na+ into the lumen leading to watery diarrhea (recall ETEC LT).

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What are the physical findings in an individual infected with V. cholerae?

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Severe dehydration from continuous watery diarrhea with a rice water appearance. Look for sunken eyes, poor skin turgor (skin tenting), and diminished pulses.

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What is the relationship between cholera and stomach acid?

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Vibrio cholerae is acid-sensitive, therefore, individuals taking medications to reduce stomach acid (eg, proton pump inhibitors) may be at increased risk for cholera.

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How are V. cholerae infections treated?

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Rehydration with intravenous (IV) fluid and electrolytes. In milder cases, treat with oral rehydration with electrolyte and glucose solution (eg, WHO oral rehydration solution). Antibiotics such as doxycycline, tetracycline, and ciprofloxacin may shorten the duration of the illness.

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How is Vibrio parahaemolyticus transmitted and what are its symptoms?

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Vibrio parahaemolyticus is transmitted by ingestion of undercooked seafood (shrimp, sushi, and the like) and is a frequent cause of seafood-associated diarrhea.

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How is Vibrio vulnificus transmitted and what are its symptoms?

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Direct inoculation of contaminated brackish water causes necrotizing wound infections (hand injuries related to opening oysters). Ingestion of raw shellfish causes gastroenteritis and sepsis with necrotizing skin lesions.

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Which groups of patients are especially sensitive to V. vulnificus septicemia?

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Cirrhotic and immunocompromised patients are very susceptible (>40% mortality rate).

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CAMPYLOBACTER

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CAMPYLOBACTER

Front 64

Describe the morphology of Campylobacter?

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Corkscrew shaped with long bipolar flagellae. Similar to Helicobacter pylori, its specialized shape helps drill through mucous membranes.

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What is the clinical progression of disease in an individual infected with Campylobacter jejuni?

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After incubation of approximately 3 days, patients usually present with abdominal pain and diarrhea. However, approximately one-third of patients present with an influenza-like prodrome (ie, fever, malaise), followed a day later by severe loose, watery, or bloody stools.

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What are the common sources of C. jejuni and how is it transmitted?

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Poultry (infrequently red meats) and in many domestic animals. Commonly transmitted via cross-contamination (eg, unwashed cutting board)

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What is the most common cause of bloody diarrhea in the United States?

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Campylobacter

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What neurological disorder is associated with C. jejuni infection?

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Guillain-Barre syndrome, an autoimmune, demyelinating ascending motor paralysis

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HELICOBACTER PYLORI

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HELICOBACTER PYLORI

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What disorder does H. pylori most commonly cause?

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Duodenal ulcers. Ninety percent of duodenal ulcers are associated with H. pylori. (Chronic nonsteroidal anti-inflammatory drug [NSAID] use accounts for the other 10%.)

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How can H. pylori be biochemically characterized?

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Catalase positive, oxidase positive, and urease positive. Urease, an important pathogenic factor, produces ammonia and bicarbonate that neutralizes gastric acids.

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How is H. pylori diagnosed?

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Invasive (endoscopy with biopsy) or noninvasive (serology or urease breath test in which patients drink C14-labeled urea which is then hydrolyzed to ammonia and labeled CO2 that is detected in their breath)

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What are the long-term consequences of H. pylori infection?

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Chronic gastritis, gastric adenocarcinoma, and mucosa-associated lymphoid tumor (MALT) type B-cell lymphoma

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What is the combination of medications used to treat H. pylori infection?

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Triple therapy originally included bismuth salts, metronidazole, and either ampicillin or tetracycline. The current regimen of choice is a proton pump inhibitor, amoxicillin, and clarithromycin.

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BACTEROIDES

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BACTEROIDES

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Bacteroides fragilis is normal colonic flora, but under what conditions does it cause disease?

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Bacteroides fragilis has very low virulence; however, intestinal perforation may lead to secondary peritonitis and abscess formation. Bacteroides fragilis may also be pathogenic in situations of gyn pathology (pelvic inflammatory disease [PID], septic abortion).

Note that 1° peritonitis = spontaneous bacterial peritonitis, 2° = peritonitis due to perforation/necrosis

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What is given as antimicrobial prophylaxis prior to abdominal surgery to prevent pathologic infection with B. fragilis among other GI pathogens?

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Used to be anti-anaerobic cephalosporins or oral metronidazole, but these have largely been replaced by ertapenem

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CLINICAL VIGNETTES

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CLINICAL VIGNETTES

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A 10-year-old girl with sickle cell disease presents with left knee pain, leukocytosis, and an increased erythrocyte sedimentation rate (ESR). What is the most likely diagnosis and what pathogen is most likely responsible?

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Osteomyelitis caused by Salmonella

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A 30-year-old man presents with fever, abdominal cramps and watery diarrhea after consuming raw oysters on the prior day. On stool examination, there are RBCs and WBCs. What is the most likely diagnosis?

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Vibrio parahaemolyticus

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A 15-year-old girl presents with abdominal pain and diarrhea after eating a hamburger at a barbeque the day before. She is afebrile but on rectal examination there is gross blood. Stool analysis is positive for RBCs and negative for fecal leukocytes. What is the most likely diagnosis? How do you confirm the diagnosis? What is a possible sequela of this infection?

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Enterohemorrhagic E. coli O157:H7. Confirm with stool culture. May lead to hemolytic uremic syndrome (HUS)