enteric bacteria Flashcards
list the enteric bacteria
Vibrionaceae: vibrio cholerae, vibrio parahemolyticus. Enterobacteriaceae: e coli, shigella, salmonella, yersinia. Campylobacter. Helicobacter pylori.
Which enteric bacteria are spread by environment
nontyphoidal salmonella, enterohemorrhagic e coli and vibrio cholera.
Which enteric bacteria are spread human to human
typhoidal salmonella, enterotoxigenic e coli, vibrio cholerae and shigella
sources of enteric pathogens
poultry, egg, milk, beef, vegetables
enteric bacteria gram staining
all are gram negative bacilli
Gram negative bacteria structure
Outer membrane contains lipopolysaccharide. LPS contains: lipid A (endotoxin), core polysaccharides (differs btw genera), O antigens (repeating oligosaccharides). They also contain H antigens (flagellar proteins in motile organisms) and K antigens ( capsular polysaccharide not found in all strains)
how do you detect fecal leukocytes
methylene blue stain
Which enteric bacteria are oxidase positive vs negative?
All enterobacteriacaea are oxidase negative, and ferment glucose. Vibrios are oxidase positive
importance of plasmids in enterics
can confer antibiotic resistance, produce enterotoxins, and confer adherence/ invasive factors
How do bacteriophage affect enteric bacteria
bacteriophage can change the phenotype of a bacterium it lysogenizes (ex. V. cholerae toxin)
define pathogenicity islands
regions of DNA found in chromosomes of pathogenic strains only which encode virulence factors such as toxins, invasion genes, etc.
What are type III secretion systems
method used by gram negative bacteria which play a role in invasion, intracellular survival and attachment
Describe watery diarrhea and the likely bacterial causes
copious, watery, no blood or pus. No tissue invasion. Small intestine. Causes: ETEC, EPEC, , cholera
Describe dysentery and likely causes
scant volume, blood pus or mucus. Tissue invasion. Large intestine. Causes: shigella, EIEC, campylobacter
Describe protracted diarrhea and likely causes
Lasts more than 14 days. Causes: EPEC
Describe bloody, watery diarrhea and likely causes
copious, some blood, pus, invasion. Ileum and colon. Causes: salmonella, campylobacter, yersiniae
describe hemorrhagic colitis and likely causes
copious, like liquid blood, no leukocytes or invasion. Large intestine. Causes: EHEC
What are the main mechanisms used by enteric bacteria
Toxigenic (vibrio cholerae, ETEC, EHEC), invasive (salmonella) or both (shigella)
define exotoxin, enterotoxin and endotoxin
Exotoxin: secreted out of cell by organism. Enterotoxin: exotoxin with specific effects on intestine. Endotoxin: LPS (lipid A + O antigen)
For each of the following, list the type of diarrhea produced upon infection and common organisms: small intestine, large intestine
small intestine: secretory diarrhea. V. cholera, ETEC, salmonella, Yersinia, campylobacter. Large intestine: inflammatory diarrhea. Shigella, EHEC
What determines relative infectivity
Organisms that are more sensitive to acid (such as vibrios) have higher infective doses and are more likely to be transmitted by food or water. Those with lower infective doses are more likely to be transmitted from person to person (such as shigella)
Describe cholera
Profuse watery diarrhea caused by an enterotoxin. Prototype for toxigenic diarrheas. No tissue invasion present - affects the small intestine
pathogenesis of cholera
Colonization of small bowel and toxin production. Bacteriophage conversion is important
Cholera colonization
Requires surface expressed adherence factor TCP pilus
Cholera toxin production
Encoded as part of a phage cholera toxin gene. This phage uses the TCP pilus as its receptor
Cholera toxin structure/function
A and B toxins- B subunit binds ganglioside GM1 of enterocytes and allows the A subunit to enter cytoplasm and constitutively activate adenylate cyclase, leading to increased cAMP then increased Cl secretion, decreased Na absorption and net secretion of fluid into gut lumen. The cholera toxin is cytotonic (does not kill the cell)
Cholera mode of transmission
fecal/oral- contaminated water> foods. Aquatic environments (shellfish). Also person to person
Cholera treatment
Restore fluid and electrolyte loss. Oral rehydrate solution (salt/sugar soln) or IV ringers lactate + KCl. Antibiotics shorten course (tetracyclines)
Vibrio parahemolyticus- mode of transmission, diseases it causes
Comes from raw or undercooke shellfish (it is a halophilic organism found in marine environments). Causes gastroenteritis, wound infections and septicemia.
Vibrio vulnificus- mode of transmission and Sx
Ingestino of contaminated seafood (oysters). Causes gastroenteritis and can proceed to extraintestinal infections in immunocompromised
Compare ETEC, EPEC and EHEC: type of diarrhea, and virulence factors
Enterotoxigenic: travelers diarrhea,heat labile and heat stable toxins. Enteropathogenic: watery persistent diarrhea, Attaches and effaces. Enterohemorrhagic: bloody dysentery, attaches and effaces and produces shiga like cytotoxin
For ETEC: Sx, treatment
Watery diarrhea, no blood or pus. Rare low grade fever. Abd cramps, vomiting. Treatment: supportive (fluids, salt), Abx not recommended, but if necessary fluoroquinolones. Pepto relieves Sx.
ETEC pathogenesis
NO tissue invasion. Heat labile enterotoxin (same mechanism as cholera) and heat stable enterotoxin (activates guanylate cyclase raising cGMP and increasing fluid secretion). Colonizes small intestine by fimbrial adhesions to overcome peristalsis
EPEC - population, Sx, treatment
infants (daycare centers). Sx: watery stools, no blood or mucus. Vomiting, low grade fever. Treatment: hydration, antibiotics.
EPEC pathogenesis
NO tissue invasion. Adhere to enterocyte surface. Type III secretion of translocated-intimin receptor initiates attaching and effacing lesion (microvilli destruction, pedestal formation). This interferes with absorption leading to diarrhea
EHEC - source,serotype, Sx
Food/water outbreaks. O157:H7 is major serotype. Sx: initially watery then bloody diarrhea and hemorrhagic colitis leading to hemolytic uremic syndrome. Fecal leukocytes uncommon (diagnostic feature)
EHEC - treatment and pathogenesis
Treatment: supportive. Abx have no benefit. Pathogenesis: Form attaching-effacing lesions, also produce shiga-like cytotoxins which bind to Gb3 sphingolipids of enteroctes and renal endothelial cells then inhibit protein synthesis and cause tissue damage
what are M cells
antigen sampling cells that overly the lymphoid follicles of the gut
Invasive pathogens Sx and pathogenesis
Bacteria invade the intestine via M cells and cause structural damage to the intestine. This produces an inflammatory diarrhea- frequent low volume mucoid and/or bloody stools with tenesmus, fever or abd pain. Stools have many leukocytes
List the invasive enteric bacteria
Shigella, salmonella and S. Typhi, EIEC, yersinia, campylobacter
List the noninvasive enteric bacteria
virbrio cholera, ETEC, EPEC, EHEC
Shigella classifications
group A: S. dysenteriae. Group B: S. flexneri. Seen primarily in male homosexuals. Group C: S. boydii primarily in India. Group D: S. Sonnei, mildest disease, most common in US
Shigella pathogenesis
Enterotoxins cause watery diarrhea. Type III secretion of effector proteins. Entry via M cells, uptake by macrophages. Induces apoptosis and released bacteria invade basal side of epithelial cells. Shigella lyse the vacuole, grow in the cytoplasm and spread to neighbors. Inflammatory response increases spread but enables clearance of infection.
Which shigella produce shiga toxin
Only S. dysenteriae type 1
Shigella Sx
Incubation period of 1-4 days. Fever, malaise, vomiting, watery diarrhea, frank dysentery, blood and mucus, cramps and tenesmus. Hemolytic uremic syndrome
Shigella infectivity
Very acid resistant so low infectious dose (10-100)
Shigella transmission
Four F’s: food, fingers, feces, flies
Shigella treatment
supportive, fluid balance. Antibiotics shorten duration of sx and shedding of bacteria- ciprofloxacin
Salmonella transmission
Fecal oral route. Typhoid: only transmitted by humans. Non-typhoid: poultry, eggs, contaminated produce
salmonella virulence factors
attachment, invasion (pathogenicity island 1) and survival inmacrophages (pathogenicity island 2)
Salmonella pathogenesis
Invasion of M cells, transient bacteremia. Uptake by mononuclear phagocytes where salmonella multiply.
Salmonella Sx
Gastroenteritis: 24-48 hrs after ingestion nausea, vomiting, headache, fever, cramps and watery diarrhea. Septicemia: prolonged fever. Typhoid fever: incubation of few days to few weeks. Constipation or inflammatory diarrhea followed by fever. Continues for 6-8 weeks untreated
Salmonella treatment
Gastroenteritis is self limiting. Typhoid requires antibiotics- ciprofloxacin and ceftriaxone.
Salmonella immunity
There are so many diff serovars that there is not good immunity. Typhoid vaccine effective in children > 2yrs
List the Yersinia species and which are enteric pathogens.
Pestis, enterocolitica and pseudotuberculosis. The last two are enteric
Yersinia transmission
domestic animals and sometimes blood transfusions (grow at low temps). Often associated with undercooked pork and dairy
Yersinia pathogenesis and Sx
Infects terminal ileum producing RLQ pain. Low grade fever, watery diarrhea, some blood, fecal leukocytes. Complications include reactive arthritis (Reiters syndrome) in HLA-B27 positive pts.
Yersinia treatment
Antibiotics - do not show major impact on outcome but still used
What is the most common cause of gastroenteritis in Western worls
campylobacter- food borne
List the campylobacters
c. jejuni and c. Coli
Campylobacter structure and growth
small curved gram negative rods. Catalase and oxidase positive. Prefer microaerophilic and increased temperature for culture. Grows best on enriched media with antimicrobials that inhibit other intestinal bacteria
Campylobacter Sx
diarrhea, fever, abd cramping, bloody stools, vomiting. Fecal leukocytes may be present. Complication- Guillain Barre (demyelinating dz) and Reiters syndrome (autoimmune reactive arthropathy)
Campylobacter pathogenesis
Invasive, enterotoxin production and cytotoxin production. Invasion of terminal ileum and proximal colon. Motility and chemotaxis are important in colonization of gut.
Campylobacter transmission
contaminated milk or water. Young pets with diarrhea, raw poulty. Highest in infants then young adult males.
Campylobacter treatment
supportive fluid replacement. Antibiotics in severe cases (erythromycin or quinolones but fluoroquinolone resistance is emerging due to antibiotic usage in poultry)
H pylori pathogenesis
colonizes mucus layer of stomach, does NOT invade epithelium. Causes inflammation, epithelial cell damage and neutrophil infiltration. Reduction in acid secretion leads to gastric atrophy which can progess to gastric carcinoma
H pylori structure and culture/isolation
curved, motile, microaerophilic gram negative rods. Strong urease activity. Isolated on campy agar wihtout antibiotics
H pylori Sx
Casues nearly all duodenal ulcers and 70% of gastric ulcers
H pylori virulence factors
High motility- rapid penetration of mucus to reach less acidic epithelium. Urease- produces ammonia to raise pH. Pathogenicity islands- encode virulence genes. Toxins- vacuolating cytotoxin causes epithelial damage
H pylori transmission
acquired in childhood. Life long without treatment. Fecal-oral transmission, with oral-oral and gastric-oral routes possible. Prevalence increases with overcrowding and lower socioeconomic status
H pylori diagnosis
Histology of biopsy is gold standard. Rapid urease test on biopsy. Urea breath tests. ELISA for IgG
H pylori treatment
Only treat those with peptic ulcers to prevent antibiotic resistance. Treatment: PPI + bismuth + tetracycline for 14 days (amoxicillin, metronidazole, clarithromycin)
