Enteric+Bacteria[1]

8/8/2019 Enteric+Bacteria[1]

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Enteric Bacteria

General Info-any bacteria that inhabit the GI tract as commensal or pathogen-few found in stomach or small intestine (except ileum)

-larger intestine has >90% anaerobe , the remainder are facultative G- rods-1 st step to identify G- rod is the ability to ferment glucose and oxidase test

Enterobacteriaceae-facultative G- rods that ferment glucose, oxidase negative , and non-spore forming

-isolation on MacConkey agar selection agars contain lactose as sole sugar source-Salmonella, Shigella, and Yersinia do not ferment lactose

-identification of isolate based on biochemical tests (citrate and indole tests)-serotypes based on agglutination to three main surface Ag

-O somatic Ag is the terminal moiety of LPS heat stable-H Ag are flagellar heat labile-Capsular Ag are acid sugars may block agglutination with anti-O serum

-K Ag of E. coli, Vi Ag of S. typhi, and serotype Ag of K. pneumoniaeShigella-non motile, non-fermenter of lactose, H 2S negative

-not considered part of the normal flora close relative of E. coli-Group A (S. dysenteriae) produce severe disease produce Shiga toxin-Group B (S. flexneri) and Group D (S. sonnei) are common in the US-clinical manifestations range from asymptomatic to bacillary dysentary

-cramps, tenesmus, and fever with low volume, bloody, mucoid stool-high number of fecal leukocytes-HUS is major complication of shiga toxin-Reiters syndrome may develop post infection polyarthritis and uveitis

-infectious dose is very low due to acid resistant travel thru stomach-transient growth in small intestine and colonization of the colon-invades colonic epithelial cells thru M cells limited to mucosal surface

-bacteremia is not common-induces apoptotic death of macrophages in the lamina propria-acute inflammation and mucosal destruction create ulcers and abcesses-cell to cell spread via release from dead cells or direct passage via vacuole

-utilizes host cell actin as a means of motility actin tail formation-virulence factors are found on a large plasmid chromosomal genes are also needed

-coordinated regulation is temperature dependent invasive at 37 C-shiga toxin is both cytotoxic and enterotoxic may act as a neurotoxin as well

-RNA N-glycosidase that inactivates ribosomes by adenine removal-transmission is fecal/oral human specific and highly contagious (ID = 200)-children are at highest risk day care center, crowding, and poor sanitation

-stool cultures used in acute stage with MacConkey agar -TSI is alkaline over acid with no gas

-usually self-limiting disease fluid replacement, do not impair GI motility-TMP/SMX used in severely ill no effective vaccine-hand washing is best method for prevention


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Salmonella-identical to Shigella except they are motile and do produce H 2S-classified based on O, H, and K Ag-typhoidal salmonella primarily infects humans -- transmission is fecal (human)/oral-non typhoidal salmonellae infects many animals transmission is fecal (animal)/oral

-salmonella cause three main types of diseases-enterocolitis diarrhea from S. enteritidis or S. typhimurium-high incident in US disease of the industrial world no vaccine-nausea, vomiting, cramps, and diarrhea (may be bloody with few leukocytes)-stomach acid kills many Salmonella colonization of small intestine-production of enterotoxin and invasion of mucosa in ileum and colon

-large virulence plasmid is present-treatment is fluid replacement no antibiotics are usually given

-enteric fever typhoid fever from S. typhi and S. paratyphi A,B-major cause of morbidity and mortality in developing countries (esp. kids)-10 to 14 day incubation followed by constitutional symptoms

-early constipation followed by bloody diarrhea abdominal rose spots-diagnosis by stool culture 80% positive 1 st week, variable beyond 1 st week -adhere to and kill M cells penetrate lymph follicles

-invade macrophages and disseminate in blood-spread to many organs especially liver and spleen

-complications include toxemia ( myocarditis ), GI lesions, and carrier state-virulence of S. typhi based on Vi capsule Ag inhibits complement killing

-lacks virulence plasmid of entercolitis causing Salmonella-Ab against Vi are protective possible vaccine

-chloramphenicol or ampicillin are used also TMP/SMX-sustained bacteremia caused by S. typhimurium and S. cholorae-suis

-often 2

infection in debilitated patients (cancer, etc...)-may lead to focal lesions in lung, bones, and meninges-increased susceptibility to endocarditis and osteomyelitis-chronic infections occur in patients with Schistosoma mansoni-chloramphenical or ampicillin are used also TMP/SMX

-humans are the sole reservoir for S. typhi asymptomatic food handlers are problematic-may persist in the gall bladder-non typhoidal salmonella exists in almost all animal species-prevention thru hand washing and improving sanitation


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Yersinia-non lactose fermenters with optimal growth at 22-25 C not motile at 37 C-Y. pestis is the causitive agent in the Plague-Y. enterolitica and Y. psuedotuberculosis are 1 animal pathogens

-fecal/oral route of transmission

-enterocolitis presents with fever, diarrhea, cramps, bloody stool with leukocytes-Reiters syndrome is possible septicemia is rare-mesenteric lymphadenitis mimics appendicitis

-similar to S. typhimurium replicate within macrophages produce heat stable toxin-Y. pseudotuberculosis may penetrate ileal mucosa to enter lymph nodes

-virulence factors include chromosomal and plamid genes-invasins are on chromosome , and outer membrane proteins are on plasmid-Y. enterocolitica also produces the heat stable toxin

-dramatic increase in incidence over last 10 years-serotypes O3, O8, and O9 of Y. entercolitica and O1 of Y. pseudotuberculosis

-O3 and O9 in Europe, O3 in Canada, and O8 in the US

-no treatment necessary unless septicemia develops aminoglycosides or tetracycline-hand washing and sanitation for prevention no vaccineEscherichia coli

-lactose fermenter that is both a normal commensal and frank pathogen may cause bacteremia-intestinal diseases caused by diarrheagenic E. coli

-evolved from commensals thru acquisition of virulence factors-each class is associated with an O:H serotype not related to virulence

Enterotoxigenic E. coli (ETEC)-causes acute secretory diarrhea watery w/o blood or leukocytes

-classic travelers diarrhea-adhere to small bowel with specific colonization fimbriae (plasmid encoded)

-produce heat labile ( LT ) or heat stable ( ST ) toxin ( plasmid encoded )-LT is similar to cholera A/B type toxin -- intracellular cAMP-ADP ribosylates GS protien of cyclase complex

-ST increases intracellular cGMP via guanylate cyclase-no bacterial invasion occurs

-children in endemic areas are at high risk (developing countries)-650 million cases of pediatric diarrhea per year

-prevention by improved sanitation no vaccine available-Ig against CF may be a means of passive protection

Enteroinvasive E. coli (EIEC) often confused with Shigella-bacillary dysentary identical to shigellosis low volume with blood and neutrophils

-carry same invasion plasmid of Shigella-human specific disease spread is from infected person-does not ferment lactose all other E. coli do ferment lactose


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Enteropathogenic E. coli (EPEC)-acute and chronic diarrhea in infants watery w/o blood, may have leukocytes-produce attaching and effacing (A/E) lesions effacement of brush border -virulence factors include:

-bundle forming pilus (BFP) plasmid encoded mediator of adherence

-not required for A/E lesions-intimin (required for A/E lesions) and other secreted proteins-encoded on chromosome pathogenicity island

-highest incident in children < 2 years old rarely found in adults-breast feeding is protective no vaccine available

Enterohemorrhagic E. coli (EHEC) and Shiga toxin-producing E. coli (STEC)-cause a spectrum of disease mild diarrhea, hemorrhagic colitis (HC), and HUS

-copious bloody diarrhea with cramps in HC no fever and non-invasive-O157:H7 is major EHEC serotype in US low infectious dose

-produces A/E lesions identical to EPEC-carry chromosomal pathogenicity island coding intimin

-produce bacteriophage-encoded Shiga toxin associated with HUS-STEC also produces the bacteriophage-encoded Shiga toxin-lacks the pathogenicity island no A/E lesions

-both reside as commensal in cows contaminate food/water or undercooked meat-no vaccine , but Ab against Shiga toxin may provide passive protection for HUS-screen for O157:H7 on SMAC agar does not ferment sorbitol-DNA probes and serotyping are necessary to identify various diarrheagenic E. coli

Vibrionaceae-comma shaped G- rods, glucose fermenters, oxidase positive with polar flagella

-abundant in marine and surface watersVibrio cholerae humans are only known host

-grows well at 37C with hi salt concentration and hi pH-classified on the basis of the O Ag

-O1 consists of Classical and El Tor-O139 genetically resembles El Tor caused epidemics in India

-codes for an additional polysaccharide capsule-acute diarrhea caused by enterotoxin-incubation period (1-4 days) followed by sudden onset of watery diarrhea no fever

-rice water stools (mucus, cells, and vibrios) with rapid fluid loss-cholera gravis may reach 1 L per hour of fluid loss

-survive acid in stomach and attach to brush border to multiply-Tcp pili required for colonization no invasion of epithelial cells occurs

-cholera toxin encoded on bacteriophage that uses Tcp pili as a receptor-heat labile toxin with similar action to E. coli LT-B subunit binds GM 1 ganglioside on epithelial cells-A subunit activates adenylate cyclase via ADP-ribosylation

-increased secretion of Cl - from crypt cells-decreased NaCl absorption from villus cells

-transmission thru contaminated water or undercooked seafood-bicarb buffer or fish and rice meals lowers ID50


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Vibrio parahemolyticus-causes acute, watery diarrhea after short incubation period (hours)

-most virulent strains produce Kanagawa toxin hemolysin-cytotoxic and cardiotoxic activities

-associated with eating undercooked seafood common in Japan and gulf states

Vibrio vulnificus-causes wound infections and gastroenteritis leading to fatal septicemia-transmission thru sea water contact (wounds) or eating raw oysters (septicemia)-liver disease and hemochromatosis are risk factors

Campylobacter jejuni-comma shaped, G- rod, oxidase positive and microaerophilic

-found in normal flora of many animals-causes enteritis with fever, cramps, and diarrhea watery or bloody with neutrophils

-acute colitis and bacteremia may also occur -Reiters syndrome is possible following infection-40% of Guillain Barre patients had Campylobacter infection prior to symptoms

-adhere to small intestine with invasion of tissue and inflammation colon may be a target-transmission by contaminated food/water or contact with infected animals (dogs)-may be more frequent than Salmonella or Shigells

-isolation from blood or stool on selective media containing antibiotics-grown at 42C in reduced O2 (5%)

-treat with fluid replacement and erythromycinHelicobacter pylori

-motile, spiral shaped microaerophilic and urease positive-cause of chronic gastritis and peptic ulcers

-implied risk for gastric carcinoma and marginal zone lymphoma-transmission is by oral ingestion found in feces, dental plaques, and gastric contents

-penetrates gastric mucus and colonizes epithelium-toxins and urease damage gastric epithelium causing an inflammatory response-vacuolation of epithelium leads to ulceration

-virulence factors include:-urease which converts urea to ammonia and CO2 helps survival in low pH-flagella may allow penetration of gastric mucus-VacA cytotoxin may damage cells-CagA protein is located within a pathogenicity island more likely to produce ulcers

-present in vast majority of people worldwide-mixed infections are uncommon within same host-husbands and wives rarely exchange strains children will have one or the other

-diagnosis by gastric biopsy and culture similar to C. jejuni except temp. at 37

C-may detect urease in biopsy or breath test to detect radiolabeled CO 2-serologic tests of plasma and salivary IgG or IgA cannot tell if infection is active

-treatment with bismuth subsalicylate and amoxicillin (tetracycline) and metronidazole-two week course vaccines are in developement


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Pseudomonadaceae-aerobic G- rods that oxidize but dont ferment glucose, oxidase postive with polar flagella

-ubiquitous in soil, water, plants, and animalsPseudomonas aeruginosa

-produce grape-like odor and may be flourescent green (pyoverdin)

-grows between 37 and 42 C-present in moist environments and can form biofilms-resistant to disinfectants and preservatives

-opportunistic pathogen causing nosocomial infections-impaired immune system or previous injury increase risk -may cause UTI, bacteremia, necrotizing pneumonia, endocarditis, and meningitis

-ear and lung infections with sepsis in compromised patients-also causes swimmers ear

-cystic fibrosis patients may develop chronic infections-produce a mucoid strain with an alginate capsule-often co-infected with Staph. Aureus

-virulence factors include:-pili that mediate adherence to host cells-exotoxin A identical to ADP-ribosylation of EF-2 by diptheria toxin

-prevents protein chain elongation-exotoxin S also ADP-ribosylates proteins unknown target site-proteases cause tissue destruction and allow access to deep within tissues

-elastase, collagenase, lecithinase, and alkaline protease-hemolysin (phospholipase C)

-drug resistance is a problem evolves resistance rapidly-use penicillin and aminoglycoside or ceftazidime

Extraintestinal Enteric Bacterial Infections

-ascending UTI (most common route) may result in cystitis or pyelonephritis-hematogenous UTI infection via bloodstream-Salmonella, Staph. Aureus, and Candida

-uncomplicated UTI caused mostly by E. coli-most common in females (during first year, then during sexual activity)-diagnosed with clean catch of midstream urine mixed species = contamination-positive with 10 5 bacteria per mL treat with TMP/SMX

-complicated UTI occur in catheterized or immunosuppressed patients-Proteus mirabilis is most common infectious agent wider spectrum of causative agents

-swarming motility on agar with predilection for upper urinary tract-associated with kidney stone formation via urease action increasing urine pH

-more common among older men prostrate hypertrophy-mixed species common in urine sample positive at 10 2 to 10 4 bacteria per mL-Uropathogenic E. coli (UPEC) carry pathogenicity island encoding P fimbriae and hemolysin-neonatal meningitis from E. coli expressing K1 antigen greatest risk within 4 weeks of life-1 lobar pneumonia caused by Klebsiella pneumonia greater risk with alcoholism

-urease positive lactose fermenter, non-motile with capsule (anti-phagocytic)-Septicemia and endocarditis from Enterobacter (encapsulated ) and Serratia marcescens

-both contaminate parenteral fluids Serratia produces a red pigment

Enteric+Bacteria[1]

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