Bacterial Causes of Diarrhea – Flashcards

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Invasion
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- may not have any diarrhea or vomiting

- dysentary may be present

- fecal leukocytes present

- blood in stool

- fever

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Inflammatory gastroenteritis pathogens
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  1. Salmonella sp.
  2. Shigella sp.
  3. Campylobacter sp.
  4. Yersinia enterocolitica
  5. Vibrio parahaemolyticus
  6. Francisella tularensis
  7. EIEC
  8. EHEC
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Salmonella sp. (general, habitat)
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Gram -, rods, motile, facultative anaerobes, non-lactose fermenting

 

Habitat:

- typhi = human

- enteritidis and choleraesuis = intestines of animals

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Salmonella sp.: transmission
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Fecal-oral route

animals to humans (Turtles)

animal food products to humans

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Salmonella sp: O Ag
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somatic
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Salmonella sp: H Ag
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Flagellar Protein
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Salmonella sp: Vi Ag
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Capsular Polysaccharide
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Salmonella Pathogenesis
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-sensitive to killing by gastric acid

-attach to gastric epithelial cells in sm. intestine and colon -> bacterial type III secretory system injects bacterial proteins into host cells -> internalization -> replication in vacuoles -> cell lysis -> enter mesenteric lymph nodes and blood stream -> fever, ab pain, diarrhea

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Type III Secretion
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used by Salmonella sp.

-bacterial needle that injects effector proteins into host cell

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Salmonella enteritidis: Virulence
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-inflammatory diarrhea due to invasion of intestinal epithelial cells

-controlled by vagocytic defenses

-risk in immunocompromised for disseminated disease

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Salmonella typhi: pathogenesis
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-cause enteric fever (typhoid fever)

-fever, nonproductive cough, bloody diarrhea, ab pain, rose spots on skin

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Salmonella typhi: Virulence
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-invasive intracellular pathogen

-reaches blood stream (better than other Salmonella sp.)

-little diarrhea

-enteric fever

-involvement of other organs

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Salmonella: Clinical manifestations - Enteritis
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- most common form of salmonellosis

- symptoms occur 6 - 48 hrs after injestions

  • nausea, ab cramps, vomiting, nonbloody diarrhea
  • fever, headache, myalgias

Symptoms last 2 days - 1 wk

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Salmonella: Clinical manifestations - septicemia
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- higher risk in pediatric, geriatric and immunocompromised

- clinical presentation like all Gram (-) sepsis

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Salmonella: clinical manifestations - Enteric fever
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S. typhi = typhoid fever

others = paratyphoid fever

-bacteria pass through the gastric epithelial cells and are engulfed by macrophages

 

-Symptoms:

  • 10 - 14 days after ingestions
  • fever, headache, myalgias, malaise, anorexia for 1 wk followed by diarrhea
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Salmonella: detection
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Non-lactose fermenter = colorless on MacConkey agar

 

motile

H2S+

 

enteritidis - isolated from stool

typhi - isolated from stool OR blood

 

fewer rectal leukocytes than shigellosis

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Shigella Sp.: general, habitat, transmission
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General:

Gram -, bacilli, non-motile, non-lactose fermenter

resistant to stomach acids = only 10 - 20 bacilli needed to cause disease

 

Habitat:

human and primate intestines

invades and survives in cytoplasm

 

Transmission:

fecal-oral, P2P

 

 

 

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Shigella sp: virulence
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-produces shiga toxin (exotoxin, cytotoxic to epithelial cell)

-attach and penetrate GI epithelial cells and M cells (use Type III)

-multiply intracellularly, spread to contiguous cells (use hemolysin to escape cell)

-use host cell actin for transport

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Shigella sp: detection
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-isolation from stool

-nonlactose fementer

Distinctive features from Salmonella:

-non-motile

-H2S negative

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Shigellosis: clinical manifestations
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-incubation period 36 - 72 hrs

-fever, cramping ab pain (both non specific)

-dysentary 2 days later

-watery diarrhea

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Shigellosis: treatment
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-usually self limited

-prevent P2P spread

-fluid and electrolyte replacement for severe cases

-antidiarrheal compunds contraindicated (b/c they inhibit peristalsis = can't get rid of toxin)

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Campylobacter sp: general
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General:

gram -, curved or comma shaped, microaerophilic, motile rods

can suvive intracellularly in monocytes and intestinal epithelial cells -; tissue necrosis and cell death

can travel to blood stream

;

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Campylobacter sp: habitat and transmission
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habitat: intestinal tract of animals

;

transmission:

-fecal-oral route

-transmitted ny contraminated food; more common in summer

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Campylobacter sp: incidence
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leading cause of bacterial diarrheal illness in US

;

most common cause in udnerdeveloped countries

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3-5 days after ingestion; diseasse only if penetrates the mucouse layer and invades GI epithelial cells

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Campylobacter sp: virulence
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-flagella

-adherence factors

-heat labile toxin = watery diarrhea

-ingestion by host cells = inflammatory colitis

-can also produce shiga toxin

-inflammatory and bloody diarrhea

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Campylobacter sp: clinical manifestations
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anywhere from 7 days to chronic infection

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periumbilical cramping, intense abdominal pain that mimics appendicitis, malaise, myalgias, headache, vomiting

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watery diarrhea = most common

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inflammatory bowel disease

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Campylobacter sp: detection
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Detection:

-WBC in feces

-isolation in stool: requires growth on Campy or Skirrow media

;

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Yersinia enterocolitica: general, habitat, transmission
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general:

aerobic, gram (-), bacilli

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habitat: domestic and farm animals

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transmission: fecal-oral route

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Yersinia enterocolitica: pathogenesis
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invades mucosa of terminal ileum -; painful enlargement of mesenteric lymp nodes

- mistaken for appendicitis

- causes inflammatory and bloody diarrhea

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transmitted by contaminated meat products, mostly during winter (can grow at 4 degrees C)

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Yersinia enterocolitica: virulence and clinical manifestations
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virulence:

-heat stable enterotoxin -; inflammatory and bloody diarrhea

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clinical:

-febrile illness with abdominal pain

-can mimic appendicitis

-lasts 2 - 3 weeks

-common in infants, occasional septicemia

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Yersinia enterocolitica: detection
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isolation from stool and blood
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Aeromonas sp.
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gram (-), motile, bacilli

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found in fresh, salt and chlorinated water habitats

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very resistant to temperatures and chemicals

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Aerolysin cytotoxic toxin (ACT)

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opportunistic pathogen in immune compromised

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Vibro sp: general
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small, curved, gram (-), bacilli, single flagellum
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V. cholerae: virulence, transmission
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virulence:

-produces cholera toxin - activates adenylate cyclase to increase cAMP -; voluminous, watery diarrhea

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transmission:

-contaminated water or food (shellfish or crabs)

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Vibro cholerae: pathogenesis
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-colonizes small bowel

-acute illness due to enterotoxin production

;;; -severe form: rapid loss of liquid and electrolytes; hypovolemic shock, metabolic acidosis and death

-acid sensitive = requires a lot to cause disease

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Cholera toxin (enterotoxin)
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- A-B type toxin

- A increases adenylate cyclase activity -; increase in cAMP

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Vibro cholera: clinical manifestations
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-abrupt, watery diarrhea (rice water)

-vomiting following diarrhea

-cyanotic, sunken eyes, high voice, unobtainable BP, etc. all because of severe dehydration

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Vibrio cholera: diagnosis
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-rice water stools

-stool culture on thiosulfate-citrate-bile salt-sucrose agar (TCBS); colonies are yellow, other Vibrio are green

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Vibrio parahaemolyticus:
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-hemolytic strains are most virulent

-enterotoxin production -; moderate bowel inflammation; mild to moderately severe diarrhea

-halophilic (salt-loving); grows in marine environments

-found in raw or undercooked shellfish

-colonizes small intestine

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Vibrio parahaemolyticus: Transmission, clinical manifestions, diagnosis
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Transmission:

-ingestion of inadequately cooked seafood or sushi

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clinical: watery diarrhea, ab cramps, nausea, vomiting, bloody diarrhea (sometimes)

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diagnosis: green on TCBS agar

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Enterotoxigenic E. Coli (ETEC)
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-Non-invasive = do not see fecal WBC's

-colonize sm. intestine

-common cause of traveler's diarrhea

-produce cholera-like (heat-labile) toxin and a heat-stable toxin -; both lead to watery diarrhea (secretion of Cl- -; osmotic diarrhea)

-abrupt onset watery diarrhea, lasts less than 24 hrs after initiation of fluid replacement

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Enteropathogenic E. Coli (EPEC)
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-non-invasive = do not see WBC in stool

-no known toxin

-adheres to epithelial cells in Sm. intestine and disrupts microvilli (effacement)

-type III secretory system

;; -makes its own receptor

;;;;;;; - when it binds to cell it forms pedestals

-watery diarrhea with mild inflammation, infants ;6 m.o.

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Enteroaggregative E. Coli (EAggEC)
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-non-invasive = do not see WBC in stool

3 stages:

  1. adhere to mucosa
  2. enhanced mucus production encases bacteria enabling biofilm formation
  3. elaboration of cytotoxin, damages intestinal cells

-may colonize sm. and lg. intestine

-cause of a more persistent diarrhea

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Diagnosis and treatment of inflammatory E. coli infections
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Diagnosis:

-isolation on MacConkey's Agar (like Vibro)(lactose fementer)

Tx: fluid and electrolytes, antibiotics

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Enteroinvasive E. coli (EIEC)
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-similar pathogenesis as for Shigella infections

-results in watery diarrhea and dysentery

-sporadic outbreaks in infants and children

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Enterohemorrhagic E. coli (EHEC)
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-mostly infects lg. bowel

-kidney damage due to Shiga toxin

 

Clinical manifestations:

-Hemolytic colitis: severe crampy ab pain, watery diarrhea followed by bloody diarrhea, no fever

-Hemolytic Uremic Syndrome: triad of acute renal failure, thrombocytopenia and microangiopathic hemolytic anemia

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Diagnosis and Treament of Invasive E. coli infections: EHEC
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Dx:

-carbohydrate sorbitol must be included in the medium

-inability to ferment sucrose

-ELISA detection of Shiga Toxins 1 and 2 in stool

 

Tx: Avoid antibiotics

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Listeria monocytogenes: Listeriosis
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-usually mild diarrhea but systemic symptoms are prominent

-pathogen can break into cytoplasm and divide

-major risk is maternal infection during pregnancy

-serious in immunocompromised

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Three most common causes of acute infectious diarrhea
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Salmonella, Shigella, Campylobacter
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E. coli: general
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  • MOST common in uncomplicated outpatient UTI's
  • Gram (-), motile, bile tolerant, lactose fermenting
  • Lab ID: pink on MacConkey Agar
  • transmission: part of normal flora
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E. coli: Virulence Factors
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  • adherence to urethroepithelial cells via fimbriae (pyelonephritis strains are the most adherent)
  • endotoxin
  • some strains have capsule adhesion
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E. coli: UTI strains
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UPEC

  • adhere to urethroepithelial cells
  • increased serum resistance
  • increased hemolysin production
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Staphylococcus saprophyticus
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  • 5-15% of cystitis cases in young, sexually active women
  • gram (+), cocci in clusters
  • transmission: normal flora of skin and GU mucosa
  • prevention: urination after intercourse
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Staphylococcus saprophyticus: Lab ID
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  • white colonies on blood agar
  • catalase (+)
  • coagulase (-)
  • mannitol non-fermenter
  • Novobiacin resistant (distinguishes from other coagulase (-) staph)
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Staphylococcus epidermidis
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  • nosocomial UTI pathogen
  • white colonies on blood agar
  • Catalase (+)
  • Coagulase (-)
  • mannitol non-fermenter
  • novobiacin sensitive
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Staphylococcus epidermidis: pathogenesis and tx/px
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  • Pathogenesis: slime production and biofilm formation; colonizes catheters and prostheses
  • Tx/Px: MDR strains exist so use catheter care
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Enterococci
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  • common in pts with recurrent infections, instrumented or have anatomic defects
  • normal flora of UG tract
  • MDR (vanco)
  • fomerly classified in Streptococcus
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Proteus mirabilis
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  • produces ureases which cause pyelonephritis
  • Highly motile (swarmer) - able to ascend the ureter against the flow of urin
  • Gram (-), rod
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Proteus mirabilis: virulence and lab ID
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Virulence Factors:

  • urease
  • endotoxin

Lab ID:

  • non-lactose fermenting
  • urease (+)
  • indole (-)
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Enterobacter sp.
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  • common in pts with recurrent infections, instrumented or have anatomic defects
  • Gram (-) rod, motile
  • lactose fermenter
  • MDR
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Pseudomonas aeruginosa
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  • common in pts with recurrent infections, instrumented or have anatomic defects
  • nosocomial pathogen
  • inherently resist to many antibiotics
  • Gram (-), rods, motile, aerobe
  • ubiquitous distribution in soil and water
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Psuedomonas aeruginosa: lab ID
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  • oxidase (+) (distinguishes from E. coli)
  • pigment production
  • fimbriae for adherence
  • endotoxin
  • biofilm formation (attaches to catheters)
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Klebsiella sp.
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  • nosocomial UTIs
  • Gram (-), non-motile, lactose fermenter
  • Transmission: normal flora, able to survive in moist environments (hands)
  • virulence: capsule, endotoxin, fimbriae
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Serratia marscescens
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  • gram (-), bacillus, facultative anaerobe
  • normal GI flora in small numbers
  • environmental bacteria
  • opportunistic pathogen (nosocomial)
  • characteristic red pigment
  • lactose - , indole - , urease - , motile, H2S -
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Candida albicans
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  • common in hospitalized pts who are on broad-spectrum antibiotics and have a bladder catheter
  • diabetic pts
  • immunosuppressed pts
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