Enterobacteriaceae, Klebsiella, Pseudomonas Flashcards
Where are enterobacteriaceae?
Widely distributed Gram neg bacilli: in soil, water, plants, GI of humans and animals
Majority of urinary isolates; large portion of blood, peritoneum, and resp cavity isolates
Morphology of enterobacter
Average size, non-spore-forming G- bacilli that may have motility (flagella) or not (Kleb, Shig, Yersinia)
Aerobic or facultative anaerobes
Enterobacter and Quellung reaction
Some positive (Kleb, Enterobacter, E. coli), some negative
Species with positive Quellung
Encapsulated: SHiNSKSS Strep pneumo H. influenza N. meningitidis Salmonella Klebsiella group B Strep
GNR infections
Enteritis (E. coli, Salmon, Shig, Yers)
Non-enteric: UTI, cellulitis, soft-tissue abscess, intra-abd abscess, bacteremia, liver/spleen abscess, foreign body infxn, pneumonia, endocarditis
*External or from gut spillage/ transmigration
Morphology & diseases of Escherichia
G-, fac anaerobe; oxidase neg, lactose fermenter
Commonest bact in gut, commonest cause of UTI
Most infections E. coli; most endogenous, enteritis exogenous
E. coli virulence factors
Fimbrial adhesins, secretion systems to export proteins for pathogenesis and toxins
E. coli causes of enteritis
ETEC (enterotoxigenic), EHEC (enterohemorrhagic), EIEC, EPEC, EAggEC
*Uropathogenic E. coli (most likely to be encapsulated, produce P fimbriae, produce cytolytic hemolysin, multiple Fe-acquiring mechanisms)
ETEC diseases, spread, tx
Leading cause bact diarrhea in developing world (Traveler’s diarrhea)
9% diarrheal deaths, 1% deaths in kids 1-2 days = sec diarrhea, n/v
Tx: rehydrate +/- abx (pregnant, immunocompromised)
Pathogenesis of ETEC
Ingestion of contaminated food, water -> attach to small intestinal epithelial cells but don’t invade -> secrete heat labile and heat stable toxins
Heat labile and heat stable toxin mechanisms
Labile: similar to cholera toxin, A-B toxin -> ADP ribosylation of Gs -> activate AC -> inc cAMP
Stable: stimulates GC -> inc cGMP
EHEC alternative name
Shiga toxin producing E. coli (STEC)
EHEC epidemiology
Undercooked meats, contaminated drinking water, foods; few organisms needed for infection
E. coli O157:H7 virulence & mechanism
EHEC with O and H antigens, Shiga like toxins Stx-1,2 encoded by phage
A subunit internalized, stops protein synthesis; B subunit binds GB3 glycolipid-R in colon, kidney
E. coli O157:H7 diseases
Common cause diarrhea/ dysentery in dev’d world
Severe abd pain, bloody diarrhea, hemorrhagic colitis, HUS
HUS
After 2-7% E. coli O157:H7 infections; mostly kids, 5-10% mortality
Thrombotic microangiopathy; acute renal failure, anemia, thrombocytopenia; can lead to HTN, renal impairment
*NO ABX - can worsen it; supportive care
Characteristics of enteritis caused by EIEC, EPEC, EAggEC
EIEC: Shigella-like dysentery w blood, mucus
EPEC: Pediatric diarrhea, esp infants; watery or bloody diarrhea in infants, person-person spread
EAgg: childhood diarrhea, more than 14 days; watery w mucus
Non-enteritis E. coli infections
UTI (CA or nosocomial), blood stream infections, pneumonias (neonatal, nosocomial), meningitis (after surgery, VP shunts), peritonitis (peritoneal dialysis)
Tx based on abx-susceptibility
Salmonella enterica serotypes and transmission
S. typhi and paratyphi are serovars - adapted to humans
2500+ serotypes based on H and O Ags
Fecal-oral spread, person-person
Epidemiology: non-typhi Salmonella
Contaminated foods, fecal-oral spread at day care or food service personnel; animal reservoirs: poultry, reptiles (TUTTLES), livestock, birds, domestic animals, rodents
Clinical syndromes of Salmonella
Enteritis (6-48 hr for 3-7d, n/v, diarrhea, cramps, +/- fever, constipation first, no blood or pus in stool, stools pos ww-yy post illness)
Septicemia, osteomyelitis, aortitis
*Especially in immunosuppressed (HIV+, malignancy, certain drugs)
Virulence of Salmonella
Endotoxin, invasion genes (chromosomal, attachment and invasion)
Entry into host: ingest contam food/water, fecal-oral spread, moderate number of bacteria
*Susceptible to low pH, antacids increase susceptibility to dz
How is Salmonella infection established?
Attach to epi cells, uptake, replication in endosome, penetrate into subepi tissue, inflam response contained -> spreads to blood = sepsis
Treating, preventing, controlling Salmonella
Sx: fluid replacement
Abx not for uncomplicated GI -> may prolong carrier state; abx for septicemia
Prev/control: sanitation, water and sewage treatment, proper food prep and storage
S. typhi epidemiology
Contaminated food or water; humans are only reservoir, but passive carriage by flies from feces to food
Chronic carriers: GB colonization, endemic reservoirs
Symptoms of S. typhi
Enteric fever; incubate 7-21 d, starts as diarrhea, bacteremia -> fever (3-4 w), malaise, anorexia, myalgia, HA, rose spots, relative bradycardia, hepatosplenomegaly, lymphocytosis
Complications: infxn of bone, heart valves, brain, Peyer’s patches bleeding (longitudinal ulcer)
Virulence factors & mechanisms of disease of S. typhi
Vi PS capsule, endotoxin
Invade M cells in PPatches, replicate and transport to subepi tissue, survive in MFs, enter blood and lymph -> replicate in liver, spleen with prolonged release of endotoxin -> GB colonization, shed in bile
Treating, preventing, controlling S. typhi
Tx: abx if complicated and susceptible
Sanitation, carriers shouldn’t handle food, vaccines against Vi capsular PS (oral or IM)
Epidemiology of Shigella
Fecal-oral spread, primarily dz of kids
Contaminated food or water
FEW organisms for infection (vs. Salmonella)
Clinical symptoms of Shigella
Watery diarrhea -> in 1-3 days: abd cramps, fever, blood/ pus in stools, tenesmus
*Identical to EIEC
Can cause HUS (toxin)
Morphology of Shigella
G- bacillus, non-motile, species classified by O Ag, n H Ag
Not a lactose fermenter, relatively biochemically inactive
Virulence factors of Shigella
Shigatoxin (some spp), virulence plasmid (attachment, invasion, intracellular replication)
Tx, prevention, control of Shigella
Tx: fluid replacement, abx to shorten duration and fecal excretion (cipro, TMP)
Prevent: wash hands, chlorinate water, sanitation
Yersinia reservoirs
Y. enterocolitica: pigs, rodents, livestock
Y. pestis: rodents
Y. entercolitica physiology, structure, epidemiology
G- bacillus, motile, flagella at low temp (22), growth at 4 C (inc metabolic activity at low temp)
Fecal-oral spread; milk, food, water
Common in Scandinavia, cold areas of N. America
Clinical syndromes of Y. entercolitica
Diarrhea, fever, abd pain (“appendicitis”); similar to Salmonella, mesenteric lymphadenitis
Complications: septicemia, hepatic abscesses
Post-infxn: reactive arthritis (HLA B27)
Pathogenesis and tx for Y. entercolitica
Invasive; heat-stable enterotoxin similar to E. coli ST
Tx: supportive care for non-complicated cases; FQs, ceph, tetras, etc. based on sensitivity
Y. pestis epidemiology
Rat fleas from rat to human; common in Africa, Asia, SW USA
1000-2000 cases in world per year
Used as biological weapon
Morphology of Y. pestis
Non-motile, non-spore forming, not lactose fermenter
Bipolar staining with Giemsa or Wright stain
Aerobic on most media, optimal at 28*
Clinical symptoms of Y. pestis
Bubonic plague: fevers, chills, HA, firm buboes (groin) w edema; 50% fatal wo tx
Pneumonic plague: 1’ or 2’, pneumonia w watery or purulent sputum w bacteria; 50% mortality (100% wo tx)
Septicemic plague: bacteremia, no buboes, fever, sepsis, 33% fatal (100% wo tx)
Tx of Y. pestis
Streptomycin, gentamicin, tetracyclines, chloramphenicol
*Many side effects
Klebsiella pneumoniae infections
Aspiration pneumonia
Abscesses in lung, liver
especially in Alcoholics, diabetics
Can get MD-ResistAnce
Klebsiella virulence & symptoms
PS capsule -> mucoid colonies
Currant jelly sputum in pneumonia (esp alcoholics)
MDR strains: ESBL, KPC
Proteus morphology & clinical syndromes
P. mirabilis most common pathogen
G- bacillus, very motile
Causes UTIs, kidney stones (alkaline urine bc urease pos -> precipitation of Mg and Ca)
Urease positive organisms
PUNCHK Proteus Ureoplasma Nocardia Cryptococcus Helicobacter Klebsiella
Enterobacter morphology & clinical syndromes
G-, lactose fermenter, fac anaerobe
Pathogens: E. cloacae, aerogenes
UTI, pneumonia, blood stream infxn, nosocomial infxn, etc.
Treatment of enterobacter & resistance mechanism
“Inducible AmpC” -> tx failure w use of routine abx
Consider FQs, carbapenems
Serratia morphology and clinical syndromes
G- enterobacteriaceae
Any infection, commonly nosocomial infections
Resistance mechanism of Serratia
Inducible AmpC -> tx failure w use of routine abx
Pseudomonas aeruginosa morphology
Aerobic, G- bacilli (single or pairs), oxidase+, non-lactose fermenter, motile with monotrichous polar flagellum, multiple cell surface pili/fimbriae
Can use wide range of carbon/energy sources
Pigmentation and hemolysis of P. aeruginosa
Blue-green phenazine (pyocyanin), red (pyorubin), or black (pyomelanin)
Colonies have metallic sheen, sometimes slimy
B-hemolysis
Grape-like odor
What is alginate?
“Mucoid exopolysaccharide”, leading to mucoid appearance of strains from CF patients and occasionally other patients w chronic P. aeruginosa infxns
Most strains of P. aeruginosa can produce it
Pseudomonas virulence factors
Adhesins, alginate, exotoxin A, exoenzyme S, elastolytic activit, phospholipase C, pyocyanin, abx resistance
What are exotoxin A, exoenzyme S, and pyocyanin of Pseudomonas?
A: inhibits protein synthesis, causes tissue damage (eye infxn, burn)
S: inhibits protein synthesis, interferes with phagocytosis
Pyo: makes ROS -> tissue damage
Where is Pseudomonas found?
Ubiquitous in water, soil, plants; can colonize anywhere in body and cause any infection
Pseudomonas infections
Wound infxn, hot tub dermatitis; chronic or malignant otitis externa; burn wound infxn, endocarditis (IVDU); bacteremia, sepsis, ecthyma gangrenosum; nosocomial, UTI, pneumonia, meningitis
PSEUDO: Pneumonia, Sepsis, External otitis, UTI, Drug use/Diabetic, Osteomyelitis
Transmission of Pseudomonas & at risk populations
Moist reservoirs
Can be normal GI flora in hospitalized pts
Contact and endogenous spread
Immunocompromised, drug users, burn patients
Pseudomonas tx and prevention
Resistant to: FQ, B-lactam, AGs; easily MDR
Endocarditis: double coverage
Good aseptic technique, avoid unnecessary use of broad-spectrum abx, remove indwelling lines asap
Isolate pts with MDR strain
Campylobacter epidemiology
Most common cause bacterial gastroenteritis
Transmitted by chickens, cattle, swine, cat/dog
Contaminated meat, fish, milk, mushrooms, raw seafood
Contaminated water (animal feces)
Campylobacter jejuni morphology
G- bacillus, very small, comma- or S-shaped
Motile: single polar flagella or darting corkscrew
Growth: reduced O2, increased CO2, elevated temp
Clinical syndromes Campylobacter
Gastroenteritis (1-7d post): watery diarrhea or dysentery (fever, and pain, bloody stool) for 1-2 w
Septicemia rarely
Autoimmune responses to Campylobacter
? IBS; reactive arthritis; Guillain-Barre syndrome (may cause 20-40% GB cases; 2-3 post febrile illness) d/t Ab to core sugars of LPS cross-rx w gangliosides
Tx and prevention Campylobacter
Self-limiting; fluid- and electrolyte replacement; multiple abx-res plasmids
Erythromycin (enteritis) or AGs (septicemia)
Prevention: proper food prep, good sanitation, pasteurize milk
H. pylori morphology
G- spiral-shaped bacillus w corkscrew motility
Epidemiology and clinical syndromes H. pylori
In 70-100% pts with gastritis, gastric ulcer, duodenal ulcer
Infxn increases with age
? also gastric adenocarcinoma?
Virulence and transmission of H. pylori
Urease, motility, mucinase, adherence factors, endotoxin, cytotoxin
No animal reservoir, likely fecal-oral spread
Dx and tx of H. pylori
Gastric biopsy or culture; serology or urea breath test (monitor tx this way)
Tx: combo abx (amox, tetra, metro); PPI, bismuth (anti-inflam)
