gram-

oxidase-

non-motile OR motile w/ peritrichous flagella

non-fastidious

all except 1 ferment glucose (some ferment lactose; some non-fermenters can be pathogenic? not a good rule)

normal animal/human intestinal flora

>70% UTIs

significant cause: food poisoning

1. Escherichia coli

2. Shigella

3. Proteus

4. Salmonella

5. Yersinia

6. Klebsiella

*all GNB

Escherichia

Klebsiella

Proteus

Salmonella

Shigella

Yersinia

pink colonies => lactose fermenters

used when testing for enterobacteriaceae

1. lipid A: w/in mem; toxic activity

2. conserved core polysaccharide: common antigen

3. variable O-polysaccharide: serologic diversity

1. capsule (antiphag/poor antigen; inhib opson/complement activation)

2. antigenic variation: K&H antigens (alternatively expressed or not at all; evade host defense)

3. nutrient trap: Fe chelators (siderophores  enterobactin, aerobactin)

4. ~20 bact proteins => "syring" (deliver virulence factors to host) *Yersinia, Salmonella, EPEC, Pseudomonas*

humoral & innate immunity

incr susceptibility w/ dysfunction/deficiencies of these parts of the immune system

Salmonella

Shigella

Yersinia

Proteus

Morganella

motility test semi-soft medium inoculated w/ straight neele

motile bacteria swim away from the line of inoculation to find nutrients/cause turbidity 

=> + is cloudy/line of inoculation not visible

and - is clear/line of inoculation visible (bacteria are growing along)

*used to test enterobacteriaceae

-citrate utilization test (citrate is sole carbon source & ammonium salts sole N source)

-organisms that metabolizae citrate use ammonium salts --> release ammonia/incr pH

-bromothymol blue: green at neutral & deep blue above pH 7.6

*all salmonella (except S. typhi are +)

this tests for the bacteria that produce urease (these organisms will break the C-N bond of amides => co2, nh3, & h20 => basic solution)

results: + is pink

examples: E. coli- & Proteus+

+ result: bacterial tryptophanase (converts tryptophan --> indole); adding Kovac's reagent leads to formation of red ring (pink color)

*E. coli+; P. vulgaris+; S. typhimurium-

combined test to determine production of: indole & H2S AND motility

inoculate organism in tube: organism w/ cysteine desulfurase (cysteine --> pyruvate + NH3 + H2S); Fe in medium rxs w/ H2S => black precip; motility (growth away from stab) is difficult to see w/ the H2S rxns

Ex: 1) E. coli does not produce H2S (no black color) & DOES prod indole (red ring)

2) Salmonells prod H2S (black color) & does NOT prod indole (no red ring)

3) Proteus vulgaris produces both H2S & indole (black color and red ring)

triple-sugar-iron (TSI) test

[medium contains: 1% sucrose, 1% lactose, 0.1% glucose, and Fe]

no fermentation (obligate aerobe): slant & butt remain red

only glucose is fermented: acid in butt turns it yellow (insuff to affect slant)

sucrose or lactose ferments: butt & slant both yellow

gas forms during fermentation: agar cracks (displaced upwards)

H2S is produced: black in butt

triple sugar iron (TSI) test results:

red-no fermentation

yellow-acid prod from fermentation

YG-gas produced

selective medium

bile salts & crystal violet inhib GPB growth

lactose (fermentable sugar) allows differentiation

neutral dye: red @ pH<6.8 & colorless @ pH>6.8

Escherichia coli

Klebsiella pneumoniae

(considered to be usually non-pathogenic)

Salmonella

Shigella

Proteus

(considered to be usually pathogenic)

1. surface antigens (confer variability)

2. adhesins (indicates cell identity: p fimbriae/pili~UTI; colonization factors~GI; aggregative adherence fimbriae~UTI)

3. capsule

4. endotoxin: LPS

5. Exotoxins: ETEC (enterotoxigenic)~heat stable & heat labile; EHEC (enterohemorrhagic)~shiga-like toxins

UTI

-dysuria, frequency, suprapubic pain

-fever and/or back px => progression to pyelonephritis

1. Streptococcus agalactiae

2. Escherichia coli

serotypes w/ P pili

attaches bacteria to cell linings of the bladder and prevents them being "flushed" out with the urine

abdomen/pelvis

may => peritonitis, diverticulitis, appendicitis or visceral abscess

more common occurrence in hospital borne pneu

(GNBs cause ~70% nosocomial pneumonia)

(E. coli is rarely a cause of community pneumonia)

frequently infects decubitus ulcer

also infects extremities in diabetic pts

1. Where does bacteremia/septicemia arise (w/ E. coli infection)?

2. What is the most common source of bacteremia?

1.at any extra-intestinal site

2. Escherichia coli UTIs

1. Escherichia coli (60%)

2. Klebsiella (20%)

3. Proteus (15%)

1. enteropathogenic E. coli (EPEC)

2. enterotoxigenic E. coli (ETEC)

3. enterohemorrhagic E. coli (EHEC)

4. enteroinvasive (EIEC)

5. enteroaggregative (EAEC)

EPEC (enteropathogenic E. coli)

mechanism: Bfp, intimin, Tir allow attachment to intest epithel cells => destruction of microvillus => malabsorption/watery diarrhea 

enterotoxigenic E. coli (ETEC)

virulence: heat-labile (LT1-cholera like toxin incr cAMP) & heat-stable (STa toxin incr cGMP) => fluid loss 

enterohemorhagic E. coli (EHEC) O157:H7 serotype most common in the US

transmission: undercooked meat, vegetables, unpasteurized milk, fruits, water

virulence: shiga toxins (Stx-1) => disrupt protein synthesis => inflammation/lesions/destruction of intestinal villus => fluid secretion

presentation: mild --> bloody diarrhea, severe abdominal px

progression: may => HUS & kidney failure

prevalence: mostly underdeveloped countries

virulence: plasmid mediated invasion & destruction of colonic epithelial cells

presentation: fever, cramp, watery diarrhea --> dysentery w/ scant bloody stools; progresses like Listeria & Shigella

=> infant bloody diarrhea (underdeveloped countries)

presentation: persistent watery diarrhea w/ vomiting, dehydration & fever

virulence: stacked bricks (plasmid-encoded behavior of rods) => short microvilli => poor reabsorption

-ETEC: traveler's diarrhea; organism in feces; toxins; LT & ST genes

-EHEC: serotype O157:H7; low amt of organism in feces; shiga toxins/genes; usually sorbitol non-fermenters

<5 yr

older adults >60 yr

1. Salmonella enterica - clinically more significant

Serovars: Typhimurium & Typhi & Paratyphi

2. Salmonella bongori

poultry & dairy products & undercooked meat

-Salmonella enterica infects the ovaries/upper oviduct tissues of hens

-phagocytic microfold (M) cells in peyer's patch => membrane ruffles in intest epithel cells => trap salmonella/induce their endocytosis (w/ salmonella present, epithelial cells secrete IL8 => attract PMNs --> PMN's toxic substances damage intest mucosa => inflammatory diarrhea)

*NTS => massive PMN infiltration (large/small bowel mucosa)

*TTSS play key role in endocytosis/intracell surviv

gastroenteritis

symptoms: fever, vomiting, water diarrhea, cramps

tx: NO antibiotics, usually self-limiting

invade: epithelium like other Salmonella --> disseminate through body via macrophages traveling through lymphatics

colonize: reticuloendothelial tissues (liver, spleen, bone marrow) --> re-enter GI tract => re-exposure => intestinal ulcers & necrosis

*Salmonella Typhi => mononuclear cell infiltration (not same as GI PMN infil during NTS infections)

Salmonella Typhi

early presentation: rose spots on trunk & chest (rash where bacteria is present), hepatosplenomegaly, epistaxis 

progression: bradycardia @ peak of fever

w/o tx: severely ill (GI bleeding/perforation <= hyperplasia & ulceration)

gram-

oxidase-

motile rod

lactose non-fermenter

produce H2S

SS agar: grilliant green, ox bile, high thiosulfate & citrate inhib normal flora (H2S production detected by using thiosulfate & iron - colonies -> black color)

Shigella dysenteriae

Shigella boydii

Shigella flexneri

Shigella sonnei

1. Name the 5 F's

2. What organism is this associated w/?

1. Food, Flies, Feces, Fingers, Fomites

2. Shigella

through M cells of Peyer's Patches

causes mucosal destruction/inflammation

rarely invades the bloodstream

Shigella dysenteriae => shiga toxin (inhib protein synthesis => cell death)

*remember, once these bacteria are inside the cells, they will stay there

Shigella sonnei

Shigella Flexneri

*neither => shiga toxin => less severe disease (watery diarrhea)

non-fermenters (white colonies on MacConkey)

H2S non-producer

neutrophils in fecal stain

1. motility: 

Shigella-not

E. coli-motile

2. H2S production (black colonies on SS agar)

Shigella-not a producer

Salmonella-yes a producer

1. Yersinia enterocolitica

2. Yersinia pseudotuberculosis

3. Yersinia pestis

gram- rod

zoonotic pathogen

non-lactose fermenter

motile only @ 28* C

*70kb plasmid essential (at least 6 genes for outer mem proteins => cytotoxicity, resist phago, apoptosis of host cells)

-chrom inv prod => translocation across epithelium

acute diarrhea <= enteritis or enterocolitis

also: low fever & cramping 

Klebsiella pneumoniae 

-causes majority of Klebsiella infections in LTCF, hospitals & community

1. Pneumonia: minor cause of community; usually lobar (acute, severe, destructive)

2. UTI: not that common

3. Soft-tissue infection: affects devitalized tissues (decubitus & diabetic ulcers & burn sites)

4. Bacteremia: can be caused from infection at any site

gram- 

encapsulated rod

intracellular pathogen

(has never been cultured)

donovan bodies w/in macrophages (pathognomonic sign)

1. Proteus mirabilis: causes ~90% of Proteus infections

2. Proteus vulgaris

normal flora in GUT, soil, & water 

adhesins

flagella 

IgA protease

urease

UTI

wound infections

kidney (from urinary tract; more commonly than E. coli)

lactose non-fermenter

do not form regular colonies

"swarming colonies" from high motility

urease+

gram-

non-spore forming

anaerobic rods

(name the two genera)

1. Bacteroides prevotella and Bacteroides porphyromonas (rod or coccobacilli)

2. Fusobacterium (longer rods tapering end)

most common cause of intra-abdominal infections

also: sinusitis, otitis, brain/liver abscesses, pneumonia, skin & soft-tissue infection

weakly gram- staining

small pleomorphic rod

strict anaerobe

foul smelling wound w/ presence of gas

Bile Esculin agar: B. fragilis (black growth) vs. Proteus mirabilis (no growth)