Lecture 8 and 9 Flashcards
Stain and shape of Enterobacteriaceae organisms
GramNeg
Rods
All have capsule (very large in Klebsiella)
O2 requirement of enterobacteriaceae
Facultatively anaerobic
How do enterobateriaceae move
Either peritrichous flagella or are nonmotile
O-antigens are what?
Part of LPS
H antigens are what?
Flagella
K/Vi antigens are what?
Capsular type
What is the main cause of foodborne illnesses?
Bacteria
What tests can you use for enterobacteriaceae
IMViC
Carbohydrate metabolism
What is IMViC
A test to identify a type of bacteria from the coliform group
What is enterotube?
A test tube to identify different enterobacteriaceae
What is unique about gut bacteria and how sense hormones?
They can response to stress-induced hormones levels (tells them this is a good time to attack)
Why do bacteria often go undetected in the body?
Many can block signaling pathways that would signal their presence
What is unique about pathogenic E. coli?
They never enter the cell but they produce protein that can facilitate entry of other bacteria and survival in a cell
What are the three diseases associated with E. coli?
Enteric
UTI
Sepsis/meningitis
What antigens are present on enterobacteriaceae
O
H
K/Vi
How can you detect E. coli in the lab?
All lac+
Copious acid production
Detected by green metallic sheen on EMB agar
What type of E. coli causes UTIs?
Uropathogenic E. coli
What type of E. coli causes sepsis and meningitis?
Meningitis associated E. coli
Why is E. coli the most common cause of UTI?
Proximity of anus to urethra
Uropathogenic E. coli interact with blood how?
Have “P” pilus will faciliates blood cell binding
How many types of diarrhea are caused by E. coli?
5
EPEC (EPEC) do what?
Bundle in the intestine against microvilli
Inhibit water uptake
EPEC stands for?
Enteropathogenic E. coli
Who can get EPEC?
Young children
Symptoms of EPEC
Watery, self-limiting diarrhea
ETEC stands for?
Enterotoxigenic E. coli “Montezuma’s Revenge”
ETEC symptoms
Watery diarrhea
Increased gut motility
Cramps
ETEC are found were?
Have CFA adhesion pili and stick to brush-border
ETEC produces what?
2 LT toxins (AB toxins like cholera)
STa toxin (activates cGMP production and water secretion)
STb toxin
EHEC stands for?
Enterohemorrhagic E. Coli (157:H7)
EHEC symptoms
Blood diarrhea without fever (hemorrhagic colitis)
What toxins does EHEC produce
Verotoxin (ABt-protein synthesis inhibitor-aquired by phage conversion)
EHEC can cause what symptoms outside of the GI tract?
Hemolytic-Uremic syndrome
What is hemolytic uremic syndrome?
Uremia and organ failure due to damage of glomerular endothelium
EIEC stands for what?
Enteroinvasive E. Colic
What is EIEC indistinguishable from?
Shigella dysenteriae type I
Symptoms of EIEC?
Blood in diarrhea
What type of E. coli should you not treat with antibiotics and why?
EHEC
The bacteria end up producing more toxin in response to Abx
How can EIEC invade and colonize?
Has invasive colonization factors (Ipas) produced from a shigella plasmid
EAEC stands for what?
Enteroaggregative E. Coli
EAEC symptoms
Noninflammatory pediatric diarrhea in developing countries
How does EAEC stick?
Aggregative pili form infective foci in intestine
Who is susceptible to E. coli meningitis
Neonates
Why can E. coli cause meningitis in neonates?
Has a K1 capsule which mimics NCAM receptor (which makes it hard to target)
Meningitis associated E. Coli is similar to what?
N. meningitidis B capsular antigen
Salmonella will have what common lab findings?
Lac-
H2s+
All salmonella belong to what species?
S. enterica
What two types of salmonella need to be considered separately?
S. typhi
S. paratyphi
These penetrate intestinal epithelium
What diseases are caused by salmonellsa?
Typhoid fever
Bacteremia/Septicemia
Enterocolitis/Gastroenteritis
What organism causes typhoid fever?
S. typhi
S. paratyphi
How does S. typhi reach blood stream?
Through intestinal mucosa
Where does S. typhi disseminate once in the blood?
Via macrophages to liver, spleen,, gallbladder
How does typhoid fever kill you
Intestinal hemorrhage
What type of salmonella causes bacteremia/septicemia?
S. Cholerasuis
What type of PT typically gets bacterermia/septicemia from S. cholerasuis?
Immuncompromised
What type of salmonella causes enterocolitis/gastroenteritis?
S. Enteriditis
What are symptoms of S. enteriditis?
N/V/D
Fever
Typically self-limiting
Can colonize the gallbladder and shed for weeks
What is a common source for S. enteriditis?
Eggs and poultry
Fecal-oral route
How does S. enteriditis cause illness?
Binds to invades gut epithelium
Can reach blood stream
Produce cytotoxic enterotoxin
Typhoid toxin enters host cells (ADP ribosylates a G protein and damages DNA)
Lab results for shigella?
Lac -
H2S -
Where is the only place shigella typically attacks?
GI
What are symptoms of shigella?
Fever and watery diarrhea for 2 days
Then, 2 days of blood and mucousy stool
Dehydration may be lethal
Shigella transmission
4 Fs
How does shigella cause illness?
Phagocytosed by M cells and given to macrophages
Lyse phagolysosome and replicate in cytoplasm
Release IL-1 and permeabilize cell junction
Spread by actin tails
Has shigella enterotoxin
How does Yersinia adhere?
YadA
What specific antigens does yersinia have and why are they significant?
V and W
Allows for intracellular growth
What bug causes “plague”
Yersinia pestis
Symptoms of yersinia pestis?
Malaise, headache, vomiting
Painful buboes in groin or other lymph nodes
What is a secondary infection from yersinia pestis?
Septicemia (may be primary or secondary to bubonic)
What is the third type of infection from yersinia pestis?
Pneumonic
Cough with blood tinged sputum
100% fatal in 24 hours
Why can fleas spread yersinia pestis?
Ymt phospholipase also the bug to live in a flea
How does yersinia pestis cause illness?
Genes turn on at 37° C
Type III inserts toxic Yops into host
Inhibits MAP kinase
When yersinia pestis inhibits MAP Kinase what subsequent pathways are effected?
Cytokine production
Cell replication
Prevents phagocytosis
Inhibits platelet aggregation
What is Tx for yersinia pestis PT if asymptomatic?
Tetracycline
Tx for y. pestis if symptomatic?
Streptomycin
Y. enterocolitica Sx?
Enterocolitis with intestinal abscesses
Severe bloody diarrhea with cramping and fever
Lasts longer
Mesenteric adenitis
Spread in feces (common in cattle and hog reservoirs)
Y. enterocolitica Tx?
Ampicillin
What enterobacteraceae is only a respiratory bug?
Klebsiella pneumoniae
K. granulomatis symtoms
This is an enterobacteriaeceae but is an STD
Genital infection that can mimic syphilis
What enterobacteriaceae is commonly associated with UTI
Proteus mirabilis, Proteus vulgaris
Urease production can result in bladder stones
Proteus mirabilis, Proteus vulgaris on agar
Swarming motility
Serratia marcescens causes what in whom?
Pneumonia, bacteremia, endocarditis in immunocompromised PTs
What is the new goal of treating enterobacteriaceae?
Return normal mucous production
MUC2 inhibits inflammatory and is carbon source for normal flora
Vibrio shape and stain
Gram neg. comma shaped rod
polar flagellum
2 circular chromosomes
Vibrio environment
Alkalophiles
Where do V. cholera live?
Copods in ocean
V. cholera antigens?
H antigens
O antigens
What is the most common form of v cholera now?
O1 El Tor Inaba
O1 El Tor Inaba produces?
Hemolysin
Why is O1 El Tor Inaba bad?
Polymyxin resistanct
How many organisms for V cholera to infect?
10^6
Who is more susceptible to cholera infections?
Antacid users
V. cholera Sx
N/V loose stools
“rice water stools”
No pain
How does V cholera cause infection?
Fibriae bind to gut epithelium
Toxin from PAI island on Chrom 1
Regulated by ToxR (activated by appropriate temp, acidity,…)
V. Cholera AB toxin mechanism
B binds as pentramer to receptor ganglioside Gm1
ADP ribosylates Gs Protein
Increase cAMP ion secretion into gut
Water follows
V. cholera Tx
Rehydration and electrolytes
Doxy can limit shedding but not stop symptoms (azithro if pregnant)
V. parahemolyticus symptoms
-12-24 hr incubation, then nausea, vomiting, watery to bloody
diarrhea, with or without gastroenteritis -self limiting, resolves in 1-4 days
V. parahemolyticus pathogenesis
-biofilms, T3SS and T6SS, hemolytic/cytotoxic enterotoxin
V. parahemolyticus control
-rehydration and electrolyte replacement, Doxycycline if necessary
V. vulnificus symptoms
very rapid (hours) cellulitis and necrosis 
V. vulnificus cause
-infected wounds from handling contaminated seafood (esp shellfish)
-bacteremia from eating raw oysters (always from contaminated seawater)
eventual liver damage (alcoholic predisposition): 50% fatal
V. vulnificus pathogenesis
-antiphagocytic capsule contributes to virulence -necrotizing cytotoxin
V. vulnificus control
-Doxycycline right away! (Cipro if pregnant) -takes 18 hours to get a positive culture; too late
Campylobacter shape and stain
Gram neg curved, helical, or gull-winged, polar flagella (sometimes bipolar)
Campylobacter oxygen requirement
Microaerophile
C. jejuni temperature
42° C
C. fetus temp
25° C
C. jejuni
-disease of the large intestine
-presents as abdominal pain (gastroenteritis), with cramps, fever,
very bloody diarrhea (sometimes blood red) (= invasive organism) -self-limiting within a week or so in typical pts.
-may invade the bloodstream and cause enteric fever in immunocomp. -sequela
-1-4 weeks after C. jejuni infection, patients (~1/2000) can develop Guillain-Barré syndrome (demyelinating neural disease, progressive flaccid paralysis) – molecular mimicry: autoantibodies to GM1 gangliosides
C. jejuni sources?
-a zoonosis (50-100% of chickens and turkeys in US infected) -human acquisition
-fecal-oral route
-consumption of contaminated poultry or milk -incidence peaks in the summer
most common in infants and young adults
C. jejuni pathogenesis
- produces an inflammatory enterotoxin
- C. jejuni bacteremia indicates an invasive potential
C. jejuni control
- rehydration therapy to treat diarrhea
- tetracycline, quinolones or clarithromycin for systemic infections
C. fetus clinical
-usually causes systemic infections, septicemia (rarely diarrhea) -spontaneous abortions in cattle
C. fetus epidemilogy
- zoonosis (cattle)
- humans acquire from eating contaminated undercooked beef -elderly, ill, and immunosuppressed especially susceptible
C. fetus pathogenesis
-major virulence factor is an S-layer protein that inhibits complement fixation by C3b; less opsonization = less phagocytosis
C. fetus control
-tetracyclines, macrolides and quinolones
Helicobacter pylori shape and stain
Gram neg spirillum
H. pylori oxygen
Microaerophile
H. pylori lab
-oxidase+, catalase+
H. pylori produces what?
produces HUGE amounts of urease (urease test positive in minutes to hours)
H pylori lives where?
not invasive; colonizes gastric mucosa, esp. antrum (Lewis blood group adhesin)
H. pylori leads to what?
stimulates gastrin production, which stimulates acid production in the fundus
H. pylori diagnosis
- serologic test (but antibodies remain after eradication)
- gram stain / culture of gastric biopsy
- urea breath test: 14C-urea is fed, detection of 14CO2 in breath is diagnostic of urease activity in stomach
Who should possibly have H. pylori and not know it
Be aware of the potential for gastritis caused by H. pylori in GERD patients being treated long-term with Proton pump inhibitors, which mask the H. pylori infection
Why do people with type O blood have more H. pylori?
Binds to Lewis antigen (antigen if you are O blood type)
H. pylori pathogenesis
H. pylori bind to base of gastric mucosal cells where pH is 7.4, rather than the pH 2 conditions of the apical border
huge amounts of urease buffer pH by forming NH3 from urea
-produce a vacuolating toxin VacA
-activated by stomach acid
-binds to sphingomyelin “lipid rafts” in gastric epithelial cells -insert into cell as selective anion channel
-cause extensive vacuolation of epithelial cells and release of urea,
also inhibition of antigen presentation pathways and T cells
What is the only one of four virulence factors in H. pylori that causes symptoms?
CagA
ulcer-assoc. strains produce a cytotoxin, CagA -secreted by T4SS
- induces apoptosis in host cells
- potential oncoprotein
- Production of both virulence factors is enhanced by salt
H. pylori control
Treat ulcer with bismuth subsalicylate
- Treat infection with tetracycline or macrolide + metronidazole
- Treat acid with PPI
- recovery from ulcer only occurs if infection treated, too (bicarbonate only allows H. pylori to spread)
How can you differentiate E. coli from salmonella?
No vomiting with E. coli
