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70 Cards in this Set

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Points of Triangular Relationship of factors contributing to infection
BACTERIAL VIRULENCE (large dose vs. small dose)
SITE OF INFECTION (mucosal vs. invasion)
HOST RESPONSE (intact vs. weakened)
compare VIRULENCE of
Shigella > Salmonella

shigella requires far fewer #s of bacteria for infection
Factors to consider in usage of antibiotics in infection
1) Bacteriocidal vs. Bacteriostatic
2) Tissue penetration by antibiotics
3) condition of the host
Characteristics of the Enterobacteriaceae family (Enterics)
-many normal part of gut flora
-gram negative rods
-facultative anaerobes
-ferment glucose
-oxidase negative (no cytochrome oxidase)
-reduce nitrates to nitrites
general properties of Salmonella
1) gram neg. rods, non-spore-forming, facultative anaerobes
2) ferment glucose under anaerobic conditions
3) DO NOT ferment lactose (distinguishing characteristics)
4) produce H2S
5) Motility (if present) due to presence fo flagella
diversity of Salmonella
1500 + "species" (serotypes)
distinguished by:
-antigenic analysis of O Ag
-analysis fo H antigen (part of flagella, either Phase I or Phase II)
-unique Ag only for Salmonella typhi called Vi antigen
3 major species of Salmonella
Salmonella typhi (typhoid fever or enteric; one serotype)
Salmonela choleraesuis (bacteremic syndrome; one serotype)
Salmonella enteritidis (many serotypes, major cause of diarrhea)
Lab ID of Salmonella
Primary isolation from feces: on differential media w/ lactose (EMB & MacConkey agar): non-lactose fermenting colones = Salmonella, lactose fermenting colones = E. coli and other nonpathogenic bacteria

Biochem and sero tests to id organism for Dx and Epidemiological purposes: using type specific sera against O, H and Vi Antigens
3 clinically distinguishable syndromes related to Salmonellosis is man:
1) enteric fevers (common in dvpg world)
2) septicemias (rare)
3) acute gastroenteritis (usually self limiting)
inoculum of Salmonella required for disease
10^5 CFU
prototype of enteric fevers caused by Salmonella typhi (or paratyphi)
Typhoid fever
both Salmonella typhi and paratyphi are what type of organisms?
facultative intracellular organisms
Phases of Typhoid Fever
7-14 day incubation
Bacteremic Phase
GI Phase
Chronic Phase (in ~3% of patients)
characteristic symptoms of Typhoid Fever
malaise, anorexia, headache, followed by fever (but LOW HR)

rose spots (blanching rash), leukopenia common, feber subsides gradually after 3rd week, severe intestinal hemorrhages in later stages (10% of untreated cases die of complications involving bowel perforation)
osteomyelitis may occur in SCA patients
Carriers of salmonella
~3% of patients, excrete large number of organisms from suppartive focus in biliary tract over extended periods, these are important sources for spreading the infection if sewage disposal is inadequate
late complicaton of Salmonella
toxic megacolon- dilation of colon > 6cm
where do Salmonella typhi multiply?
within the mononuclear cells of Peyer's patches
how do Salmonella typhi get into bloodstream?
after multiplication in Peyer's patches, they enter intestinal lymphatics and travel via thoracic duct to the blood where they are disseminated into spleen, bone marrow and GALL BLADDER
what cultures should be used when in Salmonella Typhii infection?
stool cultures are positive (very early {1st week} and again when S. typhi are excreted into the intestine from the fall bladder in the late stage or carrier state)
blood cultures become positive after 7-14 days
Lab Dx of S. typhi from blood, stool or urine
test for elevated or rising O and H agglutinins bt wks 1-3 "Febrile agglutinins"
-test rise in Ab to Vi antigen to dx typhoid fever (Vi Ag onfound in S. typhi)
Tx of S typhi
1st line of therapy: fluoroquinolones (ciproflaxacin) or 3rd generation cephalosporins (cetriaxone)
2nd line: chloramphenicol; ampicillin; trimethorpim plus sulfa.
Chronic carrier states: 1) ampicillin or ciproflaxacin 2) cholecystectomy
S. typhi infects only man not...
Prevention of S. typhi
sanitary control of h2O
pasteurization of milk and screening of food handlers
Two typhoid vaccines currently available in the US
a) oral live attenuated vaccine (4 doses, not recommendted for kids <6 years)
b) a Vi capsular polysaccharide vaccine (ViCPS) for intramuscular use (given 2 weeks prior to exposure)????
both show to protect 50-80% of recipients
Septicemia caused by Salmonella
5-10% of infections

high fever and bacteremia usually NO GI involvement, has been classically caused by S. Choleraesuis
-may occur in SCA or cancer patients, or young children
-osteomyelitis due to S. Choleraesuis may be found in a child with SCA
-suppurative lesions during bacteremia may dvp almost anywhere in the body, local absecesses, cholescytitis, pericarditis, meningitis, osteomyelitis, etc..
the most common form of salmonella infection
ENTEROCOLITIS (Gastroenteritis)

confuined to the GI tract (blood cultures are positive in ~5-10% of patients)
most common species of Salmonella causing enterocolitis
Salmonella typhimurium (S. enteritidis serotype typhimurium)
blood cultures are rarely positive in gastroenteritis (salmonella typhimurium infection) relative to what other Salmonella infections
enteric fever (S. typhi)
septicemia (S. choleraesuis)
where blood cultures are frequently positive
how long does it take for symptoms of gastroenteritis caused by Salmonella typhimurium to appear?
8 to 48 hours after contaminated food consumption

lasts 1-4 days, usually self limited
symptoms of gastroenteritis caused by Salmonella typhimurium
sudden onset with headache, chills, abdominal pain, nausea, vomiting and then diarrhea, often accompanied by fever

symptoms can be explained by endotoxin release upon invasion of epithelial tissue of the small and large intestines 6-8 hours after ingestion

lasts 1-4 days, usually self limited
oxidase test will be negative for which gastroenteritis-causing bacteria?
E. coli , Salmonell and Shigella all LACK cytochrome oxidase
oxidase test positive for which gastroenteritis-causing bacteria?
both have cytochrome oxidase
result of Salmonelle glucose fermentation test

yellow in the butt of test tube
General properties of Salmonella
1) Do not ferment lactose (distinguishes from some enterics)
2. Ferments Glucose (like other enterics)
3. Produces H2S (gas)
3. Motile- has flagella (contrast to Shigella)
number of Salmonella enteritidis serotypes
almost all cause gastroenteritis
how do S. enteritidis differ from S. typhi
transmission patterns differ from that of typhoid fever

reservoir determined by serotypes in domestic animals (contrasting with no animal reservoir in s. typhi)

domestic animals are fed salmonella-laden meat scraps

gastroenteritis common in dvpd countries, typhoid fever due to S. typhi common in developing countries
Salmonella serotype most frequently involved in egg contamination
S. enteritidis
= serotype most commonly involved in egg contamination
estimated contamination from 0.0005 to as high as 5% of eggs entering food supply
Salmonella traced to fruits or juice probably result from what?
contamination in the field by animal or human fecal matter and not sufficiently washed before serving
Lab Dx of Salmonella in gastroenteritis
absolutely dependent on finding Salmonella in feces or fecal swab
H antigen (2 types)
O antigen (arrangement of sugar specific for each serotype)

does not ferment lactose
gram-negative rod
ferments glucose anaerobically (produces acid)
usually produces H2S
motile (flagella)
Salmonella morphology on MacConkey agar
1) bile salt as selective agent
2) lactose
3) neutral red as pH indicator
(non lactose fermenting)

{contrast to pink lactose-fermenting E. coli colonies}
Salmonella morphology on EMB agar (Eosin methylene Blue agar)
-lactose-containing medium used
-eosin inhibits growth of Gram + bacteria
-methylene blue is color indicator for lactose fermentation
-similar in function to the MacConkey agar (MacConkey agar commonly used in Hospital Labs)
Salmonella (colonies are not black)
E. Coli (lactose fermentor) colonies purple/black
Kligler Iron Agar for Salmonella detection
contains sugar, but much higher percentage of lactose, allows you to detect quickly lactose fermentation more quickly, if fermenting only glucose, bacteria would generate much less acid

need to provide source of Hydrogen

Ferric citrate reacts with hydrogen sulfide (so Hydrogen sulfide can be detected)

acid (yellow) in butt
alkaline (red) in slant.. reverts to glucose fermentation under aerobic conditions at surface
Kliger Iron Agar results for:
E. coli
Salmonella: red slant/yellow butt
Shigella: red slant/yellow butt (aerobic and anaerobic glucose fermentation)
E. coli: all yellow (acid throughout, lactose fermentation)
Pseudomonas: red slant/neutral butt (no fermentation!)
How does one distinguish Salmonella from E. coli and from Proteus?
Indole negative (indole is byproduct of tryptophan hydrolysis)
Urease negative (urease splits urea into ammonea and carbon dioxide)
how can Salmonella be distinguished from Shigella (morphologically)
(salmonella can swim, shigelly stay where physically placed by loop)

salmonella has pertrichous flagella
(as do other enterobacteriaceae)

shigella has no flagella

Vibrio cholera: polar or monotrichous flagellum
Pseudomonas: lophotrichous flagella
Hallmarks of typhoid fever
episodic or high spiking fever
rose spot (on abdomen)
late GI bleed
what serotype of salmonella enteritidis comes from reptiles?
Salmonella enteritidis serotype typhimurium
Laboratory Diagnosis of Salmonella gastroenteritis
Non-Lactose fermenting, H2S producing Gram negative rod; Urease and Indole negative which distinguish it from Proteus and E. coli, respectively
Other bacterial causes of diarrhea (other than salmonella)

a. Shigella
b. Campylobacter
c. E. coli
d. C difficile
e. rare in US (i. Yersinia enterocolitica, ii) Vibrio species)
2. Toxin (food poisoning)
a. S. aureus
b. Bacillus cereus
3. Viral causes (rotavirus, norwalk virus)
4. Protozoa and helminths
Treatment of Salmonella gastroenteritis
-mostly self-limiting
-fluid replacement
-treat patients with rpedisposing conditions (ampicillin, trimethoprim sulf, 3rd generation cepholosporin, fluoroquinolone (eg ciproflaxacin)
slide #58 L6 shig/salmonella summary of clinical diseases table
incubation period
GI symptoms
blood cultures
stool culture
typical organism
Hippocrates description of dysentery
blood diarrhea
general characteristics of Shigella
-a lactose non fermentor
*nonmotile (no flagella)
*does not produce H2S
*contains O antigens only (no H antigens)
-Indole and Urease negative

*distinguish Shigella from Salmonella
morphology of Shigella colonies grown on macConkey Agar
colorless colonies
main characteristics distinguishing Shigella from Salmonella
-No H Antigens (no flagella)
-fewer organisms required to initiate infection (100 vs. 100,000 Salmonella)
-No animal reservoir (transmitted from person to person)
-Bacteremia uncommon in shigella (common in S. typhi and paratyphi and S. choleraesuis)
-4 species of Shigella (vs. >1500 Salmonella)
most common species of Shigella found in the US (responsible for 75% of infections)
Shigella sonnei
Shigella is spread by
Incubation period of Shigella
1-4 day incubation period
Where does Shigella invade?
intestinal epithelium, limited penetration

intestinal ulceration due to Shiga toxin
why does Shigella infection require such a low inoculum?
the organism is acid tolerant
Pathogenesis of Shigella infections
1) oral ingestion, invades intestinal M cells
2) Uptake by M0s into phagocytic vacules (uptake induced by secreted protein of Shigella)
3) Escape from the phagocytic vacule into the cytoplasm of M0s
4) induces apoptosis (programmed cell-death) of macrophages, infects new cells
5) LPS released, causing IL-1 and TNF release from monocytic cells --> fever/systemic symptoms
Shiga toxin released, leading to GI ulceration and bloody diarrhea
Shiga toxin
contains 2 subunits (A and B)
A interferes with fxn of 60S ribosomal RNA inhibiting protein syntehsis
Subunit B binds to receptor on intestinal cells
diarrhea ensues due to fluid malabsorption
may lead to apoptosis of mucosal cells
clinical syndromes of Shigella infections
-Fever (due to LPS), diarrhea, abdominal cramps
-bloody diarrhea w/ mucous (INVASIVE!)
-usually self-limiting, rarely fatal
-can detect organisms in feces up to 1-4 weeks after recovery (continuing risk of dissemination)
Stool Examination in Shigella
NEUTROPHILS (not monocytes)
Histology of colon in Shigellosis
mucin in glands of intestinal lining
Dx of Shigella
-Clinical symptoms not diagnostic
-Isolation of microorganism from feces
- Non-lactose fermenting Gram – rods
- no gas with glucose fermentation
- no H2S
- nonmotile
Treatment of Shigella infections
-fluid and electrolyte replacement (esp. in young)
-try ciprofloxacin and Trimethoprim-Sulfa if severe
-consider antibiotic susceptibility testing with increasing resistance
Prevention of Shigella infections
-improve sanitation (human is the only host)
- live attenuated vaccine, not very effective
-recombinant O-Ag vaccine conjucated to inactivated Shiga toxin is a promising vaccine candidate (not yet approved)
pathogenic Shigella species most common outside of US
S. dysenteriae (serogroup A)
other common and less severe Shigella serotypes (besides S. sonnei) in the US
S. flexneri and S. Boydii