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70 Cards in this Set
- Front
- Back
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Points of Triangular Relationship of factors contributing to infection
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BACTERIAL VIRULENCE (large dose vs. small dose)
SITE OF INFECTION (mucosal vs. invasion) HOST RESPONSE (intact vs. weakened) |
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compare VIRULENCE of
SHIGELLA and SALMONELLA |
Shigella > Salmonella
shigella requires far fewer #s of bacteria for infection |
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Factors to consider in usage of antibiotics in infection
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1) Bacteriocidal vs. Bacteriostatic
2) Tissue penetration by antibiotics 3) condition of the host |
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Characteristics of the Enterobacteriaceae family (Enterics)
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-many normal part of gut flora
-gram negative rods -facultative anaerobes -ferment glucose -oxidase negative (no cytochrome oxidase) -reduce nitrates to nitrites |
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general properties of Salmonella
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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 |
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diversity of Salmonella
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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 |
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3 major species of Salmonella
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Salmonella typhi (typhoid fever or enteric; one serotype)
Salmonela choleraesuis (bacteremic syndrome; one serotype) Salmonella enteritidis (many serotypes, major cause of diarrhea) |
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Lab ID of Salmonella
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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 |
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3 clinically distinguishable syndromes related to Salmonellosis is man:
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1) enteric fevers (common in dvpg world)
2) septicemias (rare) 3) acute gastroenteritis (usually self limiting) |
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inoculum of Salmonella required for disease
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10^5 CFU
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prototype of enteric fevers caused by Salmonella typhi (or paratyphi)
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Typhoid fever
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both Salmonella typhi and paratyphi are what type of organisms?
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facultative intracellular organisms
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Phases of Typhoid Fever
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7-14 day incubation
Bacteremic Phase GI Phase Chronic Phase (in ~3% of patients) |
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characteristic symptoms of Typhoid Fever
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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 |
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Carriers of salmonella
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~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
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late complicaton of Salmonella
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toxic megacolon- dilation of colon > 6cm
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where do Salmonella typhi multiply?
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within the mononuclear cells of Peyer's patches
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how do Salmonella typhi get into bloodstream?
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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
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what cultures should be used when in Salmonella Typhii infection?
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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 |
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Lab Dx of S. typhi from blood, stool or urine
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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) |
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Tx of S typhi
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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 |
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S. typhi infects only man not...
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animals!
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Prevention of S. typhi
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sanitary control of h2O
pasteurization of milk and screening of food handlers vaccination |
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Two typhoid vaccines currently available in the US
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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 |
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Septicemia caused by Salmonella
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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.. |
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the most common form of salmonella infection
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ENTEROCOLITIS (Gastroenteritis)
confuined to the GI tract (blood cultures are positive in ~5-10% of patients) |
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most common species of Salmonella causing enterocolitis
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Salmonella typhimurium (S. enteritidis serotype typhimurium)
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blood cultures are rarely positive in gastroenteritis (salmonella typhimurium infection) relative to what other Salmonella infections
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enteric fever (S. typhi)
and septicemia (S. choleraesuis) where blood cultures are frequently positive |
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how long does it take for symptoms of gastroenteritis caused by Salmonella typhimurium to appear?
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8 to 48 hours after contaminated food consumption
lasts 1-4 days, usually self limited |
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symptoms of gastroenteritis caused by Salmonella typhimurium
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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 |
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oxidase test will be negative for which gastroenteritis-causing bacteria?
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E. coli , Salmonell and Shigella all LACK cytochrome oxidase
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oxidase test positive for which gastroenteritis-causing bacteria?
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Pseudomonas
and Neisseria both have cytochrome oxidase |
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result of Salmonelle glucose fermentation test
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positive
yellow in the butt of test tube |
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General properties of Salmonella
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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) |
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number of Salmonella enteritidis serotypes
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>1500
almost all cause gastroenteritis |
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how do S. enteritidis differ from S. typhi
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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 |
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Salmonella serotype most frequently involved in egg contamination
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S. enteritidis
= serotype most commonly involved in egg contamination estimated contamination from 0.0005 to as high as 5% of eggs entering food supply |
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Salmonella traced to fruits or juice probably result from what?
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contamination in the field by animal or human fecal matter and not sufficiently washed before serving
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Lab Dx of Salmonella in gastroenteritis
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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) |
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Salmonella morphology on MacConkey agar
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1) bile salt as selective agent
2) lactose 3) neutral red as pH indicator Salmonella- WHITE COLONIES, (non lactose fermenting) {contrast to pink lactose-fermenting E. coli colonies} |
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Salmonella morphology on EMB agar (Eosin methylene Blue agar)
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-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 |
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Kligler Iron Agar for Salmonella detection
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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 |
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Kliger Iron Agar results for:
Salmonella Shigella E. coli Pseudomonas |
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!) |
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How does one distinguish Salmonella from E. coli and from Proteus?
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Indole negative (indole is byproduct of tryptophan hydrolysis)
Urease negative (urease splits urea into ammonea and carbon dioxide) |
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how can Salmonella be distinguished from Shigella (morphologically)
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MOTILITY AGAR
(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 |
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Hallmarks of typhoid fever
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episodic or high spiking fever
bradycardia rose spot (on abdomen) hepatosplenomegaly late GI bleed |
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what serotype of salmonella enteritidis comes from reptiles?
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Salmonella enteritidis serotype typhimurium
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Laboratory Diagnosis of Salmonella gastroenteritis
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Non-Lactose fermenting, H2S producing Gram negative rod; Urease and Indole negative which distinguish it from Proteus and E. coli, respectively
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Other bacterial causes of diarrhea (other than salmonella)
***FOR BOARDS |
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 |
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Treatment of Salmonella gastroenteritis
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-mostly self-limiting
-fluid replacement -treat patients with rpedisposing conditions (ampicillin, trimethoprim sulf, 3rd generation cepholosporin, fluoroquinolone (eg ciproflaxacin) |
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slide #58 L6 shig/salmonella summary of clinical diseases table
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incubation period
onset fever duration GI symptoms blood cultures stool culture typical organism |
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Hippocrates description of dysentery
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blood diarrhea
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general characteristics of Shigella
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-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 |
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morphology of Shigella colonies grown on macConkey Agar
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colorless colonies
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main characteristics distinguishing Shigella from Salmonella
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-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) |
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most common species of Shigella found in the US (responsible for 75% of infections)
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Shigella sonnei
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Shigella is spread by
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Food
Feces Fingers Flies |
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Incubation period of Shigella
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1-4 day incubation period
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Where does Shigella invade?
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intestinal epithelium, limited penetration
intestinal ulceration due to Shiga toxin |
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why does Shigella infection require such a low inoculum?
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the organism is acid tolerant
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Pathogenesis of Shigella infections
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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 AND Shiga toxin released, leading to GI ulceration and bloody diarrhea |
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Shiga toxin
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EXOTOXIN
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 |
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clinical syndromes of Shigella infections
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-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) |
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Stool Examination in Shigella
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NEUTROPHILS (not monocytes)
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Histology of colon in Shigellosis
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mucin in glands of intestinal lining
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Dx of Shigella
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-Clinical symptoms not diagnostic
-Isolation of microorganism from feces - Non-lactose fermenting Gram – rods - no gas with glucose fermentation - no H2S - nonmotile |
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Treatment of Shigella infections
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-fluid and electrolyte replacement (esp. in young)
-try ciprofloxacin and Trimethoprim-Sulfa if severe -consider antibiotic susceptibility testing with increasing resistance |
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Prevention of Shigella infections
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-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) |
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pathogenic Shigella species most common outside of US
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S. dysenteriae (serogroup A)
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other common and less severe Shigella serotypes (besides S. sonnei) in the US
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S. flexneri and S. Boydii
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