Λοιμώξεις γαστρεντερικού Ρούτσιας Γιάννης, MD, PhD Επικ καθηγητης Ανοσολογίας/Μικροβιολογιας
Λοιμώξεις γαστρεντερικού
Ρούτσιας Γιάννης, MD, PhD Επικ καθηγητης Ανοσολογίας/Μικροβιολογιας
FAMILY ENTEROBACTERIACEAE
Escherichia Klebsiella Enterobacter Salmonella Shigella Proteus Providencia
Citrobacter Morganella Serratia
IDENTIFICATION
MORPHOLOGY AND IDENTIFICATION
Short Gram negative rods May form chains In culture : circular, convex, smooth, with distinct
edges Growth characteristics : carbohydrate fermentation
patterns and activity of amino acid decarboxylases and enzymes are used in biochemical differentiation
IMViC REACTIONS
ACRONYM for the following tests: Indole Methyl Vogues-Proskauer Citrate
Patterns exhibited by groups of organisms
helpful in further differentiation
IMViC REACTIONS
Indole: Kovak's reagent
(+) E. coli Proteus vulgaris
(-) Klebsiella Enterobacter Proteus mirabilis
Indole:
Culture on differential media: allows rapid presumptive identification
Lactose fermented rapidly Escherichia coli : metallic sheen; motile; flat; non-
viscous colonies Enetrobacter aerogenes : raised colonies; no
metallic sheen; often motile; more viscous growth Klebsiella pneumonia : very viscous; mucoid growth;
nonmotile
Lactose fermented slowly Edwardsiella, Serratia, Citrobacter, Arizona,
Providencia, Erwinia
( cont. culture on differential media )
Lactose not fermented Shigella species: Nonmotile; no gas from dextrose Salmonella species: Motile; acid and usually gas from dextrose Proteus species: “ Swarming” on agar; urea rapidly hydrolyzed
(smell of ammonia )
MOTILITY, FLAGELLA
MOTILITY Escherichia coli Enterobacter Salmonella Proteus Providencia Morganella Serratia Citrobacter
PATHOGENIC FACTORS
ENDOTOXINS PART OF THE GRAM
NEGATIVE CELL WALL (LPS)
Release various mediators of inflammation IL-1 IFN TNF
Trigger humoral and enzymatic mechanisms intrinsic fibrinolytic kinin
WAYS OF CAUSING DISEASE: ATTACHMENT
ABILITY TO COLONIZE & ADHERE TO A RELEVANT REGION IN THE BOWEL
EXAMPLES: EPEC
(enteropathogenic E. coli): pili
ETEC (enterotoxigenic E. coli): CFA
WAYS OF CAUSING DISEASE: TOXIN PRODUCTION
ENTEROTOXIN alter metabolic
activity of intestinal epithelial cells
EXAMPLES: ETEC Shigella
dysenteriae Salmonella Aeromonas
WAYS OF CAUSING DISEASE: TOXIN PRODUCTION
CYTOTOXIN disrupt the structure
of individual epithelial cells
NEUROTOXIN
EXAMPLES: EHEC Shigella spp. Salmonella
Shigella spp.
WAYS OF CAUSING DISEASE: INVASION
AFTER ADHERENCE GAIN ACCESS TO
INTRACELLULAR ENVIRONMENT
REACH DEEPER TISSUES ACCESS
NUTRIENTS FOR GROWTH
AVOID HOST IMMUNE SYSTEM
EXAMPLES: EIEC & EHEC Shigella spp.
ENTERIC INFECTIONS: UPSETTING OF FLUID AND ELECTROLYTE BALANCE / NON-INFLAMMATORY
MAJOR SYMPTOMS watery diarrhea no fecal leukocytes no fever
EXAMPLE/S ETEC
(enterotoxigenic E. coli)
Vibrio cholerae
ENTERIC INFECTIONS: PENETRATION W/ SUBSEQUENT ACCESS TO THE BLOODSTREAM (ENTERIC FEVER)
MAJOR SYMPTOMS signs of systemic
infection headache, malaise,
sore throat fever
EXAMPLE/S Salmonella typi
ENTERIC INFECTIONS: INVASION AND POSSIBLE CYTOTOXIN PRODUCTION / INFLAMMATORY DYSENTERY
MAJOR SYMPTOMS dysenteric-like
diarrhea mucus, blood &
leukocytes fever
EXAMPLE/S EIEC
(enteroinvasive E. coli)
Salmonella enteritidis
Shigella spp.
Escherichia coli
Κροσσοι:pili ,fimbriae
Μαστίγια: flagella
Escherichia coli
Escherichia coli
Escherichia coli
HABITAT/ RESERVOIR
normal bowel flora soil, water, vegetation female genital tract
TRANSMISSION endogenous ingestion nosocomial
Escherichia coli
AVIRULENT strains part of the normal flora cause contiguous
infection opportunistic
PATHOGENIC strains EPEC
(enteropathogenic) ETEC
(enterotoxigenic) EIEC
(enteroinvasive) EHEC
(enterohemorrhagic) EAEC
(enteroaggregative)
Escherichia coli EXTRAINTESTINAL INFECTION
VIRULENCE FACTORS endotoxin capsule pili
DISEASE & INFECTION UTI bacteremia nosocomial infections most common cause
of Gram negative nosocomial infections
Escherichia coli EIEC (enteroinvasive E. coli)
VIRULENCE FACTORS cause disease similar to
shigellosis invades intestinal
mucosal epithelial cells
DISEASE & INFECTION Dysentery
(necrosis, ulceration, bowel inflammation )
in young children poor sanitation
Escherichia coli ETEC (enterotoxigenic E. coli)
VIRULENCE FACTORS Heat labile exotoxin
(LT)- stim Heat stable enterotoxin
(ST)
DISEASE & INFECTION Traveller’s &
childhood diarrhea profuse watery
stools
Escherichia coli EAEC (enteroaggregative E. coli) VIRULENCE
FACTORS probably binding by
pili Heat stable-like and
hemolysin-like toxins
actual mechanism not known
DISEASE & INFECTION Watery diarrhea
w/c may be prolonged
transmission not well understood
Escherichia coli EHEC (enterohemorrhagic E. coli)
VIRULENCE FACTORS toxin similar to
Shiga toxin (by S. dysenteriae)
associated w/ certain serotypes such as E. coli O157:H7 (from undercooked ground beef or raw milk)
DISEASE & INFECTION Hemorrhagic colitis
(inflammation & bleeding of the large bowel mucosa)
Hemolytic Uremic Syndrome (toxin mediated damage to kidneys)
Escherichia coli EPEC (enteropathogenic E. coli)
VIRULENCE FACTORS bundle forming pilus
mediate attachment
resulting in changes in cell surface (such as loss of microvilli)
DISEASE & INFECTION Diarrhea in infants
in developing or low-income nations
can cause chronic diarrhea
Salmonella spp.
Salmonella spp.
Salmonella spp.
VIRULENCE FACTORS factors that protect
organisms from stomach acids
attachment & phagocytosis
TRANSMISSION ingestion of
contaminated food products poultry, eggs
direct fecal-oral spread in children
Salmonella
DISEASES typhoid fever (enteric
fever), septicemia, gastroenteritis
asymptomatic carriage
animals as reservoir except typhoid & paratyphoid fevers
Laboratory Diagnosis - isolation - 1st week of illness:
best specimen is blood
- 3rd week of illness : best specimen is stool - epidemiologic studies and complete ID : serologic typing
Salmonella WHO IS AT RISK ?
anyone consuming foods with large numbers of Salmonella esp. children
Salmonella typhi & paratyphi
HABITAT not part of normal
flora only found in
humans at time of infection
MODE OF TRANSMISSION person-to-person
spread by fecal-oral route
ingestion of food / water contaminated w/ human excreta
Other Salmonella spp.
HABITAT disseminated in
nature & various animals
MODE OF TRANSMISSION ingestion of contaminated
food products from animals (poultry or dairy)
direct person-to-person transmission by fecal-oral route
in health care settings
Shigella Shigella dysenteriae
Shigella
Shigella sonnei
Shigella
Culture : facultative anaerobes but grow best aerobically : convex, circular, transparent colonies with intact edges Growth characteristics : all ferment glucose; unable to ferment lactose Antigenic structure : somatic O antigens which are lipopolysaccharides ( more than 40 serotypes )
Shigella
HABITAT: - limited to the
intestinal tracts of humans and other primates
MODE OF TRANSMISSION - person-to-person
spread by fecal-oral route
overcrowded areas poor sanitary condition
Shigella spp.
VIRULENCE FACTORS adherence invasion escape from
phagocytic vesicles intercellular spread shiga toxin
(interferes with protein synthesis )
DISEASE & INFECTION Dysentery
acute inflammatory colitis
bloody diarrhea tenesmus, bloody
mucoid stools S. sonnei
watery diarrhea
Shigella: Laboratory Diagnosis Specimens : fresh stool, mucus flecks, rectal
swabs for culture : serum ( 10 days apart to demonstrate rise in
antibody titer )
Culture : streaked on differential media (MacConkeys’ agar ) and selective ( Salmonella-Shigella agar ) Serology : rise in antibody titer
Shigella: Prevention and Control
Mass chemoprophylaxis Eliminate organisms by :
sanitary control of water, food and milk; sewage disposal; fly control
isolation of patients and disinfection of excreta detection of subclinical cases and carriers,
particularly food handlers
Vibrio cholerae
Vibrio cholerae
Vibrio cholerae
Vibrio cholerae
MORPHOLOGY Short (0.5 μm by 1.5 to
3.0 μm), gram-negative rods, comma-shaped
Has a single, thick,sheathed flagellum
CULTURE Produces convex,
smooth, round,opaque, granular colonies
Most vibrios grow well at 37oC on thiosulfate-citrate-bile-sucrose (TCBS) agar
* The cause of epidemic asiatic cholera
Vibrio cholerae
CULTURE Positive oxidase test
differentiates V.cholera from other vibrios
Ag STRUCTURE Has O lipopoly-
saccharides that confer serological specificity
BIOLOGIC CLASSIFICATION
Serotypes: Ogawa and Inaba
Biotypes: classical and El Tor (produces a hemolysin, (+) Voges-Proskauer, resistant to polymyxinB)
Vibrio cholerae
VIRULENCE FACTORS
Heat-labile enterotoxin consisting of 2 subunits (A & B)
Subunit A increases levels of intracellular cyclic AMP hypersecretion of water & electrolytes
TRANSMISSION OF INFECTION
Person-to person contact involving individuals with mild or early illness
Transmitted by water and food
Vibrio cholerae
LAB DIAGNOSIS Specimens for culture
consists of mucus flecks from stools
Dark-field or phase-contrast microscopy may show rapidly motile vibrios
Rapid growth in peptone agar, blood agar ,or TCBS agar
May be identified thru
slide agglutination test using anti-O antiserum
Vibrio cholerae
CONTROL MEASURES Education and improvement of sanitation Repeated injection of a vaccine confers
limited protection Chemoprophylaxis with antimicrobial drugs
may have a place in control
CAMPYLOBACTER
CAMPYLOBACTER
CAMPYLOBACTER
MORPHOLOGY : - slender, Gram negative, helically curved rods - morphologic forms : spirals, S shapes, commas,
coccoid - infected tissues: comma shaped - after isolation : filamentous or coccoid - cork-screw darting type of motility : best observed with
phase contrast or darkfield mic. - single unipolar or bipolar flagellum
CAMPYLOBACTER
ANTIGENIC STRUCTURE: - possess lipopolysaccharide and flagellar antigen - C. fetus : has a microcapsule or S layer ( anti-
phagocytic )
EPIDEMIOLOGY: - commensals of the intestinal tract of wild and domesticated animals * C. jejuni – found in poultry, dogs, cats, sheep, and cattle
CAMPYLOBACTER
MODE OF TRANSMISSION : 1.consumption of contaminated milk, water and food 2. fecal-oral route LABORATORY DIAGNOSIS : 1. Specimen : diarrheal stool 2. Smears : Gram stain shows comma shaped rods 3. Culture : require low oxygen tension and increased
carbon dioxide levels for growth
CAMPYLOBACTER
INFECTION: Large outbreaks of human infection traced to
contaminated milk, water, food C.jejuni frequently causes acute diarrheal diseases in
travelers visiting developing countries C.fetus causes frequently fatal septicemic illness in
debilitated patients, pregnant women and in the newborn
HELICOBACTER PYLORI
HELICOBACTER PYLORI
HELICOBACTER PYLORI
HELICOBACTER PYLORI
MORPHOLOGY: - In tissues, gram-negative, curved organisms - In culture, more rodlike, bizarre U-shaped and circular
cells - Has a tuft of sheathed polar flagella
HELICOBACTER PYLORI
Motile, and a strong producer of urease
VIRULENCE FACTORS: Strong association between presence of H.pylori in the
gastric antrum and duodenal ulceration Toxins and LPS may damage mucosal cells LABORATORY DIAGNOSIS: 1. Mucosal biopsies – routine stains will demonstrate
gastritis
H. pylori
LABORATORY DIAGNOSIS (CONT) 2. Mucosal biopsies - Giemsa or special silver stain
can show curved or spiraled organism 3. Culture: grows on media containing whole or lysed
blood : grows at 37oC in standard CO2 incubators :produces circular, translucent,colonies 4. Rapid tests to detect urease activity –for presumptive
identification in specimens
The end
Λοιμώξεις γαστρεντερικού