enteric gram-negative rods ( enterobacteriaceae )
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Enteric Gram-Negative Rods ( Enterobacteriaceae ). no. white colonies pathogenic. yes. colored colonies (red) non-pathogenic. SS plate. lactose fermentation. - PowerPoint PPT PresentationTRANSCRIPT
Enteric Gram-Negative Rods Enteric Gram-Negative Rods
((EnterobacteriaceaeEnterobacteriaceae))
SS plate
colored colonies (red)colored colonies (red) non-pathogenicnon-pathogenic
yes
nowhite colonieswhite colonies
pathogenicpathogenic
lactose fermentationlactose fermentation
•Mechanism: Non-pathogenic enteric bacilli can
ferment lactose to produce acidic by-products
while pathogenic enteric bacilli such as Shigella
and Salmonella can not.
•Media: SS-plate or EMB plate , TSI agar slants
•Basic components: lactose and a pH indicator
E. coli
Enterobacter Aerogenes
IMViC test
Indole testMethyl red (MR) testVoges-Proskauer (VP) testCitrate utilization test
Live in the intestinal tract of humans and animals
anaerobes
•opportunistic infection (E. coli)
septicemia
pneumonia
meningitis
urinary tract infections
•human pathogens (Salmonella and Shigella)
•community-acquired diseases
respiratory infections (Klebsiella pneumoniae)
urinary tract infection (E. coli and Proteus)
E. coli causes urinary tract infections such as acute cystitis and pyelonephritis
pili
capsule
enterotoxin: cause diarrhea and tissue
damage
endotoxin
H Ag (flagella)
somatic O Ag (lipopolysacchari
de)
K/Vi Ag (capsule)
Escherichia coli
Gram stain?
Motility?
lactose fermentation?
Antigens?
IMViC?
Transmission route?
virulence factors?
EnteroEnteroppathogenic athogenic E. coli E. coli ((EPECEPEC))
EnteroEnterottoxigenic oxigenic E. coli E. coli ((ETECETEC))
EnteroEnteroiinvasive nvasive E. coli E. coli ((EIECEIEC))
EnteroEnterohhemorrhagic emorrhagic E. coli E. coli ((EHECEHEC))
EnteroEnteroaggaggregative regative E.coli E.coli
((EAggECEAggEC))
Enteropathogenic E. coli (EPEC)
•Commonly associated with infant diarrhea.
•Characteristic lesion with destruction of
microvilli without invasion
•Clinical signs
Fever
diarrhea with non-bloody stools
Vomiting
nausea
Enterotoxigenic E. coli (ETEC)
•Cause "traveller’s diarrhea".
•Two types of plasmid-encoded toxins are produced:Heat labile toxins (LT), an adenyl cyclase which catalyze ATP to cAMP.
Heat stable toxins (ST), a guanyl cyclase to catalyze GTP to cGMP. cAMP/cGMP
are the intracellular second messagers. The former increases the secretion of
water and ions, and the latter inhibits ionic uptake.
•Clinical signs
watery diarrhea
Fever
nausea
Enteroinvasive E. coli (EIEC)
• Associated with elder children and adult diarrhea.
• Without flagella
• High virulence: a small number of EIEC can cause serious
illness
• Clinical signs
Acute inflammatory responses
tissue destruction
diarrhea with little fluid, a lot of blood and mucus
containing polymorphonuclear cells
•EHEC produces bacteriophage-mediated exotoxin. This toxin
is called as Vero toxin (VT) because of its cytotoxicity to
cultured Vero cells.
•In children, the disease may be progressed to a systemic
stage called as hemolytic uremic syndrome (kidney injury)
with 10% death rate.
•Clinical signs
serious abdominal pain
diarrhea which is initially watery but then becomes
bloody
Enterohemorrhagic E. coli (EHEC)
It produces enteroaggregative heat-stable toxin
(EAST) similar to the heat stable toxins of ETEC.
It produces mucous associated autoagglutinin which
causes aggregation of the bacteria and formation of
biofilm.
Clinical Signs
persistent, mucus-watery diarrhea
vomiting and dehydration in infants
Enteroaggregative E. coli (EAggEC)
ShigellaShigella
Gram stain?
motility?
Lactose fermentation?
ClassificationClassification
According to the difference of O antigen,
Shigella strains are divided into 4 groups:
S. dysenteriaeS. dysenteriae
S. flexneriS. flexneri
S. boydiiS. boydii
S. sonneiS. sonnei
Clinical findingsClinical findings Most common cause of bacterial dysentery in human
characteristic blood and mucus stools
Due to specific S-IgA, only invades intestinal mucosa and never enters bloodstream. But the endotoxin can be absorbed into bloodstream to cause endotoxemia.
Can cause toxic dysentery in children, display systemic toxic symptoms but no enteric symptoms. Has a a high death rate.
Virulent factorsVirulent factors pilus pilus
endotoxinendotoxin
exotoxin:exotoxin: Shigella dysenteriae can produce an
exotoxin called as shiga-toxin which is simmilar to
Vero toxin (VT) of EHEC. Shiga-toxin is enterotoxic,
cytotoxic and neurotoxic. So the dysentery ( 痢疾 )
caused by this microbe is more serious than that by the
other three groups.
Control transmission
Dysentery is treated with antibiotics. But multiple drug resistance mediated by plasmids are common in many Shigella strains.
SalmonellaSalmonella
Gram stain?
Motility?
Lactose fermentation?
antigenic structures?
More than 2000 serotypes based on antigenic difference
Infect human (enteric fever)S. typhi
S. paratyphi A
S. schottmuelleri (S. paratyphi B)
S. hirschfeldii
Infect animal and human
S. choleraesuis
S. typhimurium
S. enteritidis
Virulent factorsVirulent factors
Vi antigen: Vi antigen: consisted of capsular
polysacchride. It resists phagocytosis and plays
an important role during invasion of Salmonella.
endotoxinendotoxin
enterotoxinenterotoxin
DiseasesDiseases
enteric fever (typhoid fever)
S. typhi S. paratyphi AS. schottmuelleri (S. paratyphi B)S. hirschfeldii
• Enteric fever (typhoid fever) is the most serious form of salmonella infection which only occurs in human.
• Carrier state is common
•In untreated patients, the death rate is 7% to 14%.
•Antibiotic therapy is essential, vaccines are not effective and not widely used.
1. The microbe initially invades intestinal mucosal
epithelium and propagate at the local.
2. The microbe penetrates into the bloodstream to cause
the first round of bacteremia with symptoms of fever,
general discomfort and pain.
3. The microbe enters many organs such as liver, spleen,
kidney, gall and marrow for further propagation.
4. The microbe penetrates into the bloodstream again to
cause the second round of bacteremia with serious
symptoms of high fever, swell of spleen and liver, rose-
colored spots in skin, and tissue injury.
enteric fever developmententeric fever development
enteric fever Diagnosis
1. Definitive diagnosis-bacteria culture
Blood @ first week
Stool and urine @ from the second week on
Marrow can be considered because of its high and permanent positive results.
enteric fever diagnosis2. Widal testa quantitative agglutination test using the known O antigen of S.typhi , and H antigens of S. typhi and S. paratyphi A/B to detect specific serum antibodies.
• For one single serum sample, The titers of anti-O antigen IgM 1:80 and/or anti-H antigen IgG 1:160.
• For two serum samples that collected with an interval of 5~7 days, 4-fold increase in titers of specific antibody.
DiseasesDiseasesGastroenteritis (food-poisoning)
S. choleraesuisS. typhimuriumS. enteritidis
• Gastroenteritis (food poisoning):
It is the most common Salmonella infection and usually transmitted from contaminated food. However, only a few of food poisoning-causing salmonella serotypes can produce enterotoxin.
DiseasesDiseases
Septicemia: commonly caused by
– S. hirschfeldii – S. typhimurium– S. choleraesuis
•Septicemia:
Many Salmonella serotypes can cause septicemia. This disease is commonly found in children or adult with low immunity.
Vibrio cholerae CholeraCholera
IntroductionCholera caused by Vibrio cholerae is characterized by profuse watery diarrhea and serious vomiting which results in extreme loss of fluid and electrolytes, shock and kidney prostration. If patients are untreated, the death rate is as high as 60%.
Cholera: outbreak in India
IntroductionThere have been 8 great outbreaks in the world.
In 1991, a great outbreak (7th) started in Peru. There were more than a million patients in Central and South America. In 1992, another great outbreak (8th) started in India and then spread to all parts of Asia. Not serotype O1 but O139 caused this outbreak.
ClassificationClassification
O-antigen O-antigen
O1
non-O1/139
O139
classical biotype
El Tor biotype
Further typingFurther typing
Responsible for the 1st-6th great outbreaks
Responsible for the 7th great outbreak
Responsible for the 8th great outbreak in 1992
Cause cholera-like disease
high pH (pH8.5-9.0)
TCBS (thiosulfate-citrate-bile-sucrose) agar plate
Major virulent factors
Flagellum: offers an ability to penetrate enteric
mucus layer to reach the surface of host cells.
Pilus: adhesion
Cholera toxin: the most important virulent factor
which induce electrolyte and water
hypersecretion. This toxin is chromosomally
encoded and its molecule contains subunits A and
B.
Pathogenesis of cholera toxin
◇ Subunit B binds to its receptor (gangliosides) on the surface of epithelial cells and provides a channel allowing subunit A to enter host cell.
◇ Cellular proteinase lyses subunit A into peptides A1 and A2
Peptide A1 has activity of ADP-ribosylation to transfer ADP from NAD onto protein G which activates protein G
↓
Activated protein G induces cAMP overproduction
↓
A large number of cAMP induces electrolyte and water hypersecretion of cells
Dehydration!! ( 脱
水 )
the major cause of death…
Replace fluid and electrolyte !!!-most important treatment
Antibiotics such as tetracycline additionally used
Vibrio parahemolyticusexists in raw sea-food and causes food poisoning in human It is halophilic and optimal NaCl concentration in media is 3.5% It produces hemolysin Can be rapidly killed by acid (eg. acetic acid)