micro sheet # 21 - Amneh shdifat

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micro sheet # 21 - Amneh shdifat

Post by Shadi Jarrar on 15/11/2010, 4:26 am

بسم الله الرحمن الرحيم
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يوجد عطل مؤقت في موقع الرفع ميديا فير .. سيتم إصلاحه قريبا
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" بسم الله الرحمن الرحيم "
Don’t worry about this long sheet because more of it is repeated of the hand out
We will continue talk about Enterobacteriaceae
There are specific disease associated with E.coli & shigella and salmonella we will talk about it .
E.coli associated diarrheal diseases :
E.coli can cause specific disease in the form of diarrhea , and there are 5 types of diarrheal disease link with E.coli infection and these may be enterotoxins production or may be to invisible's of organism
1. enterotoxigenic E.coli (ETEC)
The enterotoxin production by The enterotoxigenic E.coli are two types of toxin :
1) heat labile exotoxin is similar to that of cholera in the fat that composed two sub unit A & B that are more important for labile toxin and it act by activate of adenylate cyclase which cause increase production of cAMP and this result in a net secretion of water , inhibition of water absorption ,with consequent diarrhea and the loss of fluid.
2)Heat stable toxin and colonization factor .
The enterotoxigenic E.coli is a common cause of traveler`s diarrhea , diarrhea travels from Jordan to Iraq and Syria ,you might develop diarrhea one to two days after you arrived . in addition it cause diarrhea in infants .
Note : the diarrhea caused by The enterotoxigenic E.coli is not associated with fever or vomiting , it's just diarrhea
2. Enteropathogenic E.coli (EPEC)
This organism is more invasive doesn’t produce entrotoxin :
* damage to the intestinal epithelium take place as consequence of invasions to intestinal epithelium .
* An important cause of diarrhea in infants especially in the developing countries .
* self limited watery diarrhea but can be chronic , so sometimes more than two weeks diarrhea and cause contracted…??... which cause sometimes development the chronic agent diarrhea associated with the loss of water .
* may cause outbreaks diarrhea in nurseries .
Its identical to enterotoxigenic E.coli which cause traveler's diarrhea but here the organism invasion the tissue and cause damage .
One of the most important pathogenic that are reported recently is :
3. Enterohemorrhagic E.coli (EHEC).
* produce verotoxin which has 2 antigenic types
Vero related to cell in kidney ..??.. cell ( verocell ) so these cells are killed as a consequence of toxin produce by Enterohemorrhagic E.coli.
* It has been associated with hemorrhage colitis, a severe form of diarrhea with hemolytic uremic syndrome, a disease resulting in acute renal failure, microangiopathic hemolytic anemia and thrombocytopenia.
This is a very serious disease , that develop in a consequence of infection of Enterohemorrhagic E.coli .
* the positive agent E. coli O157:H7 is the most common.
* Can be prevented by thorough cooking of ground beef.
The most item incorporate in infection is improperly or undercook beef burger and that's why many of restaurant in U.S & Japan are closed due to spread of infection . meat kitting(chick the spelling) that become contaminated and not cooked very well is associseated with the spread of infection .
Someone's called Enterohemorrhagic diarrhea burger king diarrhea .
4. Enteroeinvasive E.coli ( EIEC )
Invades the intestinal mucosal epithelial cells. *
* Disease is similar to shigellosis.
* Affects children in the developing countries and travelers to them.
5. Enteroaggregative E.coli ( EAEC )
* Causes acute and chronic diarrhea( >14 days) in the developing countries.
* Causes a food-borne illness and sometimes water in the developed countries.
* the name is developed from the Characteristic pattern of adherence to human cells , and these organism aggregate together .
* Elaborates an enterotoxin and cytotoxin.
So we have 5 category of diarrhea caused by E.coli that impossible to differentiated except in the developed of hemorrhage (in Enterohemorrhagic E.coli ) which become chronic and bleeding occurs and that`s why we can differentiate it . otherwise the diagnoses well be very difficult .
The salmonella :
Is organism that ..??.. in Enterobacteriaceae family
They are old and new classification :
Old :recognize genus and spices
* Serotyping & biochemical assays used to name individual species within genus. (e.g., Salmonella enteritidis, S. choleraesuis, S. typhi)
* Over 2400 O-serotypes (referred to as species)
((Kauffman-white antigenic schema
* Bioserotyping (e.g., S. typhimurium)
New :is more accurate and results into serotype
DNA homology show only two species
1. salmonella enteric with six subspecies and
2. S. bongori .
* Most pathogens in S. enterica subspecies. enterica
The serotype is :* Typhi ,
* paratyphi A &
* paratyphi B and
* choleraesuis
those ( 4 serotype ) are primarily human pathogens , they don’t cause infection in animals .but the remaining serotype cause infection in animals .
humane can be infected with any serotype but those 4 serotype the only cause disease .
* the vast majority of salmonellae are a chiefly animal pathogens ( poutry , pigs , rodents , cattle , pets , turtle ) .
pigs undercook is at a risk of developed salmonella and can be serious because salmonella can survive at this low temperature .
* infecting dose is variable depending on serotype .
those are primarily human pathogens infect at low dose .
those are primarily animal pathogens infect at high dose .
clinical syndromes :
it cause by salmonella and carrier ,
1. Enteritis (acute enterocolitis )
2. Enteric fever (prototype is typhoid fever which is more severe than paratyphoid fever )
3. Septicemia (particularly S. choleraesuis, S. typhi, and S. paratyphi )
4. Asymptomatic carriage can be take place in small intestine or gall bladder . ( gall bladder is the reservoir for Salmonella typhi)
These are difficult diagnoses : if we culture the stole for several days you may not recover the organism because it take place in gall bladder and antibiotic can't reach gall bladder , in this case gall bladder will be remove .
Enteritis :
* Most common form of salmonellosis with major foodborne outbreaks and sporadic disease
Sporadic disease is out plate of salmonella disease and in Jordan in recently year are many infected are recommended
* Enteritis require High dose (108 CFU)
* Poultry, eggs, etc. are sources of infection
* 6-48h incubation period so we can differentiate it from the diarrhea that caused by enterotoxin.
Ex. On food poison : In1989 the staff of Jordan university hospital are infected by salmonella which contaminate the mayonnaise.
* the ministration : Nausea , vomiting, nonbloody diarrhea, fever, cramps, myalgia and headache are common
* S. enteritidis bioserotypes (e.g., S. typhimurium)
In elderly and female the infection may spread and cause septicemia , Enterocolitis is limited to gastric infection , does not invade beound the gastric disease
Virulence attributable to:
1. Invasiveness
2. Intracellular survival & multiplication
3. Endotoxin
4. Exotoxins : Effects in host have not been identified
* Several Salmonella serotypes produce enterotoxins similar to both the heat-labile (LT) and heat-stable enterotoxins (ST), but their effect has not been identified
* A distinct cytotoxin is also produced and may be involved in invasion and cell destruction

Invasiveness in enteritis :
* Penetrate mucus, adhere to and invade into epithelial layer (enterocytes) of terminal small intestine and further into subepithelial tissue
* Bacterial cells are internalized in endocytic vacuoles (intracellular) and the organisms multiply
* PMN’s confine infection to gastrointestinal (GI) tract, but organisms may spread hematogenously (through blood, i.e., septicemia) to other body sites
* Inflammatory response mediates release of prostaglandins, stimulating cAMP and active fluid secretion with loose diarrheal stools; epithelial destruction occurs during late stage of disease .
This is the most common form of salmonella ( food poisoning ) , treatment is complyindicated ,if the salmonella developed this will delay the recover because antibiotic kills normal flora and in the absence of normal flora these salmonella will continue multiply and cause disease , normal flora established is necessary because they can completely rediscover and stop the disease .so if it no septicemia disease it just food poison treatment is not indicated ( the infection is self limited ).
Enteric Fever
Is the most important disease and in Jordan we give the vaccine in Jordan valley
S. typhi causes typhoid fever*
*S. paratyphi A, B (S. schottmuelleri) and C (S. hirschfeldii) cause milder form of enteric fever
* Infectious dose = 106 CFU
* Fecal-oral route of transmission
1. Person-to-person spread by chronic carrier
2. Fecally -contaminated food or water
* 10-14 day incubation period
* Initially signs of sepsis / bacteremia with sustained fever (delirium) for > one week before abdominal pain and gastrointestinal symptoms.
The first week of the disease after incubation period is associated with the complications in blood stream , the second week in GI tract , the third week in urinary tract .
Virulence attributable to :
Invasiveness
* Pass through intestinal epithelial cells in ileocecal region,
infect the regional lymphatic system (total lymph node are infected), invade the bloodstream , and infect other parts of the reticuloendothelial system.
* Organisms are phagocytosed by macrophages and monocytes,
but survive, multiply and are transported to the liver, spleen,
and bone marrow where they continue to replicate
* Second week: organisms reenter bloodstream and cause
prolonged bacteremia; biliary tree and other organs are
infected; gradually increasing sustained fever likely from
endotoxemia
* Second to third week: bacteria colonize gallbladder, reinfect
intestinal tract with diarrheal symptoms and possible necrosis
of the Peyer’s patches .
the disease should be treated with antibiotic and the fever is not self limited .
Septicemia
* Can be caused by all species, but more commonly associated with S. choleraesuis, S. paratyphi, S. typhi, and S. dublin.
* Old, young and immunocompromised (e.g., AIDS patients) at increased risk of develop septicemia because of the lake of protective mechanisms .
All organism tend to cause bacteremia , but bacteremia does not developed into continuous septicemia because of host defense mechanisms, if these defense mechanisms are bleached ( like in AIDS patient ) then the organism is established in the blood stream and cause septicemia .
Asymptomatic Carriage
* Chronic carriage in 1-5% of cases following S. typhi or S. paratyphi infection .those are require antibiotic treatment
* Gall bladder usually the reservoir.
* Chronic carriage with other Salmonella spp. occurs in <<1% of cases and does not play a role in human disease transmission.
May contaminate food in case of poor hygiene and specially in cold food .( this is exception )
Treatment, Prevention and Control
$ Enteritis:
*Antibiotics not recommended for enteritis because they prolong duration of illness
Control by proper preparation of poultry & eggs
$ Enteric fever:
*Antibiotics to avoid carrier state.
Identify & treat carriers of S. typhi & S. paratyphi.
Identified these carrier is very difficult , in the past they culture to chick the presence of these organism (S. typhi & S. paratyphi) but even if the result is –ve this is does not mean that`s carrier and so this is not very sensitive and that’s why not more recommended .
* Vaccination (as available) can reduce risk of disease for travellers in endemic areas .
Protection is not permanent it realize on production of IgA in GI tract.
The Shigellae: Epidemiology and Clinical Syndromes
* Four species: S. sonnei, S. flexneri, S. boydii, and S. dysenteriae which is the most serious .( S : mean shigella )
* Low infectious dose (102-104 CFU) which is small,
so it`s more virulence because less infection dose is required .
Humans are the only reservoir *
* Transmission by fecal-oral route
* Incubation period = 1-3 days (overlaps of salmonella )
*Increase Watery diarrhea with fever; changing to dysentery
(start with watery diarrhea then dysentery with bloody and severe pain (Abdominal pain and pain of defecation))
The bacterial pathogenic of shigella district( I'm not sure about this word ) the mesentery and cause the ameba (the parasite ameba which we called it amebic )
* Major cause of bacillary dysentery (severe 2nd stage) in pediatric age group (1-10 yrs) via fecal-oral route
* Outbreaks in daycare centers, nurseries, institutions
* Leading cause of infant diarrhea and mortality (death) in developing countries.
Pathogenesis of Shigellosis
Two-stage disease:
$ Early stage:
* Watery diarrhea attributed to the enterotoxic activity of Shiga toxin following ingestion and noninvasive colonization, multiplication, and production of enterotoxin in the small intestine Fever attributed to neurotoxic activity of toxin.
$ Second stage:
* Adherence to and tissue invasion of large intestine with typical symptoms of dysentery(which is the characteristic sign of associate disease ) .
* Cytotoxic activity of Shiga toxin increases severity.
Pathogenesis and Virulence Factors
Virulence attributable to:
1. Invasiveness
* Attachment (adherence) and internalization with complex genetic control
* Large multi-gene virulence plasmid regulated by multiple chromosomal genes (is produce in shigella which enable it to invade ).
2. Exotoxin (Shiga toxin)
3. Intracellular survival & multiplication
Invasiveness in Shigella -Associated Dysentery
* Penetrate through mucosal surface of colon (colonic mucosa) and invade and multiply in the colonic epithelium but do not typically invade beyond the epithelium into the lamina propria (thin layer of fibrous connective tissue immediately beneath the surface epithelium of mucous membranes).
* Preferentially attach to and invade into M cells which is special type of lymph cell which present in Peyer’s patches and it`s important in mucosal immunity (lymphoid tissue, i.e., lymphatic system) of small intestine.
Characteristics of Shiga Toxin
* Enterotoxic, neurotoxic and cytotoxic
* Encoded by chromosomal genes
*Two domain (A-5B) structure
* Similar to the Shiga-like toxin of enterohemorrhagic E. coli (EHEC)
NOTE: except that Shiga-like toxin is encoded by lysogenic bacteriophage.
Shiga Toxin Effects in Shigellosis
$ Enterotoxic Effect:
1. Adheres to small intestine receptors
2. Blocks absorption (uptake) of electrolytes, glucose, and amino acids from the intestinal lumen ( which result in accumulation of sugar and electrolytes in small intestine which cause diarrhea) .
$ Cytotoxic Effect:
*associate with B subunit of Shiga toxin binds host cell glycolipid
* A domain is internalized via receptor-mediated endocytosis (coated pits)
* Causes irreversible inactivation of the 60S ribosomal subunit, thereby causing:
1. Inhibition of protein synthesis
2. Cell death
3. Microvasculature damage to the intestine
4. Hemorrhage (blood & fecal leukocytes in stool)
The presence of WBC`s in stool is the important marker in differentiation between toxiogenic and bacterial diarrhea so if WBC`s is present that`s mean the bacteria is cause the diarrhea and if the result is negative so the toxiogenic is cause diarrhea .
$ Neurotoxic Effect:
Fever, abdominal cramping are considered signs of neurotoxicity .
THE END
I'm so sorry about any mistake .
The correction are more than welcome .
الرياح القوية تهشم الزجاج لكنها تصقل الحديد
Lec.#21
Lec.#3 in week # 7
Tuesday. 2 /11 /2010
Done by : Amnah shdifat



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Shadi Jarrar
مشرف عام

عدد المساهمات : 997
النشاط : 12
تاريخ التسجيل : 2009-08-28
العمر : 26
الموقع : Amman-Jordan

http://jude.my-rpg.com

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