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E. coli O157:H7 Infection

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E. coli O157:H7 Infection

E. coli O157:H7 typically causes acute bloody diarrhea, which may lead to hemolytic-uremic syndrome. Symptoms are abdominal cramps and diarrhea that may be grossly bloody. Fever is not prominent. Diagnosis is by stool culture and toxin assay. Treatment is supportive; antibiotic use is controversial.

Epidemiology

Although > 100 serotypes of E. coli produce Shiga and Shiga-like toxins, E. coli O157:H7 is the most common in North America. In some parts of the US and Canada, E. coli O157:H7 infection may be a more common cause of bloody diarrhea than shigellosis or salmonellosis. E. coli O157:H7 infection can occur in people of all ages, although severe infection is most common in children and the elderly.

E. coli O157:H7 has a bovine reservoir, so outbreaks and sporadic cases occur after ingestion of undercooked beef (especially ground beef) or unpasteurized milk. Food or water contaminated with cow manure or raw ground beef can also transmit infection. The organism can also be transmitted by the fecal-oral route, especially among infants in diapers (eg, via inadequately chlorinated children's wading pools).

After ingestion, E. coli O157:H7 and similar strains of E. coli (termed enterohemorrhagic E. coli) produce high levels of various toxins in the large intestine; these toxins are closely related to the potent cytotoxins produced by Shigella dysenteriae type 1. These toxins appear to directly damage mucosal cells and vascular endothelial cells in the gut wall. If absorbed, they exert toxic effects on other vascular endothelia (eg, renal).

Symptoms and Signs

E. coli O157:H7 infection typically begins acutely with severe abdominal cramps and watery diarrhea that may become grossly bloody within 24 h. Some patients report diarrhea as being “all blood and no stool,” which has given rise to the term hemorrhagic colitis. Fever, usually absent or low grade, occasionally reaches 39° C. Diarrhea may last 1 to 8 days in uncomplicated infections.

About 5% of cases (mostly children < 5 yr and adults > 60 yr) are complicated by hemolytic-uremic syndrome (see Thrombocytopenia and Platelet Dysfunction: Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic-Uremic Syndrome (HUS)), which typically develops in the 2nd wk of illness. Death may occur, especially in the elderly, with or without this complication.

Diagnosis


Stool cultures
Sometimes rapid stool assay for Shiga toxin

E. coli O157:H7 infection should be distinguished from other infectious diarrheas by isolating the organism from stool cultures. Often, the clinician must specifically ask the laboratory to test for the organism. Because bloody diarrhea and severe abdominal pain without fever suggest various noninfectious etiologies, E. coli O157:H7 infection should be considered in suspected cases of ischemic colitis, intussusception, and inflammatory bowel disease. A rapid stool assay for Shiga toxin may help. Patients at risk of noninfectious diarrheas may need sigmoidoscopy. If done, sigmoidoscopy may reveal erythema and edema; barium enema typically shows evidence of edema with thumbprinting.

Treatment


Supportive care

The mainstay of treatment is supportive. Although E. coli is sensitive to most commonly used antibiotics, antibiotics have not been shown to alleviate symptoms, reduce carriage of the organism, or prevent hemolytic-uremic syndrome. Fluoroquinolones are suspected of increasing release of enterotoxins.

In the week after infection, patients at high risk of developing hemolytic-uremic syndrome (eg, children < 5 yr, the elderly) should be observed for early signs, such as proteinuria, hematuria, red cell casts, and rising serum creatinine. Edema and hypertension develop later. Patients who develop complications are likely to require intensive care, including dialysis and other specific therapies, at a tertiary medical center.

Prevention

Correct disposal of the stool of infected people, good hygiene, and careful hand washing with soap limit spread of infection. Preventive measures that may be effective in the day care setting include grouping children known to be infected with E. coli O157:H7 or requiring 2 negative stool cultures before allowing infected children to attend. Pasteurization of milk and thorough cooking of beef prevent food-borne transmission.

Reporting outbreaks of bloody diarrhea to public health authorities is important because intervention can prevent additional infections.

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Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic-Uremic Syndrome (HUS)
 
 
 
 
Thrombotic thrombocytopenic purpura and hemolytic-uremic syndrome are acute, fulminant disorders characterized by thrombocytopenia and microangiopathic hemolytic anemia. Other manifestations may include alterations in level of consciousness and renal failure. Diagnosis requires demonstrating characteristic laboratory test abnormalities, including Coombs'-negative hemolytic anemia. Treatment is plasma exchange and corticosteroids in adults and supportive care (sometimes including hemodialysis) in children.

Pathophysiology

Thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome (HUS) involve nonimmunologic platelet destruction. Loose strands of von Willebrand's factor (VWF) or fibrin are deposited in multiple small vessels, which damage passing platelets and RBCs causing significant thrombocytopenia and anemia. Platelets are also destroyed within multiple small thrombi. Multiple organs develop bland platelet-VWF thrombi (without the vessel wall granulocytic infiltration characteristic of vasculitis) localized primarily to arteriocapillary junctions, described as thrombotic microangiopathy. The brain, heart, and kidneys are particularly likely to be affected.

TTP and HUS differ mainly in the relative degree of renal failure. Typically, disorders in adults are described as TTP and are less likely to involve renal failure. HUS is used to describe the disorder in children, which typically involves renal failure.

Etiology

Children

Most cases follow acute hemorrhagic colitis resulting from Shiga toxin–producing bacteria (eg, Escherichia coli O157:H7, some strains of Shigella dysenteriae).

Adults

Many cases are idiopathic. Known causes and associations include

Drugs: Quinine (most common), immunosuppressants, and cancer chemotherapy drugs (eg, cyclosporine, mitomycin C)
Pregnancy (often indistinguishable from severe preeclampsia or eclampsia)
Rarely, hemorrhagic colitis from Escherichia coli O157:H7

A predisposing factor in many patients is congenital or acquired deficiency of the plasma enzyme ADAMTS13, which cleaves VWF and thus eliminates abnormally large VWF multimers that can cause platelet thrombi;

Symptoms and Signs

Manifestations of ischemia develop with varying severity in multiple organs. These manifestations include weakness, confusion and coma, abdominal pain, nausea, vomiting, diarrhea, and arrhythmias caused by myocardial damage. Children usually have a prodrome of vomiting, abdominal pain, and diarrhea (frequently bloody). Fever may occur, but high fever with chills does not occur in TTP or HUS and suggests sepsis. The clinical syndromes of TTP and HUS are indistinguishable, except that neurologic symptoms are less common with HUS.

Diagnosis


CBC with platelets, peripheral blood smear, Coombs' test
Exclusion of other thrombocytopenic disorders

TTP-HUS is suspected in patients with suggestive symptoms, thrombocytopenia, and anemia. If the disorder is suspected, urinalysis, peripheral blood smear, reticulocyte count, serum LDH, renal function tests, serum bilirubin (direct and indirect), and Coombs' test are done. The diagnosis is suggested by:

Thrombocytopenia and anemia
Fragmented RBCs on the blood smear (helmet cells, triangular-shaped RBCs, distorted-appearing RBCs—these changes describe microangiopathic hemolysis)
Evidence of hemolysis (falling Hb level, polychromasia, elevated reticulocyte count, elevated serum LDH)
Negative direct antiglobulin (Coombs') test

Otherwise unexplained thrombocytopenia and microangiopathic hemolytic anemia are sufficient evidence for a presumptive diagnosis.

Causes

Although causes (eg, quinine sensitivity) or associations (eg, pregnancy) are clear in some patients, in most patients TTP-HUS appears suddenly and spontaneously without apparent cause. TTP-HUS is often indistinguishable, even with renal biopsy, from syndromes that cause identical thrombotic microangiopathies (eg, preeclampsia, systemic sclerosis, accelerated hypertension, acute renal allograft rejection).

Testing for ADAMTS13 activity is appropriate in patients with suspected TTP-HUS, except in children who have typical diarrhea-associated HUS. Although the results of ADAMTS13 testing do not affect initial treatment, results are important prognostically.

Stool testing (specific culture for E. coli O157:H7 or Shiga toxin assay) is done in children with diarrhea and also adults who had a prodrome of bloody diarrhea; however, the organism and toxin may have cleared by the time of presentation.

Treatment


Plasma exchange and corticosteroids in adults

Typical diarrhea-associated HUS in children caused by enterohemorrhagic infection usually spontaneously remits and is treated with supportive care and not plasma exchange; over half require renal dialysis. In other cases, untreated TTP-HUS is almost always fatal. With plasma exchange, however, > 85% of patients recover completely.

Plasma exchange is continued daily until evidence of disease activity has subsided, as indicated by a normal platelet count, which may be several days to many weeks. Adults with TTP are also given corticosteroids. In patients with recurrence when plasma exchange is stopped or in patients with relapses, more intensive immunosuppression with rituximab may be effective. Most patients experience only a single episode of TTP-HUS. However, relapses occur in about 40% of patients who have a severe deficiency of ADAMTS13 activity caused by an autoantibody inhibitor. Patients must be evaluated quickly if symptoms suggestive of a relapse develop.

 

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Γερμανία: Ανησυχία για θανατηφόρο βακτηρίδιο


Οι υγειονομικές αρχές της Γερμανίας εκφράζουν την Τρίτη ανησυχία για την ταχεία μετάδοση ενός βακτηριδίου που προκαλεί αιμορραγίες στο πεπτικό σύστημα και που έχει προκαλέσει όπως φαίνεται ήδη ένα θάνατο.

"Μια 83χρονη γυναίκα πέθανε στις 21 Μαΐου, μετά την εισαγωγή της στις 15 Μαΐου στο νοσοκομείο για αιμορραγικές κολίτιδες. Εξετάσεις σε εργαστήρια απέδειξαν τη μόλυνσή της" από εντεροαιμορραγικό E.coli (Eceh), βακτηρίδιο που ευθύνεται για σοβαρά προβλήματα υγείας, αναφέρει το υπουργείο Υγείας της Κάτω Σαξονίας σε ανακοίνωσή του.

Ωστόσο διεξάγεται έρευνα για να διαπιστωθεί με βεβαιότητα η αιτία θανάτου της 83χρονης, προσθέτει το υπουργείο.

Τις τελευταίες δύο εβδομάδες, εκατοντάδες επιβεβαιωμένα ή ύποπτα κρούσματα μόλυνσης από το βακτηρίδιο αυτό έχουν καταγραφεί στη Γερμανία, σύμφωνα με το Ινστιτούτο Ρόμπερτ-Κοχ (RKI), το ομοσπονδιακό θεσμό που είναι επιφορτισμένος με τον έλεγχο και την καταπολέμηση των ασθενειών.

Στα εκατοντάδες αυτά κρούσματα, περισσότεροι από 80 ασθενείς παρουσίασαν σοβαρά προβλήματα υγείας, τα οποία είναι γνωστά με την ονομασία Ουραιμικό Αιμολυτικό Σύνδρομο (ΟΑΣ).

"Και στο παρελθόν υπήρξαν φορές που υπήρχε έξαρση των κρουσμάτων ΟΑΣ, όμως ποτέ τόσα σε τόσο μικρό χρονικό διάστημα", αναφέρει το RKI σε σημερινή ανακοίνωσή του.

Το RKI εκφράζει επίσης ανησυχία όσον αφορά το γεγονός ότι οι ασθενείς είναι κυρίως ενήλικες, ενώ η ασθένεια αυτή πλήττει εν γένει κυρίως παιδιά σε μικρή ηλικία.

Το 2010 στα 65 κρούσματα ΟΑΣ που είχαν καταγραφεί από το ινστιτούτο RKI, ποσοστό χαμηλότερο από το 9% των ασθενών ήταν ενήλικες και δύο κρούσματα ήταν θανατηφόρα.

Δεν παρουσιάζουν το σύνδρομο αυτό όλοι όσοι έχουν προσβληθεί από το βακτηρίδιο Eceh, επισημαίνει το RKI, καθώς σύμφωνα με τα στατιστικά στοιχεία που έχει στη διάθεσή του περίπου χίλιοι άνθρωποι προσβάλλονται κάθε χρόνο στη Γερμανία από το βακτηρίδιο αυτό και συνήθως δεν παρουσιάζουν σοβαρές επιπλοκές.

Η μετάδοση του βακτηριδίου αυτού στον άνθρωπο γίνεται με την κατανάλωση μολυσμένων τροφίμων, όπως για παράδειγμα ωμού ή όχι καλά ψημένου κιμά κρέατος ή μη παστεριωμένου γάλακτος.

Ωστόσο μέχρι στιγμής δεν έχει καταστεί δυνατό να εντοπιστεί η πηγή της πρόσφατης μόλυνσης στη Γερμανία και ως εκ τούτου "δεν μπορεί να αποκλειστεί ότι εξακολουθεί να υπάρχει", καταλήγει το RKI.


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Δ. Κουναλάκης:
Δεν είναι ορατοί οι σύνδεσμοι (links). Εγγραφή ή ΕίσοδοςΓερμανία: Ανησυχία για θανατηφόρο βακτηρίδιο


Οι υγειονομικές αρχές της Γερμανίας εκφράζουν την Τρίτη ανησυχία για την ταχεία μετάδοση ενός βακτηριδίου που προκαλεί αιμορραγίες στο πεπτικό σύστημα και που έχει προκαλέσει όπως φαίνεται ήδη ένα θάνατο

.......

Πηγή:www.capital.gr

--- Τέλος παράθεσης ---

Αν το θυμάμαι καλά αυτό το βακτήριο δεν προκαλεί το θάνατο. Οι γιατροί και φαρμακοποιοί σκοτώνουν τους ασθενείς χάρις σε αυτο το στέλεχος.
Και ο τρόπος είναι απλός: Δίνεις στον ασθενή αντιβίωση. Αν δεν κάνω λάθος, είναι το γνωστό στέλεχος που όταν "αυτοκτονείται" απελευθερώνει τοξίνες που πρακτικά προκαλούν νέκρωση του εντέρου. Αυτό δεν είναι Νεκτάριε;

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Treatment


Supportive care

The mainstay of treatment is supportive. Although E. coli is sensitive to most commonly used antibiotics, antibiotics have not been shown to alleviate symptoms, reduce carriage of the organism, or prevent hemolytic-uremic syndrome. Fluoroquinolones are suspected of increasing release of enterotoxins. (   ;)  Κουναλάκης ο γάτος )

In the week after infection, patients at high risk of developing hemolytic-uremic syndrome (eg, children < 5 yr, the elderly) should be observed for early signs, such as proteinuria, hematuria, red cell casts, and rising serum creatinine. Edema and hypertension develop later. Patients who develop complications are likely to require intensive care, including dialysis and other specific therapies, at a tertiary medical center.

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