Gastrointestinal Tract Infection
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GASTROINTESTINAL TRACT INFECTIONSY. MIFTAHUL EL JANNAH
Flora normalEnterobacteriaceae, kecuali Salmonella, Shigella, Yersinia, Vibrio dan CampylobacterNon dextrose fermenting Gram negative rodsEnterococciAlpha hemolytic dan non hemolytic StreptococciDiphtheroidsSedikit S. aureusSedikit YeastBanyak anaerob
Saat lahir usus steril, mo masuk bersama makanan, tdd Streptococcus asam laktat dan Lactobacillus . For an infection to occur, the pathogen must be ingested in sufficient numbers or possess attributes to elude the host defenses of the upper gastrointestinal tract and reach the intestinePerkembangan pola makan merubah flora normal ususAsam lambung menjaga jumlah mo seminimal mungkin [103-105/g isi lambung] Seiring pH usus menjadi basa flora normal meningkat. Duodenum orang dewasa 108-1010 bakteri/g isi ususJejunum dan ileum 105-108 bakteri/g Caecum dan kolon transversum 103-105 bakteri/g Kolon sigmoid dan rektum 1011 bakteri/g
Every day we swallow large numbers of microorganisms. Because of the body's defense mechanisms, however, they rarely succeed in surviving the passage to the intestine in sufficient numbers to cause infection.
PeranSintesis vitamin KKonversi pigmen pigmen empedu dan asam asam empeduPenyerapan zat-zat makanan dan hasil pemecahannyaPerlawanan terhadap mo patogen
Figure 22.1 As well as many colloquial expressions, several different clinical terms are used to describe infections of the gastrointestinal tract. Diarrhea without blood and pus is usually the result of enterotoxin production, whereas the presence of blood and/or pus cells in the feces indicates an invasive infection with mucosal destruction.
A wide range of microbial pathogens is capable of infecting the gastrointestinal tract, and the important bacterial and viral pathogens They are acquired by the fecal-oral route, from fecally contaminated food, fluids or fingers Many different pathogens cause infections of the gastrointestinal tract. Some are found in both humans and animals while others are strictly human parasites.
Infections of the gastrointestinal tract can be grouped into those that remain localized in the gut and those that invade beyond the gut to cause infection in other sites in the body. In order to spread to a new host, pathogens are excreted in large numbers in the feces and must survive in the environment for long enough to infect another person directly or indirectly through contaminated food or fluids.
The damaging effects resulting from infection of the gastrointestinal tract
Escherichia coli is a major cause of gastrointestinal infection, particularly in developing countries and in travelers. There is a range of pathogenic mechanisms within the species, resulting in more or less invasive disease. *Specialized tests are given in italics. (LT, heat-labile enterotoxin; ST, heat-stable enterotoxin.)
Bacterial causes of diarrhea Escherichia coli This is one of the most versatile of all bacterial pathogens. Some strains are important members of the normal gut flora in man and animals, whereas others possess virulence factors that enable them to cause infections in the intestinal tract or at other sites, particularly the urinary tract Strains that cause diarrheal disease do so by several distinct pathogenic mechanisms and differ in their epidemiology
There are six distinct groups of E. coli with different pathogenetic mechanisms Initially all diarrhea-associated Escherichia coli were termed enteropathogenic E. coli (EPEC). Enteropathogenic E. coli (EPEC), enterotoxigenic E. coli (ETEC), enterohemorrhagic E. coli (EHEC) more important in developed enteroinvasive E. coli (EIEC), enteroaggregative E. coli (EAEC), and diffuse-aggregative E. coli (DAEC).
The diarrhea produced by E. coli varies from mild to severe, depending upon the strain and the underlying health of the host. EIEC and EHEC strains both cause bloody diarrhea
EPEC and ETEC are the most important contributors to global incidence of diarrhea
Enteropathogenic E. coli (EPEC) Do not appear to make any toxins. They do produce bundle-forming pili (Bfp), intimin (an adhesin) and an associated protein (translocated intimin receptor, Tir). These virulence factors allow bacterial attachment to epithelial cells of the small intestine, leading to disruption of the microvillus (an 'attaching-effacing' mechanism of action) leading to diarrhea.
Electron micrograph of enteropathogenic Escherichia coli adhering to the brush border of intestinal mucosal cells with localized destruction of microvilli. (Courtesy of S Knutton.)
The clinical features of bacterial diarrhea infection. It is difficult, if not impossible, to determine the likely cause of a diarrheal illness on the basis of clinical features alone, and laboratory investigations are essential to identify the pathogen.
Enterotoxigenic E. coli (ETEC) possess colonization factors (fimbrial adhesins. ETEC diarrhea in children in developing countries may be clinically indistinguishable from cholera
These bind the bacteria to specific receptors on the cell membrane of the small intestine. These organisms produce powerful plasmid-associated enterotoxins which are characterized as being either heat labile (LT) or heat stable (ST): Heat-labile enterotoxin LT-I is very similar in structure and mode of action to cholera toxin produced by V. cholerae, and infections with strains producing LT-I can mimic cholera, particularly in young and malnourished children.Heat-stable enterotoxins (STs) in addition to or instead of LT. STs have a similar but distinct mode of action to that of LT. STA activates guanylate cyclase activity, causing an increase in cyclic guanosine monophosphate, which results in increased fluid secretion. Immunoassays are commercially available for the identification of ETEC.
Electron micrograph of enterotoxin Escherichia coli, showing pili necessary for adherence to mucosal epithelial cells. (Courtesy of S Knutton.)
Enterohemorrhagic E. coli (EHEC)Isolates produce a verotoxin The verotoxin (i.e. toxic to tissue cultures of 'vero'cells) is essentially identical to Shiga (Shigella) toxin. After attachment to the mucosa of the large intestine (by the 'attaching-effacing' mechanism also seen in EPEC) the produced toxin has a direct effect on intestinal epithelium, resulting in diarrheaEHEC cause hemorrhagic colitis (HC) and hemolytic-uremic syndrome (HUS). In HC there is destruction of the mucosa and consequent hemorrhage; this may be followed by HUS. Verotoxin receptors have been identified on renal epithelium and may account for the kidney involvement. While there are many serotypes of EHEC, the most common one in the USA is O157:H7.HUS is characterized by acute renal failure, anemia and thrombocytopenia, and there may be neurologic complications HUS is the most common cause of acute renal failure in children in the UK and USA.
Verotoxin-producing Escherichia coli infection, showing fibrin 'thrombi' in glomerular capillaries in hemolytic-uremic syndrome. (Weigert stain.) (Courtesy of HR Powell.)
Enteroinvasive E. coli (EIEC) Attach specifically to the mucosa of the large intestine Utilizing plasmid-associated genes, they invade the cells by endocytosis. Inside the cell they lyse the endocytic vacuole, multiply and spread to adjacent cells, causing tissue destruction, inflammation, necrosis and ulceration, resulting in blood and mucus in stools
Enteroaggregative E. coli (EAEC) Derive their name from their characteristic attachment pattern to tissue culture cells .The pattern is an aggregative or 'stacked brick' formation. These organisms act in the small intestine to cause persistent diarrhea especially in children in developing countries. Their aggregative adherence ability is due to plasmid-associated fimbriae. EAEC also produce heat-labile toxins (an enterotoxin and a toxin related to E. coli hemolysin) but their role in diarrheal disease is uncertain.
Diffuse-aggregative E. coli (DAEC) Produce an alpha hemolysin and cytotoxic necrotizing factor 1 They are also known as diffuse-adherent or cell-detaching E. coli. Their role in diarrheal disease, especially in young children, is incompletely understood and somewhat controversial, with some studies reporting no association.
Specific tests are needed to identify strains of pathogenic E. coli :Because E. coli is a member of the normal gastrointestinal flora, specific tests are required to identify strains that may be responsible for diarrheal disease. Infections are more common in children and are also often travel-associated, and these factors should be considered when samples are received in the laboratory. It is important to note that specialized tests beyond routine stool cultures are required to identify specific diarrhea-associated E. coli types. Such tests are not ordinarily performed with uncomplicated diarrhea, which is usually self-limiting. Antibacterial therapy is not indicated for E. coli diarrheaFluid replacement may be necessary, especially in young children. Treatment of HUS is urgent and may involve dialysis. Provision of a clean water supply and adequate systems for sewage disposal are fundamental to the prevention of diarrheal disease. Food and unpasteurized milk can be important vehicles of infection, especially for EIEC and EHEC, but there is no evidence of an animal or environmental reservoir.
SalmonellaSalmonellae common cause of food-associated diarrhea in many developed countries, in some countries (e.g. the USA and UK) they have been relegated to second place by Campylobacter. The