Entero-aggregative E.coli (EaggEC).
Mathew and Coworkers described afifty reputed group of Enterovirulent E.coli associated with traveler’s diarrhea in Mexico. This new group was associated to more than 40% of HEP-2 cells in tissue culture assays (Janda and Abbott 1998).
Cravioto et al. (1979) observed that EPEC adhere to HEP-2 cells. However, these investigators also showed that many E.coli strains adhere to HEP-2 cells as well and, moreover, that the adherence pattern of EPEC was described as localized adherence (LA), denoting the presence of clusters or microcolonies on the surface of HEP-2 cells. In contrast, non-EPEC did not adhere in the characteristic microcolony morphology, instead displaying a phenotype initially described as (DA) (Nataro et al., 1987a).
The HEP-2 adherence properties of E.coli isolated phenotype can be sub-devided into three categories, (i)Localized (now EPEC), (ii) Aggregative (now EAEC), (iii) Diffuse (now DAEC).
Aggregative adherence (AA) distinguished by prominent, stacked brick autoagglutination of the bacterial cells to each other, which often occurred on the surface of the cells, as well as on the glass coverslip free from the HEP-2 cells.
Diffusely adherent (DA) bacteria were seen dispersed over the surface of the HEP-2 cell, with little aggregation and little adherence to the glass coverslip free from cells (Nataro, 2001).
1.3.12.1. Pathogenesis.
The pathogenicity of EAEC is not thoroughly under stood, however a characteristic histopathological lesion and several candidate virulence factors have been described.; the site of EAEC infection is not known. In an out break of EAEC diarrhea in infants, the illume was shown to be involved (Eslava et al., 1993). The short incubation period of as little as 7 hours, is most consistent with a small bowel site of infection (Nataro et al., 1995a).
Hicks et al. (1996) and Knutton et al. (1992) however shown that EAEC can adhere to small and to an even greater extent to large-bowel section vitro.
EAEC characteristically enhance mucus secretions by the mucosa, with trapping of the bacteria in a bacterium-mucus biofilm (Tzipori et al., 1992), and volenteers fed EAEC develop a diarrhea predominately mucoid in character (Nataro, 2001).
Infection with EAEC has repeatedly been shown to induce cytotoxic effects on the intestinal mucosa. In rabbit and rat ileal loop models (Vial et al., 1988).
EAEC induce a destructive lesion demonstrated by light microscopy. The lesion is characterized by shortening of the villi, hemorrhage necrosis of the villus tips and mild inflammatory response with oedema and mononuclear infiltration of the sub-mucosa (Nataro, 2001).
Thus, diarrheagenic E.coli which adhered to HEP- 2 cells but which were not of EPEC serotypes were termed (enteroadherent E.coli) (Mathewson et al., 1986). The term “enteroadherent” is still frequently used but should now be replaced by the more precise terms enteroaggregative and diffusely adherent (Vial et al., 1988).
EAEC strains are currently defined as E.coli strains that do not secrete entertoxine LT or ST and that adhere to HEP-2 cells in an AA pattern (Nataro et al., 1995a).
1.3.12.2. Cytotoxins.
The toxic effects observed in animal models, human intestinal explains and T84 cells are not accompanied by interalization of the bacteria or by intinate attachment. Therefore, several groups have attempted to identify secreted cytotoxins.
Eslava et al. (1998) have identified 108-Kda cytoxin which elicits destructive lesions in the rat ileal loop. This protein was described by serum from patients infected with EAEC (Baldwin et al., 1992).
1.3.12.3. Epidemiology.
Strains of EAEC belong to very diverse combinations of O and H type, and even within an outbreak of diarrheal disease strains with several different serotypes may be isolated. The diversity of serotypes and pathogenic mechanisms observed suggests that the genes encoding the aggregative phenotype may be accepted readily by pathogenic strains of E.coli causing these bacteria to be considered as EAEC (Green wood et al., 2002).
1.3.12.4. Clinical diagnosis.
The clinical feauters of EAEC are a watery, mucoid secretory diarrheal illness with low-grade fever and little to no vomiting. Beside bloody (Cravioto et al., 1991).
Stiner et al. (1998) have found a large percentage of patients excreting EAEC have detectable fecal lactoferrin and supernormal levels of IL-8 in the stool. This observation suggests that EAEC infection may be accompanied by a suitable form of mucosal inflammation.
1.3.12.5. Detection and diagnosis.
EAEC infection is diagnosed definitively by the isolation of E.coli from the stools of patients and the demonstration of AA pattern in the HEP-2 assay.
1.3.12.5.1. HEP-2 assay.
• HEP-2 cells assay remains the gold standard for detection of EAEC. This test involves allowing strains of E.coli to adhere to cell monolayers in vitro and observing the pattern of adhesion by microscopy. Although tissue culture tests are laborious, the pattern of adhesion remains the key assay for detecting EAEC.
• An aggregative adhesion gene probe has proved useful as a comparatively rapid means of screening strains as a prelude to HEP-2 adhesion test (Nataro and Kaper, 1998 and Green wood et al., 2002).
Wednesday, March 14, 2012
Entero-aggregative E.coli (EaggEC).
Entero-aggregative E.coli (EaggEC).
Mathew and Coworkers described afifty reputed group of Enterovirulent E.coli associated with traveler’s diarrhea in Mexico. This new group was associated to more than 40% of HEP-2 cells in tissue culture assays (Janda and Abbott 1998).
Cravioto et al. (1979) observed that EPEC adhere to HEP-2 cells. However, these investigators also showed that many E.coli strains adhere to HEP-2 cells as well and, moreover, that the adherence pattern of EPEC was described as localized adherence (LA), denoting the presence of clusters or microcolonies on the surface of HEP-2 cells. In contrast, non-EPEC did not adhere in the characteristic microcolony morphology, instead displaying a phenotype initially described as (DA) (Nataro et al., 1987a).
The HEP-2 adherence properties of E.coli isolated phenotype can be sub-devided into three categories, (i)Localized (now EPEC), (ii) Aggregative (now EAEC), (iii) Diffuse (now DAEC).
Aggregative adherence (AA) distinguished by prominent, stacked brick autoagglutination of the bacterial cells to each other, which often occurred on the surface of the cells, as well as on the glass coverslip free from the HEP-2 cells.
Diffusely adherent (DA) bacteria were seen dispersed over the surface of the HEP-2 cell, with little aggregation and little adherence to the glass coverslip free from cells (Nataro, 2001).
1.3.12.1. Pathogenesis.
The pathogenicity of EAEC is not thoroughly under stood, however a characteristic histopathological lesion and several candidate virulence factors have been described.; the site of EAEC infection is not known. In an out break of EAEC diarrhea in infants, the illume was shown to be involved (Eslava et al., 1993). The short incubation period of as little as 7 hours, is most consistent with a small bowel site of infection (Nataro et al., 1995a).
Hicks et al. (1996) and Knutton et al. (1992) however shown that EAEC can adhere to small and to an even greater extent to large-bowel section vitro.
EAEC characteristically enhance mucus secretions by the mucosa, with trapping of the bacteria in a bacterium-mucus biofilm (Tzipori et al., 1992), and volenteers fed EAEC develop a diarrhea predominately mucoid in character (Nataro, 2001).
Infection with EAEC has repeatedly been shown to induce cytotoxic effects on the intestinal mucosa. In rabbit and rat ileal loop models (Vial et al., 1988).
EAEC induce a destructive lesion demonstrated by light microscopy. The lesion is characterized by shortening of the villi, hemorrhage necrosis of the villus tips and mild inflammatory response with oedema and mononuclear infiltration of the sub-mucosa (Nataro, 2001).
Thus, diarrheagenic E.coli which adhered to HEP- 2 cells but which were not of EPEC serotypes were termed (enteroadherent E.coli) (Mathewson et al., 1986). The term “enteroadherent” is still frequently used but should now be replaced by the more precise terms enteroaggregative and diffusely adherent (Vial et al., 1988).
EAEC strains are currently defined as E.coli strains that do not secrete entertoxine LT or ST and that adhere to HEP-2 cells in an AA pattern (Nataro et al., 1995a).
1.3.12.2. Cytotoxins.
The toxic effects observed in animal models, human intestinal explains and T84 cells are not accompanied by interalization of the bacteria or by intinate attachment. Therefore, several groups have attempted to identify secreted cytotoxins.
Eslava et al. (1998) have identified 108-Kda cytoxin which elicits destructive lesions in the rat ileal loop. This protein was described by serum from patients infected with EAEC (Baldwin et al., 1992).
1.3.12.3. Epidemiology.
Strains of EAEC belong to very diverse combinations of O and H type, and even within an outbreak of diarrheal disease strains with several different serotypes may be isolated. The diversity of serotypes and pathogenic mechanisms observed suggests that the genes encoding the aggregative phenotype may be accepted readily by pathogenic strains of E.coli causing these bacteria to be considered as EAEC (Green wood et al., 2002).
1.3.12.4. Clinical diagnosis.
The clinical feauters of EAEC are a watery, mucoid secretory diarrheal illness with low-grade fever and little to no vomiting. Beside bloody (Cravioto et al., 1991).
Stiner et al. (1998) have found a large percentage of patients excreting EAEC have detectable fecal lactoferrin and supernormal levels of IL-8 in the stool. This observation suggests that EAEC infection may be accompanied by a suitable form of mucosal inflammation.
1.3.12.5. Detection and diagnosis.
EAEC infection is diagnosed definitively by the isolation of E.coli from the stools of patients and the demonstration of AA pattern in the HEP-2 assay.
1.3.12.5.1. HEP-2 assay.
• HEP-2 cells assay remains the gold standard for detection of EAEC. This test involves allowing strains of E.coli to adhere to cell monolayers in vitro and observing the pattern of adhesion by microscopy. Although tissue culture tests are laborious, the pattern of adhesion remains the key assay for detecting EAEC.
• An aggregative adhesion gene probe has proved useful as a comparatively rapid means of screening strains as a prelude to HEP-2 adhesion test (Nataro and Kaper, 1998 and Green wood et al., 2002).
Mathew and Coworkers described afifty reputed group of Enterovirulent E.coli associated with traveler’s diarrhea in Mexico. This new group was associated to more than 40% of HEP-2 cells in tissue culture assays (Janda and Abbott 1998).
Cravioto et al. (1979) observed that EPEC adhere to HEP-2 cells. However, these investigators also showed that many E.coli strains adhere to HEP-2 cells as well and, moreover, that the adherence pattern of EPEC was described as localized adherence (LA), denoting the presence of clusters or microcolonies on the surface of HEP-2 cells. In contrast, non-EPEC did not adhere in the characteristic microcolony morphology, instead displaying a phenotype initially described as (DA) (Nataro et al., 1987a).
The HEP-2 adherence properties of E.coli isolated phenotype can be sub-devided into three categories, (i)Localized (now EPEC), (ii) Aggregative (now EAEC), (iii) Diffuse (now DAEC).
Aggregative adherence (AA) distinguished by prominent, stacked brick autoagglutination of the bacterial cells to each other, which often occurred on the surface of the cells, as well as on the glass coverslip free from the HEP-2 cells.
Diffusely adherent (DA) bacteria were seen dispersed over the surface of the HEP-2 cell, with little aggregation and little adherence to the glass coverslip free from cells (Nataro, 2001).
1.3.12.1. Pathogenesis.
The pathogenicity of EAEC is not thoroughly under stood, however a characteristic histopathological lesion and several candidate virulence factors have been described.; the site of EAEC infection is not known. In an out break of EAEC diarrhea in infants, the illume was shown to be involved (Eslava et al., 1993). The short incubation period of as little as 7 hours, is most consistent with a small bowel site of infection (Nataro et al., 1995a).
Hicks et al. (1996) and Knutton et al. (1992) however shown that EAEC can adhere to small and to an even greater extent to large-bowel section vitro.
EAEC characteristically enhance mucus secretions by the mucosa, with trapping of the bacteria in a bacterium-mucus biofilm (Tzipori et al., 1992), and volenteers fed EAEC develop a diarrhea predominately mucoid in character (Nataro, 2001).
Infection with EAEC has repeatedly been shown to induce cytotoxic effects on the intestinal mucosa. In rabbit and rat ileal loop models (Vial et al., 1988).
EAEC induce a destructive lesion demonstrated by light microscopy. The lesion is characterized by shortening of the villi, hemorrhage necrosis of the villus tips and mild inflammatory response with oedema and mononuclear infiltration of the sub-mucosa (Nataro, 2001).
Thus, diarrheagenic E.coli which adhered to HEP- 2 cells but which were not of EPEC serotypes were termed (enteroadherent E.coli) (Mathewson et al., 1986). The term “enteroadherent” is still frequently used but should now be replaced by the more precise terms enteroaggregative and diffusely adherent (Vial et al., 1988).
EAEC strains are currently defined as E.coli strains that do not secrete entertoxine LT or ST and that adhere to HEP-2 cells in an AA pattern (Nataro et al., 1995a).
1.3.12.2. Cytotoxins.
The toxic effects observed in animal models, human intestinal explains and T84 cells are not accompanied by interalization of the bacteria or by intinate attachment. Therefore, several groups have attempted to identify secreted cytotoxins.
Eslava et al. (1998) have identified 108-Kda cytoxin which elicits destructive lesions in the rat ileal loop. This protein was described by serum from patients infected with EAEC (Baldwin et al., 1992).
1.3.12.3. Epidemiology.
Strains of EAEC belong to very diverse combinations of O and H type, and even within an outbreak of diarrheal disease strains with several different serotypes may be isolated. The diversity of serotypes and pathogenic mechanisms observed suggests that the genes encoding the aggregative phenotype may be accepted readily by pathogenic strains of E.coli causing these bacteria to be considered as EAEC (Green wood et al., 2002).
1.3.12.4. Clinical diagnosis.
The clinical feauters of EAEC are a watery, mucoid secretory diarrheal illness with low-grade fever and little to no vomiting. Beside bloody (Cravioto et al., 1991).
Stiner et al. (1998) have found a large percentage of patients excreting EAEC have detectable fecal lactoferrin and supernormal levels of IL-8 in the stool. This observation suggests that EAEC infection may be accompanied by a suitable form of mucosal inflammation.
1.3.12.5. Detection and diagnosis.
EAEC infection is diagnosed definitively by the isolation of E.coli from the stools of patients and the demonstration of AA pattern in the HEP-2 assay.
1.3.12.5.1. HEP-2 assay.
• HEP-2 cells assay remains the gold standard for detection of EAEC. This test involves allowing strains of E.coli to adhere to cell monolayers in vitro and observing the pattern of adhesion by microscopy. Although tissue culture tests are laborious, the pattern of adhesion remains the key assay for detecting EAEC.
• An aggregative adhesion gene probe has proved useful as a comparatively rapid means of screening strains as a prelude to HEP-2 adhesion test (Nataro and Kaper, 1998 and Green wood et al., 2002).
Enterotoxin production
Enterotoxin production.
Shigella and EIEC infections are both characterized by a period of watery diarrhea that precedes the onest of scantly dysenteric stools containing blood and mucus. Indeed, in the majority of infections with EIEC and many with Shigella, only watery diarrhea occurs.
Nataro et al. (1995b) cloned and sequenced a plasmid borne gene from EIEC (designated sen), which encodes a novel protein of predicted size 63k Da. It was shown that a mutation of the sen gene causes a significant diminution of the entertoxic activity of the parent strain. And that the purified sen protein elicits rises in ISC without a significant effect on tissue conductance (Nataro, 2001).
1.3.11.5. Clinical considerations.
The clinical infections is characterized by fever, several abdominal cramps, malaise and watery diarrhea, accompanied by toxemia. Scantly stool containing pus, muces and blood follows the watery diarrhea (Mahon and Manuselis 2000).
1.3.11.6. Detection and diagnosis.
I- EIEC strains may be non motile and do not ferment lactose, cross reactions between Shigella and EIEC O antigens have been seen. Isolates may be mistaken for non pathogenic E.coli although EIEC do not decarboxylate lysine, more than 80% of E.coli decarboxylate lysin, for this reasons cases of diarrheal illness resulting from EIEC may be underreported (Mahon and Manuselis, 2000).
Recently, DNA probes to identify EIEC strains have been studied and compared with the sereny test. DNA probes to screen stool samples for EIEC have developed which eliminate the need for various other tests to identify EIEC.
Also a PCR assay with primers derived from also effective in a multiplex PCR system to identify EIEC strains simultaneously with other E.coli categories (Nataro and Kaper 1998).
II- EIEC strains can be difficult to distinguish from Shigella spp and from other E.coli strains including nonpathogenic strains. In general identification of EIEC entails demonstrating that the organism posses the biochemical profile of E.coli, yet with the genotypic or phenotypic characteristics of Shigella spp. The classical phenotypic assay for Shigella and EIEC identification is the sereny test, which correlate the ability of the strain to invade epithelial cells and spread from cell to cell (Green Wood et al., 2002 and Mahon and Manuselis, 2000).
Shigella and EIEC infections are both characterized by a period of watery diarrhea that precedes the onest of scantly dysenteric stools containing blood and mucus. Indeed, in the majority of infections with EIEC and many with Shigella, only watery diarrhea occurs.
Nataro et al. (1995b) cloned and sequenced a plasmid borne gene from EIEC (designated sen), which encodes a novel protein of predicted size 63k Da. It was shown that a mutation of the sen gene causes a significant diminution of the entertoxic activity of the parent strain. And that the purified sen protein elicits rises in ISC without a significant effect on tissue conductance (Nataro, 2001).
1.3.11.5. Clinical considerations.
The clinical infections is characterized by fever, several abdominal cramps, malaise and watery diarrhea, accompanied by toxemia. Scantly stool containing pus, muces and blood follows the watery diarrhea (Mahon and Manuselis 2000).
1.3.11.6. Detection and diagnosis.
I- EIEC strains may be non motile and do not ferment lactose, cross reactions between Shigella and EIEC O antigens have been seen. Isolates may be mistaken for non pathogenic E.coli although EIEC do not decarboxylate lysine, more than 80% of E.coli decarboxylate lysin, for this reasons cases of diarrheal illness resulting from EIEC may be underreported (Mahon and Manuselis, 2000).
Recently, DNA probes to identify EIEC strains have been studied and compared with the sereny test. DNA probes to screen stool samples for EIEC have developed which eliminate the need for various other tests to identify EIEC.
Also a PCR assay with primers derived from also effective in a multiplex PCR system to identify EIEC strains simultaneously with other E.coli categories (Nataro and Kaper 1998).
II- EIEC strains can be difficult to distinguish from Shigella spp and from other E.coli strains including nonpathogenic strains. In general identification of EIEC entails demonstrating that the organism posses the biochemical profile of E.coli, yet with the genotypic or phenotypic characteristics of Shigella spp. The classical phenotypic assay for Shigella and EIEC identification is the sereny test, which correlate the ability of the strain to invade epithelial cells and spread from cell to cell (Green Wood et al., 2002 and Mahon and Manuselis, 2000).
Entero-invasive E.coli (EIEC).
Entero-invasive E.coli (EIEC).
Enteroinvasive strains of E.coli (EIEC) are strains produce dysentry with direct penetration, invasion, and destruction of the intestinal mucosa. This diarrheal illnesses is very similar to that produced by Shigella. The EIEC infections seem to occur in adults and children alike (Mahon and Manuselis 2000).
EIEC strains are generally lysine decarboxylase negative, non motile, and lactose negative (Brenner et al., 1973). EIEC apparently lack fimbial adhesions but do not possess a specific adhesions that as in Shigella, is thought to be an outer membrane protein. Also, like Shigella, EIEC are invasive organisms. They do not produce LT or ST and, unlike Shigella, they do not produce the Shiga-toxin (Hale et al., 1997).
1.3.11.1. Pathogenesis.
The pathogenesity is resemble to Shigella pathogenesis. Both organisms have shown to invade the colonic epithilium, a phenotype mediated by both plasmid and chromosomal loci. In addition, both EIEC and Shigella Spp elaborate one or more secretory enterotoxins that may play roles in diarrheal pathogenesis (Nataro, 2001).
1.3.11.2. Invasiveness.
The current model of Shigella and EIEC pathogenesis comprises (i) Epithelial cell penetration, (ii) Lysis, of the endocytic vacuole, (iii) intracellualr multiplication, (iv) directional movement through the cytoplasm, and (v) extension into adjacent epithelial cells (Nataro, 2001).
EIEC and Shigella both cause disease by invading intestinal epithelial. Infection is by ingestion, only a small number of bacteria need to be swallowed as they are relatively resistant to gastiric acid and bile and pass readily into the large intestine where they multiply in the gut lumen. The bacteria passes through the overlying mucus layer, attach to the intestinal epithelial cells and are carried into the cell by endocytosis into the endocytic vacuole which then lysis.
The ability to cause the vacuole to lyse is an important virulence attribute, as organisms unable to do this can’t spread to neighbouring cells. After lysis of the vacuole the bacteria multiply within the epithelial cell and kill it. Spread to neighbouring cells leads to tissue destruction and inflammation which cause dysentry. Pathogenicity in Shigellae and EIEC depends on chromosomal and plasmid genes (Green Wood et al., 2002).
1.3.11.3. Epidemiology.
Epidemiology and ecology of EIEC have been poorly studied. Documented EIEC out breaks are usually foodborne or water borne, although person to person transimission does occur. Infections are usually foodborne but there is also evidence of cross infection. The most common serogroup is O124 (Green Wood et al., 2002).
Enteroinvasive strains of E.coli (EIEC) are strains produce dysentry with direct penetration, invasion, and destruction of the intestinal mucosa. This diarrheal illnesses is very similar to that produced by Shigella. The EIEC infections seem to occur in adults and children alike (Mahon and Manuselis 2000).
EIEC strains are generally lysine decarboxylase negative, non motile, and lactose negative (Brenner et al., 1973). EIEC apparently lack fimbial adhesions but do not possess a specific adhesions that as in Shigella, is thought to be an outer membrane protein. Also, like Shigella, EIEC are invasive organisms. They do not produce LT or ST and, unlike Shigella, they do not produce the Shiga-toxin (Hale et al., 1997).
1.3.11.1. Pathogenesis.
The pathogenesity is resemble to Shigella pathogenesis. Both organisms have shown to invade the colonic epithilium, a phenotype mediated by both plasmid and chromosomal loci. In addition, both EIEC and Shigella Spp elaborate one or more secretory enterotoxins that may play roles in diarrheal pathogenesis (Nataro, 2001).
1.3.11.2. Invasiveness.
The current model of Shigella and EIEC pathogenesis comprises (i) Epithelial cell penetration, (ii) Lysis, of the endocytic vacuole, (iii) intracellualr multiplication, (iv) directional movement through the cytoplasm, and (v) extension into adjacent epithelial cells (Nataro, 2001).
EIEC and Shigella both cause disease by invading intestinal epithelial. Infection is by ingestion, only a small number of bacteria need to be swallowed as they are relatively resistant to gastiric acid and bile and pass readily into the large intestine where they multiply in the gut lumen. The bacteria passes through the overlying mucus layer, attach to the intestinal epithelial cells and are carried into the cell by endocytosis into the endocytic vacuole which then lysis.
The ability to cause the vacuole to lyse is an important virulence attribute, as organisms unable to do this can’t spread to neighbouring cells. After lysis of the vacuole the bacteria multiply within the epithelial cell and kill it. Spread to neighbouring cells leads to tissue destruction and inflammation which cause dysentry. Pathogenicity in Shigellae and EIEC depends on chromosomal and plasmid genes (Green Wood et al., 2002).
1.3.11.3. Epidemiology.
Epidemiology and ecology of EIEC have been poorly studied. Documented EIEC out breaks are usually foodborne or water borne, although person to person transimission does occur. Infections are usually foodborne but there is also evidence of cross infection. The most common serogroup is O124 (Green Wood et al., 2002).
Enteropathogenic E.coli (EPEC).
Enteropathogenic E.coli (EPEC).
The Enteropathogenic E.coli organisms are the oldest known group of coliforms recognized to cause diarrheal disease in humans and has been linked to infant diarrhea in developing world. Once defined solely on the basis of O and H serotypes, EPEC is now defined on the basis of pathogenic charcteristics. Disease is rare in older children and adults, presumably, because of specific O serogroups have been associated with out breaks of EPEC diarrhea (Lewis, 1997).
1.3.10.1. Pathogenesis.
The ability of EPEC strains to cause diarrhea has been confirmed by oral administration of the organisms to babies and incompletely under stool.
Colonilization of the upper part of the small intestine occurs in infantile entiritis associated with EPEC. In many patients, EPEC are seen by electron microscopy to be intimately associated with the mucosal surface and to be partially surrounded by cup like projections (pedestals” of the enterocyte surface and in areas of EPEC attachment the brush border microocilli are lost. Many strains are strongly adhesive to border microvill are lost. Many strains are strongly adhesive to intestinal epithelial cells, and this represents an important pathogenic mechanism. Such strains of E.coli have been termed attaching, effacing E.coli or entero adherent E.coli (EAEC) (Green Wood et al., 2002).
1.3.10.2. Epidemiology.
1.3.10.2.1. Age distribution:
The most notable feature of the epidemiology of disease due to EPEC is the striking age distribution seen in persons infected with this pathogen. EPEC infection is primarily a disease of infants younger than 2 years. As reviewed by Levine and Edelman (Edelman and Levine 1983). Numerous case-control studies in many countries have shown a strong correlation of isolation of EPEC from infants with diarrhea compared to healthy infants. The correlation is strongest with infants younger than 6 months. In children older than 2 years, EPEC can be isolated from healthy and sick individuals, but a statistically significant correlation with disease is usually not found (Nataro and Kaper 1998).
1.3.10.2.2. Transmission and reservoirs:
As with other diarrheagenic E.coli strains, transmission of EPEC is fecal-oral, with contaminated hands, contaminated weaning foods, or contaminated fomites serving as vehicles.
Unless strict decontamination procedures are followed, admission of an infant to a pediatric ward can result in contamination of crib lien, toys, hand towels, scales.
The reservoir of EPEC infection is thought to be symptomatic or asymptomatic children and asymptomatic adults carriers, including mothers and persons who handle infants. Numerous studies have documented the spread of infection through hospitals, nurseries (Bower et al., 1989).
1.3.10.2.3. EPCE in developing countries:
EPEC is a major cause of infants diarrhea in developing countries. Numerous studies have been founds EPEC to be more frequently isolated from infants with diarrhea than from matched healthy controls (Donnenberg 1995). Particulary in the 0 to 6 months age group, EPEC strains are often the most frequently isolated bacterial diarrheal pathogens (Cravioto et al., 1988).
Several studies have shown that breast feeding is protective against diarrhea due to EPEC. Both human colostrum and milk strongly inhibit the adhesion of EPEC to HEP 2 cells in vitro (Camara et al., 1994).
1.3.10.4. Clinical considerations.
EPEC cause primarily acute diarrhea and it was associated with many common symptoms such as watery diarrhea, vomiting and low-grade fever are common symptoms beside malaise (Cohen and Gianella, 1991).
Fecal leukocytes are seen only occasionally, but more sensetive tests for inflammatory diarrhea such as an anti-lactoferrin latex bead agglutination test are frequently positive with EPEC infection.
As with other diarrheal pathogens, the primary goal of treatment of EPEC diarrhea is to prevent dehydration by correcting fluid and electrolyte imblances. Oral rehydration may be sufficient for milder cases, but more severe cases require parenteral rehydration. Correction nutritional imbalance with lactose free formula or breast milk may be insufficient for some severely ill patients, and total parenteral nutrition may be required. A variety of antibiotics have been used to treat EPEC and have proved useful in many cases. There are no vaccines currently available or in clinical trails to prevent disease due to EPEC (Camara et al., 1994).
1.3.10.5. Detection and diagnosis.
The definition of EPEC has changed in recent years as our knowledge of this pathogen has grown. For many years these organisms were defined only by O serogroups, which were subsequently defined to O:H serotypes. This definition changed as additional serotypes were associated with infantile diarrhea (Edelman and Levine 1983).
Citing recent pathogensis data, the second international symposium on EPEC in 1995 reached a consensus on the basic characteristics of EPEC, the most important of these were the A/E histopathology and the absence of Shiga-toxin. Many EHEC strains also produce the A/E lesion, therefore, determining the presence (indicative of EHEC) or absence (indicative of EPEC) of Stx is essential. The sole defining micorbiological characteristic of EPEC, is no longer deemed an essential characteristic of EPEC, although the majority of EPEC strains fall into certain well-recognized O:H serotypes (Green Wood et al., 2002).
There is some debate whether EPEC strains the lack the EAF plasmid are true pathogen or not so it was found that, only EAF-positive strains and not EAF-negative strains were significantly associated with diarrhea (Echeverria et al., 1991).
Furthermore, EAF-negative strains isolated during the course of an epidemiological study could also be derivatives of EHEC that have lost the phasges that encode Stx.
So EPEC: A/E, Stx-negative strains possessing the EAF plasmid would be called “typical EPEC”, while strains doesn’t possess the EAF plasmid would be called “atypical EPEC” (Nataro and Kaper 1998).
1.3.10.6. Diagnostic tests.
Given that EPEC strains, as with other diarrheagenic E.coli strains, are defined on the basis of virulence properties, there are two approaches to the detection of EPEC in the laboratory (i) phenotypic (ii) genotypic. The phenotypic approach requires the use of cell cultures and fluorescence microscopy, and the genotypic method requires the use of DNA hyberdization or PCR (Nataro and Kaper 1998).
The Enteropathogenic E.coli organisms are the oldest known group of coliforms recognized to cause diarrheal disease in humans and has been linked to infant diarrhea in developing world. Once defined solely on the basis of O and H serotypes, EPEC is now defined on the basis of pathogenic charcteristics. Disease is rare in older children and adults, presumably, because of specific O serogroups have been associated with out breaks of EPEC diarrhea (Lewis, 1997).
1.3.10.1. Pathogenesis.
The ability of EPEC strains to cause diarrhea has been confirmed by oral administration of the organisms to babies and incompletely under stool.
Colonilization of the upper part of the small intestine occurs in infantile entiritis associated with EPEC. In many patients, EPEC are seen by electron microscopy to be intimately associated with the mucosal surface and to be partially surrounded by cup like projections (pedestals” of the enterocyte surface and in areas of EPEC attachment the brush border microocilli are lost. Many strains are strongly adhesive to border microvill are lost. Many strains are strongly adhesive to intestinal epithelial cells, and this represents an important pathogenic mechanism. Such strains of E.coli have been termed attaching, effacing E.coli or entero adherent E.coli (EAEC) (Green Wood et al., 2002).
1.3.10.2. Epidemiology.
1.3.10.2.1. Age distribution:
The most notable feature of the epidemiology of disease due to EPEC is the striking age distribution seen in persons infected with this pathogen. EPEC infection is primarily a disease of infants younger than 2 years. As reviewed by Levine and Edelman (Edelman and Levine 1983). Numerous case-control studies in many countries have shown a strong correlation of isolation of EPEC from infants with diarrhea compared to healthy infants. The correlation is strongest with infants younger than 6 months. In children older than 2 years, EPEC can be isolated from healthy and sick individuals, but a statistically significant correlation with disease is usually not found (Nataro and Kaper 1998).
1.3.10.2.2. Transmission and reservoirs:
As with other diarrheagenic E.coli strains, transmission of EPEC is fecal-oral, with contaminated hands, contaminated weaning foods, or contaminated fomites serving as vehicles.
Unless strict decontamination procedures are followed, admission of an infant to a pediatric ward can result in contamination of crib lien, toys, hand towels, scales.
The reservoir of EPEC infection is thought to be symptomatic or asymptomatic children and asymptomatic adults carriers, including mothers and persons who handle infants. Numerous studies have documented the spread of infection through hospitals, nurseries (Bower et al., 1989).
1.3.10.2.3. EPCE in developing countries:
EPEC is a major cause of infants diarrhea in developing countries. Numerous studies have been founds EPEC to be more frequently isolated from infants with diarrhea than from matched healthy controls (Donnenberg 1995). Particulary in the 0 to 6 months age group, EPEC strains are often the most frequently isolated bacterial diarrheal pathogens (Cravioto et al., 1988).
Several studies have shown that breast feeding is protective against diarrhea due to EPEC. Both human colostrum and milk strongly inhibit the adhesion of EPEC to HEP 2 cells in vitro (Camara et al., 1994).
1.3.10.4. Clinical considerations.
EPEC cause primarily acute diarrhea and it was associated with many common symptoms such as watery diarrhea, vomiting and low-grade fever are common symptoms beside malaise (Cohen and Gianella, 1991).
Fecal leukocytes are seen only occasionally, but more sensetive tests for inflammatory diarrhea such as an anti-lactoferrin latex bead agglutination test are frequently positive with EPEC infection.
As with other diarrheal pathogens, the primary goal of treatment of EPEC diarrhea is to prevent dehydration by correcting fluid and electrolyte imblances. Oral rehydration may be sufficient for milder cases, but more severe cases require parenteral rehydration. Correction nutritional imbalance with lactose free formula or breast milk may be insufficient for some severely ill patients, and total parenteral nutrition may be required. A variety of antibiotics have been used to treat EPEC and have proved useful in many cases. There are no vaccines currently available or in clinical trails to prevent disease due to EPEC (Camara et al., 1994).
1.3.10.5. Detection and diagnosis.
The definition of EPEC has changed in recent years as our knowledge of this pathogen has grown. For many years these organisms were defined only by O serogroups, which were subsequently defined to O:H serotypes. This definition changed as additional serotypes were associated with infantile diarrhea (Edelman and Levine 1983).
Citing recent pathogensis data, the second international symposium on EPEC in 1995 reached a consensus on the basic characteristics of EPEC, the most important of these were the A/E histopathology and the absence of Shiga-toxin. Many EHEC strains also produce the A/E lesion, therefore, determining the presence (indicative of EHEC) or absence (indicative of EPEC) of Stx is essential. The sole defining micorbiological characteristic of EPEC, is no longer deemed an essential characteristic of EPEC, although the majority of EPEC strains fall into certain well-recognized O:H serotypes (Green Wood et al., 2002).
There is some debate whether EPEC strains the lack the EAF plasmid are true pathogen or not so it was found that, only EAF-positive strains and not EAF-negative strains were significantly associated with diarrhea (Echeverria et al., 1991).
Furthermore, EAF-negative strains isolated during the course of an epidemiological study could also be derivatives of EHEC that have lost the phasges that encode Stx.
So EPEC: A/E, Stx-negative strains possessing the EAF plasmid would be called “typical EPEC”, while strains doesn’t possess the EAF plasmid would be called “atypical EPEC” (Nataro and Kaper 1998).
1.3.10.6. Diagnostic tests.
Given that EPEC strains, as with other diarrheagenic E.coli strains, are defined on the basis of virulence properties, there are two approaches to the detection of EPEC in the laboratory (i) phenotypic (ii) genotypic. The phenotypic approach requires the use of cell cultures and fluorescence microscopy, and the genotypic method requires the use of DNA hyberdization or PCR (Nataro and Kaper 1998).
Enterotoxigenic E.coli (ETEC).
ETEC is defined as the E.coli strains that elaborate at least one member of two defined groups of enterotoxins: a heat liable toxin (HLT) and aheat stable toxins(HST). The first is a heat-labile enterotoxin (LT) that shows approximately 80% protein sequence identify with the heat-labile cytotoxinic cholera toxin of vibrio cholerae. The second toxin produced by ETEC is a heat-stable with a molecular mass of about 2Kda. Previous studies suggested that ETEC strains carrying both toxins (HLT+ and HST+) predominate clinically followed in decreasing frequency by strains carrying HSt+ only and those carrying HLT+ only. However, a 1996 review of 700ETEC strains collected over a period of more than 30 years found that the relative prevalence of these toxine type I is not different and that individual toxin-producing patterns may be related to serogroup specificity (Sears and Kaper, 1996 and
Tamura et al., 1996).
1.3.9.1. Epidemiology.
ETEC strains are associated with two major clinical syndromes: weaning diarrhea among children in the developing world, and traveler’s diarrhea. The epidemiologic pattern of ETEC disease is determined in large part by a number of factors: (I) Mucosal immunity to ETEC infection develops in exposed individuals, (ii) Even immune asymptomatic individuals may shed large numbers of virulent ETEC organisms in the stool, and (iii) The infection requires a relatively high infectious dose (Nataro and Kaper 1998). These three feautures create a situation in which ETEC contamination of the environment in areas of endemic infections is extremely prevalent, and most infants in such areas will encounter in warm-climate countries are not well under stool, but it seems likely that water contaminated by human (or) animal sewage plays an important part in the spread of infection (Green Wood, 2002).
1.3.9.2. Clinical symptoms.
The most common symptoms associated with ETEC infection are diarrehea (91-97%) and abdominal cramps (80-94%). Stools are typically watery in consistency, often yellow-tinged, and without the presence of mucus, pus or fecal leukocytes (Cohen and Gianella, 1991).
The gastroentritis induced by ETEC infection is typically indicating guishable from secretory diarrheas elicited by other gram-negative enteropathogens. Less often nausea (39-70%), headaches (35-57%), myalgia (50%), weakness (35%). Chills (31%), and low grade fevers (13-22%) are observed (Role et al., 1995).
Vomiting (2-1%) is not commonly associated with ETEC infection, a fact that helps distinguish this illness from gastrointestinal disturbances caused by norwalk virus.
ETEC infections commonly occur in four settings. In less developed countries, ETEC infection predominate in children younger than a years of age. Unlike the relatively mild infections, ETEC gastroentritis in young children in underdeveloped nations can be serve at times, with dehydration and adverse nutritional consequences leading to retardation of normal growth development (Cohen and Gianella, 1991).
Dehydration has also been noted as a consequence of ETEC infection in industrialized countries. As children mature, the incidence of ETEC disease apparently declines, suggesting that immunity may develop in local inhabitants with advancing age (Black et al., 1981).
1.3.9.3. Detection and Diagnosis.
Detection of ETEC has long relied on detection of the enterotoxins (HLT or HST). HST was initially detected in a rabbit ligaled ileal loop assay, but the expense and lack of standarization caused this test to be replaced by the sucking-mouse assay which become the standard test for the presence of HST for many years (Cryan 1990).
The traditional bioassay for detection of HLT involves the use of cell culture, either the Y, adrenal cell assay (or) the chinese hamster ovary (CHO) cell assay (Donta et al., 1974).
DNA probes were found to be useful in the detection of HLT and HST encoding genes in stool and environmental samples. Since that time several advances in ETEC detection have been made, but genetic techniques continue to attract the most detection and use. It should be stressed that there is no perfect test for ETEC decection of colonization factors because of their great number and heterogeneity (Abdul et al., 1994).
Several PCR assays for ETEC are quite sensitive and specific when used directly on clinical samples or on isolated bacterial colonies. A useful adaptation of PCR is the “multiplex” PCR assay in which several PCR primers are combined with the aim of detecting one of several different diarrheagenic E.coli pathotypes in a single reaction (duToit et al., 1993).
Tamura et al., 1996).
1.3.9.1. Epidemiology.
ETEC strains are associated with two major clinical syndromes: weaning diarrhea among children in the developing world, and traveler’s diarrhea. The epidemiologic pattern of ETEC disease is determined in large part by a number of factors: (I) Mucosal immunity to ETEC infection develops in exposed individuals, (ii) Even immune asymptomatic individuals may shed large numbers of virulent ETEC organisms in the stool, and (iii) The infection requires a relatively high infectious dose (Nataro and Kaper 1998). These three feautures create a situation in which ETEC contamination of the environment in areas of endemic infections is extremely prevalent, and most infants in such areas will encounter in warm-climate countries are not well under stool, but it seems likely that water contaminated by human (or) animal sewage plays an important part in the spread of infection (Green Wood, 2002).
1.3.9.2. Clinical symptoms.
The most common symptoms associated with ETEC infection are diarrehea (91-97%) and abdominal cramps (80-94%). Stools are typically watery in consistency, often yellow-tinged, and without the presence of mucus, pus or fecal leukocytes (Cohen and Gianella, 1991).
The gastroentritis induced by ETEC infection is typically indicating guishable from secretory diarrheas elicited by other gram-negative enteropathogens. Less often nausea (39-70%), headaches (35-57%), myalgia (50%), weakness (35%). Chills (31%), and low grade fevers (13-22%) are observed (Role et al., 1995).
Vomiting (2-1%) is not commonly associated with ETEC infection, a fact that helps distinguish this illness from gastrointestinal disturbances caused by norwalk virus.
ETEC infections commonly occur in four settings. In less developed countries, ETEC infection predominate in children younger than a years of age. Unlike the relatively mild infections, ETEC gastroentritis in young children in underdeveloped nations can be serve at times, with dehydration and adverse nutritional consequences leading to retardation of normal growth development (Cohen and Gianella, 1991).
Dehydration has also been noted as a consequence of ETEC infection in industrialized countries. As children mature, the incidence of ETEC disease apparently declines, suggesting that immunity may develop in local inhabitants with advancing age (Black et al., 1981).
1.3.9.3. Detection and Diagnosis.
Detection of ETEC has long relied on detection of the enterotoxins (HLT or HST). HST was initially detected in a rabbit ligaled ileal loop assay, but the expense and lack of standarization caused this test to be replaced by the sucking-mouse assay which become the standard test for the presence of HST for many years (Cryan 1990).
The traditional bioassay for detection of HLT involves the use of cell culture, either the Y, adrenal cell assay (or) the chinese hamster ovary (CHO) cell assay (Donta et al., 1974).
DNA probes were found to be useful in the detection of HLT and HST encoding genes in stool and environmental samples. Since that time several advances in ETEC detection have been made, but genetic techniques continue to attract the most detection and use. It should be stressed that there is no perfect test for ETEC decection of colonization factors because of their great number and heterogeneity (Abdul et al., 1994).
Several PCR assays for ETEC are quite sensitive and specific when used directly on clinical samples or on isolated bacterial colonies. A useful adaptation of PCR is the “multiplex” PCR assay in which several PCR primers are combined with the aim of detecting one of several different diarrheagenic E.coli pathotypes in a single reaction (duToit et al., 1993).
Gastroenteritis associaed with Escherichia coli
E.coli may cause several types of diarrheal illness. There are five major categories of diarrhegenic E.coli, based on definite virulence factors, clinical manifestations produced, epidemiology, and different O:H stereotypes.
These include the following:
• Enteropathogenic Escherichia coli (EPEC), which cause infantile entritis, especially in tropical countries.
• Enteropathogenic Escherichia coli (EPEC), which are responsible for community acquired diarrheal disease in areas of poor sanitation and are the commonest cause of traveller’s diarrhea.
• Entero-invasive Escherichia coli (EIEC), which cause an illness resembling Shigella dysentery in patients of all ages.
• Enterohemorrhagic Escherichia coli (EHEC), which caused disease in developed countries. Stereotype O157:H7.
• Entero-aggregative Escherichia. coli (EaggEC), which cause chronic diarrhaeal disease in certain developing countries (Nataro, 2001).
1.3.8.11. Phenotypic assay based on virulence characteristics.
Identification of diarrheagenic E.coli strains requires that these organisms can be differentiated from nonpathogenic members of the normal flora. Serotypic markers correlate, sometimes very closely, with specific categories of diarrheagenic E.coli, however, these markers are rarely sufficient in and themselves to reliably identify a strain as diarrheagenic (an exception may be strains of serotype O157:H7, a serotype that serves as a marker for virulent enterohemorrhagic E.coli strains, nevertheless, EHEC of serotypes other than O157:H7 are being identified with increasing frequency in sporadic and epidimic cases). In addition to its limited sensitivity and specificity serotyping is tedious and expensive and is performed reliable only by a small number of reference laboratories. Thus, detection of diarrheagenic E.coli has focused increasingly on the identification of characteristics which themselves determine the virulence of these organisms. This may include detection of the genes encoding these traits (Nataro and Kaper, 1998).
These include the following:
• Enteropathogenic Escherichia coli (EPEC), which cause infantile entritis, especially in tropical countries.
• Enteropathogenic Escherichia coli (EPEC), which are responsible for community acquired diarrheal disease in areas of poor sanitation and are the commonest cause of traveller’s diarrhea.
• Entero-invasive Escherichia coli (EIEC), which cause an illness resembling Shigella dysentery in patients of all ages.
• Enterohemorrhagic Escherichia coli (EHEC), which caused disease in developed countries. Stereotype O157:H7.
• Entero-aggregative Escherichia. coli (EaggEC), which cause chronic diarrhaeal disease in certain developing countries (Nataro, 2001).
1.3.8.11. Phenotypic assay based on virulence characteristics.
Identification of diarrheagenic E.coli strains requires that these organisms can be differentiated from nonpathogenic members of the normal flora. Serotypic markers correlate, sometimes very closely, with specific categories of diarrheagenic E.coli, however, these markers are rarely sufficient in and themselves to reliably identify a strain as diarrheagenic (an exception may be strains of serotype O157:H7, a serotype that serves as a marker for virulent enterohemorrhagic E.coli strains, nevertheless, EHEC of serotypes other than O157:H7 are being identified with increasing frequency in sporadic and epidimic cases). In addition to its limited sensitivity and specificity serotyping is tedious and expensive and is performed reliable only by a small number of reference laboratories. Thus, detection of diarrheagenic E.coli has focused increasingly on the identification of characteristics which themselves determine the virulence of these organisms. This may include detection of the genes encoding these traits (Nataro and Kaper, 1998).
Friday, March 9, 2012
Rapid Laboratory Diagnosis of Mycobacterium tuberculosis
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Thursday, March 1, 2012
Meningitis
Meningitis is an inflammation of leptomeninges and underlying subarachnoid cerebrospinal fluid (CSF), whereas encephalitis is an inflammation of the brain parenchyma . Meningitis and encephalitis are life – threatening infections especially in children as any infectious agent can cause central nervous system (CNS) infection because of the inflammation's proximity to the brain and spinal cord; therefore the condition is classified as a medical emergency (CDC , 2009).
Aseptic Meningitis (AM) is a febrile meningial inflammation characterized by CSF mononuclear pleocytosis ,normal glucose, mild elevation in protein and absence of bacteria agents . Viral meningitis which is the most common form of AM is an infection of the meninges by one of different viruses or occurs as an uncommon complications of systemic viral infection ((Sergio et al., 2007 & Scheld et al ., 2004).
Human Enteroviruses (EVs) are the most common causes of adult AM and together with herpes simplex virus type 1 (HSV-1) are the main causes of meningitis in adult and children especially in areas with vaccination( Desmond et al., 2006). While in areas with low vaccination , measles and mumps viruses are often the most common causes of meningitis (Frantzidou et al ., 2008 & Moran ; 2003 ).
Approximately half cases of viral meningitis are caused by coxsackie and echovirus types of enterovirus ( Caro et al ., 2001).
Mycobacterium TB, mycoplasma and leptospira can also cause AM ( Avery et al.,2006).Tuberculous meningitis is the second most frequently cause of infectious AM in Egypt with
the highest mortality rate among the other causes of meningitis ( Van den Bos et al ., 2004).
AM may also result from infection by treponema pallidum , borrelia burgdorferi and malaria (Jordan & Durso, 2005). Cryptococcus neoformans is a form of fungal meningitis that typically seen in AIDS, while amoebic meningitis caused by Naegleria fowleri is contracted from freshwater sources (Sloan et al ., 2008 & Ginsberg ,2004).
AM may also caused by several non-infectious causes as cancer (malignant meningitis)( Chamberlain, 2005 & Tunkel et al ., 2004). Drugs as non-steroidal anti-inflammatory agents, antibiotics and intravenous immunoglobulins also can cause AM (Moris & Garcia-Monco , 1999).
Laboratory diagnosis of viral meningitis relied on virus isolation and this method has several limitations as it needs long duration from days to weeks with limited sensitivity , virus antigen and antibody detection (Kupila et al ., 2005).
For the diagnosis of M. tuberculosis , a number of laboratory techniques can be used that differ in their sensitivity, cost and time. They include acid-fast staining, isolation on Lowenstein Jensen media and radiometric method (BACTC) .Molecular methods as polymerase chain reaction (PCR) and Gen-probe identification methods can also be used (Thwaites et al. , 2005).
PCR is used to identify the pathogens in CSF . It is sensitive and specific test. It is also used in distinguishing the various causes of viral meningitis ( Pandit et al ., 2005).
Aseptic Meningitis (AM) is a febrile meningial inflammation characterized by CSF mononuclear pleocytosis ,normal glucose, mild elevation in protein and absence of bacteria agents . Viral meningitis which is the most common form of AM is an infection of the meninges by one of different viruses or occurs as an uncommon complications of systemic viral infection ((Sergio et al., 2007 & Scheld et al ., 2004).
Human Enteroviruses (EVs) are the most common causes of adult AM and together with herpes simplex virus type 1 (HSV-1) are the main causes of meningitis in adult and children especially in areas with vaccination( Desmond et al., 2006). While in areas with low vaccination , measles and mumps viruses are often the most common causes of meningitis (Frantzidou et al ., 2008 & Moran ; 2003 ).
Approximately half cases of viral meningitis are caused by coxsackie and echovirus types of enterovirus ( Caro et al ., 2001).
Mycobacterium TB, mycoplasma and leptospira can also cause AM ( Avery et al.,2006).Tuberculous meningitis is the second most frequently cause of infectious AM in Egypt with
the highest mortality rate among the other causes of meningitis ( Van den Bos et al ., 2004).
AM may also result from infection by treponema pallidum , borrelia burgdorferi and malaria (Jordan & Durso, 2005). Cryptococcus neoformans is a form of fungal meningitis that typically seen in AIDS, while amoebic meningitis caused by Naegleria fowleri is contracted from freshwater sources (Sloan et al ., 2008 & Ginsberg ,2004).
AM may also caused by several non-infectious causes as cancer (malignant meningitis)( Chamberlain, 2005 & Tunkel et al ., 2004). Drugs as non-steroidal anti-inflammatory agents, antibiotics and intravenous immunoglobulins also can cause AM (Moris & Garcia-Monco , 1999).
Laboratory diagnosis of viral meningitis relied on virus isolation and this method has several limitations as it needs long duration from days to weeks with limited sensitivity , virus antigen and antibody detection (Kupila et al ., 2005).
For the diagnosis of M. tuberculosis , a number of laboratory techniques can be used that differ in their sensitivity, cost and time. They include acid-fast staining, isolation on Lowenstein Jensen media and radiometric method (BACTC) .Molecular methods as polymerase chain reaction (PCR) and Gen-probe identification methods can also be used (Thwaites et al. , 2005).
PCR is used to identify the pathogens in CSF . It is sensitive and specific test. It is also used in distinguishing the various causes of viral meningitis ( Pandit et al ., 2005).
Meningitis
Meningitis is an inflammation of leptomeninges and underlying subarachnoid cerebrospinal fluid (CSF), whereas encephalitis is an inflammation of the brain parenchyma . Meningitis and encephalitis are life – threatening infections especially in children as any infectious agent can cause central nervous system (CNS) infection because of the inflammation's proximity to the brain and spinal cord; therefore the condition is classified as a medical emergency (CDC , 2009).
Aseptic Meningitis (AM) is a febrile meningial inflammation characterized by CSF mononuclear pleocytosis ,normal glucose, mild elevation in protein and absence of bacteria agents . Viral meningitis which is the most common form of AM is an infection of the meninges by one of different viruses or occurs as an uncommon complications of systemic viral infection ((Sergio et al., 2007 & Scheld et al ., 2004).
Human Enteroviruses (EVs) are the most common causes of adult AM and together with herpes simplex virus type 1 (HSV-1) are the main causes of meningitis in adult and children especially in areas with vaccination( Desmond et al., 2006). While in areas with low vaccination , measles and mumps viruses are often the most common causes of meningitis (Frantzidou et al ., 2008 & Moran ; 2003 ).
Approximately half cases of viral meningitis are caused by coxsackie and echovirus types of enterovirus ( Caro et al ., 2001).
Mycobacterium TB, mycoplasma and leptospira can also cause AM ( Avery et al.,2006).Tuberculous meningitis is the second most frequently cause of infectious AM in Egypt with
the highest mortality rate among the other causes of meningitis ( Van den Bos et al ., 2004).
AM may also result from infection by treponema pallidum , borrelia burgdorferi and malaria (Jordan & Durso, 2005). Cryptococcus neoformans is a form of fungal meningitis that typically seen in AIDS, while amoebic meningitis caused by Naegleria fowleri is contracted from freshwater sources (Sloan et al ., 2008 & Ginsberg ,2004).
AM may also caused by several non-infectious causes as cancer (malignant meningitis)( Chamberlain, 2005 & Tunkel et al ., 2004). Drugs as non-steroidal anti-inflammatory agents, antibiotics and intravenous immunoglobulins also can cause AM (Moris & Garcia-Monco , 1999).
Laboratory diagnosis of viral meningitis relied on virus isolation and this method has several limitations as it needs long duration from days to weeks with limited sensitivity , virus antigen and antibody detection (Kupila et al ., 2005).
For the diagnosis of M. tuberculosis , a number of laboratory techniques can be used that differ in their sensitivity, cost and time. They include acid-fast staining, isolation on Lowenstein Jensen media and radiometric method (BACTC) .Molecular methods as polymerase chain reaction (PCR) and Gen-probe identification methods can also be used (Thwaites et al. , 2005).
PCR is used to identify the pathogens in CSF . It is sensitive and specific test. It is also used in distinguishing the various causes of viral meningitis ( Pandit et al ., 2005).
Aseptic Meningitis (AM) is a febrile meningial inflammation characterized by CSF mononuclear pleocytosis ,normal glucose, mild elevation in protein and absence of bacteria agents . Viral meningitis which is the most common form of AM is an infection of the meninges by one of different viruses or occurs as an uncommon complications of systemic viral infection ((Sergio et al., 2007 & Scheld et al ., 2004).
Human Enteroviruses (EVs) are the most common causes of adult AM and together with herpes simplex virus type 1 (HSV-1) are the main causes of meningitis in adult and children especially in areas with vaccination( Desmond et al., 2006). While in areas with low vaccination , measles and mumps viruses are often the most common causes of meningitis (Frantzidou et al ., 2008 & Moran ; 2003 ).
Approximately half cases of viral meningitis are caused by coxsackie and echovirus types of enterovirus ( Caro et al ., 2001).
Mycobacterium TB, mycoplasma and leptospira can also cause AM ( Avery et al.,2006).Tuberculous meningitis is the second most frequently cause of infectious AM in Egypt with
the highest mortality rate among the other causes of meningitis ( Van den Bos et al ., 2004).
AM may also result from infection by treponema pallidum , borrelia burgdorferi and malaria (Jordan & Durso, 2005). Cryptococcus neoformans is a form of fungal meningitis that typically seen in AIDS, while amoebic meningitis caused by Naegleria fowleri is contracted from freshwater sources (Sloan et al ., 2008 & Ginsberg ,2004).
AM may also caused by several non-infectious causes as cancer (malignant meningitis)( Chamberlain, 2005 & Tunkel et al ., 2004). Drugs as non-steroidal anti-inflammatory agents, antibiotics and intravenous immunoglobulins also can cause AM (Moris & Garcia-Monco , 1999).
Laboratory diagnosis of viral meningitis relied on virus isolation and this method has several limitations as it needs long duration from days to weeks with limited sensitivity , virus antigen and antibody detection (Kupila et al ., 2005).
For the diagnosis of M. tuberculosis , a number of laboratory techniques can be used that differ in their sensitivity, cost and time. They include acid-fast staining, isolation on Lowenstein Jensen media and radiometric method (BACTC) .Molecular methods as polymerase chain reaction (PCR) and Gen-probe identification methods can also be used (Thwaites et al. , 2005).
PCR is used to identify the pathogens in CSF . It is sensitive and specific test. It is also used in distinguishing the various causes of viral meningitis ( Pandit et al ., 2005).
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