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).
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Wednesday, March 14, 2012
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
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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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