Rotavirus, Enteropathogenic Escherichia coli (EPEC) and Parasitic Etiology of Pediatric Diarrhea in Kirkuk city

Abstract

Diarrheal disease continues to be an important cause of morbidity and mortality among young children in developing countries [1]. Acute gastroenteritis is one of the leading causes of illness and death in infants and children throughout the world, especially in developing countries. An estimated 2.5 million gastroenteritis deaths occur each year in children less than 5 years of age [2]. Diarrheal infections may be caused by bacterial, viral, or parasitic pathogens. Some cases have a single defined cause; others do not have any defined cause, and a substantial number (one third) are caused by multiple pathogens, because such known diarrheal pathogen fulfills Koch's postulates and is capable of being the sole etiologic agent causing disease. Multiple pathogens are not essential for causing disease. How additional pathogens cause and contribute to the disease process is unknown. The source of the multiple pathogens in a patient could simply result from multiple pathogens in an urban environment of crowded impoverished conditions. If the various pathogens occurred independently in cases of disease, then each pathogen in a polymicrobial infection would be expected to occur in proportion to its presence in all patients with severe diarrhea [3]. Rotavirus remains the commonest cause of severe dehydrating diarrhea among children worldwide. Children in developing countries die more because of several factors including poorer access to hydration therapy. The reported prevalence of rotavirus diarrhea from global surveillance networks and hospital-based studies ranges from 6% to 56%. [4] Rotavirus was coined from the Latin word (rota – meaning wheel), and is given because the viruses have a distinct wheel-like shape [5]. Rotaviruses are non-enveloped, double-stranded RNA viruses (dsRNA) comprising a genus within the family Reoviridae. The 11 segments of dsRNA genome code for 6 structural and 6 non-structural proteins. Seven groups of rotavirus (A–G) have been described, with group A rotaviruses being the leading cause of severe dehydrating gastroenteritis in children < 5 years of age worldwide. [6] It is not possible to diagnose rotavirus infection by clinical presentation because the clinical features of rotavirus gastroenteritis do not differ from those of gastroenteritis caused by other pathogens. Confirmation of rotavirus infection by laboratory testing is necessary for reliable rotavirus surveillance and can be useful in clinical settings to avoid inappropriate use of antimicrobial therapy. Rotavirus is shed in high concentrations in the stool of children with gastroenteritis and a fecal specimen is the preferred specimen for diagnosis [4]. The main symptoms of rotavirus gastroenteritis (RVGE) are fever, abdominal pain, lethargy, diarrhea and vomiting that may lead to hypovolemic shock and dehydration. Severe cases may lead to death. The World Health Organization (WHO) estimates that 527,000 children under the age of five years die of rotavirus disease each year. Children in the poorer countries account for 82% of rotavirus deaths [7]. There is increasing evidence that polymicrobial infections in which microorganisms present specific pathologies may act in a synergistic or inhibitory fashion, impacting on either tissue, host cell destruction or the maintenance of health; among these, bacterial-bacterial, viral-viral, parasitic-parasitic, or viral-bacterial interactions have been well documented. For example, enteroaggregative Escherichia coli (EAEC) or enteropathogenic E. coli (EPEC) may provide a second pathogen with better conditions to invade the intestine and cause diarrhea [8]. Enzyme immunoassays (EIA) have replaced electron microscopy (EM) as the standard method for the detection of rotaviruses in stool samples in the 1980s [9].