The Causative Agent of Amoebiasis
A Primer on One of the Most Notorious Protozoan Parasite
Jun 27, 2007
A large number of protozoan species spend a part if not all of their life cycle inside the body of higher organisms either as parasites or symbionts (Stevens and Hume, 1998). Although protozoans have been known to be endosymbionts of some ruminants, they are notably known for being parasites causing a variety of infections in their hosts. Protozoans are responsible for many known diseases that have inflicted humans – amoebiasis, giardiasis, sleeping sickness, malaria and many others (Cox, 2002). The blood and the gastrointestinal tract are usual sites of infection and proliferation of protozoan parasites (Herwaldt, 2001). Entry of cysts into these systems in humans is facilitated by vectors (insects, flies, mosquitoes) that carry and introduce them directly to the host or through the food and water supply (Graczyk, 2005). Those that infect the gastrointestinal tract are called enteric protozoa.
Enteric protozoans are transmitted by the fecal-oral route and tend to exhibit similar life cycles consisting of a cyst stage and a trophozoite stage. Fecal-oral transmission involves the ingestion of food or water contaminated with cysts. After ingestion by an appropriate host, the cysts transform into trophozoites which exhibit an active metabolism and are usually motile (Garcia, 2001). The parasite takes up nutrients and undergoes asexual replication during the trophic phase. Some of the trophozoites will develop into cysts instead of undergoing replication. Cysts are characterized by a resistant wall and are excreted with the feces (Garcia, 2001). Such is the mechanism of infection of one of the most notorious of pathogenic protozoans – Entamoeba histolytica.
Humans harbor at least eight species of amoebae in the intestinal lumen, of which only one, E. histolytica, is a pathogen; the others being commensal (Leber, 1999). These amoebae live and multiply in the gut and form cysts that are passed out in the feces and infect new individuals when they are consumed in contaminated water and food. Most infections are asymptomatic, but some strains of E. histolytica can invade the gut wall, causing severe ulceration and amoebic dysentery characterized by bloody stools (Cox, 2002). If the parasites gain access to damaged blood vessels, they may be carried to extraintestinal parts anywhere in the body, the most important of which is the liver, where the amoebae cause hepatic amoebiasis (Tanyuksel and Petri, 2003).
It has been estimated in 1986 by Walsh that E. histolytica causes 50 million cases and 100,000 deaths annually. Hence, for several years, researchers have been searching for methods that will allow an accurate and reliable assessment of amoebiasis. Laboratory diagnosis is usually based on microscopy and serological methods; but there have been remarkable developments in molecular biology-based detection procedures over the last decade.
The sensitivity and specificity of conventional microscopy on a single stool specimen for different species of Entamoeba has been shown in many studies to be less than optimal (Garcia and Bruckner, 1997). For the serological methods, the presence of IgG antibodies in a single sample of serum does not indicate whether the infection is recent or past (Caballero-Salcedo et al., 1994; Gathiram and Jackson, 1987). The inhibitory effect of some fecal components on PCR resulting to false negatives (Orlandi and Lampel, 2000) and the lack of uniformity in the technique make molecular methods of detection less popular. Thus, not one of the methods is sufficient, a combination of these diagnostic methods is often necessary for the accurate diagnosis of recently acquired infection.
References
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Cox, F.E.G. 2002. History of human parasitology. Clin. Micro. Rev. 15(4): 595–612
Garcia, L.S. and D.A. Bruckner. 1997. Diagnostic medical parasitology, 3rd ed. ASM Press, Washington, D.C.
Garcia, L. S. 2001. Diagnostic medical parasitology, 4th ed. ASM Press, Washington DC
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Leber, A.L., and S.M. Novak. 1999. Intestinal and urogenital amoebae, flagellates and ciliates, p. 1391-1405. In P.R. Murray, E.J. Baron, M.A. Pfaller, F.C. Tenover, and R.H. Yolken (ed.), Manual of clinical microbiology, 7th ed. ASM Press, Washington, D.C.
Orlandi, P.A. and K.A. Lampel. 2000. Extraction-free, filter-based template preparation for rapid and sensitive PCR detection of pathogenic parasitic protozoa. J. Clin. Microbiol. 38:2271-2277
Tanyuksel, M. and Petri, W.A. 2003. Laboratory Diagnosis of Amebiasis. Clinical Microbiology Reviews 16(4):713-729.
Walsh, J.A. 1986. Prolems in recognition and diagnosis of amoebiasis: Estimation of the global magnitude of morbidity and mortality. Rev. Infect. Dis. 8:228-238
