Entamoeba hystolytica is a protozoan pathogen

Entamoeba histolytic is a protozoan pathogen that causes human amoebiasis. The protozoa occur in two forms: a cyst, which is dormant and persists for a long time outside the human host, and an active trophozoite, which is the diving type. Trophozoites occur as commensals in the majority of infected humans and become invasive in a limited number of cases by invading the intestinal mucosa, resulting in ulcers. Trophozoites may penetrate other areas of the body, such as the liver, where they cause necrosis of tissue, resulting in abscesses. Notably, the pathogenesis of disease by Entamoeba histolytic is associated with attachment of the trophozoite to the targeted cell, lysis of the targeted cell, and necrosis of the targeted cell with a number of identified molecules involved in this process. For instance, chief molecules found at the surface of the trophozoite and implicated in the adherence of the trophozoite to the targeted cell are the N-acetyl-D-galactosamine and a lectin inhibited by galactose. Moreover, there has been an extensive study of several amoebic performing proteins referred to as 5kDa amoebapore. The amoebapore can form ion-channels by inserting into the lipid bilayers of the target cells. Markedly, as measured in animal models, the phagocytic potential of trophozoites relies on virulence. In this regard, factors such as the association of trophozoites with bacteria similarly affect virulence. Therefore, there are multiple key determining factors and a unifying picture of pathogenesis, which are ideal when the relative contributions of each factor are manageable. Further understanding of the mechanism of pathogenesis of amoebiasis is applicable through the development of a transfection system that introduces genes into trophozoites in the recent technical advances.

Key words: trophozoite, amoebapore, cyst, abscess, necrosis, lysis, virulence.

Pathogenesis of Disease by Entamoeba Hystolytica

Entamoeba hystolytica is a protozoan existing worldwide and causes amoebiasis in which developing countries shows the highest prevalence of the disease due to inadequate barriers between human feces and the supplies of water and food. The picture below (see Fig.1) shows an Entamoeba hystolytica trichrome strain in amoebiasis with two observable diagnostic characteristics. Foremost, there is ingestion of erythrocytes by two trophozoites. Secondly, the three trophozoites have nuclei with small karyosomes that are centrally located.



Fig. 1. Trichome strain of amoebiasis (Bennett et al., 2015).

Even though most cases of amoebiasis asymptomatic, the occurrence of invasive and dysentery extraintestinal infection is still possible. For example, amoebic liver abscess is a frequent symptom of invasive amoebiasis although other organs including cerebral, cutaneous, cardiac, peritoneal, pleuropulmonary and genitourinary sites are also involved. In well-established nations, Amoebiasis ultimately affects travelers to and migrants from endemic regions with institutionalized and immunosuppressed individuals as well as homosexuals.

The transmission of Entamoeba hystolytica occurs via ingestion of infective stage (cyst form) of the protozoa, which remains viable in fecal contaminated hands of food handlers, fertilizer, soil, or water for weeks to months. Fecal to oral transmission of the protozoan can also occur through activities such as anal sex, or a one on one inoculation of the rectum via colonic rinsing equipment. The trophozoite (invasive form) appears through excystation that occurs in the terminal colon or ileum. The parasite’s invasive form is able to invade and infiltrate the mucosal barrier of the colon thereby resulting in secretory diarrhea, tissue destruction, and a bowel related colitis inflammation. Additionally, there may be a hematogenous spread of the trophozoites to deeply suited organs such as the liver through portal circulation. Entamoeba hystolytica has the ability to cause a broad spectrum of intestinal conditions and illnesses, which include the following:

Toxin Megacolon

Ameboma

Asymptomatic infection

Perianal ulceration

Symptomatic noninvasive infection

Chronic nondysenteric colitis

Fulminant colitis with perforation

Entamoeba hystolytica also results in extraintestinal conditions including the following:

Genitourinary disease

Liver abscess

Brain abscess

Pleuropulmonary disease

Pericarditis

Peritonitis

The demonstration of Entamoeba hystolytica or employing immunologic techniques is the most preferable laboratory diagnosis of amoebiasis. Concisely, other laboratory studies apart from standard blood tests employed in the diagnosis of amoebiasis include culture, polymerase chain reaction (PCR) assay, microscopy, and serologic testing. The treatment of the disease includes surgical intervention, pharmacologic therapy, and preventive measures where appropriate. Several clinical scenarios are suitable for an inpatient care even though majority of patients with amoebiasis are on an outpatient care. This report will thus focus on the lifecycle, pathophysiology, epidemiology, diagnosis, and medication of amoebiasis caused by Entamoeba hystolytica.

Entamoeba Hystolytica

The Lifecycle of Entamoeba hystolytica in Human Host

As Bennett et al. (2015) observes the life cycle of Entamoeba hystolytica is complete in one human host since the protozoon is monogenetic. The life cycle is complete through the following:



Fig. 2. Life Cycle of Entamoeba hystolytica (Bennett et al., 2015).

Encystment. Entamoeba only remains in the intestinal lumen in the precystic forms in which the parasite round up, dissolves food vacuoles, and takes in a considerable quantity of food materials in form of black rod-like chromatid and glycogen granules. Subsequently, the parasite undergoes encystment and secret a thin, round, resistant and transparent cyst wall around it that varies in size. The cyst is mononucleate with a very clear cytoplasm at this stage. The availability of chromatid bodies which occur in multiples of either two or more or singly is a manifestation of the cyst wall of the parasite in the human host (Bennett et al., 2015). The small karyosomes of the cysts undergoes two division so that each becomes tetra nucleate and afterwards, the cyst is infective to a new human host after which they pass out with the human fecal waste.

Transfer to new human host. The infective encysted forms from the human waste stay viable outside the human intestine for a long duration of time if conditions in the environment become favorable. The infection of the new host occurs by taking in the infective cysts with contaminated drinks and food.

Excystment. The intestinal contents of the human host such as tissue elements and bacteria provide nutrients to the metacystic trophozoites, which grow to maximum size to form the trophozoites of the subsequent generation. Ideally, a long period passes by as the trophozoites stay in the lumen after which they may attack the intestinal wall and commence the life cycle for the second time.

In other words, the lifecycle of the parasite occurs in three stages including the trophozoite, precystic and cystic stage. The feeding, motile, and pathogenic trophozoites are the adult stages of the parasite. They undergo binary fission in the intestinal wall thus producing tetra nucleate daughtercells, which come out with fecal matter and remain viable for about 2 weeks. They find their way into the host through contaminated water and drinks.

Pathophysiology of Entamoeba hystolytica once in Human host

As Feldman, Friedman and Brandt (2016) note, only small fractions of the cysts cause amoebiasis although there is a poor interpretation of encystation and excystation processes. A Lectin inhibited by glucose and N-acetyl-D-galactosamine mediates the attachment of trophozoites to colonic epithelial cells although the response against the lectin by a mucosal immunoglobulin may result in fewer recurrent infections. Moreover, a peptide family with the ability to form pores in lipid bilayers (amebapores) undertakes cytolysis in which apoptosis induces by trophozoites through a non-tumor and non-Fas necrosis factor receptor pathways. Apoptosis is also inducible through sublytic concentrations of the amebapores. The inflammation and invasion of the gut occurs through cysteine proteinases. Similarly, as cysteine proteinase mimics the human interleukin (IL)-1-converting enzyme action, there is increased amplification of inflammation mediated by IL-1 thereby cleaving the precursor of IL-1 to its active form. Additionally, it can plow and deactivate the immunoglobulin (IgG) and (IgA) and anaphylatoxins C3a and C5a.

The parasite possesses approximately 98 putative transmembrane kinases expressed in proliferating trophozoites and inducible via serum (Feldman, Friedman & Brandt, 2016). The main causes of phagocytosis are transmembrane kinases and they play a key role as virulence factor in amebic colitis as studies in animal model. The study concludes that transmembrane kinases may be significant factors towards the future considerations of drug development. Furthermore, the epithelial cell of the parasite secretes some inflammatory mediators including cyclooxygenase and interleukin (IL-8and IL-beta) thereby resulting in the attraction of macrophages and neutrophils. Due to the blunting effect of innate immune system, corticosteroid therapy tends to worsen the clinical outcome of amoebiasis. The trophozoites may directly inhibit additional human defenses such as the complement system due to CD59 cross reactivity, which is the red blood cells inhibiting membrane for C5b-9 inflammation complex in the human host.

The pathogenic strains of the parasite evade the complement-mediated lysis as the amoebiasis spreads to the liver through the portal blood. The trophozoites that manage to reach the liver forms unique abscesses with well-circumscribed locus of dead hepatocytes encompassed by a fraction of trophozoites, inflammatory cells and active hepatocytes. Accordingly, the parasite has the ability to kill red blood cells without coming in direct contact with them (Feldman, Friedman & Brandt, 2016; Lamps, 2009). On the contrary, limitation of the disease occurs by cell-mediated immunity, which helps to prevent its recurrences. In this regard, the killing of the trophozoites occurs through antigen-specific blastogenic responses that produce lymphokines such as delta interferon, which initiate the killing by macrophages. The death of the trophozoites depends on oxidative and non-oxidative pathways, contact, and nitric oxide. On the same note, the activation of amebicidal activity of neutrophils occurs through the intervention of lymphokines such as TNF- α. Moreover, cytotoxic T-cell activity against the trophozoites occurs through in vitro incubation of CD8+ lymphocytes with the parasitic antigen. However, T-cell response to the parasitic antigens during acute invasive amoebiasis undergoes depression a serum factor induced by the parasite.

The Epidemiology of Entamoeba hystolytica

Generally, the prevalence of amoebiasis is about 5% in the United States with asymptomatic Entamoeba dispar infection being the most prevalent as opposed to Entamoeba hystolytica (Clark, 2011). In addition, approximately 9% of Entamoeba hystolytica result in amoebiasis implying that only 1% of individuals with fecal microscopy results that shows the presence of the parasite develop symptomatic amoebiasis. Conversely, some individuals including recipients of corticosteroid, young patients, malnourished individuals, and pregnant women are predisposed to amebic colitis. In this respect, there were approximately 3000 cases of amoebiasis in 1993 from the CDC that involved over 30% of Hispanic immigrants and 20% of Asian immigrants (Lamps, 2009). Notably, the prevalence of amoebiasis increases significantly among male homosexuals, mentally retarded individuals and individuals living in communal settings. People at the risk of infection are travelers to endemic areas where amebic colitis less common in short term travelers whereas amebic liver abscess is common among less than four days to a minimum of three months travel exposures.

One particular study shows that out of the number of people returning with diarrhea from travel exposures, 10% of them have amoebiasis (Lamps, 2009). Conversely, 2.5% of travelers from Southeast Asia and Central America in another case study revealed an increase in acute amebic diarrhea. The certificate of mortality data in United States from 1991 to 2008 observed 135 deaths from amoebiasis with Texas and California registering a 40% decline in morality (Clark, 2011; Lamps, 2009). However, more amoebiasis deaths were common among citizens born in the United States. On the contrary, over 55 million cases of invasive amoebiasis appear globally on an annual scale thus resulting in more than 0.1 million deaths, which is a representation of a tip of an iceberg considering that only 15% to 25% of infected people end up being symptomatic. Briefly, developing nations tends to have a higher prevalence of amoebiasis as opposed to already developed nations. In this regard, polymerase chain reactions and enzyme-linked immunosorbent assay of feces from asymptomatic individuals helps to determine the prevalence of amoebiasis in developing nations.

According to Clark (2011), Entamoeba dispar colonizes approximately 500,000,000 people with the parasitic infection with the disease being less frequent in children than in adults although children are more predisposed to fulminant colitis. Markedly, invasive amoebiasis is more prevalent in adult males that females although the disease affects both sexes while amebic liver abscess occurs more than ten times among men aged between 20 to 55 years as opposed to women. Even though the disparity for the infection between the two sexes is unclear, it may be due to implication of hormonal effects and alcohol. Nevertheless, the disease increases among postmenopausal women. Amebic liver abscess and the asymptomatic infection is more common and equally distributed among prepubertal children and adults of both sexes and an increased proportion of invasive amoebiasis in adult males may be due to susceptibility of males to the disease (Clark, 2011).

Signs and Symptoms of Human Host

The signs mostly appear one month after ingestion of the cysts by human and according to CDC, only 15% to 20% of the individuals who have the disease become ill (Bennett et al., 2015). The signs are still mild at this stage involving stomach cramps and loose as well as bloody stool although the parasite can produce amebic dysentery when it invaded the intestinal lining. The parasite can cause tissue abscesses and destruction if it invades the bloodstream and ends up in the heart, brain, liver and the heart. Since the liver is the frequent destination of the parasite, the signs and symptoms of liver abscess includes tenderness and fever in the upper-right part of the human torso. Moreover, mild symptoms may include, fatigue, rectal pain during bowel movement, excessive gas, and unintentional weight loss. On the other hand, severe symptoms include nausea and vomiting, abdominal, bloody stools of up to stools each day, abdominal tenderness, jaundice of the brain and lungs, and intermittent fever.

Required Medication

A luminal agent such as paromomycin, iodoquinol, and diloxanide furoate is appropriate in the treatment of asymptomatic amoebiasis such as Entamoeba dispar infections in nonendemic areas. Nitroimidazole derivative and luminal agent is significant in the treatment of amebic colitis in order to eradicate colonization. Similarly, paromomycin is significant in the treatment of intestinal amoebiasis occurring among individuals with HIV infection. On the other hand, medicine such as diloxanide, a derivative of dichlorocetamide that is amebicidal against cyst and trophozoite forms of the parasite is important in the treatment of the disease. However, this medicine is accessible within the United States. Metronidazole is vital in curing amebic liver abscess without drainage after which addition of a luminal agent follows in the treatment. Additionally, metronidazole that can infiltrate the brain-blood barrier is significant in the treatment of disseminated amoebiasis. Nonetheless, in cases where perforated bowel is a concern, empirical antibacterial therapy is applicable.

Conclusion

In retrospect, scientific studies of Entamoeba hystolytica are increasingly becoming significant in light of the pathogenesis of amoebiasis. The infectious disease affects millions of people every single year. To that end, it is crucial for future research studies to focus towards the diagnosis of patients from endemic regions like Central America, Southeast Asia and the tropical regions of Africa. Future research should focus in these regions due to high rate of water and food contamination. Therefore, there is an urgent need to avail medical regiments to affected countries.

References

Clark, C.G. (2011). Entamoeba hystolytica and Entamoeba Dispar, the Non-Identical Twins. World Class Parasites, 7(4), 15-26.

Bennett, J.E., Dolin, R., Blaser, M.J., Mandell, G.L., & Douglas, R.G. (2015). Mandell, Douglas, and Bennett’s Principles and practice of infectious diseases. Philadelphia: Elsevier/Saunders.

Feldman, M., Friedman, L.S., & Brandt, L.J. (2016). Sleisenger and Fordtran’s gastrointestinal and liver disease: Pathophysiology/diagnosis/management. Philadelphia: Saunders/Elsevier.

Lamps, L.W. (2009). Entamoeba hystolytica. Surgical Pathology of the Gastrointestinal System: Bacterial, Fungal, Viral, and Parasitic Infections, 5(3), 169-175.

Mead, J.R., & Okhuysen, P. (2010). Rationale Approaches to Treating Cryptosporidium, Cyclospora, Giardia, and Entamoeba. World Class Parasites, 8(5), 103-115.

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