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Chapter 22 : Colonization and Invasion of Humans by

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Abstract:

parasites have a two-stage life cycle consisting of a disease-causing trophozoite stage and an infectious cyst stage. Ingestion of cysts from fecally contaminated food or water initiates infection in humans. The ingested cyst is quadrinucleate and is resistant to chlorination, gastric acidity, and desiccation. The first line of defense against invasion is provided by the intestinal mucins, which are high-molecular-weight glycoproteins lining the mucosal epithelium. DNA fragmentation characteristic of apoptosis is observed in host cells upon intestinal invasion by . Apoptosis occurs when a signal activates effectors such as caspases (cysteine proteinases with specificity for aspartate residues) to degrade cell components. The role of caspases in vivo on amoebic liver abscesses has been studied by using a mouse model of infection. Infection with usually results in asymptomatic colonization, but there is an approximately 10% risk of developing invasive disease. Interestingly, there was actually an increased rate of new infections in children with serum IgG antibodies to the lectin: children with serum anti-lectin IgG antibodies had 53% more new infections. The discovery that humans naturally acquire partial immunity gives hope that an effective vaccine can be made, and the Gal/GalNac lectin, which mediates adherence, is an intriguing vaccine candidate. Importantly, since humans are the only significant reservoir for infections, a vaccine that blocks colonization could lead to the elimination of amoebiasis.

Citation: Peterson K, Petri, Jr. W. 2005. Colonization and Invasion of Humans by , p 313-324. In Nataro J, Cohen P, Mobley H, Weiser J (ed), Colonization of Mucosal Surfaces. ASM Press, Washington, DC. doi: 10.1128/9781555817619.ch22
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Figure 1

(A) Trophozoite of . Trophozoites are 10 to 30 μm in diameter. They are the invasive form of the parasite and are the only form seen in invasive lesions due to . (B) Cyst of . Cysts are approximately 12 μm in diameter. They are the infectious form of the parasite and are environmentally stable, being resistant to desiccation and chlorination. Reprinted from reference with permission from the publisher. © 2003 Massachusetts Medical Society. All rights reserved.

Citation: Peterson K, Petri, Jr. W. 2005. Colonization and Invasion of Humans by , p 313-324. In Nataro J, Cohen P, Mobley H, Weiser J (ed), Colonization of Mucosal Surfaces. ASM Press, Washington, DC. doi: 10.1128/9781555817619.ch22
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Image of Figure 2
Figure 2

The Gal/GalNAc lectin of . The lectin mediates the adherence of to host immune cells, intestinal epithelium, and colonic mucins and is required for contact-dependent cytolysis and serum resistance. It is composed of three major subunits, each of which is encoded by gene families. By a combination of monoclonal antibody epitope mapping and in vitro expression studies, domains of the lectin involved in carbohydrate binding, host recognition, serum resistance, and cell signaling have been identified. Mϕ, macrophage.

Citation: Peterson K, Petri, Jr. W. 2005. Colonization and Invasion of Humans by , p 313-324. In Nataro J, Cohen P, Mobley H, Weiser J (ed), Colonization of Mucosal Surfaces. ASM Press, Washington, DC. doi: 10.1128/9781555817619.ch22
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Figure 3

Murine model of amebic colitis. A section of the cecum from a C3H mouse infected with is shown at magnification of ×40 (A) and ×1,000 (B) with hematoxylin and eosin stain. The large amebic ulceration seen in panel A is shown under higher power in panel B, where individual amebic trophozoites are demonstrated invading the intestine. Reprinted from reference with permission. © 2002. The American Association of Immunologists, Inc.

Citation: Peterson K, Petri, Jr. W. 2005. Colonization and Invasion of Humans by , p 313-324. In Nataro J, Cohen P, Mobley H, Weiser J (ed), Colonization of Mucosal Surfaces. ASM Press, Washington, DC. doi: 10.1128/9781555817619.ch22
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Figure 4

DNA fragmentation of murine intestinal cells at the site of colonic invasion by . Magnification, ×1,000. Reprinted from reference with permission from Blackwell Publishing.

Citation: Peterson K, Petri, Jr. W. 2005. Colonization and Invasion of Humans by , p 313-324. In Nataro J, Cohen P, Mobley H, Weiser J (ed), Colonization of Mucosal Surfaces. ASM Press, Washington, DC. doi: 10.1128/9781555817619.ch22
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Figure 5

Gross appearance of amebic liver abscess. Reprinted from reference . © 2003 Massachusetts Medical Society. All rights reserved.

Citation: Peterson K, Petri, Jr. W. 2005. Colonization and Invasion of Humans by , p 313-324. In Nataro J, Cohen P, Mobley H, Weiser J (ed), Colonization of Mucosal Surfaces. ASM Press, Washington, DC. doi: 10.1128/9781555817619.ch22
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Figure 6

Acquired immunity of children to amebiasis. Children who developed stool IgA anti-CRD antibodies in the first year of the study ( = 81) had a lower incidence of new infections in the second year compared to children who remained IgA anti-CRD negative ( = 149). The two groups are statistically significantly different ( < 0.04) at every time point. Reprinted from reference with permission from University of Chicago Press. © 2002 by the Infectious Disease Society of America. All rights reserved.

Citation: Peterson K, Petri, Jr. W. 2005. Colonization and Invasion of Humans by , p 313-324. In Nataro J, Cohen P, Mobley H, Weiser J (ed), Colonization of Mucosal Surfaces. ASM Press, Washington, DC. doi: 10.1128/9781555817619.ch22
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