I. Causes of Disease
The colonic acanthamoeba was first described by Malmsten in1857In the year2was found in the feces of patients with acute dysentery, and then LeuKart in1861In the same year, the worm was also found in the large intestine of pigs.1862In the year, Stein classified it into the genus Bag and named it colonic acanthamoeba, its taxonomic status is Protozoa Subkingdom, Ciliate Phylum, Kinetoplastid Class, Vorticella Subclass, Trichocerca Order, Trichocerca Suborder, Bag Genus, colonic acanthamoeba (Balantidium coli).
1The morphological colonic acanthamoeba is the only ciliate discovered to be parasitic in humans and the largest protozoan parasitic in the human body. Its life cycle includes two basic forms: the trophozoite and the cyst.
(1) The trophozoite is round or oval, colorless and transparent or faintly gray with a green tinge, about (30 to200 μm × (25~120 μm. The ventral surface is slightly flattened, and the dorsal surface is elevated. The body surface has ridges and grooves, extending from the anterior to the posterior end. The ridges have folds on their surface, and the grooves are located between the ridges. The surface cilium extends outward from the grooves, and the movement of the cilium can cause the body to move forward and backward. The body surface is covered with a membrane, below which is the transparent ectoplasm, and inside is the endoplasm. The anterior end is slightly pointed, with a food vesicle formed by the inward indentation of the membrane on the ventral surface, where food is digested. The remaining substances are excreted through a small, inconspicuous triangular anal pore at the posterior end of the body. The trophozoite has electron-dense bodies. There are also two contractile vacuoles in the cytoplasm that can regulate osmotic pressure. The cytoplasm also contains polysaccharide granules, food vesicles, etc. The mitochondria are distributed around the body surface.
(2)The cyst is round or oval, with a size of about40 to60μm. The cyst wall is thick and transparent, pale yellow or light green. Active trophozoites can be seen in fresh cysts. The cyst has strong resistance to the external environment and can survive at room temperature for2weeks to2months, under direct sunlight for3h later and then die; it also has strong resistance to chemical drugs, in10% formaldehyde solution can survive4h.
2The cyst stage is the infective stage of this organism. Humans become infected by ingesting food or drinking water contaminated with cysts. The cyst is digested by digestive juices in the digestive tract, and the organism emerges from the cyst and transforms into a trophozoite. The trophozoite falls into the large intestine and feeds on intestinal food residues, intestinal wall cells, and bacteria. The trophozoite reproduces mainly by transverse binary fission in the intestines, but can also reproduce by budding. Some trophozoites become rounded due to the dehydration of fecal formation, and the organism secretes a cyst wall that surrounds the trophozoite, forming a cyst that is excreted with the feces. Trophozoites in the porcine intestinal lumen can form a large number of cysts, but in the human intestinal lumen, cyst formation is rare. In addition, the nucleus does not divide during cyst formation, so when the cyst is digested in the digestive tract, only one trophozoite can be produced from a single cyst.
Second, Pathogenesis
Many people believe that Entamoeba coli has pathogenic properties. When the human body has chronic diseases, malnutrition, or intestinal dysfunction, the organism can invade and reproduce, causing disease. After the organism invades the human body, it needs a period of time to adapt to the intestinal symbiotic flora. Once adapted, it can reproduce rapidly and in large numbers. Some bacteria in the intestines, such as Klebsiella, Staphylococcus aureus, and Enterobacter, as well as other parasites, have the effect of promoting the growth of this organism and causing pathological changes. Entamoeba coli invades intestinal tissue by means of the mechanical movement of the organism's cilia and the action of hyaluronidase secretion. The organism dissolves the intercellular matrix through hyaluronidase and penetrates the intestinal tissue. In severe infections, glycogenolytic enzymes and hemolysins have been isolated from pig feces. The organism causes colonic mucosal inflammation, necrosis, and ulcers by means of the aforementioned factors, and can lead to secondary bacterial infections, thereby aggravating mucosal lesions. The pathological changes are similar to those caused by invasive amebae in intestinal lesions. The lesions are mainly located in the cecum and sigmoid colon, occasionally involving the distal ileum and appendix, and in some cases, the organism can invade mesenteric lymph nodes, liver, lungs, pleura, and urinary and reproductive tracts. The intestinal mucosa is congested and edematous, and sometimes there are pinpoint hemorrhagic spots. In the early stage of the lesion, the intestinal mucosa may have volcanic crater-like ulcers with a diameter of a few millimeters, which gradually expand and fuse to form ulcers with a small mouth, large base, and irregular edges. Unlike amebic ulcers, the ulcers formed in this disease have a slightly larger opening and a short, thick neck. The bottom of the ulcer is generally located in the submucosa, but a large number of trophozoites can also be seen in the surrounding intestinal mucosa. The mucosa between the ulcers can be normal or edematous and hemorrhagic, and there is infiltration of lymphocytes and eosinophils.