One, etiology
The colonic acanthamoeba was first discovered by Malmsten in 1857 in the feces of 2 patients with acute dysentery. Subsequently, LeuKart found the same worm in the large intestine of pigs in 1861. In 1862, Stein classified it into the genus Balantidium and named it Balantidium coli, its taxonomic status is Protozoa Subkingdom, Ciliate Phylum, Kinetoplastida Class, Parabasalia Subclass, Trichomonadida Order, Trichomonadida Suborder, Balantidium Genus, Balantidium coli.
1. The colonic acanthamoeba is the only ciliate discovered to be parasitic in humans and also the largest protozoan parasitic in humans. Its life cycle includes two basic forms: the trophozoite and the cyst.
(1) The trophozoite is circular or oval, colorless, transparent, or faintly gray with a green tinge, with a size of about (30~200) μm × (25~120) μm. The ventral surface is slightly flattened, and the dorsal surface is elevated. The surface of the organism has ridge-like elevations and groove-like depressions, extending from the anterior to the posterior end. The surface of the ridge-like elevations has folds, and the groove-like depressions are located between the two ridges. The surface纤毛 all extend outward from the grooves, and the movement of the flagella can cause the organism to move forward and backward. The surface of the organism is covered with a pellicle, below which is the transparent ectoplasm, and inside is the endoplasm. The anterior end of the organism is slightly pointed, with a food vacuole formed by the invagination of the pellicle on the ventral surface. Food is digested within the vacuole, and the residual substances are excreted out of the body through a small and not obvious triangular anal pore at the posterior end of the organism. 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 vacuoles, and so on. Mitochondria are distributed around the periphery of the organism.
(2) The cyst is round or oval, about 40-60μm in size. The cyst wall is thick and transparent, light yellow or light green. Active trophozoites can be seen in fresh cysts. The cyst has strong resistance to the external environment and can survive for 2 weeks to 2 months at room temperature, and it will die after 3 hours in direct sunlight; it also has strong resistance to chemical drugs and can survive for 4 hours in a 10% formalin solution.
2. The cyst is the infective stage of this worm. Humans become infected by eating food or drinking water contaminated with cysts. The cyst is digested by digestive juices in the digestive tract, and the worm escapes from the cyst to become a trophozoite. The trophozoite falls into the large intestine and feeds on intestinal waste, intestinal wall cells, and bacteria. The trophozoite reproduces mainly by transverse binary fission in the intestine, but can also reproduce by budding. Some trophozoites are affected by desiccation during the formation of feces, and the worm becomes round, secreting a cyst wall to enclose the worm, forming a cyst and excreted with feces. Trophozoites in the pig intestinal lumen can form a large number of cysts, but it is rare in the human intestinal lumen. In addition, the nucleus does not divide during cyst formation, so when the cyst is excreted from the digestive tract, only one trophozoite can be produced from a single cyst.
2. Pathogenesis
Most people believe that the colon bag mucus has pathogenicity. When the human body has chronic diseases, malnutrition, and intestinal dysfunction, the worm can invade and reproduce to cause disease. After the worm invades the human body, it needs a period of time to adapt to the intestinal symbiotic flora. Once adapted, it can reproduce rapidly 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 worm and causing pathological changes. The colon bag mucus invades the intestinal tissue must rely on the mechanical movement of the worm's cilia and the action of hyaluronidase secreted. The worm dissolves the intercellular matrix with hyaluronidase and penetrates the intestinal tissue. In severely infected pig feces, glycogen phosphorylase and hemolysin have also been isolated. The worm uses the above factors to cause colonic mucosal inflammation, necrosis, and ulcers, and can also secondary bacterial infection, thereby aggravating mucosal lesions. The pathological changes are similar to those caused by intracellular amebae. The lesions are mainly located in the cecum and sigmoid colon, occasionally involving the distal ileum and appendix, and in some cases, the worm can invade mesenteric lymph nodes, liver, lung, pleura, urinary and reproductive tract, etc. The intestinal mucosa is congested and edematous, and sometimes there are pinpoint bleeding 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 small openings, large bases, and irregular edges. Unlike amebic ulcers, the ulcers formed by this disease have slightly larger openings and short, thick necks. 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 are also lymphocytes and eosinophils infiltrating.