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eFigure 35–11. Multiple lesions of Leishmania major infection. (Used, with permission, from J El-On.)

Current Medical Diagnosis & Treatment 2018 > Protozoal & Helminthic Infections

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eFigure 35–15. Life cycle of Plasmodium vivax, the agent of vivax (tertian) malaria. The female Anopheles mosquito, shown in the typical biting angle, injects sporozoites into the human bloodstream. 1–3: Exoerythrocytic phase of asexual division (schizogony). Within an hour, the sporozoites enter liver cells to initiate the exoerythrocytic phase. Penetration of a hepatocyte is followed by growth and multiplication within a few days (2a), or the parasite may become a hypnozoite, with development delayed for as long as 1–2 years. Asexual multiplication fills the enlarging infected liver cell with merozoites (2a). The cell then ruptures, releasing thousands of parasites (3) to initiate either a second hepatic generation or the erythrocytic phase. 4–9: Erythrocytic phase of schizogony. Invasion of the bloodstream and penetration of red blood cells initiate the blood phase of schizogony. Penetration of the red blood cell may begin as a surface or appliqué (accolé) form (4), after which it enters the cell, rounds up, and ingests hemoglobin to form the ring stage (5), which enlarges and becomes an ameboid trophozoite, with numerous cytoplasmic granules (Schüffner dots) (6) produced as a by-product of hemoglobin breakdown. Nuclear division follows (7), eventually filling the infected cell as the parasites' cytoplasm surrounds each nucleus (8), rupturing it to release more merozoites (9) about 48 hours after onset of the red cell infection (tertian cycle). This asexual erythrocytic schizogony repeats itself with a 48-hour synchronous periodicity. 10a, 10b: Gametogony. Some sporozoites give rise to sexual parasites, gametocyte-producing merozoites that form male (microgametocyte) (10a) or female (macrogametocyte) stages (10b). When taken up in another Anopheles mosquito blood meal, the asexual forms are killed but the sexual stages quickly complete gamete formation. 11–13: Fertilization. "Exflagellation" is the release of male microgametes, which scatter, find a female macrogamete, and fuse. The zygote elongates, becomes a motile ookinete (13), and travels to the mosquito's stomach wall. 14–16: Sporogony. In the stomach wall of the mosquito, the ookinete becomes an oocyst (14). Masses of these oocysts may cover the mosquito's stomach. The oocyst nucleus divides innumerable times (15), and the progeny develop into elongated sporozoites, a process termed sporogony. The oocysts rupture (16), passing sporozoites throughout the female body. Most eventually concentrate in the salivary glands, after which the mosquito becomes infective and can initiate a new malaria cycle. (Reproduced, with permission, from Goldsmith R, Heyneman D [editors]. Tropical Medicine and Parasitology. Originally published by Appleton & Lange. Copyright © 1989 by The McGraw-Hill Companies, Inc.)

Current Medical Diagnosis & Treatment 2018 > Protozoal & Helminthic Infections

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eFigure 35–17. Life cycle of Entamoeba histolytica. Transmission of infective cysts of this abundant amebic parasite of humans (with pathologic results in 10–20% of infections) may involve fecally contaminated flies, water, fingers, or food. The damage caused by these parasites can involve ulceration of the colon or passage through the intestinal mucosa and spread to other organs. Ingested cysts are acted on by stomach and duodenal enzymes and rapidly excyst. The tetranucleated trophozoite (1) separates into four uninucleated amebae (2), each of which divides mitotically, resulting in eight uninucleated amebulae (3). Occasionally, trophozoites penetrate the mucosa, ingest red blood cells (4), and initiate the ulceration process, which may spread extraintestinally. Normally, the trophozoites multiply in the lumen of the colon and form a commensal colony, feeding on fecal bacteria (5). The trophozoites complete their vegetative phase and begin cyst formation by a process consisting of loss of water and rounding up (6), formation of a central vacuole with chromatoidal particles (7), an early cyst maturation stage with development of typical round-ended chromatoidals (binucleated stage) (8), and final maturation, often completed after passage in the feces, to form the tetranucleated cyst (9), which loses its chromatoidals and becomes infective to humans. (Reproduced, with permission, from Goldsmith R, Heyneman D [editors]. Tropical Medicine and Parasitology. Originally published by Appleton & Lange. Copyright © 1989 by The McGraw-Hill Companies, Inc.)

Current Medical Diagnosis & Treatment 2018 > Protozoal & Helminthic Infections

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eFigure 35–28. Life cycles of Fasciola hepatica and F gigantica (liver flukes). A grazing cow ingests vegetation contaminated with metacercariae. Young flukes excyst, penetrate through the intestine, and pass directly into the liver parenchyma and bile ducts, where maturation of flukes follows. Undeveloped eggs are excreted via bile into stool. If this occurs in marshy or wet areas inhabited by host snails (Lymnaea), the miracidia within the eggs develop, hatch, and infect the snails by penetration. In the snail, miracidia become sporocysts that produce rediae that multiply and finally produce swarms of cercariae. These motile larvae emerge, swim from the snail, and encyst on nearby aquatic vegetation. 1–10: After excystation (1), the fluke passes through the gut wall directly into the liver and bile ducts (3). The mature fluke (2) produces large numbers of undeveloped eggs (4) that pass in feces from the host, mature in water (5), hatch, and release miracidia (6) that invade a suitable snail in which multiplication occurs through sporocyst formation and successive generations of rediae (7, 8), resulting finally in shedding from the snail of great numbers of cercariae (9). These swimming larvae encyst on aquatic or immersed vegetation (10), the source of infection of cattle and other herbivores or of humans. (Reproduced, with permission, from Goldsmith R, Heyneman D [editors]. Tropical Medicine and Parasitology. Originally published by Appleton & Lange. Copyright © 1989 by The McGraw-Hill Companies, Inc.)

Current Medical Diagnosis & Treatment 2018 > Protozoal & Helminthic Infections

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eFigure 35–40. Life cycle of Diphyllobothrium latum (broad fish tapeworm). Ingestion of raw or inadequately cooked fish containing plerocercoid larvae is followed by development of a tapeworm in the small bowel and passage of feces containing operculated eggs. Eggs deposited in a freshwater pond or lake hatch and infect the first intermediate host, a copepod (water flea). The infected copepod conveys the early larval form to a small fish, which can in turn infect a number of piscivorous fish until a human or other piscivorous mammal feeds on the larger fish and acquires the infection. 1–6: The scolex (1) of an adult worm attaches by sucking grooves to the wall of the small intestine. Mature segments (2) deposit eggs in the gut lumen that are passed in stool (3). Eggs that reach a freshwater pond hatch after a period of development, releasing the ciliated coracidium (4), which develops in the first intermediate (copepod) host into the procercoid (5). Fish—often minnows—feed on the copepods and digest the procercoids free. The procercoids penetrate the gut, pass to the fish musculature, and mature into a nonencysted plerocercoid (6) capable of passing from the gut of one transport fish host to the flesh of a larger piscivorous host. The final transfer occurs when a human or other piscivorous mammal feeds on the infected fish and digests the plerocercoid free. The young worm attaches by its scolex and grows into an adult tapeworm, often 8 m or more in length and up to 2 cm in breadth. (Reproduced, with permission, from Goldsmith R, Heyneman D [editors]. Tropical Medicine and Parasitology. Originally published by Appleton & Lange. Copyright © 1989 by The McGraw-Hill Companies, Inc.)

Current Medical Diagnosis & Treatment 2018 > Protozoal & Helminthic Infections

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