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eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

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eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

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eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

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eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

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eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

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eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

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eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

View in Context

eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

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eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

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eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

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eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

View in Context

eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

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eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

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eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

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eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

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eFigure 37–9. Life cycle of Plasmodium. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host . Sporozoites infect liver cells and mature into schizonts , which rupture and release merozoites . (Of note, in Plasmodium vivax and Plasmodium ovale a dormant stage [hypnozoites] can persist in the liver and cause relapses by invading the bloodstream weeks or even years later.) After this initial replication in the liver (exo-erythrocytic schizogony ), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony ). Merozoites infect RBCs . The ring stage trophozoites mature into schizonts, which rupture releasing merozoites . Some parasites differentiate into sexual erythrocytic stages (gametocytes) . Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal . The parasites’ multiplication in the mosquito is known as the sporogonic cycle . While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes . The zygotes in turn become motile and elongated (ookinetes) , which invade the midgut wall of the mosquito where they develop into oocysts . The oocysts grow, rupture, and release sporozoites , which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of malarial parasite.

Current Medical Diagnosis & Treatment 2024 > Malaria

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eFigure 37–15. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2024 > Amebiasis

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eFigure 37–15. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2024 > Amebiasis

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eFigure 37–15. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2024 > Amebiasis

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eFigure 37–15. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2024 > Amebiasis

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eFigure 37–15. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2024 > Amebiasis

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eFigure 37–15. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2024 > Amebiasis

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eFigure 37–15. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2024 > Amebiasis

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eFigure 37–15. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2024 > Amebiasis

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eFigure 37–15. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2024 > Amebiasis

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eFigure 37–15. Life cycle of Entamoeba histolytica. Cysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body and would not survive exposure to the gastric environment if ingested. In many cases, the trophozoites remain confined to the intestinal lumen (: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients, the trophozoites invade the intestinal mucosa (: intestinal disease) or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (: extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E histolytica and E dispar. These two species are morphologically indistinguishable unless E histolytica is observed with ingested RBCs (erythrophagocytosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Entamoeba histolytica.

Current Medical Diagnosis & Treatment 2024 > Amebiasis

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eFigure 37–25. Adult trematodes. Clonorchi sinensis adults are flattened and measure approximately 10–25 mm long by 3–5 mm wide. Like other flukes, they are hermaphroditic, with a single ovary situated anterior to two branches testes. Adults reside in the biliary passages of the liver of the definitive host. A: Adult of C sinensis. B: Adult of C sinensis stained with carmine. Clearly visible in this image are the oral sucker (OS), pharynx (PH), ceca (CE), acetabulum, or ventral sucker (AC), uterus (UT), vitellaria (VT) and testes (TE). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A photo and a diagram of adult trematodes.

Current Medical Diagnosis & Treatment 2024 > Clonorchiasis & Opisthorchiasis

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eFigure 37–25. Adult trematodes. Clonorchi sinensis adults are flattened and measure approximately 10–25 mm long by 3–5 mm wide. Like other flukes, they are hermaphroditic, with a single ovary situated anterior to two branches testes. Adults reside in the biliary passages of the liver of the definitive host. A: Adult of C sinensis. B: Adult of C sinensis stained with carmine. Clearly visible in this image are the oral sucker (OS), pharynx (PH), ceca (CE), acetabulum, or ventral sucker (AC), uterus (UT), vitellaria (VT) and testes (TE). (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A photo and a diagram of adult trematodes.

Current Medical Diagnosis & Treatment 2024 > Clonorchiasis & Opisthorchiasis

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–32. Hydatid cysts in the liver on CT scan. Hydatid cysts in the liver are caused by parasitic infection by the Echinococcus tapeworm. On CT, they appear as low density, fluid-filled masses, often with septations. The cyst walls may enhance with contrast or may be calcified (arrows). (Used, with permission, from Nicholas Fidelman, MD.) An abdominal CT scan shows a large muscular outgrowth from the lower lobe of the liver.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–33. Echinococcosis of the liver with hepatobronchial fistula. This CT scan of the upper portion of the liver demonstrates a large, well-circumscribed, sharply demarcated cystic lesion of the right lobe of the liver near the diaphragm—typical of echinococcal cysts. The additional finding here is a change in the right lung at the posterior sulcus so that instead of the lung around the cyst being aerated, there is increased density within this area. This finding proved to be the result of a fistula from the echinococcal cyst through the diaphragm and into the right lung base. An abdominal CT scan shows a large lesion in the upper lobe of the liver, and an outgrowth from the right lobe.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 9–20. Normal lung ventilation with xenon-133. With the patient’s single full breath, inhaled radioxenon is evenly distributed to all lung areas, reaching the terminal airways and alveoli in the normal patient (A, posterior view). There is a less noticeable gradient of activity from the upper to the lower lung fields than is seen in perfusion lung images. Fifteen-second images obtained during closed-system rebreathing of a xenon–oxygen mixture show uniform distribution at 120 seconds (B). Serial 15-second frames after switching the patient to room air breathing (C to G) show a homogeneous pattern of washout from all lung areas. This sequence mainly evaluates the posterior lung regions. To better localize gas trapping in specific lung segments or more anterior regions, the acquisition may be modified after the rebreathing phase by rotating the patient into posterior oblique positions. Selected images from a complete study include single breath (H, posterior view), the late phase of rebreathing (I, posterior view), posterior washout (J), left posterior oblique washout (K), and right posterior oblique washout (L). No gas is retained in this patient, which is normal, but in obstructive airway disease gas retention persists and is better localized in the oblique views than in a posterior view alone. A small amount of alveolar xenon normally crosses the alveolar membrane to reach the blood and be distributed throughout the body. Because it is highly soluble in lipids, xenon accumulates in adipose tissue, including the liver, which is faintly seen with prolonged rebreathing. Liver activity should not be mistaken for delayed washout of xenon from the base of the lung. Occasionally, splenic blood pool radioactivity or swallowed xenon in the stomach may also be seen. (SIN BRE = single breath, L REB = late rebreathe, WO = washout.) (Reproduced with permission from Grippi MA, Elias JA, Fishman JA, Kotloff RM, Pack AI, Senior RM, Siegel MD. Fishman’s Pulmonary Diseases and Disorders, 5e. 2015.) Four examples of normal ventilation scans compared with eight examples of abnormal scans.

Current Medical Diagnosis & Treatment 2024 > Pulmonary Venous Thromboembolism

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eFigure 18–8. Dilated bile ducts. A: CT shows a dilated distal bile duct (arrowhead). L, liver; k, kidney. B: CT demonstrates dilated intrahepatic bile ducts (arrow) and a liver mass (M). (Reproduced, with permission, from Barth KH. Percutaneous biliary drainage for high obstruction. Radiol Clin North Am. 1990;28:1226.) An axial CT scan shows an enlarged bile duct adjacent to liver and kidney. An axial CT scan shows enlarged bile ducts on either side of a liver mass.

Current Medical Diagnosis & Treatment 2024 > Jaundice & Evaluation of Abnormal Liver Biochemical Tests

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eFigure 18–8. Dilated bile ducts. A: CT shows a dilated distal bile duct (arrowhead). L, liver; k, kidney. B: CT demonstrates dilated intrahepatic bile ducts (arrow) and a liver mass (M). (Reproduced, with permission, from Barth KH. Percutaneous biliary drainage for high obstruction. Radiol Clin North Am. 1990;28:1226.) An axial CT scan shows an enlarged bile duct adjacent to liver and kidney. An axial CT scan shows enlarged bile ducts on either side of a liver mass.

Current Medical Diagnosis & Treatment 2024 > Jaundice & Evaluation of Abnormal Liver Biochemical Tests

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eFigure 18–10. Schematic diagram of a percutaneous transhepatic cholangiogram, here used to provide drainage for an obstructing pancreatic carcinoma. A: A dilated peripheral intrahepatic bile duct is entered percutaneously with a fine needle (arrow). B: A long guidewire is passed through the needle into the intrahepatic duct, common hepatic duct, and common bile duct, and then advanced past the tumor into the duodenum. C: The needle is withdrawn, and a plastic catheter has been passed over the guidewire to create a channel through the liver parenchyma. D. An external-internal drainage catheter is inserted over the guidewire and through the channel, then advanced via the bile ducts and through the tumor to empty into the duodenum. (Reproduced, with permission, from James TW, Baron TH. Endoscopic and Radiologic Treatment of Biliary Disease. In: Feldman M, Friedman LS, Brandt LJ [editors]. Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 2 vol set, 11th edition. Philadelphia, Elsevier; 2023.) Four diagrams of the liver and gall bladder depict the steps in a percutaneous transhepatic cholangiogram.

Current Medical Diagnosis & Treatment 2024 > Jaundice & Evaluation of Abnormal Liver Biochemical Tests

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eFigure 18–18. Cirrhosis: macronodular and postnecrotic (low power). An image shows a layer of fatty cells. A histology shows a section of the liver with scar tissue.

Current Medical Diagnosis & Treatment 2024 > Cirrhosis

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eFigure 18–18. Cirrhosis: macronodular and postnecrotic (low power). An image shows a layer of fatty cells. A histology shows a section of the liver with scar tissue.

Current Medical Diagnosis & Treatment 2024 > Cirrhosis

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eFigure 18–25. Cirrhosis. Ultrasonogram shows increased echogenicity in the liver (L). Arrowhead shows ascitic fluid. (Reproduced, with permission, from Krebs CA, Giyanani VL, Eisenberg RL. Ultrasound Atlas of Disease Processes. Originally published by Appleton & Lange. Copyright © 1993 by The McGraw-Hill Companies, Inc.) An ultrasonogram shows a highly reflective liver under ascitic fluid.

Current Medical Diagnosis & Treatment 2024 > Cirrhosis

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eFigure 18–26. Cirrhosis. A: Longitudinal ultrasonogram through the right upper abdomen in a patient with alcohol-associated liver disease. A markedly nodular liver (arrows) is seen in addition to a large amount of ascites (A). B: Transverse ultrasonogram from the same patient in which dilated tortuous vessels (arrows) adjacent to the spleen (S) are seen. These are typical for splenic varices in a patient with portal hypertension. (Courtesy of Peter W. Callen, MD.) An ultrasonogram shows ascites located above the markedly nodular liver. An ultrasonogram shows spleen located over the tortuous vessels of the liver.

Current Medical Diagnosis & Treatment 2024 > Cirrhosis

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eFigure 18–26. Cirrhosis. A: Longitudinal ultrasonogram through the right upper abdomen in a patient with alcohol-associated liver disease. A markedly nodular liver (arrows) is seen in addition to a large amount of ascites (A). B: Transverse ultrasonogram from the same patient in which dilated tortuous vessels (arrows) adjacent to the spleen (S) are seen. These are typical for splenic varices in a patient with portal hypertension. (Courtesy of Peter W. Callen, MD.) An ultrasonogram shows ascites located above the markedly nodular liver. An ultrasonogram shows spleen located over the tortuous vessels of the liver.

Current Medical Diagnosis & Treatment 2024 > Cirrhosis

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eFigure 18–28. Cirrhosis. Contrast-enhanced CT demonstrates the classic features of cirrhosis–a nodular contour to the liver (yellow arrows) along with features of portal hypertension including ascites (red arrow), splenomegaly (black arrow), and distal esophageal varices (green arrow). (Used, with permission, from Nicholas Fidelman, MD.) An axial CT scan shows the features of abdominal organs during cirrhosis.

Current Medical Diagnosis & Treatment 2024 > Cirrhosis

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eFigure 18–39. Liver biopsy—centrilobular congestion (nutmeg liver). An image from the liver biopsy shows a circular body adjacent to the liver.

Current Medical Diagnosis & Treatment 2024 > Hepatic Venous Outflow Obstruction (Budd-Chiari Syndrome)

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eFigure 18–40. Liver abscess. CT shows the abscess as a low-density mass (A). S, spleen; L, liver. (Reproduced, with permission, from Krebs CA, Giyanani VL, Eisenberg RL. Ultrasound Atlas of Disease Processes. Originally published by Appleton & Lange. Copyright © 1993 by The McGraw-Hill Companies, Inc.) An axial CT scan shows an enlarged abscess adjacent to the liver. Spleen is located opposite to the abscess.

Current Medical Diagnosis & Treatment 2024 > Pyogenic Hepatic Abscess

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eFigure 18–41. Multiple hepatic and splenic pyogenic abscesses. The liver contains multiple lucent fluid collections with irregular margins and abnormal septations. These collections were the result of a staphylococcal infection and represent pyogenic abscesses. The spleen also contains abscesses. An axial scan shows an enlarged liver, consisting of lucent fluid collections, irregular margins, and abnormal septations.

Current Medical Diagnosis & Treatment 2024 > Pyogenic Hepatic Abscess

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eFigure 18–42. Hemangioma. Postcontrast CT scans demonstrate (A) early peripheral enhancement (arrow) and (B) delayed central filling (arrowhead). L, liver; S, spleen. (Reproduced, with permission, from Krebs CA, Giyanani VL, Eisenberg RL. Ultrasound Atlas of Disease Processes. Originally published by Appleton & Lange. Copyright © 1993 by The McGraw-Hill Companies, Inc.) An axial CT scan shows an enlargement in the lateral edge of the liver. Spleen is located in the opposite side of the body. An axial CT scan shows a filled enlargement in the lateral edge of the liver. Spleen is located in the opposite side of the body.

Current Medical Diagnosis & Treatment 2024 > Benign Liver Neoplasms

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eFigure 18–42. Hemangioma. Postcontrast CT scans demonstrate (A) early peripheral enhancement (arrow) and (B) delayed central filling (arrowhead). L, liver; S, spleen. (Reproduced, with permission, from Krebs CA, Giyanani VL, Eisenberg RL. Ultrasound Atlas of Disease Processes. Originally published by Appleton & Lange. Copyright © 1993 by The McGraw-Hill Companies, Inc.) An axial CT scan shows an enlargement in the lateral edge of the liver. Spleen is located in the opposite side of the body. An axial CT scan shows a filled enlargement in the lateral edge of the liver. Spleen is located in the opposite side of the body.

Current Medical Diagnosis & Treatment 2024 > Benign Liver Neoplasms

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eFigure 18–44. Focal nodular hyperplasia on MRI (post-contrast). A post-contrast MRI image shows a bright, well-circumscribed hyperenhancing lesion in the right lobe of the liver that has a "central stellate scar" (arrow) without findings of cirrhosis. These characteristics are typical of focal nodular hyperplasia. (Used, with permission, from Nicholas Fidelman, MD.) An axial post-contrast MRI image shows a large lesion in the center of the liver, with a scar across its center.

Current Medical Diagnosis & Treatment 2024 > Benign Liver Neoplasms

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eFigure 18–45. Focal nodular hyperplasia. A histology shows irregular bright patches amidst small dense spots. A photo shows liver tissue with small nodules.

Current Medical Diagnosis & Treatment 2024 > Benign Liver Neoplasms

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eFigure 18–45. Focal nodular hyperplasia. A histology shows irregular bright patches amidst small dense spots. A photo shows liver tissue with small nodules.

Current Medical Diagnosis & Treatment 2024 > Benign Liver Neoplasms

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eFigure 18–46. Hepatic adenoma. A histology shows a white patch amidst small dark spots. A photo of a liver tissue shows a large opaque structure on the cut surface.

Current Medical Diagnosis & Treatment 2024 > Benign Liver Neoplasms

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eFigure 18–46. Hepatic adenoma. A histology shows a white patch amidst small dark spots. A photo of a liver tissue shows a large opaque structure on the cut surface.

Current Medical Diagnosis & Treatment 2024 > Benign Liver Neoplasms

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eFigure 18–57. Acute pancreatitis. CT shows diffuse enlargement of the pancreas (P) with dilated bile duct (arrow) and pancreatic duct (arrowheads). L, liver; a, aorta; K, kidneys; s, superior mesenteric artery. (Reproduced, with permission, from Krebs CA, Giyanani VL, Eisenberg RL. Ultrasound Atlas of Disease Processes. Originally published by Appleton & Lange. Copyright © 1993 by The McGraw-Hill Companies, Inc.) A radiograph of the abdomen in a transverse view reveals a mass on the pancreas.

Current Medical Diagnosis & Treatment 2024 > Acute Pancreatitis

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eFigure 21–1. Biometric measurements in a fetus. A: The biparietal diameter is measured on an axial image through the fetal head at the level of the hypoechoic thalamui (asterisks) and the cavum septum pellucidum (arrows). Head circumference is measured on the same plane of imaging as the biparietal diameter. B: Femur length. C: Abdominal circumference is measured in a transverse plane through the abdomen at the level of the stomach (S) and right portal vein of the liver (arrows); spine is seen at 3 o'clock. The ultrasound age is usually an average of the four measurements—biparietal diameter, head circumference, abdominal circumference, and femur length—and is reported in menstrual weeks. The result is compared with the patient's reported first day of her last normal menstrual period. (Reproduced, with permission, from Fetal Imaging. In: Cunningham F, Leveno KJ, Bloom SL, Dashe JS, Hoffman BL, Casey BM, Spong CY (editors). Williams Obstetrics, 25th ed. McGraw Hill; 2018.) Three sonograms show the biometric measurements of a fetus inside the uterus.

Current Medical Diagnosis & Treatment 2024 > Essentials of Prenatal Care

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