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eFigure 30–2. Clinical manifestations of hyperlipidemias. A: Xanthomas of extensor tendons of the hands. B: Xeroradiogram of Achilles tendon xanthoma. C: Xanthoma of Achilles tendon (normal Achilles tendons do not exceed 7 mm in diameter in the region between the calcaneus and the point at which the tendon fibers begin to radiate toward their origins). (Reproduced with permission from Gardner DG, Shoback D. Greenspan's Basic & Clinical Endocrinology, 10th ed, McGraw-Hill Education, 2018.) Eight photos depict clinical manifestations of hyperlipidemias.

Current Medical Diagnosis & Treatment 2024 > Lipid Disorders: Clinical Presentations

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eFigure 30–2. Clinical manifestations of hyperlipidemias. A: Xanthomas of extensor tendons of the hands. B: Xeroradiogram of Achilles tendon xanthoma. C: Xanthoma of Achilles tendon (normal Achilles tendons do not exceed 7 mm in diameter in the region between the calcaneus and the point at which the tendon fibers begin to radiate toward their origins). (Reproduced with permission from Gardner DG, Shoback D. Greenspan's Basic & Clinical Endocrinology, 10th ed, McGraw-Hill Education, 2018.) Eight photos depict clinical manifestations of hyperlipidemias.

Current Medical Diagnosis & Treatment 2024 > Lipid Disorders: Clinical Presentations

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eFigure 30–2. Clinical manifestations of hyperlipidemias. A: Xanthomas of extensor tendons of the hands. B: Xeroradiogram of Achilles tendon xanthoma. C: Xanthoma of Achilles tendon (normal Achilles tendons do not exceed 7 mm in diameter in the region between the calcaneus and the point at which the tendon fibers begin to radiate toward their origins). (Reproduced with permission from Gardner DG, Shoback D. Greenspan's Basic & Clinical Endocrinology, 10th ed, McGraw-Hill Education, 2018.) Eight photos depict clinical manifestations of hyperlipidemias.

Current Medical Diagnosis & Treatment 2024 > Lipid Disorders: Clinical Presentations

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector’s midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2024 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector’s midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2024 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector’s midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2024 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector’s midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2024 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector’s midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2024 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector’s midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2024 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector’s midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2024 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector’s midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2024 > American Trypanosomiasis (Chagas Disease)

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eFigure 37–2. Life cycle of Trypanosoma cruzi. An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucous membranes, such as the conjunctiva . Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes . The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes . Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites . The ingested trypomastigotes transform into epimastigotes in the vector’s midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut . T cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of T cruzi bug.

Current Medical Diagnosis & Treatment 2024 > American Trypanosomiasis (Chagas Disease)

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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

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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

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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 28–14. Hands of patient with pseudohypoparathyroidism. A: Note the short fourth finger. B: Note the "absent" fourth knuckle. C: Film shows the short fourth metacarpal. (Reproduced, with permission, from Potts JT. Pseudohypoparathyroidism: Clinical features; signs and symptoms; diagnosis and differential diagnosis. In: The Metabolic Basis of Inherited Disease, 4th ed. Stanbury JB, Wyngaarden JB, Frederickson DS [editors]. McGraw-Hill, 1978.) A photo shows stubby fingers of a patient, with the fourth finger as short as the fifth one. A photo shows a patient's hands balled into a fist. The fourth knuckle in each hand is missing. An x-ray shows that the metacarpal of the fourth finger is short.

Current Medical Diagnosis & Treatment 2024 > Hypoparathyroidism & Pseudohypoparathyroidism

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eFigure 28–14. Hands of patient with pseudohypoparathyroidism. A: Note the short fourth finger. B: Note the "absent" fourth knuckle. C: Film shows the short fourth metacarpal. (Reproduced, with permission, from Potts JT. Pseudohypoparathyroidism: Clinical features; signs and symptoms; diagnosis and differential diagnosis. In: The Metabolic Basis of Inherited Disease, 4th ed. Stanbury JB, Wyngaarden JB, Frederickson DS [editors]. McGraw-Hill, 1978.) A photo shows stubby fingers of a patient, with the fourth finger as short as the fifth one. A photo shows a patient's hands balled into a fist. The fourth knuckle in each hand is missing. An x-ray shows that the metacarpal of the fourth finger is short.

Current Medical Diagnosis & Treatment 2024 > Hypoparathyroidism & Pseudohypoparathyroidism

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eFigure 28–14. Hands of patient with pseudohypoparathyroidism. A: Note the short fourth finger. B: Note the "absent" fourth knuckle. C: Film shows the short fourth metacarpal. (Reproduced, with permission, from Potts JT. Pseudohypoparathyroidism: Clinical features; signs and symptoms; diagnosis and differential diagnosis. In: The Metabolic Basis of Inherited Disease, 4th ed. Stanbury JB, Wyngaarden JB, Frederickson DS [editors]. McGraw-Hill, 1978.) A photo shows stubby fingers of a patient, with the fourth finger as short as the fifth one. A photo shows a patient's hands balled into a fist. The fourth knuckle in each hand is missing. An x-ray shows that the metacarpal of the fourth finger is short.

Current Medical Diagnosis & Treatment 2024 > Hypoparathyroidism & Pseudohypoparathyroidism

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