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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 37–18. Life cycle of Giardia lamblia. Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages) . The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) . Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces . Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Giardia.

Current Medical Diagnosis & Treatment 2024 > Giardiasis

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eFigure 37–18. Life cycle of Giardia lamblia. Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages) . The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) . Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces . Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Giardia.

Current Medical Diagnosis & Treatment 2024 > Giardiasis

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eFigure 37–18. Life cycle of Giardia lamblia. Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages) . The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) . Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces . Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Giardia.

Current Medical Diagnosis & Treatment 2024 > Giardiasis

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eFigure 37–18. Life cycle of Giardia lamblia. Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages) . The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) . Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces . Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Giardia.

Current Medical Diagnosis & Treatment 2024 > Giardiasis

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eFigure 37–18. Life cycle of Giardia lamblia. Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages) . The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) . Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces . Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Giardia.

Current Medical Diagnosis & Treatment 2024 > Giardiasis

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eFigure 37–18. Life cycle of Giardia lamblia. Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages) . The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (hands or fomites) . In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites) . Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk . Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in nondiarrheal feces . Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Giardia.

Current Medical Diagnosis & Treatment 2024 > Giardiasis

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eFigure 37–19. Giardia lamblia trophozoite: Giardia duodenalis trophozoites in Kohn stain. G duodenalis trophozoites are pear-shaped and measure 10–20 mcM in length. In permanent, stained specimens, two large nuclei are usually visible. The sucking disks (used for attaching to the host’s mucosal epithelium), median bodies, and flagella (8) may also be seen. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A photomicrograph of Giardia lamblia trophozoite in a Kohn stain.

Current Medical Diagnosis & Treatment 2024 > Giardiasis

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eFigure 37–35. Trichuris trichiura. Note copulatory bursa and single terminal spicule in male (above). Female at right. The worms inhabit the large intestine, with their narrow anterior ends sewn into the mucosa. (Reproduced, with permission, from Goldsmith R, Heyneman D [editors]. Tropical Medicine and Parasitology. Originally published by Appleton & Lange. Copyright © 1989 by The McGraw-Hill Companies, Inc.) An illustration shows male Trichuris trichiura with bursa and spicule. The female has a long tail.

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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eFigure 37–36. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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eFigure 37–36. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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eFigure 37–36. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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eFigure 37–36. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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eFigure 37–36. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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eFigure 37–36. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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eFigure 37–36. Life cycle of Trichuris trichiura. The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15–30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60–70 days after infection. Female worms in the cecum shed between 3000 and 20,000 eggs per day. The life span of the adults is about 1 year. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of nematode or roundworm, Trichuris trichiura.

Current Medical Diagnosis & Treatment 2024 > Trichuriasis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 8–3. Sinusitis. A: Axial CT section reveals opacification of the left maxillary sinus. B: Axial T2-weighted MR image (TR [equals] 2000 ms, TE [equals] 80 ms) in the same patient. There is a peripheral zone of high signal intensity representing thickened mucosa with submucosal fluid. The central zone reveals slightly lower signal intensity. The mucoproteinaceous secretions show variable signals depending on the protein content. (Reproduced, with permission, from Rao VM, Flanders AE, Tom BM. MRI and CT Atlas of Correlative Imaging in Otolaryngology. Originally published by Appleton & Lange. Copyright © 1992 by The McGraw-Hill Companies, Inc.) A CT scan shows an axial view of the opaque left maxillary sinus. A T2 weighted MRI shows an axial view of opaque left maxillary sinus filled with submucosal fluid.

Current Medical Diagnosis & Treatment 2024 > Infections of the Nose & Paranasal Sinuses

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eFigure 8–3. Sinusitis. A: Axial CT section reveals opacification of the left maxillary sinus. B: Axial T2-weighted MR image (TR [equals] 2000 ms, TE [equals] 80 ms) in the same patient. There is a peripheral zone of high signal intensity representing thickened mucosa with submucosal fluid. The central zone reveals slightly lower signal intensity. The mucoproteinaceous secretions show variable signals depending on the protein content. (Reproduced, with permission, from Rao VM, Flanders AE, Tom BM. MRI and CT Atlas of Correlative Imaging in Otolaryngology. Originally published by Appleton & Lange. Copyright © 1992 by The McGraw-Hill Companies, Inc.) A CT scan shows an axial view of the opaque left maxillary sinus. A T2 weighted MRI shows an axial view of opaque left maxillary sinus filled with submucosal fluid.

Current Medical Diagnosis & Treatment 2024 > Infections of the Nose & Paranasal Sinuses

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Figure 8–8. Severe angular cheilitis in a man with HIV with oral thrush. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H. The Color Atlas of Family Medicine, 2nd ed. McGraw-Hill, 2013.) A photo of severe angular cheilitis in an H I V-positive man with oral thrush. White curd-like patches overly the erythematous mucosa.

Current Medical Diagnosis & Treatment 2024 > Oral Candidiasis

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eFigure 17–1. Duodenal angioectasia characterized by its bright red, stellate appearance. (Used, with permission, from Richard W. Mclean I, MD.) An endoscopy image of the colon reveals a localized patch of bright red, spider-like vessels on the mucosa.

Current Medical Diagnosis & Treatment 2024 > GI Bleeding

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eFigure 17–2. A: Colonic angioectasia characterized by its bright red appearance. B: Same lesion following cautery with a bipolar probe. (Used, with permission, from A. Huang.) An endoscopy image of the colon reveals a bright red, irregular patch of angioectasia on the mucosal lining. An endoscopy image reveals an angioectasia lesion, appearing as an opaque white spot with a yellow center.

Current Medical Diagnosis & Treatment 2024 > GI Bleeding

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eFigure 17–2. A: Colonic angioectasia characterized by its bright red appearance. B: Same lesion following cautery with a bipolar probe. (Used, with permission, from A. Huang.) An endoscopy image of the colon reveals a bright red, irregular patch of angioectasia on the mucosal lining. An endoscopy image reveals an angioectasia lesion, appearing as an opaque white spot with a yellow center.

Current Medical Diagnosis & Treatment 2024 > GI Bleeding

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eFigure 17–4. Normal appearing "Z line": the junction of squamous esophageal mucosa and columnar gastric mucosa. (Used, with permission, from Y. Chen.) An endoscopy image of a normal squamocolumnar junction. There is smooth, pink mucosa at the opening between the esophagus and the stomach.

Current Medical Diagnosis & Treatment 2024 > Gastroesophageal Reflux Disease

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eFigure 17–6. Distal esophagus (squamocolumnar junction) with 2 linear erosions > 5 mm in length at 2 and 10 o'clock (LA Grade B). (Used, with permission, from Y. Chen.) An endoscopy image reveals two erosions at the squamocolumnar junction of the esophagus. The erosions appear as rough, pale pink patches spreading into the smooth, bright pink mucosa.

Current Medical Diagnosis & Treatment 2024 > Gastroesophageal Reflux Disease

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eFigure 17–7. Distal esophagus with ulceration involving less than 75% of circumference (LA Grade C). (Used, with permission, from A. Huang.) An endoscopy image of the esophagus reveals irregular, bright red ulcerated lesions spread across 50 to 60 percent of the mucosal circumference.

Current Medical Diagnosis & Treatment 2024 > Gastroesophageal Reflux Disease

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eFigure 17–8. Distal esophagus with ulceration involving >75% of the esophageal circumference consistent with LA Grade D. (Used, with permission, from A. Huang.) An endoscopy image of the esophagus reveals bright red ulcerated lesions covering 80 to 90 percent of the mucosal circumference.

Current Medical Diagnosis & Treatment 2024 > Gastroesophageal Reflux Disease

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eFigure 17–11. A: A smooth, benign appearing peptic stricture in the distal esophagus. (Used, with permission, from A. Huang.) B: A balloon has been placed across the stricture in preparation for dilation. C: Following balloon dilation, there is mucosal disruption of the stricture with mild bleeding. (Used, with permission, from Richard W. Mclean I, MD.) An endoscopy image reveals a narrowed, smooth opening between esophagus and stomach. An endoscopy image of a balloon positioned across the peptic stricture. An endoscopy image reveals a widened opening and bleeding of the mucosa at the stricture.

Current Medical Diagnosis & Treatment 2024 > Gastroesophageal Reflux Disease

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eFigure 17–11. A: A smooth, benign appearing peptic stricture in the distal esophagus. (Used, with permission, from A. Huang.) B: A balloon has been placed across the stricture in preparation for dilation. C: Following balloon dilation, there is mucosal disruption of the stricture with mild bleeding. (Used, with permission, from Richard W. Mclean I, MD.) An endoscopy image reveals a narrowed, smooth opening between esophagus and stomach. An endoscopy image of a balloon positioned across the peptic stricture. An endoscopy image reveals a widened opening and bleeding of the mucosa at the stricture.

Current Medical Diagnosis & Treatment 2024 > Gastroesophageal Reflux Disease

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eFigure 17–11. A: A smooth, benign appearing peptic stricture in the distal esophagus. (Used, with permission, from A. Huang.) B: A balloon has been placed across the stricture in preparation for dilation. C: Following balloon dilation, there is mucosal disruption of the stricture with mild bleeding. (Used, with permission, from Richard W. Mclean I, MD.) An endoscopy image reveals a narrowed, smooth opening between esophagus and stomach. An endoscopy image of a balloon positioned across the peptic stricture. An endoscopy image reveals a widened opening and bleeding of the mucosa at the stricture.

Current Medical Diagnosis & Treatment 2024 > Gastroesophageal Reflux Disease

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eFigure 17–12. These white fluffy exudates are typical of Candida esophagitis. (Used, with permission, from Richard W. Mclean I, MD.) An endoscopy image of the esophagus reveals slightly raised, white, fluffy irregular patches lining the mucosa.

Current Medical Diagnosis & Treatment 2024 > Infectious Esophagitis

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eFigure 17–13. A Mallory Weiss tear with active oozing is evident at the squamocolumnar junction. (Used, with permission, from Y. Chen.) An endoscopy image of the squamocolumnar junction reveals bleeding and bubbling from a mucosal tear.

Current Medical Diagnosis & Treatment 2024 > Benign Esophageal Lesions

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eFigure 17–15. Fine, concentric mucosal rings ("trachealization") seen in some patients with eosinophilic esophagitis. (Used, with permission, from Richard W. Mclean I, MD.) An endoscopy image of the esophagus reveals numerous, fine, slightly raised concentric lines on the mucosal lining.

Current Medical Diagnosis & Treatment 2024 > Benign Esophageal Lesions

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eFigure 17–19. Clean based duodenal white 1-cm ulcer of duodenal bulb. (Used, with permission, from Y. Chen.) An endoscopy image reveals a duodenal ulcer as a white, pitted lesion on the mucosal surface.

Current Medical Diagnosis & Treatment 2024 > Peptic Ulcer Disease

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eFigure 17–21. A soft, gelatinous clot is adherent to an underlying duodenal ulcer. (Used, with permission, from Y. Chen.) An endoscopy image of a white jelly-like mass of tissue over top a bleeding ulcerous lesion in the duodenal mucosa.

Current Medical Diagnosis & Treatment 2024 > Peptic Ulcer Disease

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eFigure 17–23. In the duodenum, the mucosa has a 'scalloped' or 'mosaic' appearance. Biopsies are consistent with celiac disease. (Used, with permission, from Richard W. Mclean I, MD.) An endoscopy image reveals a scalloped appearance to the mucosal layer, with multiple wavy, concentric rings along the length of the esophagus.

Current Medical Diagnosis & Treatment 2024 > Malabsorption

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eFigure 17–24. Clostridioides difficile colitis with pseudomembranes (adherent, yellow mounds). (Used, with permission, from Y. Chen.) An endoscopy image reveals numerous yellow, round lesions scattered along the mucosal lining.

Current Medical Diagnosis & Treatment 2024 > Antibiotic-Associated Colitis

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eFigure 17–25. Crohn disease of colon characterized by scattered ulcers with adherent mucopus and intervening normal appearing mucosa. (Used, with permission, from A. Huang.) An endoscopy image of the colon reveals glossy yellow and white streaks on the mucosa.

Current Medical Diagnosis & Treatment 2024 > Inflammatory Bowel Disease

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eFigure 17–26. Crohn involvement of terminal ileum with extensive linear and stellate ulcers. (Used, with permission, from A. Huang.) An endoscopy image of the colon reveals several white and yellow raised patches scattered over the mucosa.

Current Medical Diagnosis & Treatment 2024 > Inflammatory Bowel Disease

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eFigure 17–28. Mild ulcerative colitis characterized by loss of normal vascularity and scattered small erosions. (Used, with permission, from A. Huang.) An endoscopy image of the colon reveals abnormally pale pink mucosa with a granular, white surface.

Current Medical Diagnosis & Treatment 2024 > Inflammatory Bowel Disease

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eFigure 17–29. Severe ulcerative colitis is characterized by granularity, loss of normal vascularity, diffuse erosions and ulcerations, and spontaneous bleeding. (Used, with permission, from Y. Chen.) An endoscopy image of the colon reveals profuse bleeding in the mucosa. The lining appears rough with brown and yellow patches. There is no apparent bleeding.

Current Medical Diagnosis & Treatment 2024 > Inflammatory Bowel Disease

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eFigure 17–31. A diminutive rectal hyperplastic polyp characterized by size, white color, lack of vascularity, and smooth surface. (Used, with permission, from A. Huang.) An endoscopy image reveals a smooth, white mass protruding as a shallow bump on the mucosal surface.

Current Medical Diagnosis & Treatment 2024 > Polyps of the Colon

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eFigure 17–32. Diminutive sessile colonic adenoma characterized by a variegated mucosal surface. (Used, with permission, from Y. Chen.) An endoscopy image reveals a large, round white mass protruding from the mucosa. Irregular wavy, yellow streaks cover the mucosal surface.

Current Medical Diagnosis & Treatment 2024 > Nonfamilial Adenomatous & Serrated Polyps

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eFigure 17–33. Diminutive sessile colonic adenoma visualized under blue light imaging to characterize a prominent mottled vascular pattern. (Used, with permission, from Y. Chen.) An endoscopy image reveals a round, mass protruding as a smooth bump from the mucosa. The surface of the mass has red streaks of vasculature.

Current Medical Diagnosis & Treatment 2024 > Nonfamilial Adenomatous & Serrated Polyps

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eFigure 17–35. A large sessile colonic adenoma; pathologic assessment confirmed tubulovillous features. (Used, with permission, from A. Huang.) An endoscopy image of the colon reveals a large, lobed polyp in the mucosa.

Current Medical Diagnosis & Treatment 2024 > Nonfamilial Adenomatous & Serrated Polyps

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eFigure 17–36. A 1-cm bi-lobed adenoma is visible that is attached to a long stalk (pedunculated polyp). (Used, with permission, from A. Huang.) An endoscopy image of the colon reveals a large smooth, lobed mass of cells attached to a slender stalk protruding from the mucosa.

Current Medical Diagnosis & Treatment 2024 > Nonfamilial Adenomatous & Serrated Polyps

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