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

Current Medical Diagnosis & Treatment 2024 > Amebiasis

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

Current Medical Diagnosis & Treatment 2024 > Amebiasis

View in Context

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

Current Medical Diagnosis & Treatment 2024 > Amebiasis

View in Context

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

Current Medical Diagnosis & Treatment 2024 > Amebiasis

View in Context

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

Current Medical Diagnosis & Treatment 2024 > Amebiasis

View in Context

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

Current Medical Diagnosis & Treatment 2024 > Amebiasis

View in Context

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

Current Medical Diagnosis & Treatment 2024 > Amebiasis

View in Context

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

Current Medical Diagnosis & Treatment 2024 > Amebiasis

View in Context

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

Current Medical Diagnosis & Treatment 2024 > Amebiasis

View in Context

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

Current Medical Diagnosis & Treatment 2024 > Amebiasis

View in Context

eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

View in Context

eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

View in Context

eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

View in Context

eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

View in Context

eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

View in Context

eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

View in Context

eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

View in Context

eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

View in Context

eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

View in Context

eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

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eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

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eFigure 37–26. Life cycle of Paragonimus westermani (lung fluke). The eggs are excreted unembryonated in the sputum, or alternately, they are swallowed and passed with stool . In the external environment, the eggs become embryonated , and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues . Miracidia go through several developmental stages inside the snail : sporocysts , rediae , with the latter giving rise to many cercariae , which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian host . Human infection with P westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite . The metacercariae excyst in the duodenum , penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults  (7.5–12 mm by 4–6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycle is not achieved because the eggs laid cannot exit these sites. Time from infection to oviposition is 65–90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P westermani. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of P westermani.

Current Medical Diagnosis & Treatment 2024 > Paragonimiasis

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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eFigure 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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eFigure 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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eFigure 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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eFigure 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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eFigure 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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eFigure 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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eFigure 37–34. Life cycle of Ascaris lumbricoides (the giant roundworm of humans). Adult worms , live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10–14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1–2 years. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Ascaris lumbricoides.

Current Medical Diagnosis & Treatment 2024 > Ascariasis

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eFigure 37–37. Life cycles of Ancylostoma duodenale and Necator americanus (human hookworms). Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1–2 days. The released rhabditiform larvae grow in the feces or the soil, or both , and after 5–10 days (and two molts) they become filariform (third-stage) larvae that are infective . These infective larvae can survive 3–4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed . The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host . Most adult worms are eliminated in 1–2 years, but the longevity may reach several years. Some A duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A duodenale may probably also occur by the oral and transmammary route. N americanus, however, requires a transpulmonary migration phase. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of intestinal hookworm.

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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eFigure 37–37. Life cycles of Ancylostoma duodenale and Necator americanus (human hookworms). Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1–2 days. The released rhabditiform larvae grow in the feces or the soil, or both , and after 5–10 days (and two molts) they become filariform (third-stage) larvae that are infective . These infective larvae can survive 3–4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed . The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host . Most adult worms are eliminated in 1–2 years, but the longevity may reach several years. Some A duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A duodenale may probably also occur by the oral and transmammary route. N americanus, however, requires a transpulmonary migration phase. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of intestinal hookworm.

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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eFigure 37–37. Life cycles of Ancylostoma duodenale and Necator americanus (human hookworms). Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1–2 days. The released rhabditiform larvae grow in the feces or the soil, or both , and after 5–10 days (and two molts) they become filariform (third-stage) larvae that are infective . These infective larvae can survive 3–4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed . The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host . Most adult worms are eliminated in 1–2 years, but the longevity may reach several years. Some A duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A duodenale may probably also occur by the oral and transmammary route. N americanus, however, requires a transpulmonary migration phase. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of intestinal hookworm.

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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eFigure 37–37. Life cycles of Ancylostoma duodenale and Necator americanus (human hookworms). Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1–2 days. The released rhabditiform larvae grow in the feces or the soil, or both , and after 5–10 days (and two molts) they become filariform (third-stage) larvae that are infective . These infective larvae can survive 3–4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed . The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host . Most adult worms are eliminated in 1–2 years, but the longevity may reach several years. Some A duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A duodenale may probably also occur by the oral and transmammary route. N americanus, however, requires a transpulmonary migration phase. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of intestinal hookworm.

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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eFigure 37–37. Life cycles of Ancylostoma duodenale and Necator americanus (human hookworms). Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1–2 days. The released rhabditiform larvae grow in the feces or the soil, or both , and after 5–10 days (and two molts) they become filariform (third-stage) larvae that are infective . These infective larvae can survive 3–4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed . The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host . Most adult worms are eliminated in 1–2 years, but the longevity may reach several years. Some A duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A duodenale may probably also occur by the oral and transmammary route. N americanus, however, requires a transpulmonary migration phase. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of intestinal hookworm.

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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eFigure 37–37. Life cycles of Ancylostoma duodenale and Necator americanus (human hookworms). Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1–2 days. The released rhabditiform larvae grow in the feces or the soil, or both , and after 5–10 days (and two molts) they become filariform (third-stage) larvae that are infective . These infective larvae can survive 3–4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed . The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host . Most adult worms are eliminated in 1–2 years, but the longevity may reach several years. Some A duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A duodenale may probably also occur by the oral and transmammary route. N americanus, however, requires a transpulmonary migration phase. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of intestinal hookworm.

Current Medical Diagnosis & Treatment 2024 > Hookworm Disease

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–38. Life cycle of Strongyloides stercoralis (small roundworm of humans). The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist. Free-living cycle: The rhabditiform larvae passed in the stool  (see “Parasitic cycle” below) can either become infective filariform larvae (direct development) , or free-living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch  and eventually become infective filariform larvae . The filariform larvae penetrate the human host skin to initiate the parasitic cycle (see below) . Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin , and by various, often random routes, migrate to the small intestine . Historically it was believed that the L3 larvae migrate via the bloodstream to the lungs, where they are eventually coughed up and swallowed. However, there is also evidence that L3 larvae can migrate directly to the intestine via connective tissues. In the small intestine, they molt twice and become adult female worms . The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs , which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool  (see “Free-living cycle” above), or can cause autoinfection . In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may disseminate throughout the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in S stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Strongyloides.

Current Medical Diagnosis & Treatment 2024 > Strongyloidiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

Current Medical Diagnosis & Treatment 2024 > Loiasis

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eFigure 37–52. Life cycle of Loa loa. The vector for L loa filariasis is flies from two species of the genus Chrysops: C silacea and C dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound . The larvae develop into adults that commonly reside in subcutaneous tissue . The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 mcm by 6–8 mcm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluids, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs . The fly ingests microfilariae during a blood meal . After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod . There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae . The third-stage infective larvae migrate to the fly’s proboscis  and can infect another human when the fly takes a blood meal . A flowchart of the life cycle of loa loa.

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eFigure 9–2. Oxygen-hemoglobin dissociation curve, pH 7.40, temperature 38°C. (Reproduced, with permission, from Comroe JH Jr et al. The Lung: Clinical Physiology and Pulmonary Function Tests, 2nd ed. Year Book Medical Publishers, 1962.) A graph shows the oxygen-hemoglobin dissociation curve.

Current Medical Diagnosis & Treatment 2024 > Pulmonary Function Tests

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eFigure 9–3. Emphysematous bullae of left lung. A: Posteroanterior projection. B: Pulmonary angiogram. (Reproduced, with permission, from Way LW [editor]. Current Surgical Diagnosis & Treatment, 10th ed. Originally published by Appleton & Lange. Copyright © 1994 by The McGraw-Hill Companies, Inc.) A posteroanterior projection of the human lungs shows a bullae in the medial walls of the left lung. A pulmonary angiogram of the lungs shows a bullae in the medial walls of the left lung.

Current Medical Diagnosis & Treatment 2024 > Chronic Obstructive Pulmonary Disease

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eFigure 9–3. Emphysematous bullae of left lung. A: Posteroanterior projection. B: Pulmonary angiogram. (Reproduced, with permission, from Way LW [editor]. Current Surgical Diagnosis & Treatment, 10th ed. Originally published by Appleton & Lange. Copyright © 1994 by The McGraw-Hill Companies, Inc.) A posteroanterior projection of the human lungs shows a bullae in the medial walls of the left lung. A pulmonary angiogram of the lungs shows a bullae in the medial walls of the left lung.

Current Medical Diagnosis & Treatment 2024 > Chronic Obstructive Pulmonary Disease

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eFigure 9–4. Bullous disease. There is almost a complete paucity of lung markings in both lungs. The edge of some bullae can be seen in the left lung. An image of the lungs shows markings in the lower side of each lung.

Current Medical Diagnosis & Treatment 2024 > Chronic Obstructive Pulmonary Disease

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eFigure 9–12. Pneumonia with loculated empyema. A: CT shows a loculated pleural effusion in the left hemithorax (arrows). B: More caudally, dense consolidation with air bronchograms secondary to pneumonia is present in the left lower lobe. The consolidated lung enhances with contrast and is easily distinguished from the surrounding pleural effusion. (Reproduced, with permission, from Bongard FS, Sue DY [editors]. Current Critical Care Diagnosis & Treatment. Originally published by Appleton & Lange. Copyright © 1994 by The McGraw-Hill Companies, Inc.) An axial CT scan shows pleural effusion in the left hemithorax. An axial CT scan shows a consolidated lower left lung with air bronchograms secondary to pneumonia.

Current Medical Diagnosis & Treatment 2024 > Pneumonia

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eFigure 9–12. Pneumonia with loculated empyema. A: CT shows a loculated pleural effusion in the left hemithorax (arrows). B: More caudally, dense consolidation with air bronchograms secondary to pneumonia is present in the left lower lobe. The consolidated lung enhances with contrast and is easily distinguished from the surrounding pleural effusion. (Reproduced, with permission, from Bongard FS, Sue DY [editors]. Current Critical Care Diagnosis & Treatment. Originally published by Appleton & Lange. Copyright © 1994 by The McGraw-Hill Companies, Inc.) An axial CT scan shows pleural effusion in the left hemithorax. An axial CT scan shows a consolidated lower left lung with air bronchograms secondary to pneumonia.

Current Medical Diagnosis & Treatment 2024 > Pneumonia

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eFigure 9–14. Hamartoma of the lung. Incidentally identified on a chest CT scan in a young, otherwise health 31-year-old male, the hamartoma appears as a round and well-demarcated left lower lobe mass with areas of dense calcification and much lower density fat. An axial CT scan shows flagellated nodules in both lungs and a dense, calcified mass in the lower left lobe.

Current Medical Diagnosis & Treatment 2024 > Solitary Pulmonary Nodule

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Figure 9–4. Idiopathic pulmonary fibrosis. CT scan of the lungs showing the typical radiographic pattern of idiopathic pulmonary fibrosis, with a predominantly basilar, peripheral pattern of traction bronchiectasis, reticulation, and early honeycombing. A C T scan for Idiopathic pulmonary fibrosis.

Current Medical Diagnosis & Treatment 2024 > Diffuse Interstitial Pneumonias

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eFigure 9–15. A: Eosinophilic pneumonitis. This patient with parasite-induced eosinophilic pneumonitis has ill-defined nodular and fluffy, patchy densities scattered throughout both lungs. B: The lateral film from the same patient shows a better-defined infiltrate at the left lung base. An image shows nodular and fluffy patches in both lungs. A lateral view of the left lung shows nodular and fluffy patches in the base of the left lung.

Current Medical Diagnosis & Treatment 2024 > Eosinophilic Pulmonary Syndromes

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eFigure 9–15. A: Eosinophilic pneumonitis. This patient with parasite-induced eosinophilic pneumonitis has ill-defined nodular and fluffy, patchy densities scattered throughout both lungs. B: The lateral film from the same patient shows a better-defined infiltrate at the left lung base. An image shows nodular and fluffy patches in both lungs. A lateral view of the left lung shows nodular and fluffy patches in the base of the left lung.

Current Medical Diagnosis & Treatment 2024 > Eosinophilic Pulmonary Syndromes

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eFigure 9–16. Eosinophilic pneumonia. The pulmonary infiltrate in this case is confined to the lingular portion of the left lung and extends into the upper lobe. There is also a small pleural effusion. This is one of the manifestations of eosinophilic pneumonia. An image shows pulmonary inflitrate in the central portion of the left lung.

Current Medical Diagnosis & Treatment 2024 > Eosinophilic Pulmonary Syndromes

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eFigure 9–17. A: Pulmonary embolism (CXR). The heart is significantly enlarged, with prominence of main pulmonary arterial outflow as indicated by fullness in the region of the pulmonary hila. However, there are no other changes in the peripheral lung suggestive of a pulmonary embolus. B: PE (pulmonary angiogram). A large embolus is present in the right main pulmonary artery at its point of bifurcation between the upper and middle and the lower lobe vessels, resulting in a paucity of perfusion of vessels distal to the embolus. A chest radiograph shows that the heart located between the lungs is enlarged. A pulmonary angiogram shows a large mass present in the right main pulmonary artery, at the point of its branching.

Current Medical Diagnosis & Treatment 2024 > Pulmonary Venous Thromboembolism

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eFigure 9–17. A: Pulmonary embolism (CXR). The heart is significantly enlarged, with prominence of main pulmonary arterial outflow as indicated by fullness in the region of the pulmonary hila. However, there are no other changes in the peripheral lung suggestive of a pulmonary embolus. B: PE (pulmonary angiogram). A large embolus is present in the right main pulmonary artery at its point of bifurcation between the upper and middle and the lower lobe vessels, resulting in a paucity of perfusion of vessels distal to the embolus. A chest radiograph shows that the heart located between the lungs is enlarged. A pulmonary angiogram shows a large mass present in the right main pulmonary artery, at the point of its branching.

Current Medical Diagnosis & Treatment 2024 > Pulmonary Venous Thromboembolism

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eFigure 9–18. Pulmonary emboli. Pulmonary CT angiogram demonstrating multiple segmental and subsegmental pulmonary emboli (arrows) in the right lung in a patient with a spontaneous upper extremity deep venous thrombosis. A pulmonary CT angiogram shows emboli present in the vessels branching into the right lung.

Current Medical Diagnosis & Treatment 2024 > Pulmonary Venous Thromboembolism

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eFigure 9–19. Normal lung perfusion. A routine examination may include as many as eight views– anterior, posterior, right and left anterior and posterior obliques, and both right and left laterals (A to H). Some physicians prefer to omit the anterior obliques; others do not include the laterals. There is general agreement that the posterior obliques are the most valuable views. When the patient is injected in the supine position, the radioactive particles are evenly distributed throughout the lungs, with a gently increasing gradient of activity from the upper anterior to the lower posterior lung fields. The cardiac and mediastinal spaces between the lungs have a configuration in the combined anterior and posterior views similar to that of the respective area in the posteroanterior CXR. Cardiomegaly and mediastinal masses will cause distortions that are common to both examinations. An enlarged cardiac space may be caused by cardiomegaly and by effusions or other conditions of the pericardial sac and adjacent pleural cavity. If the patient is rotated, the lung images may override and cause a false defect, which will disappear when the patient is repositioned accurately. However, a true lesion is unlikely if seen in only one view of a complete study. (Reproduced, with permission, from Baum S et al. Atlas of Nuclear Medicine Imaging, 2nd ed. Originally published by Appleton & Lange. Copyright © 1992 by The McGraw-Hill Companies, Inc.) A normal lung perfusion scan shows normal perfusion in six different views of the lungs.

Current Medical Diagnosis & Treatment 2024 > Pulmonary Venous Thromboembolism

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

Current Medical Diagnosis & Treatment 2024 > Pulmonary Venous Thromboembolism

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eFigure 9–22. Diffuse alveolar hemorrhage. CT scan of the lungs with bilateral ground glass opacities resulting from diffuse alveolar hemorrhage in a patient with ANCA-associated vasculitis caused by microscopic polyangiitis. An axial CT scan shows opaque spots in both lungs.

Current Medical Diagnosis & Treatment 2024 > Alveolar Hemorrhage Syndromes

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eFigure 9–23. Asbestosis. Calcified pleural plaques at both lung bases are typical. An image shows calcified pleural plaques at the bases of both lungs.

Current Medical Diagnosis & Treatment 2024 > Occupational Pulmonary Diseases

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eFigure 9–26. Spontaneous pneumothorax on the right side. (Reproduced, with permission, from Way LW [editor]. Current Surgical Diagnosis & Treatment, 10th ed. Originally published by Appleton & Lange. Copyright © 1994 by The McGraw-Hill Companies, Inc.) An image shows that the right lower lung is collapsed.

Current Medical Diagnosis & Treatment 2024 > Pneumothorax

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eFigure 9–28. A: Pneumomediastinum secondary to esophageal perforation (posteroanterior CXR). B: Pneumomediastinum (lateral CXR). A posteroanterior chest radiograph shows bubbles in the lateral edge of left lung. An image shows emphysema in the subcutaneous region of the lungs.

Current Medical Diagnosis & Treatment 2024 > Pneumothorax

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eFigure 9–28. A: Pneumomediastinum secondary to esophageal perforation (posteroanterior CXR). B: Pneumomediastinum (lateral CXR). A posteroanterior chest radiograph shows bubbles in the lateral edge of left lung. An image shows emphysema in the subcutaneous region of the lungs.

Current Medical Diagnosis & Treatment 2024 > Pneumothorax

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eFigure 9–29. Barotrauma in ARDS. A: CXR demonstrates diffuse lung consolidation secondary to ARDS. Parenchymal stippling is present, with lucent perivascular halos secondary to pulmonary interstitial emphysema. B: On CXR 4 days later, pneumomediastinum is now identified with extensive subcutaneous emphysema. C: I n another patient with ARDS, subpleural cysts (arrow) and parenchymal stippling due to pulmonary interstitial emphysema are present. (Reproduced, with permission, from Bongard FS, Sue DY [editors]. Current Critical Care Diagnosis & Treatment. Originally published by Appleton & Lange. Copyright © 1994 by The McGraw-Hill Companies, Inc.) A normal chest radiograph. A chest radiograph shows diffuse parenchymal opacification of the lungs due to ARDS. A chest radiograph shows an arrow pointing toward cysts in subpleural region of lower right lung.

Current Medical Diagnosis & Treatment 2024 > Acute Respiratory Failure

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eFigure 9–29. Barotrauma in ARDS. A: CXR demonstrates diffuse lung consolidation secondary to ARDS. Parenchymal stippling is present, with lucent perivascular halos secondary to pulmonary interstitial emphysema. B: On CXR 4 days later, pneumomediastinum is now identified with extensive subcutaneous emphysema. C: I n another patient with ARDS, subpleural cysts (arrow) and parenchymal stippling due to pulmonary interstitial emphysema are present. (Reproduced, with permission, from Bongard FS, Sue DY [editors]. Current Critical Care Diagnosis & Treatment. Originally published by Appleton & Lange. Copyright © 1994 by The McGraw-Hill Companies, Inc.) A normal chest radiograph. A chest radiograph shows diffuse parenchymal opacification of the lungs due to ARDS. A chest radiograph shows an arrow pointing toward cysts in subpleural region of lower right lung.

Current Medical Diagnosis & Treatment 2024 > Acute Respiratory Failure

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eFigure 9–29. Barotrauma in ARDS. A: CXR demonstrates diffuse lung consolidation secondary to ARDS. Parenchymal stippling is present, with lucent perivascular halos secondary to pulmonary interstitial emphysema. B: On CXR 4 days later, pneumomediastinum is now identified with extensive subcutaneous emphysema. C: I n another patient with ARDS, subpleural cysts (arrow) and parenchymal stippling due to pulmonary interstitial emphysema are present. (Reproduced, with permission, from Bongard FS, Sue DY [editors]. Current Critical Care Diagnosis & Treatment. Originally published by Appleton & Lange. Copyright © 1994 by The McGraw-Hill Companies, Inc.) A normal chest radiograph. A chest radiograph shows diffuse parenchymal opacification of the lungs due to ARDS. A chest radiograph shows an arrow pointing toward cysts in subpleural region of lower right lung.

Current Medical Diagnosis & Treatment 2024 > Acute Respiratory Failure

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eFigure 9–30. ARDS secondary to sepsis in an immunocompromised patient following bone marrow transplantation. A: Stage I ARDS. The initial CXR is normal despite marked dyspnea and hypoxemia. B: Stage II ARDS. Within 24 hours, the CXR shows diffuse parenchymal opacification consistent with ARDS. (Reproduced, with permission, from Bongard FS, Sue DY [editors]. Current Critical Care Diagnosis & Treatment. Originally published by Appleton & Lange. Copyright © 1994 by The McGraw-Hill Companies, Inc.) A normal chest radiograph. A chest radiograph shows diffuse parenchymal opacification of the lungs due to ARDS.

Current Medical Diagnosis & Treatment 2024 > Acute Respiratory Distress Syndrome

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eFigure 9–30. ARDS secondary to sepsis in an immunocompromised patient following bone marrow transplantation. A: Stage I ARDS. The initial CXR is normal despite marked dyspnea and hypoxemia. B: Stage II ARDS. Within 24 hours, the CXR shows diffuse parenchymal opacification consistent with ARDS. (Reproduced, with permission, from Bongard FS, Sue DY [editors]. Current Critical Care Diagnosis & Treatment. Originally published by Appleton & Lange. Copyright © 1994 by The McGraw-Hill Companies, Inc.) A normal chest radiograph. A chest radiograph shows diffuse parenchymal opacification of the lungs due to ARDS.

Current Medical Diagnosis & Treatment 2024 > Acute Respiratory Distress Syndrome

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Figure 33–2. Pneumocystis pneumonia in a Haitian woman suspected of having underlying HIV/AIDS. Typical CXR showing bilateral diffuse interstitial infiltrates extending out from the hilar areas. (Reproduced, with permission, from Grippi MA, Elias JA, Fishman JA et al (editors). Fishman’s Pulmonary Diseases and Disorders, 5th ed. McGraw-Hill, 2015.) A chest X ray image shows diffuse infiltrates in the lower medial lungs, more so in the left lobe.

Current Medical Diagnosis & Treatment 2024 > HIV Infection & AIDS: Complications

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Figure 33–3. A 36-year-old man with pulmonary tuberculosis. There is an opacification of a portion of the left upper lung in association with a cavity, findings consistent with pulmonary tuberculosis. Also, there is an infiltrate in the right lung. The extent of his disease raises the specter that he has underlying HIV/AIDS. (Reproduced with permission from Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux EJ Jr, Chumley H. The Color Atlas of Family Medicine, 3rd ed. McGraw-Hill, 2019) A chest X ray image shows opaque infiltrates in the upper left lung, which extend medially, represented by a large opaque area from the center of the chest extending into the lower left lung.

Current Medical Diagnosis & Treatment 2024 > HIV Infection & AIDS: Complications

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eFigure 38–1. Pneumocystis jirovecii pneumonia. CXR shows bilateral ill-defined hazy airspace opacities. A chest radiograph of a patient affected by Pneumocystis jirovecii pneumonia. Yeast like fungus is seen on the chest with bilateral hazy airspace opacities, represented by cloudy white patches scattered across the lungs.

Current Medical Diagnosis & Treatment 2024 > Pneumocystosis (Pneumocystis Jirovecii Pneumonia)

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eFigure 38–2. CT scan of the lungs demonstrating bilateral patchy and ground-glass opacities and tree-in-bud nodular opacities. A C T scan of the lungs shows the bilateral patch and tree in bud nodular opacities.

Current Medical Diagnosis & Treatment 2024 > Pneumocystosis (Pneumocystis Jirovecii Pneumonia)

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Figure 36–5. Ascending saccular aneurysm of the thoracic aorta in tertiary syphilis. (Public Health Image Library, CDC.) A scan shows white portion engulfing the lungs in the left side of the chest.

Current Medical Diagnosis & Treatment 2024 > Clinical Stages of Syphilis

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eFigure 10–2. A: Close-up of CXR showing Kerley B lines. B: Normal chest film. C: HF stage II with Kerley B lines due to interstitial edema. Source: https://radiologyassistant.nl/chest/chest-x-ray-heart-failure. Used with permission. A chest x-ray provides a close-up view of Kerley B lines, appearing as small, horizontal straight lines at the periphery of lungs. Two chest x-rays compare the findings under normal conditions with those of a heart failure.

Current Medical Diagnosis & Treatment 2024 > Common Symptoms

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eFigure 10–2. A: Close-up of CXR showing Kerley B lines. B: Normal chest film. C: HF stage II with Kerley B lines due to interstitial edema. Source: https://radiologyassistant.nl/chest/chest-x-ray-heart-failure. Used with permission. A chest x-ray provides a close-up view of Kerley B lines, appearing as small, horizontal straight lines at the periphery of lungs. Two chest x-rays compare the findings under normal conditions with those of a heart failure.

Current Medical Diagnosis & Treatment 2024 > Common Symptoms

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eFigure 10–14. Schematic drawing of pulmonary stenosis. See text for details. LA, left atrium; RA, right atrium; Ao, aorta; PA, pulmonary artery. Reproduced with permission from Obgyn Key. Obgyn Key Website, https://obgynkey.com/pulmonary-stenosis-pulmonary-atresia-with-intactventricular-septum-and-ductus-arteriosus-constriction/. A schematic diagram depicts pulmonary stenosis.

Current Medical Diagnosis & Treatment 2024 > Pulmonary Valve Stenosis

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eFigure 10–20. Atrial septal defect, secundum type. Frontal (A) and lateral (B) views show mild to moderate cardiomegaly (without left atrial enlargement) and increased pulmonary vascularity. Source: http://mirc.luriechildrens.org/storage/ss4/docs/20060510122114531/MIRCdocument.xml. Used with permission from Cynthia Rigsby, MD. A chest radiograph shows the frontal view of lungs affected with Atrial septal defect, secundum type. The defect causes a hole in the wall between the two chambers of the heart. A chest radiograph shows the lateral view of lungs affected with Atrial septal defect, secundum type. The size of the heart is visibly, abnormally large. There is no enlargement of the left atrium.

Current Medical Diagnosis & Treatment 2024 > Atrial Septal Defect & Patent Foramen Ovale

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eFigure 10–20. Atrial septal defect, secundum type. Frontal (A) and lateral (B) views show mild to moderate cardiomegaly (without left atrial enlargement) and increased pulmonary vascularity. Source: http://mirc.luriechildrens.org/storage/ss4/docs/20060510122114531/MIRCdocument.xml. Used with permission from Cynthia Rigsby, MD. A chest radiograph shows the frontal view of lungs affected with Atrial septal defect, secundum type. The defect causes a hole in the wall between the two chambers of the heart. A chest radiograph shows the lateral view of lungs affected with Atrial septal defect, secundum type. The size of the heart is visibly, abnormally large. There is no enlargement of the left atrium.

Current Medical Diagnosis & Treatment 2024 > Atrial Septal Defect & Patent Foramen Ovale

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