History
Schistosomiasis
Acute manifestations
Cercarial dermatitis, also known as swimmer's itch, is an allergic reaction caused by the penetration of cercariae in persons who have been exposed to cercariae in fresh water. Cercarial dermatitis manifests as petechial hemorrhages with edema and pruritus, followed by maculopapular rash, which may become vesicular. The process is usually related to avian schistosomal species of the genera Trichobilharzia,Gigantobilharzia, and Orientobilharzia, which do not develop further in humans.
Katayama syndrome corresponds to maturation of the fluke and the beginning of oviposition. This syndrome is caused by high worm load and egg antigen stimuli that result from immune complex formation and leads to a serum sickness–like illness. This is the most severe form and is most common in persons with S mansoni and S japonicum infections. Symptoms include high fever, chills, headache, hepatosplenomegaly, lymphadenopathy, eosinophilia, and dysentery. A history of travel in an endemic area provides a clue to the diagnosis.
Chronic manifestations
Symptoms depend on the Schistosoma species that causes the infection, the duration and severity of the infection, and the immune response of the host to the egg antigens.
Terminal hematuria, dysuria, and frequent urination are the main clinical symptoms of urinary schistosomiasis.
The earliest bladder sign is pseudotubercle, but, in longstanding infection, radiography reveals nests of calcified ova (sandy patches) surrounded by fibrous tissue in the submucosa.
Dysentery, diarrhea, weakness, and abdominal pain are the major symptoms of intestinal schistosomiasis.
A reaction to schistosomal eggs in the liver causes a periportal fibrotic reaction termed Symmers clay pipestem fibrosis.
Hemoptysis, palpitation, and dyspnea upon exertion are the symptoms of schistosomal cor pulmonale that develops as a complication of hepatic schistosomiasis.
Headache, seizures (both generalized and focal), myeloradiculopathy with lower limb and back pain, paresthesia, and urinary bladder dysfunction are the noted symptoms of CNS schistosomiasis due to S japonicum infection.
Neuroschistosomiasis is a severe manifestation of schistosomal infection. The neurological symptoms result from the inflammatory response of the host to the deposition of eggs in the brain and spinal cord. Myelopathy is the most common neurological complication of Smansoni infection. [18]
Paragonimiasis
Acute manifestations include acute pulmonary infection is characterized by low-grade fever, cough, night sweats, chest pain, and blood-stained rusty-brown sputum.
Chronic manifestations can include lung abscess or pleural effusion. [19] Fever, hemoptysis, pleurisy pain, dyspnea, and recurrent attacks of bacterial pneumonia are the common symptoms. The condition mimics pulmonary tuberculosis.
Fever, headache, nausea, vomiting, visual disturbances, motor weakness, and localized or generalized paralysis are the symptoms of cerebral paragonimiasis.
Pulmonary paragonimiasis has been found to mimic metastatic pulmonary tumors on evaluation with imaging methods such as computed tomography (CT) and positron emission tomography (PET) scanning. [20]
Paragonimiasis can affect all parts of the human body, and reports have described cerebral paragonimiasis in the last few years. The rate of cerebral paragonimiasis has been found to be about 0.8% of all active cases of paragonimiasis. [21]
Liver fluke infections
Acute manifestations
Fascioliasis is mostly subclinical. Acute manifestations are due to migration of larva through lung parenchyma. Malaise, intermittent fever, night sweats, and pain in the right costal area are early symptoms of acute infection.
Clonorchiasis is frequently asymptomatic. A serum sickness–like illness with symptoms of high fever, eosinophilia, and rash occurs in individuals with acute infection.
Chronic manifestations
Chronic fascioliasis is frequently asymptomatic. In symptomatic patients, irregular fever, anemia, hepatobiliary manifestations (colicky pain, jaundice), and secondary bacterial infections are present.
In its end stage, chronic clonorchiasis may be complicated by recurrent pyogenic cholangitis and jaundice associated with cholangiocarcinoma.
Intestinal fluke infections
These infections are frequently asymptomatic. Diarrhea and abdominal pain are common symptoms in individuals with acute infection.
Generalized abdominal pain; ascites; and edema of the face, abdomen wall, and lower limbs are the main symptoms.
Physical
Schistosomiasis
Acute infections manifest hepatosplenomegaly, lymphadenopathy, and rashes.
Chronic schistosomiasis manifests anemia, pedal edema, ascites, and abdominal distension with distended abdominal veins. Patients may also have intestinal polyposis and signs of malnutrition.
Paragonimiasis
Abdominal mass, pain in the abdomen, and mucosanguineous diarrhea characterize abdominal paragonimiasis.
Liver fluke infections
Patients with chronic clonorchiasis may have tender hepatomegaly, progressive ascites, catarrhal cholecystitis, progressive edema, and jaundice.
Intestinal fluke infections
Patients with mild infection are usually asymptomatic. Patients with severe infections may have ascites and edema of the face, abdomen wall, and lower limbs.
Causes
See Pathophysiology.
Complications
Schistosomiasis complications can include the following:
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Cor pulmonale
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Portal hypertension
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Urinary bladder carcinoma
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Neurological complications: Cerebral and cerebellar tumour–like neuroschistosomiasis can present with increased intracranial pressure, headache, nausea and vomiting, and seizures. Myelopathy (acute transverse myelitis and subacute myeloradiculopathy) is the most common neurological complication of S mansoni infection. Schistosomal myelopathy tends to occur early after infection and is more likely to be symptomatic than cerebral schistosomiasis. The conus medullaris and cauda equina are the most common sites of involvement. Severe schistosomal myelopathy can provoke a complete flaccid paraplegia with areflexia, sphincter dysfunction, and sensory disturbances. [18]
Lung fluke complications can include the following:
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Lung abscess
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Pleural effusion
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Ectopic lesions in the brain
Liver fluke complications can include the following:
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Intercurrent bacterial infections
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Less commonly, pancreatitis in fascioliasis [22]
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Anemia
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Recurrent pyogenic cholangitis and cholangiocarcinoma in clonorchiasis
Intestinal fluke complications can include asthenia with ascites in fasciolopsiasis.
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Adult worms in humans reside in the veins in various locations: Schistosoma mansoni in the inferior mesenteric veins, Schistosoma japonicum in the superior mesenteric veins, and Schistosoma haematobium in the vesical veins (these locations are not absolute). The females (size 7-20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and they are eliminated with feces or urine, respectively. Under optimal conditions, the eggs hatch and release miracidia, which swim and penetrate specific snail intermediate hosts. The stages in the snail include 2 generations of sporocysts and the production of cercariae. Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host, and migrate through several tissues and stages to their residence in the veins. Human contact with water is thus necessary for infection by schistosomes. Various animals serve as reservoirs for S japonicum and Schistosoma mekongi. Image courtesy of the US Centers for Disease Control and Prevention.
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These are small operculated eggs. Size is 27-35 μm X 11-20 μm. The operculum, at the smaller end of the egg, is convex and rests on a visible "shoulder." At the opposite (larger, abopercular) end, a small knob or hooklike protrusion is often visible (as here). The miracidium is visible inside the egg. Image courtesy of the US Centers for Disease Control and Prevention.
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Wet mounts with iodine. The eggs are ellipsoidal. They have a small, barely distinct operculum (upper end of the eggs in panel A). The operculum can be opened (egg in panel B), for example, when slight pressure is applied to the coverslip. The eggs have a thin shell that is slightly thicker at the abopercular end. They are passed unembryonated. Size range is 120-150 μm X 63-90 μm. Image courtesy of the US Centers for Disease Control and Prevention.
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Adult flukes size range is 20-75 mm by 8-20 mm. Image courtesy of the US Centers for Disease Control and Prevention.
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Eggs are excreted unembryonated in the sputum, or, alternately, they are swallowed and passed with stool (1). In the external environment, the eggs become embryonated (2), and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues (3). Miracidia go through several developmental stages inside the snail (4): sporocysts (4a), rediae (4b), with the latter giving rise to many cercariae (4c), which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, in which they encyst and become metacercariae. This is the infective stage for the mammalian host (5). Human infection with Paragonimus westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasite (6). The metacercariae excyst in the duodenum (7), penetrate through the intestinal wall into the peritoneal cavity, and then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adults (8) (7.5-12 mm X 4-6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this occurs, 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. Image courtesy of the US Centers for Disease Control and Prevention.
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The average egg size is 85 μm by 53 μm (range, 68-118 μm X 39-67 μm). They are yellow-brown, ovoidal or elongate, have a thick shell, and are often asymmetrical with one end slightly flattened. At the large end, the operculum is clearly visible. The opposite (abopercular) end is thickened. The eggs of P westermani are excreted unembryonated. Image courtesy of the US Centers for Disease Control and Prevention.