Tissue Cestodes



Tissue Cestodes



Objectives



1. Describe and compare the life cycles of the tissue cestodes, including reservoir and intermediate hosts.


2. Describe the clinical manifestations and complications of cysticercus in the human host.


3. List the various methods used to diagnose cystericercus infection.


4. Define and describe the morphologic characteristics of the following: oncosphere, brood capsule, hydatid cyst, and hydatid sand.


5. Describe hydatid disease, including laboratory diagnosis and the best course of treatment.


6. Compare and contrast the pathogenesis and spectrum of disease associated with direct tissue damage versus the immune response to Echinococcus spp.


7. Describe the tapeworm that causes coenurosis, including hosts and symptoms of disease.


8. Describe the preventive measures recommended to avoid infection with tissue cestodes.



Parasites to be Considered



Tissue cestodes do not reach the adult stage in the human host. The organisms infect the human in their intermediate or cyst stage. The infections are much more serious than those caused by the adult tapeworm. The parasites can cause serious disease, or even death. Larval cestodes cause infection by accidental ingestion of eggs excreted from the intermediate host (Table 55-1), and they lodge in various organs and tissues in the human body. Diagnosis of larval infections can be problematic.




Taenia Solium


General Characteristics


Taenia solium, also known as the pork tapeworm, causes an intestinal infection from eating contaminated pork, as discussed in Chapter 54. The adult worm usually causes no clinical disease. Humans may accidentally become the intermediate host and ingest eggs from human feces. This typically occurs when an individual is already infected with adult T. solium. Autoinfection occurs when the individual swallows eggs from improper hand washing. Humans may develop the larval infection, which could result in cysticercosis. Cysticercosis is usually asymptomatic unless larvae invade the central nervous system (CNS), the globe of the eye, or other muscle and tissues.



Epidemiology


T. solium is found worldwide, with a higher incidence in Latin America. The larval form of the infection rarely occurs in the United States, but may be found among immigrants from Mexico. Following ingestion of T. solium eggs, the oncospheres hatch in the intestine and invade the intestinal wall. Once the larvae invade the tissue the organism is capable of spreading systemically by migration to the brain, liver, and other tissues, causing human cysticercosis. Cysticercosis is defined as larval forms distributed throughout the body. Human cysticercosis may also occur when reverse peristalsis returns gravid segments into the intestine, where the eggs hatch and release oncospheres. Cysticerci develop and may live many years. Cysticerci will eventually die and may calcify, which will aid in diagnosis.



Pathogenesis and Spectrum of Disease


Clinical signs and symptoms depend on the location, viability, and number of the cysticerci present. Cysticerci can develop in any organ or tissue of the body. The severity of the symptoms depends on the body site involved and may not appear for years after the initial infection. The most severe cases are found in the central nervous system and the eye. Once cysticerci localize in the brain, the organism causes a condition referred to as neurocysticercosis. Infection can cause epileptic-type seizures, headaches, mental disturbances, meningitis, or sudden death. Cysticerci can also be found in the eye and must be removed to avoid permanent eye damage, including blindness. Much of the damage from cysticercosis is caused by the severe inflammatory host response that occurs after the cysticerci have died. Antibodies are produced and offer the patient secondary immunity.



Laboratory Diagnosis


Cysticercosis can be difficult to diagnose. T. solium eggs are found in stools in fewer than half the patients with cysticercosis. Demonstration of eggs or proglottids in the feces is an indication of Taenia infection but does not provide a diagnosis for cysticercosis. Definitive diagnosis usually requires the identification of cysticercus in the tissue. The organism is surgically removed and microscopically examined for the presence of suckers and hooks on the scolex. The cysticercus is round to oval, translucent, and about 5 mm or more in diameter. The organism has a scolex with four suckers and a rostellum with a circle of hooks. Fine needle aspiration cytology may be helpful in the diagnosis and eliminates the need for surgical biopsy. Diagnosis may also be made using computed tomography (CT) scans and magnetic resonance imaging (MRI). Radiographs may also be useful in detecting calcifying cysticerci within tissue. Ocular cysticercosis may be diagnosed by visual identification of the larval worm. Serologic procedures (such as enzyme-linked immunosorbent assay [ELISA]) may also be used as a useful tool to aid in diagnosis, but may not be sensitive enough in light infections. The Centers for Disease Control and Prevention (CDC) offers an immunoblot assay that has demonstrated 100% specificity and 98% sensitivity. The assay uses purified antigen from T. solium containing seven different major glycoproteins. It is by far the test of choice over an ELISA. Nucleic acid-based methods and species-specific polymerase chain reaction (PCR) have been described to differentiate Taenia species.





Echinococcus Granulosus


General Characteristics


Echinococcus is the smallest of all tapeworms (3 to 9 mm long) with three to five proglottids. It contains a scolex with four suckers and a rostellum with hooks to attach to the intestinal wall. E. granulosus is a tapeworm found in the small intestine of the definitive host, the canine. Eggs are ingested by the intermediate hosts and include a variety of mammals including sheep, cattle, moose, and humans. There are several strains of Echinocococcus granulosus that have been identified, with the dog-sheep strain being the most common. Humans are typically accidental hosts and are considered a dead-end since the life cycle of the organism is unable to continue in a human host. Oncospheres hatch in the intestine of the intermediate host and invade the circulatory system, where they develop into hydatid cysts. Disease symptoms vary with the site and size of the cyst. Echinococcosis (hydatid disease) results from the presence of one or more cysts (hydatids), which can develop in any tissue.




Pathogenesis and Spectrum of Disease


Hydatid disease in humans is potentially dangerous depending on the size and location of the cyst. Some cysts may remain undetected for many years until they grow large enough to affect other organs. Many humans live day-to-day without ever knowing they are infected. The cyst is very slow growing in humans. It is usually fluid-filled and has a germinal layer from which many thousands of scolices are budded. These are known as daughter cysts (brood capsules), which attach to the germinal layer or free-float in the cyst. The scolices in the hydatid fluid resemble grains of sand and are called hydatid sand (Figures 55-2, A and 55-3). The result is a unilocular cyst containing future adult worms. The cyst may resemble a slow-growing tumor. Infections in the liver or lungs may be asymptomatic for many years, but the pressure eventually causes noticeable symptoms. The majority of the hydatid cysts occur within the liver. Cysts within the liver cause chronic abdominal pain and allergic reactions and may result in cholangitis (infection of the common bile duct) and cholestasis (interference with flow of bile from the liver). Cysts that develop in the lungs may cause infections and abscesses and result in chronic cough, shortness of breath, and chest pain. During the life cycle of the cyst, there may be occasional seepage of fluid into the host tissue and circulation causing sensitization or activation of the immune response from the presence of the parasite. The rupture and release of the fluid of a hydatid cyst may cause anaphylactic shock as a result of the primary sensitization in a previously asymptomatic individual. If a cyst bursts within the human body, many new cysts may be released that are typically eliminated via the host’s cellular immune response. Leaking fluid from a cyst may cause notable eosinophilia.


image
Figure 55-2 A, Echinococcus granules. B, Ovum. C, Scolex. (Courtesy Dr. Henry Travers, Sioux Falls, S.D.)

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Aug 25, 2016 | Posted by in MICROBIOLOGY | Comments Off on Tissue Cestodes

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