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Nematodes !!navigator!!

The nematodes, or roundworms, that are of medical significance can be broadly classified as either tissue or intestinal parasites.

Tissue Nematode Infections

With the exception of trichinellosis, these infections are due to invasive larval stages that do not reach maturity in humans.

TRICHINELLOSIS-
MICROBIOLOGY AND EPIDEMIOLOGY- Eight species of Trichinella cause human infection; two-T. spiralis and T. pseudospiralis-are found worldwide.
  • Infection results when humans ingest meat (usually pork) that contains encysted Trichinella larvae.
    • The larvae invade the small-bowel mucosa.
    • After 1 week, female worms release new larvae that migrate to striated muscle via the circulation and encyst.
  • The host immune response has few deleterious effects on muscle-dwelling larvae.
  • About 12 cases of trichinellosis are reported annually in the United States.
CLINICAL MANIFESTATIONS- Most light infections (<10 larvae per gram of muscle) are asymptomatic. A burden of >50 larvae per gram can cause fatal disease.
  • In the first week of infection, large numbers of parasites invading the gut usually cause diarrhea, abdominal pain, constipation, nausea, and/or vomiting.
  • In the second week of infection, pts develop symptoms related to larval migration and muscle invasion: hypersensitivity reactions with fever and hypereosinophilia; periorbital and facial edema; and hemorrhages in conjunctivae, retina, and nail beds. Deaths are usually due to myocarditis with arrhythmias or heart failure.
  • Approximately 2-3 weeks after infection, larval encystment in muscle causes myositis, myalgias, muscle edema, and weakness (especially in extraocular muscles; the biceps; and muscles of the jaw, neck, lower back, and diaphragm).
  • Symptoms peak at 3 weeks; convalescence is prolonged.
DIAGNOSIS- Eosinophilia develops in >90% of pts, peaking at a level of >50% at 2-4 weeks after infection.
  • An increase in parasite-specific antibody titers after the third week of infection confirms the diagnosis.
  • Detection of larvae by microscopic examination of ≥1 g of fresh muscle tissue (i.e., not routine histopathologic sections) also confirms the diagnosis. Yields are highest near tendon insertions.
TREATMENT

Trichinellosis

  • Mebendazole (200-400 mg tid for 3 days; then 400 mg tid for 8-14 days) or albendazole (400 mg bid for 8-14 days) is active against enteric-stage parasites; the efficacy of these drugs against encysted larvae is inconclusive.
  • Glucocorticoids (e.g., prednisone at 1 mg/kg daily for 5 days) may reduce severe myositis and myocarditis.
PREVENTION- Cooking pork until it is no longer pink or freezing it at -15°C (5°F) for 3 weeks kills larvae and prevents infection by most Trichinella spp.
VISCERAL AND OCULAR LARVA MIGRANS-
MICROBIOLOGY AND EPIDEMIOLOGY- Humans are incidental hosts for nematodes that cause visceral larva migrans. Most cases are caused by the canine ascarid Toxocara canis. Infection results when humans-most often preschool children-ingest soil contaminated by puppy feces that contains infective T. canis eggs. Larvae penetrate the intestinal mucosa and disseminate hematogenously to a wide variety of organs (e.g., liver, lungs, CNS), provoking intense eosinophilic granulomatous responses.
CLINICAL MANIFESTATIONS- Symptomatic infections result in fever, malaise, anorexia, weight loss, cough, wheezing, rashes, hepatosplenomegaly, and occasional profound eosinophilia (up to 90%). Ocular disease usually develops in older children or young adults and includes an eosinophilic mass that mimics retinoblastoma, endophthalmitis, uveitis, and/or chorioretinitis.
DIAGNOSIS- The clinical diagnosis can be confirmed by an ELISA for toxocaral antibodies. Stool examination for eggs is ineffective because larvae do not develop into adult worms in humans.
TREATMENT

Visceral and Ocular Larva Migrans

  • The vast majority of Toxocara infections are self-limited and resolve without specific therapy.
  • For pts with severe disease, glucocorticoids can reduce inflammatory complications.
  • Anthelmintic drugs, including mebendazole and albendazole, have not been shown to alter the course of larva migrans.
  • Ocular disease can be treated with albendazole (800 mg bid) and glucocorticoids for 5-20 days.
CUTANEOUS LARVA MIGRANS- This disease is caused by larvae of animal hookworms, usually the dog and cat hookworm Ancylostoma braziliense. Larvae in contaminated soil penetrate human skin; intensely pruritic, erythematous lesions form along the tracks of larval migration and advance several centimeters each day. Ivermectin (a single dose of 200 µg/kg) or albendazole (200 mg bid for 3 days) can relieve the symptoms of this self-limited infestation.

Intestinal Nematode Infections

Intestinal nematodes infect >1 billion persons worldwide, most commonly in regions with poor sanitation and particularly in developing countries in the tropics or subtropics. Because most helminthic parasites do not self-replicate, clinical disease (as opposed to asymptomatic infection) generally develops only with prolonged residence in an endemic area and is typically related to infection intensity.

ASCARIASIS-
MICROBIOLOGY- Ascariasis is caused by Ascaris lumbricoides, the largest intestinal nematode, which reaches lengths up to 40 cm.
  • Humans-primarily younger children-are infected by ingestion of fecally contaminated soil that contains ascarid eggs.
  • Larvae hatch in the intestine, invade the mucosa, migrate to the lungs, break into the alveoli, ascend the bronchial tree, are swallowed, mature in the small intestine, and produce up to 240,000 eggs per day that pass in the feces.
CLINICAL MANIFESTATIONS- Most infections have a low worm burden and are asymptomatic. During lung migration of the parasite (∼9-12 days after egg ingestion), pts may develop a cough and substernal discomfort, occasionally with dyspnea or blood-tinged sputum, fever, and eosinophilia.
  • Eosinophilic pneumonitis (Löffler's syndrome) may be evident.
  • Heavy infections with numerous entangled worms can occasionally cause pain, small-bowel obstruction, perforation, volvulus, biliary obstruction and colic, or pancreatitis.
LABORATORY FINDINGS- Ascaris eggs (65 by 45 µm) can be found in fecal samples. Adult worms can pass in the stool or, much less commonly, through the mouth or nose.
TREATMENT

Ascariasis

A single dose of albendazole (400 mg), mebendazole (500 mg), or ivermectin (150-200 µg/kg) is effective; these medications are contraindicated in pregnancy.

HOOKWORM-
MICROBIOLOGY- Two hookworm species, Ancylostoma duodenale and Necator americanus, cause most human infections, although A. ceylanicum is being recognized as a major hookworm pathogen in Asia. Infectious larvae present in soil penetrate the skin, reach the lungs via the bloodstream, invade the alveoli, ascend the airways, are swallowed, reach the small intestine, mature into adult worms, attach to the mucosa, and suck blood (0.2 mL/d per Ancylostoma adult) and interstitial fluid.
CLINICAL MANIFESTATIONS- Most infections are asymptomatic. Chronic infection causes iron deficiency and-in marginally nourished persons-progressive anemia and hypoproteinemia, weakness, and shortness of breath. Larvae may cause pruritic rash (“ground itch”) at the site of skin penetration as well as serpiginous tracks of SC migration (similar to those of cutaneous larva migrans).
LABORATORY FINDINGS- Hookworm eggs (40 by 60 µm) can be found in the feces. Stool concentration may be needed for the diagnosis of light infections. PCR can provide a species-specific diagnosis.
TREATMENT

Hookworm

  • Albendazole (400 mg once) or mebendazole (500 mg once) is effective, although there is significant concern that these agents are becoming much less effective. Nutritional support, iron replacement, and deworming are undertaken as needed.
STRONGYLOIDIASIS-
MICROBIOLOGY AND EPIDEMIOLOGY- Unlike other helminths, Strongyloides stercoralis can replicate in the human host, permitting ongoing cycles of autoinfection from endogenously produced larvae.
  • Infection results when filariform larvae in fecally contaminated soil penetrate the skin or mucous membranes.
    • Larvae travel through the bloodstream to the lungs, break through into alveolar spaces, ascend the bronchial tree, are swallowed, reach the small intestine, mature into adult worms, and penetrate the mucosa of the proximal small bowel; eggs hatch in the intestinal mucosa.
    • Rhabditiform larvae can pass with the feces into the soil or can develop into filariform larvae that penetrate the colonic wall or perianal skin and enter the circulation to establish ongoing autoinfection.
  • Autoinfection is constrained by unknown factors of the host immune system, disruption of which (e.g., by glucocorticoid therapy) can lead to hyperinfection.
CLINICAL FEATURES- Uncomplicated disease is associated with mild cutaneous and/or abdominal manifestations such as recurrent urticaria, larva currens (a pathognomonic serpiginous, pruritic, erythematous eruption along the course of larval migration that may advance up to 10 cm/h), abdominal pain, nausea, diarrhea, bleeding, and weight loss.
  • Disseminated disease involves tissues outside the GI tract and lungs, including the CNS, peritoneum, liver, and kidney.
    • Gram-negative sepsis, pneumonia, or meningitis can complicate or dominate the clinical course.
    • Disease can be fatal in pts given glucocorticoids; disseminated infection is uncommon among pts with HIV-1 infection.
  • Fluctuating eosinophilia is common in uncomplicated disease but is uncommon in disseminated disease.
DIAGNOSIS- A single stool examination detects rhabditiform larvae (∼250 µm long) in about one-third of uncomplicated infections. PCR is available and provides increased diagnostic specificity.
  • Duodenojejunal contents can be sampled if stool examinations are repeatedly negative.
  • Antibodies can be detected by ELISA.
  • In disseminated infection, filariform larvae can be found in stool or at sites of larval migration (e.g., sputum, bronchoalveolar lavage fluid, surgical drainage fluid).
TREATMENT

Strongyloidiasis

  • Ivermectin (200 µg/kg daily for 2 days) is more effective than albendazole (400 mg daily for 3 days). Asymptomatic pts should be treated, given the potential for later fatal hyperinfection.
  • Disseminated disease should be treated with ivermectin for at least 5-7 days (or until the parasites are eradicated).
  • In immunocompromised hosts, the course of ivermectin should be repeated 2 weeks after initial treatment.
ENTEROBIASIS-
MICROBIOLOGY AND EPIDEMIOLOGY- Enterobiasis (pinworm) is caused by Enterobius vermicularis and affects ∼40 million people in the United States (primarily children).
  • Gravid female worms migrate nocturnally from the cecum to the perianal region, each releasing up to 2000 immature eggs that become infective within hours.
  • Autoinfection and person-to-person transmission result from perianal scratching and transport of infective eggs to the mouth.
CLINICAL MANIFESTATIONS- Perianal pruritus is the cardinal symptom and is often worst at night. Eosinophilia is uncommon.
DIAGNOSIS- Eggs (55 by 25 µm and flattened on one side) are detected by microscopic examination of cellulose acetate tape applied to the perianal region in the morning.
TREATMENT

Enterobiasis

  • One dose of mebendazole (100 mg) or albendazole (400 mg) is given, with the same treatment repeated after 2 weeks. Household members should also be treated to avoid reservoirs of potential reinfection.

Filarial and Related Infections

Filarial worms, which infect >170 million people worldwide, are nematodes that dwell in the SC tissue and lymphatics. Usually, infection is established only with repeated and prolonged exposures to infective larvae; however, filarial disease is characteristically more intense and acute in newly exposed individuals than in natives of endemic areas.

  • Filarial parasites have a complex life cycle, including infective larval stages carried by insects and adult worms that reside in humans.
    • The offspring of adults are microfilariae (200-250 µm long, 5-7 µm wide) that either circulate in the blood or migrate through the skin.
    • Microfilariae are ingested by the arthropod vector and develop over 1-2 weeks into new infective larvae.
  • A bacterial endosymbiont, Wolbachia, is found in all stages of Brugia, Wuchereria, Mansonella, and Onchocerca spp. and has become a target for antifilarial chemotherapy.
LYMPHATIC FILARIASIS-
MICROBIOLOGY- Lymphatic filariasis is caused by Wuchereria bancrofti (most commonly), Brugia malayi, or B. timori, which can reside in and cause inflammatory damage to lymphatic channels or lymph nodes.
CLINICAL MANIFESTATIONS- Subclinical microfilaremia, hydrocele, acute adenolymphangitis (ADL), and chronic lymphatic disease are the main clinical presentations.
  • ADL is associated with high fever, lymphatic inflammation, and transient local edema. Both the upper and lower extremities can be involved in both bancroftian and brugian filariasis, but W. bancrofti almost exclusively affects genital lymphatics.
  • ADL may progress to more chronic lymphatic obstruction and elephantiasis with brawny edema, thickening of the SC tissues, and hyperkeratosis. Superinfection is a problem.
DIAGNOSIS- Detection of the parasite is difficult, but microfilariae can be found in peripheral blood, hydrocele fluid, and occasionally other body fluids.
  • Timing of blood collection is critical and should be based on the periodicity of the microfilariae in the endemic region involved (primarily nocturnal in many regions).
  • Two assays are available to detect W. bancrofti circulating antigens, and a PCR has been developed to detect DNA of both W. bancrofti and B. malayi in the blood.
  • High-frequency ultrasound (with Doppler techniques) of the scrotum or the female breast can identify motile adult worms.
  • The presence of antifilarial antibody supports the diagnosis, but cross-reactivity with other helminthic infections makes interpretation of this finding difficult.
TREATMENT

Lymphatic Filariasis

  • Pts with active lymphatic filariasis (defined by microfilaremia, antigen positivity, or adult worms on ultrasound) should be treated with diethylcarbamazine (DEC, 6 mg/kg daily for 12 days), which has macro- and microfilaricidal properties. Albendazole (400 mg bid for 21 days), albendazole and DEC both given daily for 7 days, doxycycline (100 mg bid for 4-6 weeks), and the addition of DEC to a 3-week course of doxycycline are alternative regimens with macrofilaricidal efficacy.
  • A single dose of albendazole (400 mg) combined with DEC (6 mg/kg) or ivermectin (200 µg/kg) has sustained (≥2 years) microfilaricidal activity and is used in lymphatic filariasis eradication campaigns.
  • For pts with chronic lymphatic filariasis, treatment regimens should focus on hygiene, prevention of secondary bacterial infections, and physiotherapy. Drug treatment should be reserved for individuals with evidence of active infection, although a 6-week course of doxycycline improves filarial lymphedema irrespective of disease activity.
ONCHOCERCIASIS-
MICROBIOLOGY AND EPIDEMIOLOGY- Onchocerciasis (“river blindness”) is caused by Onchocerca volvulus, which infects 37 million people worldwide and is transmitted by the bite of an infected blackfly near free-flowing rivers and streams.
  • Larvae deposited by the blackfly develop into adult worms (females and males are ∼40-60 cm and ∼3-6 cm in length, respectively) that are found in SC nodules (onchocercomata). About 7 months to 3 years after infection, the gravid female releases microfilariae that migrate out of the nodules and concentrate in the dermis.
  • In contrast to lymphatic filariasis, onchocerciasis is characterized by microfilarial induction of inflammation.
CLINICAL MANIFESTATIONS- Onchocerciasis most commonly presents as dermatologic manifestations (an intensely pruritic papular rash or firm nontender onchocercomata), but visual impairment is the most serious complication in pts with moderate or heavy infections.
  • Conjunctivitis with photophobia is an early ocular finding.
  • Sclerosing keratitis (the leading cause of onchocercal blindness in Africa, affecting 1-5% of pts), anterior uveitis, iridocyclitis, and secondary glaucoma due to pupillary deformities are more serious ocular complications.
DIAGNOSIS- A definitive diagnosis is based on the finding of an adult worm in an excised nodule or of microfilariae in a skin snip.
  • Specific antibody assays and PCR to detect onchocercal DNA are available in reference laboratories.
  • Eosinophilia and elevated serum IgE levels are common but nonspecific.
TREATMENT

Onchocerciasis

  • Ivermectin (a single dose of 150 µg/kg), given yearly or semiannually, is microfilaricidal and is the mainstay of treatment.
    • In African regions where O. volvulus is coendemic with Loa loa, ivermectin is contraindicated because of the risk of severe posttreatment encephalopathy.
    • Doxycycline therapy for 6 weeks is macrofilaristatic, rendering adult female worms sterile for long periods, and also targets the Wolbachia endosymbiont.
  • Nodules on the head should be excised to avoid ocular infection.

Trematodes !!navigator!!

  • The trematodes, or flatworms, may be classified according to the tissues invaded by the adult stage of the fluke: blood, liver (biliary tree), intestines, or lungs.
  • The life cycle involves a definitive mammalian host (e.g., humans), in whom adult worms produce eggs through sexual reproduction, and an intermediate host (e.g., snails), in which miracidial forms undergo asexual reproduction to form cercariae. Worms do not multiply within the definitive host.
  • Human infection results from either direct penetration of intact skin or ingestion.
  • Infections with trematodes that migrate through or reside in host tissues are associated with a moderate to high degree of peripheral-blood eosinophilia.
SCHISTOSOMIASIS-
MICROBIOLOGY AND EPIDEMIOLOGY- Five species cause human schistosomiasis: Schistosoma mansoni, S. japonicum, S. mekongi, and S. intercalatum cause intestinal and hepatic schistosomiasis, and S. haematobium causes urogenital schistosomiasis.
  • After infective cercariae penetrate intact skin, they mature into schistosomula and migrate through venous or lymphatic vessels to the lungs and ultimately the liver parenchyma. Sexually mature worms migrate to the veins of the bladder and pelvis (S. haematobium) or the mesentery (S. mansoni, S. japonicum, S. mekongi, S. intercalatum) and deposit eggs.
    • Some mature ova are extruded into the intestinal or urinary lumina, from which they may be voided and ultimately may reach water and perpetuate the life cycle.
    • The persistence of ova in tissues leads to a granulomatous host response and fibrosis.
  • These blood flukes infect ∼230 million persons (mostly children and young adults), with >70% of infected people living in sub-Saharan Africa.
CLINICAL MANIFESTATIONS- Schistosomiasis occurs in three stages that vary by species, intensity of infection, and host factors (e.g., age, genetics).
  • Cercarial dermatitis causes a pruritic maculopapular rash (“swimmers' itch”) that lasts for 1-2 weeks.
  • Acute schistosomiasis (Katayama fever) presents between 2 weeks and 3 months after parasite exposure with fever, myalgia, general malaise, fatigue, headache, cough, abdominal tenderness, eosinophilia, and transient pulmonary infiltrates.
  • Chronic schistosomiasis causes manifestations that depend primarily on the schistosome species.
    • Intestinal schistosomiasis involves mucosal granulomatous inflammation with microulcerations, superficial bleeding, and sometimes pseudopolyposis. Disease due to S. mansoni and S. japonicum is generally more severe and may also involve hepatosplenic manifestations that can progress to periportal fibrosis.
    • Urogenital schistosomiasis due to S. haematobium consists of an inflammatory active stage (dysuria; hematuria, particularly at the end of voiding; urinary egg excretion; obstructive uropathy) in children and young adults that progresses in later life to a fibrotic chronic stage (nocturia, urine retention, dribbling, and incontinence).
    • Pulmonary disease (e.g., pulmonary hypertension, cor pulmonale) and CNS disease (e.g., seizures, encephalopathy, transverse myelitis) can occur and are due to granulomas and fibrosis.
DIAGNOSIS- Diagnosis is based on geographic history, clinical presentation, and presence of schistosome ova in excreta.
  • Serologic assays for schistosomal antibodies (available through the CDC in the United States) may yield positive results before eggs are seen in excreta.
  • Infection may also be diagnosed by examination of rectal biopsies (S. mansoni and S. haematobium) and occasionally Pap smears and semen samples (S. haematobium).
TREATMENT

Schistosomiasis

  • Praziquantel (20 mg/kg bid for S. mansoni, S. intercalatum, and S. haematobium infections; 20 mg/kg tid for S. japonicum and S. mekongi infections) is the drug of choice. In pts not cured by initial treatment, the same dose can be repeated at weekly intervals for 2 weeks.
    • Since praziquantel is ineffective against the young migrating schistosome stages, treatment may need to be repeated in 6-12 weeks if eosinophilia or symptoms persist.
    • Glucocorticoids can be added in Katayama fever to suppress the hypersensitivity reaction.
    • Late established manifestations, such as severe fibrosis, do not improve with treatment.
PREVENTION- Travelers to endemic regions should avoid contact with all freshwater bodies.
LIVER (BILIARY) FLUKES-
  • Clonorchiasis (due to Clonorchis sinensis) and opisthorchiasis (due to Opisthorchis viverrini and O. felineus) occur in Southeast Asia and Eastern Europe.
    • Infection is acquired by ingestion of contaminated raw or undercooked freshwater fish; larvae travel through the ampulla of Vater and mature in biliary canaliculi.
    • Most infected individuals are minimally symptomatic; chronic or repeated infection causes cholangitis, cholangiohepatitis, and biliary obstruction and is associated with cholangiocarcinoma.
    • Therapy for acute infection consists of praziquantel administration (25 mg/kg tid for 2 days).
  • Fascioliasis is due to Fasciola hepatica and F. gigantica, which commonly infect sheep and cattle.
    • Infection is acquired by ingestion of contaminated aquatic plants (e.g., watercress).
    • Acute disease develops 1-4 weeks after infection and causes high fever, weight loss, RUQ pain, and sometimes urticaria. Chronic infection is infrequently associated with bile duct obstruction due to fibrosis.
    • For treatment, triclabendazole is given as a single dose of 10 mg/kg.
  • Stool ova and parasite (O & P) examination diagnoses infection with liver flukes. Serologic testing is helpful, particularly in lightly infected pts.
LUNG FLUKES-
  • Infection with Paragonimus spp. is acquired by ingestion of contaminated crayfish and freshwater crabs.
  • Acute infection presents with fever, cough, hemoptysis, and peripheral eosinophilia, although pts with low parasite burdens may remain relatively asymptomatic for prolonged periods.
  • Chronic infection is associated with dyspnea, bloody (“rusty”) sputum, and bronchitis-, asthma-, and tuberculosis-like symptoms.

    Pts may develop pulmonary cyst formation or ectopic infection in the CNS and other organs.

  • The diagnosis is made by O & P examination of sputum or stool; serology can be helpful.
  • Praziquantel (25 mg/kg tid for 2 days) is the recommended therapy.

Cestodes !!navigator!!

The cestodes, or tapeworms, are segmented worms that can be classified into two groups according to whether humans are the definitive or the intermediate host. The tapeworm attaches to intestinal mucosa via sucking cups or hooks located on the scolex. Proglottids (segments) form behind the scolex and constitute the bulk of the tapeworm.

TAENIASIS SAGINATA AND TAENIASIS ASIATICA-
MICROBIOLOGY- Humans are the definitive host for Taenia saginata, the beef tapeworm, and T. asiatica, the swine tapeworm, which inhabit the upper jejunum. Eggs are excreted in feces and ingested by cattle or other herbivores (T. saginata) or pigs (T. asiatica); larvae encyst (cysticerci) in the striated muscles of these animals. When humans ingest raw or undercooked meat, the cysticerci mature into adult worms in ∼2 months.
CLINICAL MANIFESTATIONS- Pts become aware of the infection by noting passage of motile proglottids in their feces. They may experience perianal discomfort, mild abdominal pain, nausea, change in appetite, weakness, and weight loss.
DIAGNOSIS- The diagnosis is made by detection of eggs or proglottids in the stool; eggs may be detected in the perianal area by the cellophane-tape test (as in pinworm infection). Eosinophilia and elevated IgE levels are usually absent.
TREATMENT

Taeniasis Saginata and Taeniasis Asiatica

Praziquantel is given in a single dose of 10 mg/kg.

TAENIASIS SOLIUM AND CYSTICERCOSIS-
MICROBIOLOGY AND PATHOGENESIS- Humans are the definitive host and pigs the usual intermediate host for T. solium, the pork tapeworm.
  • The disease has two forms, which depend on the form of parasite ingested.
    • By ingesting undercooked pork containing cysticerci, humans develop intestinal tapeworms and a disease similar to taeniasis saginata.
    • If humans ingest T. solium eggs (e.g., as a result of close contact with a tapeworm carrier or via autoinfection), they develop cysticercosis as a result of larval penetration of the intestinal wall and migration to many tissues.
CLINICAL MANIFESTATIONS- Intestinal infections are generally asymptomatic except for fecal passage of proglottids. The presentation of cysticercosis depends on the number and location of cysticerci as well as the extent of associated inflammatory responses or scarring.
  • Cysticerci can be found anywhere in the body but most often are detected in the brain, skeletal muscle, SC tissue, or eye.
  • Neurologic manifestations are most common and include seizures (due to inflammation surrounding cysticerci in the brain), hydrocephalus (from obstruction of CSF flow by cysticerci and accompanying inflammation or by arachnoiditis), and signs of increased intracranial pressure (e.g., headache, nausea, vomiting, changes in vision).
DIAGNOSIS- Intestinal infection is diagnosed by detection of eggs or proglottids in stool. A consensus conference has delineated criteria for the diagnosis of neurocysticercosis (Table 111-1 Revised Diagnostic Criteria for Neurocysticercosisa ). Findings on neuroimaging include cystic lesions with or without enhancement, one or more nodular calcifications, or focal enhancing lesions.
TREATMENT

Taeniasis Solium and Cysticercosis

  • Intestinal infections respond to a single dose of praziquantel (10 mg/kg), but this treatment may evoke an inflammatory response in the CNS if there is cryptic cysticercosis.
  • Neurocysticercosis can be treated with albendazole (15 mg/kg per day for 8-28 days) or praziquantel (50-100 mg/kg daily in three divided doses for 15-30 days). A combination of albendazole and praziquantel (50 mg/kg in three divided doses per day) is more effective in pts with more than two cystic lesions.
    • Given the potential for an inflammatory response to treatment, pts should be carefully monitored, and high-dose glucocorticoids should be used during treatment.
    • Since glucocorticoids induce praziquantel metabolism, cimetidine should be given with praziquantel to inhibit this effect.
    • Supportive measures include antiepileptic administration and treatment of hydrocephalus as indicated.
ECHINOCOCCOSIS-
MICROBIOLOGY AND EPIDEMIOLOGY- Humans are an intermediate host for larvae of Echinococcus granulosus sensu lato, E. multilocularis, and E. vogeli. Pts acquire disease due to E. granulosus sensu lato by ingesting eggs spread by canine feces.
  • After ingestion, embryos escape from the eggs, penetrate the intestinal mucosa, enter the portal circulation, and are carried to many organs but particularly the liver and lungs. Larvae develop into fluid-filled unilocular hydatid cysts within which daughter cysts develop, as do germinating cystic structures (brood capsules). Cysts expand over years.
  • Echinococcosis is prevalent on all continents, particularly in areas where livestock is raised in association with dogs.
  • E. multilocularis, found in Arctic or sub-Arctic regions, is similar to E. granulosus, but wild canines (e.g., foxes) are the definitive hosts and rodents are the intermediate hosts. The parasite is multilocular, and vesicles progressively invade host tissue.
CLINICAL MANIFESTATIONS- Expanding cysts exert the effects of space-occupying lesions, causing symptoms in the affected organ (usually liver and lung); the liver is involved in two-thirds of E. granulosus sensu lato infections and ∼100% of E. multilocularis infections.
  • Pts with hepatic disease most commonly present with abdominal pain or a palpable mass in the RUQ. Compression of a bile duct may mimic biliary disease, and rupture or leakage from a hydatid cyst may cause fever, pruritus, urticaria, eosinophilia, or anaphylaxis.
  • Pulmonary cysts may rupture into the bronchial tree or pleural cavity and cause cough, salty phlegm, chest pain, or hemoptysis.
  • Rupture of cysts may result in multifocal dissemination.
  • E. multilocularis disease may present as a hepatic tumor, with destruction of the liver and extension into adjoining (e.g., lungs, kidneys) or distant (e.g., brain, spleen) organs.
DIAGNOSIS- Radiographic imaging is important in detecting and evaluating echinococcal cysts.
  • Daughter cysts within a larger cyst are pathognomonic of E. granulosus sensu lato. Eggshell or mural calcification on CT is also indicative of E. granulosus infection.
  • Serologic testing yields positive results in ∼90% of pts with hepatic disease, but results can be negative in up to half of pts with lung cysts.
  • Aspiration of cysts usually is not attempted because leakage of cyst fluid can cause dissemination or anaphylactic reactions.
TREATMENT

Echinococcosis

  • Therapy is based on considerations of the size, location, and manifestations of cysts and the overall health of the pt. Ultrasound staging is recommended for cystic echinococcosis infection.
  • For some uncomplicated lesions, PAIR (percutaneous aspiration, infusion of scolicidal agents [95% ethanol or hypertonic saline], and reaspiration) is recommended.
    • Albendazole (7.5 mg/kg bid for 2 days before the procedure and for at least 4 weeks afterward) is given for prophylaxis of secondary peritoneal echinococcosis due to inadvertent spillage of fluid during this treatment.
    • PAIR is contraindicated for superficial cysts, for cysts with multiple thick internal septal divisions, and for cysts communicating with the biliary tree.
  • Surgical resection is the treatment of choice for complicated cystic echinococcosis.
    • Albendazole should also be given prophylactically, as just described. Praziquantel (50 mg/kg daily for 2 weeks) may hasten the death of protoscolices.
    • Medical therapy alone with albendazole for 12 weeks to 6 months results in cure in ∼30% of cases and in clinical improvement in another 50%.
  • E. multilocularis infection is treated surgically, and albendazole is given for at least 2 years after presumptively curative surgery. If surgery is not curative, albendazole should be continued indefinitely.
DIPHYLLOBOTHRIASIS- Diphyllobothrium latum, the longest tapeworm (up to 25 m), attaches to the ileal and occasionally the jejunal mucosa. Humans are infected by consumption of infected raw or smoked fish. Symptoms are rare and usually mild, but infection, particularly in Scandinavia, can cause vitamin B12 deficiency because the tapeworm absorbs large amounts of vitamin B12 and interferes with ileal B12 absorption. Up to 2% of infected pts, especially the elderly, have megaloblastic anemia resembling pernicious anemia and can suffer neurologic sequelae due to B12 deficiency. The diagnosis is made by detection of eggs in the stool. Praziquantel (5-10 mg/kg once) is highly effective.

Outline ⬆

Section 7. Infectious Diseases