Essentials of Diagnosis

• Blood flukes: demonstration of eggs in feces, urine, or rectal biopsy

• Liver flukes: demonstration of eggs in feces

• Intestinal flukes: demonstration of adult worms or eggs in feces

• Lung flukes: demonstration of eggs in sputum or feces

All trematode species that are parasitic for humans are digenetic. Sexual reproduction in the adult fluke is followed by asexual multiplication in the larval stage. Most species of adult trematodes have an oral and ventral sucker. The life cycles of trematodes that are important human pathogens are similar among all five major species. Eggs are excreted in the feces of the host, hatch in fresh water, and require a primary host in snails before infection occurs in humans. Trematode infection may be classified into four general groups based on the final habitat of the adult flukes in humans as follows: blood flukes, liver flukes, intestinal flukes, and lung flukes (Table 1).

CLINICAL SYNDROMES

BLOOD FLUKE INFECTION (SCHISTOSOMIASIS)

General Considerations

The final habitat for blood flukes is the venous system of the bowel mesentery or the urinary bladder.

A. Epidemiology. It is estimated that schistosomiasis occurs in > 200 million people worldwide and is endemic in Asia, Africa, South America, and other parts of the world where the population is engaged in freshwater agriculture. The total number of infected individuals in the United States is estimated to exceed 500,000, and these cases are most often in immigrants from South America, Asia, and the Caribbean. The disease cannot spread in the United States because the specific snail that serves as an intermediate host does not yet exist in the United States. Unlike most other trematodes that are pathogenic for humans, adult schistosomes have separate sexes. The female fluke resides within a groove created by the fold of the lateral edges of the male fluke.

Each of the five blood fluke species that are pathogenic for humans has a specific geographic distribution as follows: Schistosoma mansoni, Arabian peninsula, Africa, Caribbean, and South America; Schistosoma haematobium, Middle East and Africa; Schistosoma japonicum, Japan, China, and The Philippines; Schistosoma mekongi, Southeast Asia; and Schistosoma intercalatum, west and central Africa. The specific geographic distribution depends on the presence of the specific snail intermediate host.

B. Microbiology and Pathogenesis. The life cycle of the five major species of blood flukes is as follows: adult flukes (1-2 cm in length) inhabit the venous system of the mesentery or urinary bladder; sexual reproduction results in the characteristically shaped eggs that are excreted in the feces; the eggs hatch in fresh water, releasing ciliated motile miracidia, which penetrate the body of the snail that serves as the intermediate host (a specific snail and geographic distribution exist for each species of blood fluke); within the snail, the miracidia multiply asexually and, 4-6 weeks later, hundreds of fork-tailed cercariae emerge; the cercariae penetrate human skin, lose their tails, and become schistosomes that migrate to the lungs and liver where maturation occurs; and ~ 6 weeks later, the mature adult fluke migrates to its final habitat in the venous systems. The mean life span of adult flukes in humans is estimated to be 5-10 years.

Clinical Findings

The three different stages (cercariae, mature flukes, and eggs) of the blood fluke in humans result in three major disease syndromes in chronologic order: dermatitis (swimmers’ itch), fever and constitutional complaints (Katayama fever), and finally chronic fibro-obstructive disease (Box 88-1).

A. Signs and Symptoms. Dermatitis (swimmers’ itch) is the acute form of schistosomiasis and is characterized by a pruritic and papular rash that usually occurs within 1-3 days after penetration of the cercariae. Swimmers’ itch rarely occurs after primary exposure and is more common in individuals who have been sensitized by earlier exposure.

Katayama fever occurs 4-8 weeks after penetration of the skin in humans and coincides with the production of eggs by the flukes. Katayama fever is most severe after S japonicum infection, but occasionally occurs in patients infected with S mansoni and rarely S haematobium. Patients experience an acute onset of fever, chills, headache, and cough. Physical findings often include lymphadenopathy and hepatosplenomegaly. Eosinophilia is common. Symptoms usually disappear within a few weeks after onset, but, rarely, death may occur, usually in association with S japonicum infection. Katayama fever may be the result of immune complex formation from massive antigenic challenge from exposure to fluke eggs.

In chronic fibro-obstructive schistosomiasis, tissue damage occurs from chronic inflammatory response to the deposition of eggs. This results in chronic granulomatous disease and eventual fibrosis. Liver and bowel are the sites most commonly affected in patients with infection caused by S mansoni, S japonicum, S mekongi, or S intercalatum. Patients often experience chronic abdominal pain and diarrhea. In the liver, fibrosis may result in portal hypertension, hepatosplenomegaly, esophageal varices, and variceal bleeding. Liver function tests usually remain normal for an extended period of time after infection. In chronic untreated cases, hepatic dysfunction, jaundice, ascites, and liver failure may occur.

In patients with S haematobium infection, the flukes are located in the vesicular plexus, and granulomatous formation occurs in the bladder and ureters. Hematuria is the most common complaint. With prolonged infection, fibrosis, ureteral obstruction, and chronic renal failure may occur. The frequency of bladder cancer may be higher in patients with chronic S haematobium infection.

Pulmonary schistosomiasis may occur in patients with advanced liver cirrhosis and portal hypertension. The development of portosystemic shunts enables fluke eggs to bypass the liver and enter the pulmonary circulation. Patients with S haematobium may also develop pulmonary schistosomiasis; the eggs may enter the inferior vena cava from the vesicular plexus and enter the pulmonary venous system.

Of patients with S japonicum, ~ 3% develop central nervous system schistosomiasis manifested by space-occupying lesions that may cause focal seizures. Rarely, granulomatous lesions resulting from ectopic eggs in the vasculature of the spinal cord may cause transverse myelitis.

B. Laboratory Findings. The most common laboratory findings seen in patients with schistosomiasis include eosinophilia, hematuria, anemia, and — in chronic end-stage infection — abnormal liver function tests, elevated serum creatinine, and uremia. The diagnosis is established by identifying the characteristic schistosomal eggs in the feces, urine, or a rectal biopsy specimen. Skin tests or serologic tests are helpful for epidemiologic studies but are not diagnostic of active infection.

Differential Diagnosis

Hepatic schistosomiasis may resemble any process that causes chronic hepatosplenomegaly and portal hypertension including alcoholic cirrhosis, Wilson’s disease, chronic hepatitis C infection, and many other conditions. S haematobium must be differentiated from bladder or ureteral cancer, reflux disease, and other syndromes that cause hematuria or chronic renal failure.

Treatment

The treatment for patients with schistosomiasis is shown in Box 88-2. Praziquantel is safe and effective therapy for all five species of schistosoma that infect humans. Eggs may be shed for some time after treatment, and follow-up stool or urine examination should be obtained several months after therapy to ensure eradication.

Prognosis

The prognosis of schistosomiasis is excellent among patients who are treated before end-stage hepatic or renal disease develops. In these patients, prognosis depends on the magnitude of end-organ disease.

Prevention

The only effective means of prevention is to avoid contact with fresh water in areas where schistosomiasis is endemic.

LIVER FLUKE INFECTIONS (CLONORCHIASIS, OPISTHORCHIASIS, & FASCIOLIASIS)

General Considerations

The final common habitat for the liver flukes is the bile ducts. The liver flukes that are the most common cause of human infections are Clonorchis sinensis (clonorchiasis), Opisthorchis spp. (opisthorchiasis), and Fasciola hepatica (fascioliasis).

C sinensis (Chinese or oriental liver fluke) is a flat, elongated fluke (~ 15 mm ( 3 mm) that inhabits the distal biliary capillaries. Humans are incidental hosts, and the infection is endemic in China, Hong Kong, Korea, and Southeast Asia. Eggs eliminated in the feces are then ingested by the specific snail intermediate host. After ingestion, the eggs hatch into miracidia. The organisms multiply and produce extremely high numbers of cercariae that exit the snail and penetrate the skin of freshwater fish. Once the cercariae are on the fish skin, they encyst as metacercariae, which are infective for humans. Humans and fish-eating mammals acquire infection by ingestion of raw or undercooked fish that contain metacercariae. After ingestion, metacercariae excyst in the duodenum of humans and pass through the ampulla of Vater, where the flukes mature into adults in the bile ducts.

O felineus and other species are endemic in Southeast Asia, Eastern Europe, and Russia and are common liver flukes of dogs and cats that may be transmitted to humans. The life cycle is similar to that of C sinensis.

F hepatica is a common liver fluke in sheep and cattle and is endemic in South America, Europe, Africa, Australia, and China. Humans are incidental hosts. Eggs are deposited in the biliary system and excreted in the feces. In fresh water, the eggs hatch, and the miracidia must reach and penetrate their specific snail host within 8 h. The cercariae emerge from snails and encyst on aquatic plants and sometimes in soil. The plants are consumed by humans, sheep, or cattle. The organisms excyst in the duodenum. The larvae penetrate through the intestinal wall into the peritoneum, enter through the capsule of the liver, and migrate to the bile ducts.

Clinical Findings

The majority of patients with C sinensis and O felineus infections are asymptomatic (Box 1). With heavy infection, biliary obstruction and cholangitis may occur. The frequency of cholangiocarcinoma may be increased in patients with chronic C sinensis infection. Diagnosis depends on demonstration of the characteristic eggs in the feces.

Unlike clonorchiasis or opisthorchiasis, patients parasitized by F hepatica are usually symptomatic, and there are two distinct clinical stages of infection. In the early stage, symptoms correspond to the hepatic migration of the larvae, and patients experience fever, right upper quadrant pain, hepatomegaly, and eosinophilia. Acute symptoms subside as the larvae enter the bile ducts, and most patients become asymptomatic in this later stage of infestation. Biliary obstruction, cholangitis, or biliary cirrhosis may occur rarely with heavy infestation. The definitive diagnosis is made by identifying the characteristic eggs in the feces or bile. A positive serologic test suggests infection. Computed tomography of the liver may show small nodules and tortuous tracts made by the migrating larvae.

Differential Diagnosis

In the acute phase of F hepatica infection, patients may resemble those with acute cholangitis, cholecystitis, liver abscess, or Neisseria gonorrhoeae infection (Fitz-Hugh and Curtis syndrome). However, the presence of eosinophilia suggests F hepatica infection.

Treatment

Praziquantel is effective therapy for symptomatic patients with C sinensis or O felineus infection. Bithionol is the drug of choice for F hepatica infection (Box 2).

Prognosis

The prognosis for treated patients with liver fluke infection is excellent.

Prevention

Avoiding consumption of raw or undercooked freshwater fish is the only effective means of prevention of C sinensis or O felineus infection. Individuals should avoid consumption of undercooked aquatic plants and grasses in areas where F hepatica is endemic.

INTESTINAL FLUKE INFECTION (FASCIOLOPSIASIS)

General Considerations

The final habitat of intestinal flukes is the small bowel. Fasciolopsis buski is endemic in the Far East and southeast Asia. Eggs are excreted in the feces, develop into cercariae in fresh water, and encyst on freshwater plants. After human consumption, the organisms excyst in the bowel and mature into adult flukes that measure 2-8 cm ( 1-2 mm. They reside in the upper portion of the small intestine where they attach to the mucosa.

Clinical & Laboratory Findings

Most patients are asymptomatic, but, with heavy infection, abdominal pain, diarrhea, and occasionally malabsorption may occur (Box 1). Diagnosis may be made by the demonstration of the characteristic eggs or adult flukes in the stool.

Differential Diagnosis

Most patients are asymptomatic, and the differential diagnosis is that of patients with diarrhea and abdominal pain caused by bacteria and other parasites.

Treatment

Praziquantel is effective therapy for intestinal flukes (Box 2).

Prognosis

The Prognosis is excellent.

Prevention

Individuals residing in endemic areas should avoid consumption of undercooked aquatic plants and grasses.

LUNG FLUKE INFECTION (PARAGONIMIASIS)

General Considerations

Paragonimus westermani is endemic in the Far East Indian subcontinent, Central and South America, and West Africa. Human lung flukes produce eggs in sputum that are swallowed, excreted in the feces, and mature in fresh water into miracidia, which penetrate snails. The mature cercariae exit the snail, penetrate into freshwater crayfish and crabs, and encyst. Infection in humans occurs after ingestion of raw, undercooked, or pickled freshwater crustacea. After ingestion, the organisms excyst in the duodenum, penetrate through the bowel wall, enter the peritoneal cavity, pass through the diaphragm into the pleural space, and enter the lungs where they mature into flukes that measure 7-15 mm ( 5-8 mm. Ectopic eggs in the brain may result in space-occupying lesions and focal seizures.

Clinical Findings

Many patients with minimal to moderate infection are asymptomatic (Box 88-1). With acute infections, symptomatic patients experience cough productive of brown sputum or hemoptysis and eosinophilia. Heavy untreated infection may progress to chronic bronchitis or bronchiectasis with large-volume sputum production, pleuritic chest pain, pleural effusion, and lung abscess. Diagnosis is made by identifying the characteristic eggs in the sputum or feces. A positive serology may be helpful in the diagnosis of ectopic infection. The diagnosis should also be suspected in individuals who do not reside in endemic areas but have a history of consumption of undercooked crustacea imported from endemic areas.

Differential Diagnosis

Pulmonary paragonimiasis resembles chronic bacterial infection, mycobacterial infection, or carcinoma of the lung. The presence of eosinophilia in these patients who reside in or have traveled to an endemic area should suggest the diagnosis of paragonimiasis.

Treatment

Praziquantel is effective therapy (Box 2).

Prognosis

The prognosis is excellent in patients who are treated before the development of chronic bronchitis or bronchiectasis.

Prevention

Individuals should avoid the consumption of raw or undercooked freshwater crustacea from areas where P westermani is endemic.

Table 1. Important trematodes parasitic for humans.

Intermediate Host

Type

Infection

Species

Primary

Secondary

Site Parasitic in Humans

Blood

Schistosomiasis

S mansoni

S japonicum

S haematobium

S mekongi

S intercalatum

Snails

Snails

Snails

Snails

Snails

None

None

None

None

None

Inferior mesenteric veins

Superior mesenteric veins

Urinary bladder, venous plexus

Mesenteric veins

Mesenteric veins

Liver

Clonorchiasis

Opisthorchiasis

Fascioliasis

C sinensis

O felineus

F hepatica

Snails

Snails

Snails

Fish

Fish

Watercress

Bile ducts

Bile ducts

Bile ducts

Intestinal

Fasciolopsiasis

F buski

Snails

Fresh water plants

Small bowel

Lung

Paragonimiasis

P westermani

Snails

Crabs and crayfish

Lungs

BOX 1. Signs and Symptoms of Trematode Infection

Trematode

More Common

Less Common

Blood flukes

S mansoni

S japonicum

S makongi

S intercalatum

S haematobium

• Dermatitis (swimmers itch), Katayama fever;

• Chronic granulomatous disease of liver, hepatobiliary system, hepatosplenomegaly

• Portal hypertension, esophageal bleeding from varices

• Dermatitis (swimmers itch), Katayama fever, hematuria, chronic granulomatous disease of bladder with ureteral obstruction, chronic renal failur

• Pulmonary schistosomiasis, central nervous system involvement with seizures

• Transverse myelitis

Liver flukes

C sinensis

D felineus

F hepatica

• Most patients have no symptoms

• Early stage — Right upper quadrant pain, hepatomegaly, eosinophilia

• Biliary obstruction, cholangitis

Intestinal flukes

F buski

• Most patients have no symptoms

• Abdominal pain, diarrhea, malabsorption

Lung flukes

P westermani

• Many patients have not symptoms

• Cough productive brown sputum, hemoptysis, eosinophilia

• Chronic bronchitis, bronshiectasis, lung abscess

BOX 2. Treatment of Trematode Infections

Species

First Choice

Second Choice

S mansoni

• Praziquantel, 20 mg/kg twice daily × 1 day

Oxamniquine, 15 mg/kg single dose. African-acquired infection, 20 mg/kg daily × 3 days

S haematobium

• Praziquantel, 20 mg/kg twice daily × 1 day

Metrifonate, 7.5 mg/kg single dose, weekly × 2 weeks

S intercalatum

• Praziquantel, 20 mg/kg twice daily × 1 day

No satisfactory alternative therapy

S japonicum

S mekongi

• Praziquantel, 20 mg/kg three times daily × 1 day

No satisfactory alternative therapy

C sinensis

O felineus

• Praziquantel, 25 mg/kg three times daily × 1 day

No satisfactory alternative therapy

F hepatica

• Bithionol 30-50 mg/kg on alternate days, × 10-15 doses (maximum dose, 2 g day)

No satisfactory alternative therapy

F buski

P westermani

• Praziquantel, 25 mg/kg three times daily × 1 day

• Praziquantel, 25 mg/kg three times daily × 2 days

No satisfactory alternative therapy

Cestodes attach themselves to the intestinal mucosa by means of a specialized organ called the scolex, which has a distinctive morphology for each species of cestode. Attached to the scolex are one to several hundred segments called proglottids. Proglottids each contain both male and female reproductive organs and may be classified as immature, mature, or gravid, based on the state of maturation of their sex organs. A gravid proglottid contains a fully developed uterus, full of eggs. The uterine structure of a gravid proglottid helps to differentiate species of cestode.

Diphyllobothrium Latum Infection

Taenia Solium Infection

Cysticercosis (Cysticercus Cellulosea Infection)

Taenia Saginata Infection

HYMENOLEPIS NANA INFECTION

Essentials of Diagnosis

• Adult worms and proglottids are rare.

• Spheroidal and thin-walled eggs (30-47 mm).

• Eggs contain two polar elements from which 4-8 filaments project (diagnostic).

• Scolex has hooklets and four suckers.

General Considerations

H nana is distributed worldwide and is called the dwarf tapeworm because of its small size (2-4 cm). Endemic areas include Asia, Africa, South and Central America, and southern and eastern Europe. Infection with H nana is acquired by the ingestion of eggs, commonly from human stool. The eggs hatch within the stomach or small intestine, and the resultant larvae attach to the bowel wall, where adult worms develop in several weeks. Eggs are released directly from the gravid proglottids while these proglottids are still attached to the adult worm; therefore proglottids are rarely seen on stool examination. Various arthropods such as fleas can serve as alternate intermediate hosts for H nana. Eggs produced within infected humans can lead to internal autoinfection, and poor fecal-oral hygiene can cause infection to be passed from one person to another.

Clinical Findings

A. Signs and Symptoms. Infection with H nana is most often asymptomatic, yet some patients may complain of headache, dizziness, anorexia, or abdominal pain. Whether these symptoms are related to the infection is uncertain. Children may have headache or sleep and behavioral disturbances, which resolve after successful treatment of the infection.

B. Laboratory Findings. As for patients with other cestode infections, examination of blood from patients with H nana infection is typically normal, although a mild leukocytosis with eosinophilia may be present. Microscopic stool examination will frequently reveal eggs, but finding proglottids is uncommon with H nana infection.

Differential Diagnosis

Since infection with H nana is usually asymptomatic, patients most often discover H nana infection as an incidental finding on stool examination done for another reason. In patients with nonspecific gastrointestinal complaints, peptic ulcer disease and malignancy need to be ruled out. Similarly, in children with behavioral symptoms, a variety of neurologic disorders of organic and psychologic origins need to be considered.

Complications

Through a mechanism that is still unclear, seizures have been reported with H nana infections.

Treatment

Cysts of H nana are more resistant to therapy than adult worms. Therefore higher doses or longer courses of therapy are required to eradicate cysts than with other cestode infections. Therapy for infection by H nana consists of a single dose of either praziquantel or niclosamide (see Box 2). Follow-up examinations of stool should be performed at 2 weeks and 3 months after therapy.

Prognosis

Since infection with H nana is usually asymptomatic and infection responds to therapy, the prognosis is excellent.

Prevention & Control

Infection with H nana can be prevented with good fecal-oral hygiene and adherence to the principles of sanitation (eg, appropriate disposal of human sewage) (Box 3). Incidental ingestion of arthropod hosts may also produce infection, although this mechanism of infection is uncommon.

HYMENOLEPIS DIMINUTA

Essentials of Diagnosis

• Proglottids are rare in stool, but adult worms may be present.

• Ovoid and thick-walled eggs (70-85 um by 60-80um).

• Eggs contain no polar elements.

• Scolex has no hooklets and four suckers.

General Considerations

H diminuta is also distributed worldwide, but the incidence of infection is much less common than with H nana. Infection with H diminuta is acquired by the ingestion of eggs, produced from an obligatory arthropod intermediate host. The eggs hatch within the stomach or small intestine, and the adult worms develop in several weeks. Eggs are similar in size to the eggs of H nana but may be distinguished by their lack of polar filaments and ovoid shape. In contrast to H nana, the life cycle of H diminuta requires an intermediate arthropod host, and adult worms may be passed in the stool of humans.

Clinical Findings

A. Signs and Symptoms. Infection with H diminuta is not associated with clinical symptoms.

B. Laboratory Findings. Microscopic stool examination will frequently reveal eggs and adult worms. Blood examination may demonstrate mild leukocytosis with eosinophilia.

Differential Diagnosis

The finding of H diminuta in human infection is commonly an incidental finding that is asymptomatic.

Complications

No complications have been reported.

Treatment

Therapy for infection for H diminuta consists of niclosamide in a one-time dose (see Box 87-2).

Prognosis

H diminuta responds promptly to therapy, so the prognosis is excellent.

Prevention & Control

Infection with H diminuta can be reduced by decreasing exposure to arthropod vectors, such as by rat control measures (Box 3).

Dipylidium Caninum Infection

Echinococcal Infection

BOX 1.

Syndrome

More Common

Less Common

Diphyllobothrium latum infection

Bloating, abdominal pain, diarrhea

Intestinal obstruction, vitamin B12 deficiency

Taenia solium infection

Asymptomatic

Indigestion, nausea

Cysticercosis (extraintestinal T solium infection)

Headache, seizures, neurologic deficits

Myositis, liver or heart failure

Taenia saginata infection

Asymptomatic

Abdominal cramps, malaise

Hymenolepis nana infection

Abdominal pain

Dizziness, anorexia; children — behavioral disturbance

Hymenolepis diminuata infection

Asymptomatic

Dypylidium caninum infection

Asymptomatic

Indigestion, anorexia, anal pruritis

Echinococcal infection

Abdominal pain, mass

Seizures, headache, neurologic deficits, bone pain

BOX 2.

Syndrome

Adult treatment

Pediatric treatment

Diphyllobothrium latum infection

• Praziquantel, 10-20 mg/kg once

OR

• Niclosamide 2 g once

• Praziquantel, 10-20 mg/kg once

OR

• Niclosamide (11-34 kg), 1 g once; (>34 kg), 1.5 g once

Taenia solium infection

• Praziquantel, 10-20 mg/kg once

OR

• Niclosamide, 2 g once

• Praziquantel, 10-20 mg/kg once

OR

• Niclosamide (11-34 kg), 1 g once; (>34 kg), 1.5 g once

Cysticercosis (extraintestinal T solium infection)

• Surgery and either Praziquantel, 20 mg/kg three times daily × 15-30 d

OR

• Albendazole, 7.5 mg/kg three times daily × 8 d

Surgery and either Praziquantel, 20 mg/kg three times daily × 15-30 d

OR

• Albendazole, 7.5 mg/kg three times daily × 8 d

Taenia saginata infection

• Praziquantel, 10-20 mg/kg once

OR

• Niclosamide, 2 g once

• Praziquantel, 10-20 mg/kg once

OR

• Niclosamide (11-34 kg), 1 gm once; (>34 kg), 1.5 g once

Hymenolepis nana infection

• Praziquantel, 10-20 mg/kg once

OR

• Niclosamide, 2 g once

• Praziquantel, 10-20 mg/kg once

OR

• Niclosamide (11-34 kg), 1 gm once; (>34 kg), 1.5 g once

Hymenolepis diminuta infection

• Niclosamide, 2 g once

• Niclosamide (11-34 kg), 1 g once; (>34 kg), 1.5 g once

Dypylidium caninum infection

bull; Niclosamide, 2 g once

• Niclosamide (11-34 kg), 1 g once; (>34 kg), 1.5 g once

Echinococal infection

• Surgery and albendazole, 400 mg divided into 2 daily doses × 3 mo

OR

• Mebendazole, 50 mg/kg/d divided into 3 daily doses × 3 mo

• Surgery and albendazole, 15 mg/kg/d divided into 2 daily doses × 3 mo

OR

• Mebendazole, 50 mg/kg/d divided into 3 daily doses × 3 mo

BOX 3.

Syndrome

Preventative Measures

Diphyllobothrium latum infection

Adequate cooking of fish or freezing fish for 48 h

Taenia solium infection

Adequate cooking of pork or pork products

Cysticercosis (extraintestinal T solium infection)

As for T solium

Taenia saginata infection

Adequate cooking of beef and beef products; inspection of beef and destruction of infected carcasses

Hymenolepis nana infection

Adherence to good fecal-oral hygiene

Hymenolepis diminuta infection

Arthropod control measures (such as rat control)

Dypylidium caninum infection

Screening of dogs and cats; treatment of infected animals

Echinococcal infection

• Screening of household pets; treatment of infected animals

• Destruction of infected carcasses

• Education on routes of transmission (in endemic areas)

Buy also with tablets (capsules, pills) no prescription:

• cestodesonlinepharmacey
• niclosamide online pharmacy/canada
• Niclosamide without a Prescription

Essentials of Diagnosis

• Radiographic finding of cyst

• Positive echinococcal serology

• Aspiration of cyst revealing echinococcal sand or hooks

• Typical histologic appearance of cyst wall

General Considerations

The normal life cycle of Echinococcus species does not involve humans. Human disease occurs when humans become an accidental intermediate host for the parasite, and tissue invasion is followed by the formation of cysts (hydatid cysts). The definitive hosts for echinococcal species are canines (usually dogs), in whom the adult worms live. There may be several hundred worms within a host, and the worms are small, usually 3-6 mm long.

The scolex is attached to the dog intestine, and to each scolex is attached a single proglottid. As the proglottids mature and become gravid proglottids containing several eggs, they detach and are passed in the stool. The eggs are resistant to desiccation and may remain viable for weeks. Eggs are ingested by intermediate hosts, commonly sheep and cattle but occasionally humans. The eggs hatch in the duodenum, and the larval forms penetrate the intestinal mucosa and disseminate through the blood stream to distant sites, most commonly the liver. Within tissues, the larva develops an encasing cyst composed of an outer layer and an inner fluid-filled layer. Within 1 year, cysts may reach 5-10 cm in diameter.

Inside the inner layer, daughter cysts form which may detach and float within the fluid, and daughter scolices may form. Ingestion of meat containing hydatid cysts leads to infection of definitive hosts, and adult worms develop. Infections with Echinococcus granulosus cause the formation of unilocular cysts. In contrast, infections with Echinococcus multilocularis are associated with multilocular cysts. E multilocularis also differs from E granulosus in that definitive hosts include foxes, wolves, cats, and dogs, and intermediate hosts include small rodents. Endemic areas for E granulosus include Africa, the Middle East, southern Europe, Latin America, and the southwestern United States. For E multilocularis, forested areas of Europe, Asia, and North America are endemic.

Clinical Findings

A. Signs and Symptoms. In humans, the presentation of infection depends on where the hydatid cyst forms. The principle locations for cysts in humans include liver (60%), lung (20%), muscle (4%), kidney (4%), spleen (3%), soft tissues (3%), brain (3%), bone (2%), and other (1%). Within the liver, cysts may be incidentally diagnosed or may present as pain or a visible mass. Pulmonary cysts are usually asymptomatic, but if sufficiently large, may cause cough, dyspnea, or pleuritic pain.

Although rare, hydatid cysts in the brain are potentially the most serious and may cause obstructive hydrocephalus with ataxia and dementia or mass effect with seizures, headache, or focal neurologic deficits. Bony hydatid cysts most commonly involve vertebrae and present with bone pain. Other presentations include soft tissue swelling and bone pain or pathologic fractures secondary to cysts weakening cortical bone. In = 20% of infected patients, cysts will be multiple, so a thorough evaluation is required of all patients in whom the diagnosis is suspected.

B. Laboratory Findings. Eosinophilia may be present in = 25% of patients, but it is a nonspecific marker. Serologic testing is available, by a variety of techniques, and, if positive, the results provide supportive evidence of echinococcal infection. However, a negative result of serologic testing does not rule out hydatid cyst disease. More recent serologic techniques may help to differentiate E granulosus infection from E multilocularis infection. Cross-reaction between cysticercosis and hydatid cyst disease has been noted with some serologic assays. Another potential diagnostic procedure is cyst aspiration, although it poses some risk for anaphylaxis (see complications). This test is potentially useful to diagnose E granulosus hydatid cysts. A small volume of fluid is removed and examined microscopically for the presence of hydatid sand (daughter cysts and scolices). If a cyst is old, sand may not be present, in which case a centrifuged specimen should be examined for the presence of hooks.

C. Imaging. Radiographically, cysts appear as either unilocular cysts with an air fluid level (E granulosus) or as multiloculated cysts with little or no fluid (E multilocularis).

Differential Diagnosis

Since the usual presentation of hydatid cysts is either liver pain or mass, lung mass with irritative symptoms of obstruction, or seizures with focal neurologic symptoms, the primary differential diagnosis is to rule out primary or metastatic malignancy of each of these organs. In a unilocular hydatid cyst, the radiographic appearance is often sufficient to exclude malignancy. In contrast, multilocular cysts caused by E multilocularis are slow growing, often with little or no fluid, and frequently have central necrosis, all suggestive of malignancy. Therefore biopsy and histologic examination are necessary for definite differentiation from malignancy.

Complications

On occasion, hydatid cysts may leak fluid into the systemic circulation of the host, causing sensitization of the host. Subsequent fluid leaks may then be responsible for the induction of an allergic response or even anaphylaxis. In addition, release of cyst tissue may be associated with embolization and the development of additional cysts at distant alternate sites. Cysts also may become secondarily infected, producing abscesses. Mechanical complications of the cyst are also possible, most commonly leading to portal hypertension, ascites, and portosystemic shunting.

Treatment

Therapy for hydatid cysts caused by infection with E granulosus combines surgical and pharmacological interventions (see Box 2). Solitary unilocular cysts at operable sites are generally treated with surgical excision, percutaneous drainage, or both. Extreme care must be taken to avoid spillage of cyst contents and subsequent seeding of other sites. One approach has been to remove a portion of the cyst fluid and instill a cystocidal agent such as 95% ethanol before removing the entire cyst. Some authorities also recommend pre- and postoperative therapy with either albendazole or mebendazole.

Recent experience with albendazole is a promising alternative. Mebendazole is an alternate therapy but may be less effective that albendazole. Complicated or multiloculated cysts (caused by E multilocularis) require surgery, often in association with albendazole as above. An experimental approach to inoperable cysts involves oral therapy with albendazole or mebendazole, combined with percutaneous aspiration and instillation of 95% ethanol. Although promising, this approach has not been validated in large trials.

Prognosis

The prognosis of hydatid disease is variable. With early diagnosis and treatment of simple unilocular cysts, the outlook is excellent; in contrast, advanced multilocular disease at multiple sites with advanced portal hypertension is a potentially lethal condition. Medical therapy of inoperable E granulosus cysts is associated with cure in 30% of cases and improvement in 50%. Inoperable E multilocularis is associated with a 10-year mortality rate in 90% of cases. In such cases, indefinite treatment with albendazole or mebendazole is recommended by some authorities.

Prevention & Control

In areas endemic for hydatid disease, the disease is commonly transmitted incidentally during activities such as camping and picking berries. Education is the best prevention for transmission in these settings (Box 3). Routine screening of household pets and appropriate treatment of animals found to carry Echinococcus spp. is another important control measure. Pet owners should be educated as to techniques of good hygiene to prevent accidental inoculation of eggs from dog stools. Lastly, carcasses of infected hosts must be disposed of in ways that prevent transmission to canines.

Essentials of Diagnosis

• Motile proglottids 23 by 8 mm.

• Proglottids have genital pores at either end and contain egg clusters.

• Eggs occur in compartmented clusters (diagnostic).

• Scolex has 4-7 rows of hooklets and 4 suckers.

General Considerations

D caninum is distributed worldwide and is associated with wild and domesticated cats and dogs. The life cycle is similar to that of H diminuta, with an obligatory arthropod intermediate host. The adult worm lives in dogs, cats, or humans, and gravid proglottids are released from the adult worm either singly or in short chains. Eggs are passed in the stool, and ingestion of eggs by the intermediate host results in the development of the larval form within the arthropod host. Ingestion of the arthropod that contains larvae results in the development of an adult worm in dogs, cats, or humans. Adult worms may reach 10-80 cm in length.

Clinical Findings

A. Signs and Symptoms. Infection with D caninum is not commonly associated with clinical symptoms, although indigestion or anorexia may be present. Also anal pruritus has been reported.

B. Laboratory Findings. Microscopic stool examination will frequently reveal characteristic egg clusters and proglottids. As with other cestode infections, blood examination may demonstrate mild leukocytosis with eosinophilia.

Differential Diagnosis

Since D caninum infection in humans is often asymptomatic, most patients do not seek medical care. Once eggs are found in the stool, the appearance of egg clusters is so characteristic that no other parasite could be confused with D caninum. When a patient does seek the care of a physician for indigestion or anorexia, a variety of gastric pathologies need to be ruled out (eg, peptic ulcer disease and gastric outlet obstruction).

Complications

No complications are associated with D caninum infection.

Treatment

Therapy for D caninum infection is niclosamide in a one-time dose (see Box 87-2).

Prognosis

The prognosis for D caninum infections is excellent.

Prevention & Control

Infection with D caninum can be reduced by screening domestic dog and cat stools and treating pets found to be infected (Box 3).

Essentials of Diagnosis

• Stool examination reveals spheroidal yellow-brown eggs (31-43 mm).

• Motile proglottids that appear singly in stool.

• Mature proglottids are square.

• Scolex has no hooklets and four suckers.

• Gravid proglottid has 15-20 lateral branches.

General Considerations

T saginata infection is commonly associated with the ingestion of undercooked beef. This is distinguished from infection with T solium because human infection with the larval form (as in cysticercosis) is extremely rare with T saginata infection. T saginata infection is common in areas of the world with intensive cattle breeding, such as central Asia and central and eastern Africa. Alternative intermediate hosts for T saginata include llamas, buffalo, and giraffes. The life cycle for T saginata is similar to that of T solium; larvae are ingested in infected meat, and the tapeworm attaches to the intestinal epithelium and matures in 12 weeks. Mature tapeworms produce gravid proglottids with characteristic 15-20 lateral branches, which contain numerous eggs. Ingestion of eggs or proglottids by cows leads to hatching of eggs, and larvae that migrate into striated muscle. Case reports exist about T saginata cysticercosis in humans, although the incidence is exceedingly uncommon.

Clinical Findings

A. Signs and Symptoms. Infection with T saginata is most often asymptomatic, although a minority of patients may report nonspecific abdominal cramps or malaise. The proglottids of T saginata are motile, and patients may report seeing moving segments in the stool.

B. Laboratory Findings. Examination of the blood in patients with T saginata infection typically reveals no abnormalities, although a mild leukocytosis with eosinophilia may be present. Otherwise all laboratory tests except the microscopic stool examination will be normal. The stool examination will frequently reveal eggs and proglottids. The main basis for differentiating T saginata from T solium is the gravid proglottid, which for T solium has 7-13 lateral branches on each side of the uterus, whereas T saginata has 15-20 lateral branches.

Differential Diagnosis

Infection with T saginata is usually not associated with clinical symptoms. Patients most often seek medical attention after finding T saginata proglottids in stools or on clothing. The main differential diagnosis is to differentiate T saginata proglottids from T solium proglottids. If no gravid proglottids are present, then differentiation may not be possible, in which case patients should be treated as though they have infection with T solium.

Complications

Usually no complications are associated with T saginata; however, regurgitation and aspiration of proglottids may occur.

Treatment

Therapy for infection with T saginata is similar to treatment of intestinal T solium, a single dose of either praziquantel or niclosamide (see Box 2). Follow-up examinations of stool should be performed 1 month after treatment.

Prognosis

The prognosis for patients with intestinal T saginata infection is excellent.

Prevention & Control

Prevention of infection with T saginata involves thorough cooking of beef and beef products to > 65 °C core temperature (Box 3). Beef should also be inspected for the presence of cysts, and infected carcasses destroyed.

Essentials of Diagnosis

• Surgical excision of involved tissue, with microscopic identification of parasite.

• Frequently calcified cysts present on x-ray or computed tomography (CT) scans.

• Positive serology indicating previous exposure to T solium.

• Fine-needle aspiration of cysts (characteristic cytomorphology).

General Considerations

Cysticercosis is caused by invasion of tissue by the larval forms of T solium, which have been referred to as Cysticercus cellulosea, although the name is not taxonomically correct and introduces confusion. Within a host infected by the adult T solium, eggs or proglottids are passed in the stool. Once eggs or proglottids are ingested by either pigs (intermediate hosts) or humans (definitive and intermediate hosts), eggs hatch in the gastric juice, allowing the cysticercus to migrate from the intestine to disseminated sites, via efferent mesenteric venules. Autoinfection may also occur in humans, wherein eggs produced by the adult intestinal worm hatch and invade the intestinal epithelium.

Clinical Findings

A. Signs and Symptoms. The symptoms associated with cysticercosis relate to the organ that is invaded by cysticerci and to the inflammatory reaction that occurs in response to the larva. Within the brain, cysticercosis may cause arachnoiditis or chronic meningitis, with associated headache, vertigo, vomiting, and cranial neuropathies. Alternate presentations include obstructive hydrocephalus with ataxia and dementia, intracranial vasculitis with focal neurologic signs and neuropsychiatric changes, or mass effect with seizures, headache, or focal neurologic deficits. In addition, cord compression with lower limb weakness and loss of bowel and bladder continence may occur. Cysts outside the central nervous system tend to occur within muscle, are most often asymptomatic, and eventually die, calcify, and may be incidentally detected on radiographs. Occasionally, muscle cysts will cause pseudohypertrophy that may be associated with myositis, high fever, and eosinophilia. Cysts may also occur within critical organs (commonly heart and liver) where they present as mass lesions with pain or obstructive symptoms.

B. Laboratory Findings. Patients with cysticercosis may have a mild elevation on leukocyte count, possibly with eosinophilia. In patients with meningitis associated with neurocysticercosis, cerebrospinal fluid examination may show either lymphocytic or eosinophilic pleocytosis, hypoglycorrhachia, and elevated protein. Recently a serologic test for T solium has been developed, but its performance characteristics remain to be validated. False positive results have been associated with infections caused by other cestodes. A negative serologic test does not exclude the diagnosis of cysticercosis.

C. Imaging. Living cysts associated with cysticercosis are often multiple and have a characteristic appearance on CT scans or magnetic resonance images, both enhancing and nonenhancing unilocular cysts. Patients with extraneurologic cysticercosis may have painless subcutaneous nodules, often on the shins, which are calcified and have a characteristic appearance on plain radiographs.

Differential Diagnosis

Patients who seek care for symptoms of infection with T solium most commonly do so because of the neurologic symptoms associated with neurocysticercosis. The most common neurologic symptoms are mass effect and seizures (related to intraparenchymal lesions), hydrocephalus (related to intraventricular cysts), chronic meningitis (related to subarachnoid cysts), and cord compression (owing to spinal cord cysts). The differential diagnosis of each of these symptoms is beyond the scope of this discussion, but malignancy may present in identical ways, and so it must be ruled out.

Complications

Visceral cysticercosis is also commonly asymptomatic, but may obstruct local structures (eg, biliary obstruction in hepatic cysticercosis). Neurocysticercosis may lead to permanent neurologic impairment, coma, or even death.

Treatment

Therapy for cysticercosis includes surgery when feasible and necessary, in combination with praziquantel or albendazole (see Box 2). Therapy of cysticercosis commonly increases the local inflammation, thereby transiently causing a paradoxical worsening of the patient’s symptoms. Whether corticosteroids should be used as adjunctive therapy for patients being treated for neurocysticercosis remains in debate.

Prognosis

The mortality rate for untreated neurocysticercosis approaches 50%, but treatment decreases this rate to 5-15%.

Prevention & Control

Guidelines for the prevention of cysticercosis are the same as for the prevention of T solium infection (Box 3).

Essentials of Diagnosis

• Spheroidal yellow-brown eggs (31-43 um).

• Scolex has hooklets and four suckers.

• Proglottids usually appear as short chains.

• Mature proglottids are square and nonmotile.

• Gravid proglottid has 7-13 lateral branches on each side of uterus.

General Considerations

T solium infection occurs worldwide; endemic areas include Mexico, South and Central America, Africa, Southeast Asia, India, and the Philippines. T solium infection is commonly linked to the ingestion of undercooked pork, although other animals may harbor the larval form of the parasite. Infection may be intestinal, which is typically asymptomatic, or extraintestinal (called cysticercosis, see below), which is caused by larval forms of T solium within the tissues of the human host. Ingestion of encysted T solium larvae is followed by the parasite scolex attaching to the intestinal mucosa, which allows the worm to grow into an adult within 12 weeks. There may be one or more adult worms present for = 25 years, and these may reach lengths of 2 to 7 m. Each worm contains < 1000 proglottids. Identification of species is by the number of lateral branches on the side of the uterus within a gravid uterus.

Clinical Findings

A. Signs and Symptoms. Infection with the adult worm of T solium is usually asymptomatic, but nonspecific abdominal symptoms including indigestion and nausea may be present.

B. Laboratory Findings. Patients with intestinal T solium infection will frequently have abnormal results of stool examinations for ova and parasites and occasionally will have a mild leukocytosis with eosinophilia.

Differential Diagnosis

Since infection with the adult worm of T solium is asymptomatic, the main diagnostic concern in a patient with intestinal T solium is whether the patient has cysticercosis. If the results of evaluation suggest that there is extraintestinal infection, then specific therapy for cysticercosis is required.

Complications

T solium infection of the intestine is not commonly associated with symptoms; however, in patients with high parasite loads, obstruction may occur.

Treatment

Therapy for T solium infection of the intestine consists of either praziquantel or niclosamide (see Box 2). Follow-up examinations of stool should be performed 1 month after treatment.

Prognosis

The prognosis for patients with intestinal T solium infection is excellent.

Prevention & Control

Prevention from infection with T solium involves adequate cooking of pork and pork products to a > 65 °C core temperature (Box 3). Freezing, pickling, and salting do not prevent infection. Immunization of swine and provision of animal feed that is free of eggs and proglottids are other preventative measures that have been reported to be effective in controlling infection. Since infected humans are capable of transmitting cysticercus to others, enteric precautions should be used, and stool specimens should be handled with attention to decontamination. In addition, adequate facilities for disposal of human sewage should be available.

Essentials of Diagnosis

• Stool examination reveals ovoid, yellow-brown eggs (60-75 um by 40-50 um).

• Chains of proglottids (up to 50 cm long) may be passed in stool.

• Proglottids are wider than long (3 by 11 mm).

• Scolex has no hooklets and two grooves (bothria).

• Gravid proglottid contains rosette-shaped central uterus.

General Considerations

D latum is found worldwide, and infection is acquired by ingestion of contaminated raw or improperly cooked freshwater fish. Because of enthusiasm for raw or undercooked fish, Siberia, Europe, Canada, Alaska, and Japan are endemic regions for D latum infection. Once the D latum cyst has been ingested, the worm matures within the human intestine and begins to produce eggs after 5 weeks. A mature D latum may reach lengths of several meters and contain = 30,000 proglottids. Eggs and proglottids that are passed in stool hatch after 14 days in fresh water into ciliated coracidium larvae, which are ingested by the intermediate host, the aquatic copepod. Inside the copepod, the larvae develop into a second larval form, the procercoid. Once the copepod is ingested by a freshwater fish, the procercoid larva matures into the plerocercoid larva, which may encyst within fish tissues. Human ingestion of improperly prepared fish initiates infection by the plerocercoid larva cyst. Bears, seals, cats, mink, foxes, and wolves are alternate definitive hosts for D latum.

Clinical Findings

A. Signs and Symptoms. Infection with D latum is most often asymptomatic, but symptoms such as bloating, abdominal pain, or diarrhea may be present. More rarely, intestinal obstruction may occur. A rare complication of chronic, small-intestinal involvement with D latum is the development of Vitamin B12 deficiency, characterized by anemia with or without neurologic sequelae. This syndrome occurs most often in patients with a genetic predisposition to the development of pernicious anemia, commonly people of Scandinavia.

B. Laboratory Findings. Frequently the only abnormal finding in a patient infected with D latum is the presence of eggs or proglottids on examination of stool for ova and parasites. Blood examination may reveal a slight leukocytosis with eosinophilia and occasionally a megaloblastic anemia associated with B12 deficiency.

C. Imaging. Contrast studies of the gastrointestinal tract may reveal ribbonlike filling defects corresponding to the adult worm.

Differential Diagnosis

The most usual manifestation of D latum infection is asymptomatic carriage, which is incidentally discovered. If patients present with abdominal pain and diarrhea, the differential diagnosis includes a variety of infectious and noninfectious causes. Diarrhea from D latum infection will not be associated with stool leukocytes; this aids in formulating a differential diagnosis. Noninfectious etiologies to consider include osmotic (eg, lactose intolerance) and secretory (eg, villous adenoma) etiologies, malabsorption syndromes (eg, celiac sprue), and motility disorders (eg, irritable bowel syndrome). Infectious etiologies causing diarrhea without stool leukocytes include rotavirus, Norwalk virus, Giardia lamblia, Entamoeba histolytica, Cryptosporidium spp., and toxigenic diarrhea caused by Staphylococcus aureus, Bacillus cereus, Clostridium perfringens, and enterotoxigenic Escherichia coli.

Complications

The complications vary with the clinical syndrome associated with infection. Chronic diarrhea may lead to malnutrition. Megaloblastic anemia secondary to B12 deficiency results when the parasite disrupts the B12-intrinsic factor complex, resulting in B12 becoming unavailable for absorption by the host. B12 deficiency may lead to neurologic sequelae including peripheral neuropathy, dementia, and possible severe combined degeneration of the posterior columns. Also, infection with D latum may rarely result in intestinal obstruction caused by a mass of entangled worms.

Treatment

Therapy for infection with D latum consists of either praziquantel or niclosamide (Box 2). Follow-up examinations of stool should be performed 1 and 3 months after treatment.

Prognosis

Since the disease is not commonly associated with severe symptoms, the prognosis of infected individuals is excellent. One exception is with patients who manifest B12 deficiency, in whom the neurologic complications are reversible only if recognized and treated early.

Prevention & Control

Prevention of infection from D latum is achieved through adequate cooking of all freshwater fish or freezing of fish for 24-48 h at -18 °C (Box 3). Isolation of infected persons is not required.

Essentials of Diagnosis

• Intestinal nematodes: demonstration of characteristic eggs or parasites in stool.

• Bloodstream nematodes (filariasis): clinical diagnosis can be made; fresh blood smear may be confirmatory.

• Tissue nematodes: clinical diagnosis can be made; skin snip or other tissue examination may show organism.

General Considerations

Nematodes (roundworms) are nonsegmented, tapered, bilaterally symmetrical, cylindrical organisms that have complete digestive tracts and reproduce sexually. Although > 500,000 species of nematodes have been described, only a small number are commonly encountered as human parasites. Most nematodes have complex life cycles, sometimes involving several larval forms and intermediate hosts or free-living stages. The pathogenic nematodes may be categorized as primarily intestinal or extraintestinal tissue parasites (Box 1).

Intestinal Nematode Infections

Tissue Nematode Infections

OTHER TISSUE NEMATODE INFECTIONS

1. TRICHINOSIS

Trichinella species are unique among the tissue-dwelling nematodes in that there is no intermediate arthropod vector stage. Trichinella nematodes parasitize carnivores. Adult worms parasitize the small intestine; infective larvae are released and migrate from the intestine to muscle tissues in the host, where the larvae encyst and remain viable and infectious for several years. When the host tissues are eaten, the cyst walls are digested and the larvae again mature within several days in the intestine of the new host, perpetuating the life cycle. Normal hosts of Trichinella spp. include swine, rats, bears, foxes, walrus, and other carnivorous mammals. Humans are an incidental host. Cooking meat to 55 °C core temperatures or freezing (-15 °C) for 3 wk kills Trichinella spp. larvae.

Clinical & Laboratory Findings

Mild infection is usually asymptomatic. Early (1 wk) after infection, gastrointestinal symptoms predominate, including diarrhea, nausea or vomiting. After the second week, during the muscle invasion stage, systemic symptoms predominate including fever, myalgias, and malaise in most patients. Periorbital edema with conjunctival chemosis and edema of the eyelids is characteristic and common. Symptoms last between 4 and 8 weeks. Rarely, myocarditis or encephalitis may complicate the clinical course. In the laboratory, eosinophilia after the 10th day, sometimes marked, is characteristic, as is elevated immunoglobulin E. Serum creatine phosphokinase and lactic dehydrogenase concentrations reflect myositis. Trichinella serology becomes positive at = 3 wk after infection.

Treatment

Treatment for trichinosis remains controversial and is primarily supportive. If ingestion is known to occur within 24 h, albendazole (400 mg twice daily, (60 days), mebendazole (200-400 mg 3 times daily for 3 days, then 400-500 mg 3 times daily for 10 days), or thiabendazole (25 mg/kg/day for 1 wk) has been proposed to prevent infection. The drug is not beneficial for established infection or muscle larvae. No specific therapy has been unequivocally demonstrated to be of benefit during the muscle invasion stage.

Prognosis

Spontaneous recovery is the rule, although full recovery may require weeks to months. Death, typically from myocarditis, encephalitis, or pneumonitis, is rare.

Prevention

The incidence of human trichinosis has declined in developed countries with measures designed to reduce the prevalence of trichinosis in hogs. Trichina in wild game (or pork) can be killed by thorough cooking (internal temperature > 62 °C) throughout all parts of the meat or to > 56 °C for > 15 min, freezing < -15 °C for = 20 d, or gamma radiation.

3. TOXOCARIASIS (VISCERAL LARVA MIGRANS)

Toxocariasis, or visceral larva migrans, is a syndrome caused by invasion of human extraintestinal tissues by larvae of Ascaris spp. for which humans are not the usual host of the adult worms. Toxocara canis, commonly found in dogs, is the most commonly implicated species; Toxocara catis (cats) and Belascaris procyonis (raccoons) have also been implicated. Puppies can be infected transplacentally or transmammarily. Pregnancy in dogs reactivates latent infections in the bitch. Animals harboring adult ascarids in the intestine shed copious numbers of eggs into the environment. The eggs become infectious after 3-4 wk and are highly resistant to harsh environmental conditions. Toxocara eggs may remain infectious for months to years. Human infection results from ingestion of eggs from fecally contaminated soil, as may occur for example in children with pica. Direct transmission from pets to humans does not occur, because the eggs require maturation in soil before they become infective.

In young animals, ingested eggs hatch in the intestine and the larvae migrate through extraintestinal tissues, including liver and lung. Larvae induce coughing and are swallowed and then mature into adults in the small intestine to complete the life cycle, which resembles that of A lumbricoides in humans. In older animals, humans, and other hosts such as mice or rats, larvae also hatch from ingested eggs and invade extraintestinal tissues, but the larvae are unable to fully mature and may continue to persist and migrate in tissues as “second-stage” larvae for = 6 months. If these second-stage larvae are ingested by a dog or cat, the larvae may complete their life cycle and develop into adult intestinal worms. Eosinophilic granulomas caused by toxocariasis most often involve the liver or lungs; brain, eye, muscle, and skin involvement has also been reported.

Clinical & Laboratory Findings

Visceral larva migrans is predominately seen in children < 7 years old, and it may be associated with pica. Most cases appear to be asymptomatic. When present, symptoms are variable and depend on the organ systems involved but may include fever, cough or wheezing, and urticarial rash or skin nodules. Hepatomegaly is relatively common. Splenomegaly, lymphadenopathy, and evidence of myocarditis are less common.

Marked leukocytosis, sometimes exceeding 100,000 leukocytes/ul, and hypereosinophilia are common in visceral larva migrans. Polyclonal hypergammaglobulinemia and anti-A or anti-B antibodies to isohemagglutinin antigens (cross-reacting to T canis larval antigens) may occur. An eosinophilic spinal fluid pleocytosis may occur with central nervous system involvement. Chest x-ray abnormalities may be seen in one-third of patients. Toxocara serology may be helpful in confirming the diagnosis, but it should be remembered that in some populations the background prevalence of seropositivity in patients without clinically apparent visceral larva migrans may be high. Identification of larvae in tissue biopsy samples is diagnostic, but not sensitive. Stool examination is not usually helpful.

Ocular visceral larva migrans deserves special consideration. Infection of the eye with Toxocara larvae usually presents as a solitary finding in patients with no known history of visceral larva migrans and without concurrent multifocal, systemic symptoms or signs. The ocular findings are typically a unilateral posterior or peripheral eosinophilic inflammatory mass. Serologies may be negative. The ocular lesion may be mistaken for a retinoblastoma.

Treatment

No specific therapy has been proven effective. In many cases, symptoms are self-limited and supportive, symptomatic treatment is all that is required. Treatment with a variety of antihelminthic agents has been tried with limited success. These agents include albendazole, thiabendazole, mebendazole, diethylcarbamazine, or ivermectin. Corticosteroids may be of benefit in some patients, especially subconjunctival applications in ocular visceral larva migrans.

Prevention & Prognosis

Puppies, kittens, and household dogs and cats, especially when pregnant or nursing, should be screened and treated as necessary to prevent transmission to humans. Pica should be prevented. Most cases are self-limited although symptoms may persist for months to several years.

4. DRACUNCULIASIS

Dracunculiasis, or guinea worm infection, is caused by infection by the tissue nematode Dracunculus medinensis. The parasite has been widely distributed in the Indian subcontinent, the Arabian Peninsula, and certain areas of West and central Africa north of the equator. Human infection is acquired by drinking water that contains tiny copepods (Cyclops spp.; “water fleas”) that carry the infectious third-stage larvae. The larvae migrate to subcutaneous connective tissue, usually in the lower extremities, where they develop into adult worms over an extended incubation period that can last up to a year. The adult female may reach 60-80 cm in length. When the extremities are exposed to water, the head of the gravid female protrudes through an ulceration in the host’s extremity, a loop of uterus prolapses and discharges large numbers of first-stage larvae into the water. These are ingested by copepods to complete the life cycle.

An active eradication program by the World Health Organization has led to a dramatic reduction in the incidence of dracunculiasis world-wide. Because no nonhuman reservoir is recognized, the disease may be eradicable in the near future.

Clinical Findings

A peripheral chronic cutaneous ulceration, from which the worm may protrude, is the hallmark of dracunculiasis. A local painful, stinging or burning papule may be the first indication of impending ulceration. Generalized symptoms including fever, nausea, vomiting, dyspnea, urticaria or pruritus, or periorbital edema may be associated with development of ulceration. Ulcers on the foot frequently prevent ambulation and may result in long-lasting deformity and secondary infection (including ankle or knee joint infection). Tetanus may also complicate dracunculiasis. Dead or dying worms may result in intense inflammatory reactions. Diagnosis in endemic areas is based on the typical clinical findings.

Treatment

No specific antihelminthic therapy is available to kill adult worms. Mechanical removal of worms has been practiced for centuries. General treatment is focused on controlling complications, including bed rest, elevation of the affected extremity, wound care, and antibacterial therapy for secondary bacterial wound infections. Metronidazole, 250 mg orally 3 times daily, mebendazole, 400-800 mg orally daily, or thiabendazole 25 mg/kg twice daily may be helpful in promoting the expulsion of the worm, as is immersion of the affected limb in water several times daily.

Prevention

Noncontaminated drinking water is the key to prevention of dracunculiasis. The World Health Organization prevention program has focused on provision of clean drinking water by using tube wells, hand pumps, or cisterns, by treating drinking water supplies with temephos (to eliminate the copepods), or by boiling water. Water can also by filtered to remove particles > 100 5m.

BOX 1. Nematodes Pathogenic in Human1

Intestinal

• Ascaris lumbricoides

• Ancylostoma braziliense or A. caninum (dog and cat intestinal hookworms; cutaneous larva migrans in humans)

• Enterobius vermicularis (pinworm)

• Ancylostoma duodenale (“Old World”), Necator americanus (“New World”) (hook-worms)

• Strongyloides stercoralis

• Trichuris trichiura (whipworm)

• Capillaria philippinensis (intestinal capillariasis)

• Trichostrongylus spp.

• Anisakiasis (larval fish nematode)

Tissue dwelling

Filariasis

• Wuchereria spp. (lymphatic filariasis)

• Brugia spp. (lymphatic filariasis)

• Loa loa (African eye worm)

• Mansonella spp.

• Onchocerca volvulus

Other tissue nematodes

• Dracunculus medinensis (Guinea worm)

• Trichinella spiralis

• Toxocara spp. (larval stages — visceral larva migrans)

• Angiostrongylus cantonensis (meningitis)

1A particular nematode’s presence is extremely dependent on the geographic location. For example, tissue-dwelling nematodes are uncommon or nonexistent in the United States.

BOX 2. Treatment of Selected Intestinal Nematode Infections

First Choice

Second Choice

Ascariasis

• Pyrantel pamoate, 10-11 mg/kg once

• Mebendazole, 200-500 mg once (light infection) up to 100 mg twice daily for 3 d

• Albendazole, 400 mg once (light infection) up to 400 mg once daily for 3 d

• Ivermectin, 100-200 µg/kg once daily for 32 d

• Piperazine, 75 mg/kg once daily for 2 d

• Levamisole, 150 mg once

Enterobiasis

• Pyrantel pamoate, 10-11 mg/kg once

• Mebendazole, 100 mg once, repeat in 2 wk

• Albendazole, 400 mg once, repeat in 2 weeks

• Pyvinium pamoate, 5 mg/kg once, repeat in 2 weeks

Hookworm

• Pyrantel pamoate, 10-11 mg/kg once daily for 3 d

• Mebendazole, 100 mg twice daily for 3 d

• Albendazole, 400 mg once (Ancylostoma1) or once daily for 3 d (Necator1)

Strongyloidiasis

• Albendazole, 400 mg/d once or twice daily for 3-7 d, may repeat in1 wk

• Ivermectin, 200 µg/kg once daily for 2 d

• Thiabendazole, 25 mg/kg twice daily for 3 d; continue for 5-7 d in disseminated infection

Trichuriasis

• Albendazole, 600 mg once

• Mebendazole, 100 mg twice daily for 3 d

• Oxantel pamoate, 15 mg/kg once

1Ancylostoma, “Old World” hookworm: Necator, “New World” hookworm.

LYMPHATIC FILARIASIS

Lymphatic filariasis is a bloodstream and lymphatic infection caused by the filarial nematodes Wuchereria bancrofti, Brugia malayi, and Brugia timori. The disease is endemic in the tropics and subtropics of both hemispheres. A mosquito serves as an intermediate host and vector; the peak blood parasitemia and optimum time of the day or night for obtaining blood smears differ in various parts of the world, corresponding to the feeding pattern of the local mosquito vectors. After deposition by mosquitoes of infectious microfilariae into humans during a blood meal, 6-12 mo are required before adult worms mature and begin producing numerous circulating microfilariae to continue the life cycle. Symptoms of acute disease generally occur 8-16 mo after infection in nonindigenous peoples, but the incubation period may be longer in indigenous peoples.

Clinical & Laboratory Findings

Indigenous persons with filariasis are often asymptomatic. In the first few years after infection, variably present clinical manifestations include recurrent episodes of lymphangitis, notable for progression proximally to distally, unlike typical bacterial lymphangitis. These episodes may be accompanied by high fever and resolve within 7-10 d. Epididymitis or orchitis may occur intermittently. Other patients, especially travelers, may have allergic symptoms including urticaria, rashes, and eosinophilia. Chronic infection may result in lymphatic insufficiency, with lymphedema involving the extremities or external genitalia. Hydroceles may also occur. The term elephantiasis refers to advanced changes of chronic lymphedema, including subcutaneous thickening, skin hyperkeratosis, and fissuring.

Tropical pulmonary eosinophilia refers to a syndrome of nocturnal cough and wheezing with diffuse miliary chest x-ray infiltrates, eosinophilia, elevated immunoglobulin E concentrations, and high antifilarial antibody titers. The syndrome is caused by sequestration of W bancrofti or B malayi microfilariae in the lungs and responds to treatment with diethylcarbamazine citrate (DEC).

Diagnosis of filariasis is usually clinical in endemic areas. Confirmation requires demonstration of microfilaria in filtered blood samples, the timing of which should be adjusted to match the nocturnal or diurnal periodicity of the peak parasitemia in the region in which the infection was acquired. The organisms adapt their periodicity to local time zones, but this requires 10-14 d.

Microfilariae are more commonly seen in the bloodstream during the early stages of disease (1-2 years after infection) and are rare in the bloodstream during the lymphatic obstructive stage of disease. Administration of 50 mg of DEC may result in positive blood smears immediately (within 1 h) after administration in otherwise smear-negative individuals. Serologic testing may also be helpful, but both false positive and false negative test results occur.

Treatment

Symptomatic treatment of acute filarial lymphangitis (eg, antihistamines and aspirin) may be helpful in reducing the intensity of symptoms. DEC is an effective microfilaricidal drug, but the adult worms require a longer course of therapy and sometimes multiple courses of therapy to be eradicated. DEC (2 mg/kg) is administered 3 times daily for 2-3 wk. Allergic reactions (eg, fever, urticaria, or lymphangitis) to injured parasites may occur early in therapy; some authorities suggest smaller doses of DEC (50 mg on the first day, increasing to full dosage over 3-4 d) to minimize these reactions. Antihistamines may also be of benefit. Nonspecific side effects include headache, vertigo or dizziness, malaise, fever, or myalgias. Onchocerciasis should be excluded before DEC treatment. DEC is available in the United States from Lederle Laboratories (800-934-5556).

Prevention

Because transmission depends on mosquito vectors, control measures are directed at reducing mosquito populations and reducing the number of bites by mosquitoes.

OTHER FILARIAL INFECTIONS

1. LOIASIS

Loiasis (African eye worm infection) occurs in rainy areas of central and West Africa. The filarial parasites are transmitted by the bite of an infected Chrysops spp. horsefly. Organisms mature in the subcutaneous tissues, where adult worms may live for more than a decade and release microfilariae into the circulation.

Clinical Findings

Adult worms migrate through subcutaneous tissues at rates = 1 cm/min. This may be asymptomatic, or, especially when migration occurs around or across the eye, noted as conjunctivitis or eyelid edema. Calabar swellings are subcutaneous edematous areas of 3-10 cm that are nonerythematous and do not pit; local pain, pruritus, and mild fever may be present. Calabar swellings are transient, resolving after 2-3 d or 1 wk, only to reappear at irregular intervals in different locations. Calabar swellings do not necessarily contain worms at the time that they appear.

Symptoms of loiasis vary depending on the host. Indigenous populations typically have relatively mild symptoms or are asymptomatic even though they are microfilaremic. Travelers typically have a more symptomatic course, with an increased number and severity of Calabar swellings, marked eosinophilia, leukocytosis, hypergammaglobulinemia, and elevated immunoglobulin E antibodies.

Treatment

Treatment is with DEC, 3 mg/kg 3 times daily for 21 d. Localized inflammatory reactions to dying adult worms in tissues are common. In patients with microfilaremia, reactions may be more severe including severe neurologic complications and death. Gradually escalating doses of DEC and in some patients systemic corticosteroids may be used. Ivermectin and albendazole have been investigated as alternative therapies to DEC.

2. ONCHOCERCIASIS

Infection with Onchocerca volvulus causes African river blindness, which is the second leading cause of blindness worldwide. Onchocerciasis is transmitted by the Simulium spp. blackfly and is found in equatorial West, central, and East Africa and portions of Central and South America. Larval forms penetrate the skin after the bite of the blackfly, where they mature into adults in the subcutaneous tissues. Microfilariae from mature females migrate back to the dermis where they are ingested by blackflies to continue the life cycle.

Clinical Findings

Cutaneous and connective tissue manifestations of onchocerciasis include the formation, usually within a year, of mobile nodules encapsulating the adult worms in a fibrous tissue mass. Multiple nodules may be present in subcutaneous or connective tissues, especially over bony prominences. Depigmentation, wrinkling, and thickening of skin may be seen with chronic infection. Visual loss is the most serious complication. The earliest eye lesions are punctate keratitis associated with microfilariae within the cornea and anterior chamber. Iridocyclitis and posterior synechiae may develop, which may result in a fixed and distorted pupil. Lesions of the posterior chamber of the eye are less common, including optic atrophy and choroiditis.

Diagnosis is suspected clinically and confirmed by examination of a skin snip obtained without anesthesia from the shoulder or buttock areas, demonstrating microfilariae. Adult worms may be found in biopsied or excised nodules. Slit-lamp examination of the cornea or anterior chamber of the eye may demonstrate microfilariae. Microfilariae are identifiable in urine in 17%-30% of patients > 10 years old.

Treatment

The treatment of choice is ivermectin, 150 5g/kg orally as a single dose, which kills microfilariae but is less effective against adult worms. Treatment is repeated at 3-mo intervals for 2-3 years. Diethylcarbamazine has been used historically but is less effective and more toxic than ivermectin, and it is no longer recommended by the World Health Organization. Cutaneous nodules, especially on the scalp, may be surgically excised.