Newly arrived immigrants to the United States may present with nematodal ailments, such as strongyloidiasis, hookworm infection, clonorchiasis or cysticercosis, or they may have diseases that are not clearly of infectious etiology, such as tropical pancreatitis. The manifestations of and treatments for these illnesses may be unfamiliar to family physicians. In particular, albendazole (Albenza) and ivermectin (Stromectol) are two medications that are now available in the United States for the treatment of some worm infections (Table 1).
|Urticaria, abdominal pain, diarrhea, pulmonary involvement
|Stool or sputum microscopy, Serology
|Dermatitis, pulmonary symptoms, gastrointestinal disturbance
|Seizures, focal neurologic deficit, hydrocephalus, intracranial hypertension
|Stool microscopy or pathologic examination of cysts
|Anorexia, epigastric pain, diarrhea
|Stool or bile microscopy
|Abdominal pain, diarrhea, steatorrhea, weight loss
|Clinical and laboratory presentation, pancreatic calcifications on radiographs
|Pancreatic enzymes and specialized diet
A 47-year-old Vietnamese woman with adenocarcinoma of the lung received radiotherapy for brain and bony metastases. Because her complete blood count showed eosinophilia, stool samples were examined for ova and parasites. This testing revealed the rhabditiform larvae of Strongyloides stercoralis.
Two courses of thiabendazole were prescribed but were not completed because the patient experienced vomiting and abdominal cramps. Subsequently, linear, raised erythematous skin lesions were noted on her lower back. The patient was then treated with ivermectin, which she tolerated well.
Strongyloidiasis is acquired when infectious larvae in the soil penetrate human skin, migrate within the circulation and develop into adult worms in the gut. Female worms shed larvae in the gut, the larvae in the stool reach the soil, and the cycle is completed. The worms can also complete a life cycle within a human host without a soil phase. The number of worms may increase greatly in immunosuppressed persons.
The classically recognized triad of symptoms in chronic strongyloidiasis are urticaria (episodic, rapidly moving urticarial skin eruptions, most often on the buttocks and perianal area), abdominal pain and diarrhea. Pulmonary involvement with wheezing, chest pain and cough can also occur. Eosinophilia is usually present, unless the patient is immunosuppressed. Overwhelming infection in untreated immunosuppressed persons can be fatal.
Stool microscopy may reveal the rhabditiform larvae of S. stercoralis. (Strongyloides eggs may be found in the mucosa of the small intestine but are rarely present in feces.) These larvae, which have a short buccal capsule, can be infrequently detected despite multiple investigations. Furthermore, unless high power is used, Strongyloides larvae can be difficult to distinguish from hookworm larvae, which have a longer buccal capsule. Serology can be helpful in confirming the diagnosis.
Strongyloidiasis should be considered in patients from tropical areas who are immunosuppressed (e.g., because of corticosteroid use or malignancy). S. stercoralis can survive 40 years or more in a human host. In fact, strongyloidiasis has been found in U.S. military veterans who served in Southeast Asia during the 1960s. However, fatal S. stercoralis infection can occur in persons who have never left the United States, because the infection is endemic in parts of Appalachia.3,4
A 62-year-old Vietnamese man presented with a sore throat and bloody sputum in September 1997. He had arrived in the United States in 1994 with a history of bright red blood passed rectally. In early 1995, examination by barium enema and flexible sigmoidoscopy was unremarkable. His medical history included six years in a reeducation camp in northern Vietnam, where he had lived in near-starvation conditions. In May 1996, his blood count was significant for an absolute eosinophil level of 559 per mm3 (0.6 × 109 per L). Dry cough was noted in June 1997.
Physical examination revealed a well-developed, well-nourished patient with minimal pharyngeal erythema. The chest radiograph showed a parenchymal opacity at the base of the right lung. The blood count was unremarkable except for an eosinophil level of 1,870 per mm3 (1.9 × 109 per L). Three stool samples were negative for occult blood, but all showed hookworm eggs. The patient was treated with 10 days of oral penicillin, multivitamins and a single 400-mg dose of albendazole.
Hookworm infection is acquired when larvae from the soil penetrate the skin and enter the circulation. The spread of this nematode infection is aided by poor sanitary practices in which infected persons defecate in areas where others walk without shoes.
Patients may develop dermatitis when filariform hookworm larvae penetrate the skin. Pulmonary symptoms and signs, such as cough, wheezing and pulmonary infiltrates, may occur when the larvae pass through the lungs after entering the circulation. In addition, patients may complain of gastrointestinal discomfort when the larvae are coughed up, swallowed and then reach adult form in the small intestine, where the worms attach and suck blood.
The diagnosis of hookworm infection is based on the presence of ova in stool. Laboratory findings may also include iron-deficiency anemia and eosinophilia.
Albendazole is a synthetic nitroimidazole with broad-spectrum antinematodal activity plus anticestodal activity and some antiprotozoal activity. A single dose of albendazole is effective treatment for most forms of intestinal helminthiasis. However, the drug is officially labeled in the United States only for the treatment of neurocysticercosis and Echinococcus infection.5 Mebendazole (Vermox), another drug used to treat hookworm, must be given for three days.
Patients with iron-deficiency anemia related to hookworm infection also require iron supplementation.6 Albendazole and mebendazole should not be used in pregnant women.
A 57-year-old Cambodian woman with a seven- to eight-year history of headaches was admitted because of worsening headaches, right-sided weakness and the vomiting of clear fluid. On her first hospital day, she displayed jerking of the right upper extremity.
Magnetic resonance imaging of the brain showed multiple bihemispheric, parenchymal nodules along with edematous lesions in the posterior parietal, occipital and right basal ganglia. A slight mass effect was created by the edematous changes at the lateral location, with effacement of the frontal horn of the right lateral ventricle. A single lesion was noted in the right cerebellar hemisphere.
An ophthalmic examination was unremarkable. A radiograph of the left forearm, taken because of left arm pain, revealed multiple soft tissue calcifications the size of rice grains.
The patient was treated with dexamethasone (Decadron), cimetidine (Tagamet) and ongoing phenytoin (Dilantin). Praziquantel (Biltricide) was also administered for presumed neurocysticercosis. (Albendazole was not available at the time this patient was treated.)
Cysticercosis is caused by the immature stages of Taenia solium (pork tapeworm). Humans acquire the disease by ingesting the eggs of T. solium. Infection most commonly occurs in areas where pigs and people are in close contact, hygienic standards are low and undercooked pork is eaten.
INFECTION IN HUMANS
After using their hooks to break out of the eggs, the activated oncospheres (larvae) penetrate the intestinal epithelium of the duodenum to enter the lymphatic and vascular systems. They are subsequently carried to the brain and other tissues. Eventually, the oncospheres lose their hooks and develop into fluid-filled bladder worms (cysticerci).
The manifestations of neurocysticercosis include seizure disorders, focal deficits, hydrocephalus, arachnoiditis and intracranial hypertension. Cysticerci, sometimes calcified, are also found in muscles of various structures, including the buccal mucosa, tongue, eye and subcutaneous tissues.
The definitive diagnosis of cysticercosis is based on the pathologic examination of cysts. Stool examinations positive for adult T. solium constitute supporting evidence.
An 18-year-old Vietnamese woman who had arrived in the United States eight months previously was admitted with nausea, vomiting (clear emesis) and right upper quadrant and epigastric pain that alternated between being constant and colicky in character. She stated that curling into a fetal position partially relieved the abdominal pain.
On physical examination, the patient was found to have a temperature of 37.1°C (98.8°F) and right upper quadrant guarding. Some laboratory values were elevated: white blood cell count, 13,600 per mm3 (13.6 × 109 per L); serum alanine transaminase (ALT), 63 U per L; total serum bilirubin, 3.2 mg per dL (55 μmol per L); serum alkaline phosphatase (ALP), 142 U per L; serum aspartate transaminase (AST), 112 U per L; and serum lipase, 84 U per L.
Ultrasound examination revealed a dilated common bile duct and multiple, markedly dilated tubular structures in the liver. A black, mushy, common bile duct stone was removed during endoscopic retrograde cholangiopancreatography, and intrahepatic ducts with areas of stricture and possible proximal dilatation were noted.
The patient was treated with praziquantel for a bile duct disorder that was probably caused by Clonorchis sinensis (Chinese liver fluke) infection. Her gastrointestinal symptoms responded to treatment.
Infection with C. sinensis follows the consumption of raw fish, particularly fish raised in ponds that were fertilized with human or animal feces. Clonorchiasis is endemic in many areas of the Far East, including southern China, Hong Kong, Taiwan, Japan, Korea and Vietnam.
Anorexia, epigastric pain, diarrhea and leukocytosis (sometimes with eosinophilia) typically begin 10 to 26 days after inadequately cooked, infected fish is consumed. These symptoms generally last two to four weeks. Cholangitis, cholelithiasis, pancreatitis and cholangiocarcinoma are common complications of chronic infection.
The differential diagnosis of the acute phase of C. sinensis infection includes acute schistosomiasis. The diagnosis is established when Clonorchis eggs are found in feces or bile.
Clonorchiasis is treated with oral praziquantel, in a dosage of 25 mg per kg after each of three meals on one day. Albendazole can also be used, but a seven-day treatment course is required.
Conservative medical treatment is effective in most patients with clonorchiasis. In some patients, however, the bile ducts may continue to be inflamed after presumed eradication of the parasite.
A 31-year-old southern Sudanese man came to the United States after living in a refugee camp where food was scarce. He was hospitalized for abdominal pain that occurred between meals and also awakened him from sleep. He described his alcohol use as minimal.
His temperature was 38.4°C (101.1°F), and the abdominal examination showed periumbilical and epigastric tenderness. A number of laboratory values were elevated: serum amylase, 230 U per L; serum lipase, 54 U per L; serum ALT, 37 U per L; and serum bilirubin, 2.4 mg per dL (41 μmol per L). The serum ALP value was normal.
Ultrasound examination showed swelling and edema around the pancreas but no cysts, pseudocysts or gallstones. Stool examination was negative for ova and parasites. Hepatitis B surface antigen, antibody to hepatitis C virus and hemoglobin studies were negative. The patient declined endoscopy, and empiric treatment with clarithromycin (Biaxin) and omeprazole (Prilosec) did not improve his condition. The patient's abdominal pain decreased after he began taking pancreatic enzyme supplements orally with low-fat meals.
Tropical pancreatitis is a disorder associated with malnutrition and overcrowding in tropical areas (e.g., refugee camps). The exact cause of this condition is unknown but is suspected to be either a virus or a nutritional factor.
The major findings in tropical pancreatitis include postprandial abdominal pain (usually aggravated by the intake of fatty foods), diarrhea with steatorrhea, and weight loss. The illness is sometimes complicated by diabetes mellitus. An abdominal plain-film radiograph may reveal pancreatic calcification.
Diagnosis of tropical pancreatitis is based on the clinical, laboratory and radiographic findings.
Postprandial abdominal distress may improve when the patient follows a specialized diet and takes pancreatic enzyme supplements.