Strongyloides stercoralis

Leuckart, 1883; van Durme 1901; Looss, 1905; Fülleborn, 1914.

Strongyloides stercoralis and Strongyloides fuelleborni, dwarf threadworms of the genus Strongyloides, are the causative agents of strongyloidosis. The pathogens can be both parasitic and free in the soil.

The pathogens bore percutaneously into the tissue of the host, find a connection to the host's blood system and enter the lungs in this way. Here they leave the bloodstream into the alveoli of the lungs. From here they follow the airways cranially, are swallowed on arrival in the pharynx, and thus enter the intestine.

There, only the female individuals develop. These are 2.0-2.5mm long and 30-50um thick (see Fig.). They are predominantly located in the mucosa of the duodenum and upper jejunum and lay about 1000 fully embryonated eggs daily in the mucosa and crypts of the intestinal wall. The small (0.7mm x 14um) males are found only occasionally or are absent altogether.

The 300-500um long first larvae hatch while still in passage through the intestinal tract. They are called "rhabditiform" because of their esophagus equipped with a terminal bulb. During further development 2 ways are possible:

1. direct development (autoinvasion): The initial larvae develop within a few days into 500-700um large, vividly mobile filiariform infective larvae. These can either immediately penetrate the intestinal wall (endoautoinvasion) or leave the intestine. They then bore into the anal mucosa or surrounding skin (exoautoinvasion). They then in turn undergo a migratory phase with pulmonary passage and maturation into adult dwarf nematodes.

2. indirect development (development in the open): However, under suitable conditions, these initial larvae can mature into free-living, non-parasitic adults about 1.0mm in size. These lay eggs, which in turn can hatch into rhabditiform larvae. The survival of the free-living infective larvae depends on external conditions. If they dry out, they die quickly. As with hookworms (see Ancylostomatidae below), infection again occurs by penetration through the skin. Subsequent migration is through the right heart, lungs, bronchial system, and passage into the esophagus. 2-3 weeks after infection, the adults reach the small intestine and begin egg production.

Hyperinfection syndrome: In immunosuppression (e.g. HIV infection), massive autoinfection may occur with dissemination of larvae to all organs.

Mostly found in subtropical or tropical regions, especially Southeast Asia, Africa and South America. Rarely in Europe (especially in mines). More than 70 million people are infected worldwide; in endemic areas up to 60% of the population are infected.

Frequent occurrence in patients with HIV infection.

Internal and external autoinfection leads to chronic persistent infection. In the case of immune incompetence, a threatening hyperinfection syndrome can develop.

The pathogens bore percutaneously into the tissue of the host, find a connection to the host's blood system and enter the lungs in this way. Here they leave the bloodstream into the alveoli of the lungs. From here they follow the airways cranially, are swallowed on arrival in the pharynx, and thus enter the intestine.

There, only the female individuals develop. These are 2.0-2.5mm long and 30-50um thick (see Fig.). They are predominantly located in the mucosa of the duodenum and upper jejunum and lay about 1000 fully embryonated eggs daily in the mucosa and crypts of the intestinal wall. The small (0.7mm x 14um) males are found only occasionally or are absent altogether.

The 300-500um long first larvae hatch while still in passage through the intestinal tract. They are called "rhabditiform" because of their esophagus equipped with a terminal bulb. During further development 2 ways are possible:

1. Direct development (autoinvasion): The initial larvae develop within a few days into 500-700um large, vividly mobile filiariform infectious larvae. These can either immediately penetrate the intestinal wall (endoautoinvasion) or leave the intestine. They then bore into the anal mucosa or surrounding skin (exoautoinvasion) and in turn undergo a migratory phase involving pulmonary passage and maturation into adult dwarf nematodes.
2. Indirect development (development in the open): However, under suitable conditions, these initial larvae can mature into free-living, non-parasitic adults about 1.0mm in size. These lay eggs, which in turn can hatch into rhabditiform larvae. The survival of the free-living infective larvae depends on external conditions. If they dry out, they die quickly. As with hookworms (see Ancylostomatidae below), infection again occurs by penetration through the skin. Subsequent migration is through the right heart, lungs, bronchial system, and passage into the esophagus. 2-3 weeks after infection, the adults reach the small intestine and begin egg production.

Hyperinfection syndrome: In immunosuppression (e.g. HIV infection), massive autoinfection may occur with dissemination of larvae to all organs.

The incubation period for strongyloidiasis is:

• 12-18 hours for skin reaction
• 7 days for pulmonary reaction
• 14 days for intestinal symptoms.

At the ports of entry of the filiariform infection larvae, linerar, serpiginous, itchy erythema and plaques often form, corresponding to a cutaneous larva migrans cutanea syndrome, especially in people who have already been sensitized by previous infections. Strongyloides larvae penetrate the skin very rapidly at a rate of about 10cm/h. They are therefore also known as "cutaneous larvae". They are therefore also called "racing larves" or "Larva currens". These regress within a few days. In infections by free-living larvae, these typical linear structures occur preferentially on the foot and ankle. In external autoinoculation, they are found on the buttocks and perianally.

During pulmonary passage, pneumonitis with dry cough and other symptoms of Löffler 's syndrome may occur about 1 week after infection if the infestation is extensive.

Uncomplicated intestinal infection is associated with variable symptoms: most common are anahltende or recurrent abdominal pain, often in the epigastrium with alternating diarrhea, occasionally with mucous or bloody admixtures. Furthermore nausea or vomiting.

The dermatological picture is that of larva currens. It is not uncommon for urticaria to accompany the disease.

Extensive infections may be accompanied by alternating fever, signs of a pronounced pneumonia with respiratory distress, weakness and weight loss.

In the hyperinfection syndrome, dissemination of larvae to all organs occurs (disseminated strongyloidiasis). Larvae may be present in large numbers: lungs, liver, intestinal wall, less frequently in the CNS.

Specifically:

• Gastrointestinal: Sprue-like symptomatology, colitis, steatorrhea, hypalbuminemia, generalized edema. Complicative: necrotizing jejunitis.
• Lung: severe pneumonia with fever, cough dysplneo, hemoptysis, obstructive-restrictive ventilatory disorder.
• CNS (rare): headache, mental syndromes, meningismus, convulsions, paralysis
• Laboratory: massive signs of inflammation; often no eosinophilia!

Mebendazole (e.g. Vermox) 2 times/day 300 mg p.o. on 3 consecutive days; repeat after 2-4 weeks.

Alternative: Tiabendazole (Mintezol) 2 times/day 2-3 tbl. p.o. (= 25 mg/kg bw) for 2-3 days, max. daily dose of 3 g. Stool controls monthly for at least 3 months.

In severe cases: ivermectin (e.g. Mectizan) 170-200 μg/kg bw as ED, if necessary repeated every 2 weeks if larvae are detected in the stool.

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