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Strongyloides stercoralis (Pathogen – Intestinal Nematode)

Organism:
Strongyloides stercoralis belong to the nematodes, are pathogenic, and cause disease.  A series of workers dealt with the classification, life cycle differentiation, and possible pathogenesis of this worm during the early 1900s. Early work led to demonstration of the internal autoinfective portion of the life cycle, which has become extremely important, particularly when one is working with immunocompromised patients. It is very important to consider this infection in military personnel and travelers who, many years earlier, were in an area where the infection is endemic. More than 30 to 40 years after acquisition of the original infection, persistent, undiagnosed disease can be found in these individuals. If for any reason they become immunocompromised, the result can be disseminated disease leading to the hyperinfection syndrome and death.
NOTE:  All patients who are going to receive immunosuppressive drugs should be screened for strongyloidiasis before therapy.

 
        
                                                                                   

Agar Plate Culture

Filariform larva in sputum  Genital packet of cells  Hookworm and Strongyloides Rhabditiform larvae
     

Life Cycle:
Human infection is acquired by skin penetration of the filariform larvae (infective larvae) from the soil. These larvae are long and slender (up to 630 μm long by 16 μm wide) and may remain viable in soil or water for several days. After penetration of the skin, the larvae are carried via the cutaneous blood vessels to the lungs, where they break out of the pulmonary capillaries into the alveoli. They then migrate via the respiratory tree to the trachea and pharynx, are swallowed, and enter the mucosa in the duodenum and upper jejunum. Development of the female worms to adults usually takes about 2 weeks, after which the females begin egg production by parthenogenesis.
The eggs are oval and thin shelled, and they measure 50 to 58 μm long by 30 to 34 μm wide (generally a bit smaller than hookworm eggs). The eggs usually hatch, and the rhabditiform larvae (noninfective larvae) pass out of the intestinal tract in the feces. These larvae are passed out onto the soil in the feces and develop into free‑living male and female worms, eventually producing infective filariform larvae (egg, noninfective larvae, and infective larvae). In temperate climates, the free‑living male and female worms do not develop; however, the rhabditiform larvae that pass out in the stool develop into the filariform (infective) larvae, which are then ready to infect the next host through skin penetration.
In situations in which autoinfection occurs, some of the rhabditiform larvae that are within the intestine develop into the filariform larvae while passing through the bowel. These larvae can then reinfect the host by (i) invading the intestinal mucosa, traveling via the portal system to the lungs, and returning to the intestine or (ii) being passed out in the feces and penetrating the host on reaching the perianal or perineal skin.

Acquired:
Infection in humans is acquired through skin penetration of infective larvae (filariform larvae) from contaminated soil.

Epidemiology:
S. stercoralis is most commonly found in the warm areas but can survive in colder climates. The infection is most often found to overlap the geographic range of hookworm infections and has been reported as the most commonly diagnosed helminth infection at the University of Kentucky Medical School. It is important to remember that internal autoinfection allows for maintenance of the parasite within the host for years following the initial exposure. Since all infected individuals are at risk for hyperinfection and disseminated disease, the identification of people who may have contracted their infection many years earlier is of great clinical significance.

Clinical Features:
The pathologic changes associated with strongyloidiasis can vary, both in severity and in the areas of the body involved. Some individuals may remain totally asymptomatic, with the only abnormal clinical finding being a peripheral eosinophilia. Considering the life cycle, the three areas of primary involvement would be the skin (cutaneous), the lungs (pulmonary), and the intestinal mucosa (intestinal).  Debilitated or immunocompromised patients should always be suspected of having strongyloidiasis, particularly if there are unexplained bouts of diarrhea and abdominal pain, repeated episodes of sepsis or meningitis with intestinal bacteria, or unexplained eosinophilia.
Cutaneous.  Initial skin penetration usually causes very little reaction, although there may be some pruritus and erythema if the number of penetrating larvae is large. In some patients, the reaction at the site of larval penetration may last several weeks.  With repeated infections, the patient may mount an allergic response that will prevent the parasite from completing the life cycle. The larvae may be limited to skin migration (larva migrans). The term larva currens (racing larva) was proposed in 1958 and is now generally accepted for cases of strongyloidiasis in which there is one or more rapidly progressing linear urticarial tracks starting near the anus. There is speculation that some of these cases may involve larvae of other species of Strongyloides. These tracks may progress as fast as 10 cm/h, with an intermittent movement, usually on the thighs. Onset is sudden, and the lesions may disappear within 12 to 18 h.
Pulmonary.  Larval migration through the lungs may stimulate symptoms, depending on how many larvae are present and the intensity of the host immune response. Some patients may be asymptomatic, while others may present with pneumonia. With a heavy infective dose or in the hyperinfection syndrome, individuals often develop cough, shortness of breath, wheezing, fever, and transient pulmonary infiltrates (Loeffler's syndrome). There have been cases reported in which the larvae were found in the sputum during this larval migration.
Intestinal.  Although the timing may vary from person to person, gastrointestinal symptoms such as diarrhea, constipation, anorexia, and abdominal pain usually begin about 2 weeks after infection with larvae detectable in the stool after 3 to 4 weeks.  In heavy infections, the intestinal mucosa may be severely damaged with sloughing of tissue, although this type of damage is unusual. Parasitized individuals may show villous atrophy and crypt hyperplasia.
Hyperinfection Syndrome.  Autoinfection is probably the mechanism responsible for long‑term infections that persist years after the person has left the area where the infection is endemic. The parasite and host reach a status quo so that neither suffers any serious damage. If for any reason this equilibrium is disturbed and the individual becomes immunosuppressed, then the infection proliferates, with large numbers of larvae being produced and found in every tissue of the body, including the gastric mucosa. Several conditions, including increased use of immunosuppressive therapy, predispose an individual to the hyperinfection syndrome.  However, the distinction between autoinfection and hyperinfection tends to be quantitative rather than being specifically defined.
HTLV-1 infection.  The prevalence of S. stercoralis is significantly higher in HTLV‑1 carriers than HTLV‑1 noncarriers in Japan and elsewhere. Since cellular immunity plays a major role in the host defense against strongyloidiasis, infection with HTLV‑1 appears to change the immune system capability, leading to severe clinical manifestations and disseminated disease.
HIV infection.  Although it is well known that many people are coinfected with AIDS and S. stercoralis, there have been few cases of hyperinfection documented in this patient group, many of whom previously received steroids for Pneumocystis pneumonia or non-Hodgkin’s lymphoma.

Clinical Specimen:
Stool:  Confirmation of the infection depends on recovery and identification of the adult worms, larvae, or eggs from the stool, duodenal material, or sputum.

Laboratory Diagnosis:
Stool:  Confirmation of the infection depends on recovery and identification of the adult worms, larvae, or eggs from the stool, duodenal material, or sputum. Fecal specimens may not be positive, even after the routine ova and parasite examination, including the concentration procedure, is performed. Numbers of larvae found in the stool will also vary from day to day. It is well known that the detection of S. stercoralis larvae in the stools may be very difficult, particularly in patients with chronic, low‑level infection.
Culture:  Agar plate cultures are also recommended and tend to be more sensitive than some of the other available diagnostic methods; stool is placed onto agar plates, and the plates are sealed to prevent accidental infections and held for 2 days at room temperature. As the larvae crawl over the agar, they carry bacteria with them, thus creating visible tracks over the agar. The plates are examined under the microscope for confirmation of larvae, the surface of the agar is then washed with 10% formalin, and final confirmation of larval identification is made via wet examination of the sediment from the formalin washings.

Organism Description:
Rhabditiform Larva:       The rhabditiform larvae that normally pass out in the stool measure up to 380 μm long by 20 μm wide, with a muscular esophagus (club‑shaped anterior, then a restriction, and a posterior bulb). There is a genital primordium packet of cells, which is fairly obvious and can be seen about two‑thirds of the way back from the anterior end. One of the key morphologic differences between these larvae and those of hookworm is the length of the mouth opening (buccal capsule). The opening in the rhabditiform larvae of S. stercoralis is extremely short (only a few micrometers), while the mouth opening in hookworm rhabditiform larvae is approximately three times as long (See above). These differences can be seen by examining the larvae under the microscope with the low (10´) or high dry (40´) objectives.
Filariform Larva:  To differentiate the Strongyloides filariform larvae from those of the hookworm, one should examine the tail under the microscope. Strongyloides filariform larvae will have a slit in the tail, while hookworm filariform larvae will have a pointed tail

Laboratory Report:
Strongyloides stercoralis (eggs and/or larvae present). Eggs are rarely seen in the stool unless the patient has disseminated disease and the hyperinfection syndrome) present.

Treatment:
At present, the recommended drug of choice is ivermectin; however thiabendazole has been used very successfully for many years. In some cases, repeated therapy is necessary, and the cure rates vary.  Albendazole has also been used to treat patients with strongyloidiasis, as well as those with the hyperinfection syndrome.
The possibility of hyperinfection also puts patients with asthma and intestinal strongyloidiasis at significant risk if their lung disease is treated with systemically administered corticosteroids.  Apparently, fewer than 10 days of therapy with corticosteroids has led to disseminated strongyloidiasis
Garcia, L.S. 2007.  Diagnostic Medical Parasitology, 5th ed., ASM Press, Washington, D.C.

Control:
Contact with contaminated infective soil, feces, or surface water should be avoided. Communities where close living conditions and poor sanitation facilities exist, including both rural and urban areas in the developing world, often have high prevalence rates of strongyloidiasis. Also, closed communities such as institutions for the mentally handicapped, may have high rates of infection and transmission.