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Two recent outbreaks of acute schistosomiasis (AS) are described in this issue of the journal.1,2 These cases bring to light the difficulties in the diagnosis and management of AS as it has been recently addressed in the literature.3,4

Diagnosis

  1. Top of page
  2. Diagnosis
  3. Treatment
  4. Declaration of Interests
  5. References

The diagnosis of AS remains difficult, although molecular tools may be helpful as illustrated during one of the reported outbreaks.1 Clinically, the association of fever, angioedema, dry cough, urticaria and high blood eosinophilia clearly points to an allergic reaction to the migrating and maturing helminth larvae such as in AS.4

Diagnosis during this very early phase of the parasitic lifecycle classically relies on serological testing. The sensitivity and specificity of serological tests for AS diagnosis reach 80 and 97%, respectively when a combination of ELISA and indirect hemagglutination assays are used.5 However, following exposure, the median time to seroconversion is about 46 days, whereas clinical signs appear after about 30 days and ranges can be broad (1–12 wk).6,7 Therefore, there is an approximate 2-week seronegative window, requiring further serological testing to confirm seroconversion. The low sensitivity and delayed positivity of serological tests during the early phase of AS are due to the types of antigens (worm and egg) used for the tests.

This lack of sensitivity and delayed positivity could be improved by new diagnostic tools. Cell-free parasite DNA detection of schistosoma in plasma is a promising solution for AS. The specificity is about 100% for Schistosoma mansoni, although the intrinsic quality of the test remains elusive given that the ideal primers are yet to be defined.8 Furthermore, this new tool needs more testing with Schistosoma haematobium and Schistosoma japonicum infection. Nonetheless this test should be used when facing a typical clinical situation after exposure in an endemic area. This test is not currently available.

Culprit species are identified by analyzing eggs in human excreta (stools and urine), but this test lacks sensitivity. When testing is performed soon after infection the results are negative. The median detection time varies from 5 to 10 weeks after exposure. Early treatment with praziquantel (PZQ) delays oviposition by several weeks.7,9 It is worth noting that different phases of the parasitic lifecycle may overlap in a patient who is infected with many schistosomulae. Migrating schistosomulae may spend some time in the blood circulation before finding their way to the hepatic portal system and then to the peri-intestinal or peri-vesical blood vessels where they settle.4,10 This is not a synchronous process, and schistosomulae of different stages of maturity coexist at a given time. In AS, schistosome egg excretion by mature schistosomes may thus coincide for several weeks with circulating schistosomulae.8,10 This has important treatment implications.9,11

Treatment

  1. Top of page
  2. Diagnosis
  3. Treatment
  4. Declaration of Interests
  5. References

Treatment of AS Remains Not Well Defined

PZQ, which is the major treatment of chronic schistosomiasis is ineffective on young (7- to 28-d-old) schistosomulae.12 Unsurprisingly, it does not prevent the chronic phase of the disease.7,13 Moreover, the use of PZQ during AS may be associated with paradoxical reaction (or Jarish Herxheimer-like reaction) in 40% of 10 French patients and 56% of 9 Belgian patients, respectively.7,9 Therefore, we should wait at least 3 months after exposure before initiating PZQ treatment when the chronic stage has been reached. In addition it will be necessary to repeat the administration of PZQ to ensure effective treatment to take into account the schistosomulae that may not yet have reached the adult stage.

Corticosteroids may be prescribed in association with PZQ to avoid or attenuate this paradoxical reaction. Nonetheless there are some data arguing against this association. First, corticosteroids such as dexamethasone decrease plasma level of PZQ by 50%.14 Second, occult strongyloidiasis cannot be ruled out easily and a presumptive treatment against strongyloidiasis should also be considered.15 Finally, the timing of corticosteroids use is unclear. In one of these outbreaks its use was postponed in case of worsening evolution.1

According to our experience and as previously underlined we believe that corticosteroids use should be restricted to patients with severe forms (neurovasculitis, myocarditis, etc.) and PZQ only initiated when ova are detected in stools or urines according to the culprit species or when there is no more symptoms of AS.4,16

An effective and well-tolerated treatment for the management of patients with AS is still needed. A promising treatment could be artemisinin derivatives as they showed some activity against young schistosomulae.17,18 Therefore, a prospective study should be implemented to evaluate the use of artemisin derivatives in AS.

In conclusion, AS is difficult to diagnose and treat. The current diagnostic tools lack in sensitivity, the current treatment lack in efficacy and could cause complications. Therefore, research in diagnosis and treatment is needed.

Declaration of Interests

  1. Top of page
  2. Diagnosis
  3. Treatment
  4. Declaration of Interests
  5. References

The authors state they have no conflicts of interest to declare.

References

  1. Top of page
  2. Diagnosis
  3. Treatment
  4. Declaration of Interests
  5. References