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CASE REPORT
Year : 2016  |  Volume : 43  |  Issue : 2  |  Page : 102-105

Intestinal strongyloidiasis in a psoriatic patient following immunosuppressive therapy: Seeing the unforeseen


1 Department of Microbiology, Tirunelveli Medical College, Tirunelveli, Tamil Nadu, India
2 Department of Dermatology, Tirunelveli Medical College, Tirunelveli, Tamil Nadu, India

Date of Web Publication18-May-2016

Correspondence Address:
Poongodi Lakshmi Santhana Kumaraswamy
Department of Microbiology, Tirunelveli Medical College, Tirunelveli - 627 011, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-5009.182610

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  Abstract 

Strongyloides stercoralis , an intestinal nematode, has a complicated life cycle. Mostly asymptomatic, if symptomatic it has nonspecific, transient clinical manifestations. The two aggressive forms of the disease are: Hyperinfection syndrome (HS) or disseminated syndrome (DS). Several risk factors have been associated with strongyloidiasis including immunosuppressive therapy, human immunodeficiency virus (HIV) infection, diabetes, alcoholism, tuberculosis, impaired bowel motility, surgically created intestinal blind loops, chronic obstructive pulmonary disease, and chronic renal failure. We describe a case of intestinal strongyloidiasis in a psoriatic patient treated with immunosuppressive therapy.

Keywords: Immunosuppressive therapy, psoriasis, Strongyloides stercoralis


How to cite this article:
Kumaraswamy PL, Chinnachamy R, Palanivel N, Rajamani N. Intestinal strongyloidiasis in a psoriatic patient following immunosuppressive therapy: Seeing the unforeseen. J Sci Soc 2016;43:102-5

How to cite this URL:
Kumaraswamy PL, Chinnachamy R, Palanivel N, Rajamani N. Intestinal strongyloidiasis in a psoriatic patient following immunosuppressive therapy: Seeing the unforeseen. J Sci Soc [serial online] 2016 [cited 2019 Sep 15];43:102-5. Available from: http://www.jscisociety.com/text.asp?2016/43/2/102/182610


  Introduction Top


Strongyloidiasis is endemic in subtropical and tropical areas and infects approximately 100-200 million people worldwide. [1] It is caused by Strongyloides stercoralis, an intestinal nematode, which has a complicated life cycle. S. stercoralis can remain undetected within an individual for many years or possibly the individual's life span perpetuating parasite dispersal and the risk of infection among the community. Warm moist temperatures, lower socioeconomic status, and poor sanitation leading to fecal contamination of the soil contribute to increased prevalence in the tropics. [2] Further, it is facilitated by international travel, immigration, and increasing numbers of immunosuppressed or immunocompromised patients. Several risk factors have been associated with strongyloidiasis, including immunosuppressive therapy for rheumatic diseases, malignancy (especially lymphomas), human immunodeficiency virus (HIV) infection, human T-cell lymphotropic virus type 1 (HTLV-1) infection, diabetes, hypochlorhydria, alcoholism, tuberculosis, impaired bowel motility, surgically created intestinal blind loops, gastric ulcers, antacid use, H2 receptor antagonists such as ranitidine, age >65 years, malnourishment, chronic obstructive pulmonary disease, leprosy, and chronic renal failure. [3] Most infected individuals are asymptomatic or may have intermittent symptoms, mostly affecting the intestine (from mild pain, intermittent or persistent diarrhea to more severe conditions that can mimic inflammatory bowel disease), lungs (cough, wheezing and asthma, chronic bronchitis), and skin (pruritus, rash). Systemic symptoms such as weight loss and cachexia may also occur. Immunocompromised patients tend to develop hyperinfection syndrome (HS) and disseminated strongyloidiasis (DS) that are potentially fatal. [2],[3],[4]

We describe a case of intestinal strongyloidiasis in a psoriatic patient treated with corticosteroid and methotrexate.


  Case report Top


A 45-year-old male driver, a known case of psoriatic erythroderma of 7 months duration, was admitted with acute exacerbation of redness, scaling, and exfoliation present all over the body for 10 days. He had intense itching and a burning sensation. He had edema of both the upper limbs and lower limbs. He had fever with chills, abdominal pain, diarrhea, and cough with expectoration for 1 week. There was no history of bladder disturbances. He had loss of weight and appetite. He was treated for psoriasis with tablet prednisolone 5 mg once daily (OD) and tablet methotrexate 15 mg/week for 1 year. He was not a diabetic or hypertensive. There was no history of tuberculosis or bronchial asthma. On examination, the patient was conscious, oriented, and afebrile. He had no anemia or jaundice or cyanosis. Bilateral pedal edema was present. Pulse rate was 88 beats/min, Blood pressure was 110/80 mmHg. The central nervous system, cardiovascular system, respiratory system, and abdominal examinations were clinically normal. Dermatological examination revealed diffuse erythema and exfoliation all over the body including the scalp. Multiple erythematous, hyperkeratotic, fissured plaques were present over the palms and soles. Loss of cuticle was found over all the nails associated with chronic paronychia and dystrophy of all the fingers and toes. Glossitis was present. Oral and genital mucosae were normal.

He was treated with tablets erythromycin, prednisolone 5 mg, methotrexate 25 mg/week, ranitidine, cetirizine, chlorpheniramine, capsule Astymin Forte, syrup potassium chloride, vitamins, mineral supplements, and liquid paraffin for external application.

Laboratory investigations revealed the following: Total count - 9,800 cells/mm 3 , differential count - neutrophils - 67%, lymphocytes - 30%, eosinophils - 3%, absolute eosinophil count - 410 cells/mm 3 , hemoglobin - 13.4 g%, red blood cell (RBC) - 4.37 million/cumm, packed cell volume (PCV) - 39.2%, platelets - 2.67 lakh/mm 3 ; erythrocyte sedimentation rate (ESR) - 4 mm/30 min and 10 mm/1 h; blood sugar - 60 mg%, urea - 18 mg%, creatinine - 0.9 mg%; sodium - 138 mEq/L, potassium - 4.0 mEq/L; liver function test - total bilirubin - 1.0 mg%, direct bilirubin - 0.6 mg%, indirect bilirubin - 0.4 mg%, serum glutamic oxaloacetic transaminase (SGOT) - 24 IU/L, serum glutamic pyruvic transaminase (SGPT) - 18 IU/L, alkaline phosphatase - 86 IU/L, total protein - 5.0 g%, albumin - 3.0 g%, globulin - 2.0 g%. X-ray of the chest and electrocardiography (ECG) were normal; ultrasound of the abdomen was normal. Serum HIV antibody was nonreactive. Serum immunoglobulin E (IgE) was 2338 IU/mL. T3 was 1.2 ng/mL, T4 was 10.5 mcg/dL, thyroid-stimulating hormone (TSH) was 4.8 microIU/mL; sputum examination showed no larva, stool examination by direct wet mount revealed motile larvae identified as S. stercoralis [Figure 1]. Ethical clearance was obtained from institutional ethical committee.
Figure 1: Strongyloides stercoralis larvae in stool

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  Discussion Top


S. stercoralis infects humans percutaneously and has a direct, autoinfective, and a nonparasitic free living developmental cycle. The two aggressive forms of the disease are: Hyperinfection syndrome (HS) occurs with a heavy worm burden or disseminated strongyloidiasis (DS) in which the larvae penetrate the intestinal wall and the gut flora reach the blood stream, causing bacteremia, meningitis, and septic shock. [5] The prevalence is underreported owing to the nonspecific clinical manifestations and lack of sensitive diagnostic methods and aggressive survey.

Glucocorticoids constitute a powerful drug in the therapeutic arsenal for several diseases, which predispose to chronic strongyloidiasis. Treatment with glucocorticoids induces an increase in the fertility of the adult female nematode in vivo, and this resulted in an increase in the production of eggs. These eggs not only hatch but also release infective larvae within the intestinal mucous membranes, which facilitates dissemination of larvae to distal organs in the infected host. The mechanisms underlying the effects of glucocorticoids are being explained by various hypotheses. The first hypothesis is that worms express receptors for host-derived eicosanoids, cytokines, or chemokines in their cuticles and respond to their mediators by the synthesis of their own reproductive and growth hormones. The second hypothesis is that the parasites benefit from the suppressed innate and adaptive immune responses of glucocorticoid-exposed patients, which foster parasite reproduction, invasion, and dissemination. [6]

Symptomatic strongyloidiasis is usually transient and nonspecific; clinical diagnosis of this parasitosis is hard to establish. Diagnosis is usually by direct microscopic examination of stool specimen for rhabditiform larvae, the diagnostic stage of the parasite. However, in chronic infection larvae excretion may be low and sporadic. [7] The diagnostic sensitivity of direct microscopic examination from single specimen is low (30-50%), and repeat sampling (up to seven specimens) may be necessary to rule out infection. [3],[8],[9] Aspiration of duodenal contents or Enterotests are also used in microscopic examination. Other diagnostic methods such as concentration of stool, Baermann technique, Harada-Mori filter paper strip culture, and agar plate culture are more sensitive compared to direct microscopy. Since the egg of Ancylostoma develops into larvae in stored specimens, it is difficult to differentiate the larvae of Ancylostoma from that of Strongyloides. [10] Hence, fresh stool specimen should be examined in suspected strongyloidiasis. Patients with disseminated strongyloidiasis may have large numbers of larvae demonstrated in the stool, sputum, urine, and lung fluids as well as in organ biopsies.

Though eosinophilia is common in strongyloidiasis ranging 25-35% in acute cases and 6-8% in chronic cases, the eosinophil count may be low in some immunocompromised conditions as was the case in this patient. Absence of eosinophilia indicates poor prognosis. [11]

Serological test detecting IgG directed against filariform larval antigen by enzyme-linked immunosorbent assay (ELISA) would be useful in chronic infections before hyperinfection and/or dissemination occur while in immunosuppressed patients, its sensitivity is probably lower. [12]

It is mandatory to treat patients in the chronic phase, before HS/DS develops. If possible, previous exposure to the parasite should be screened with serology before corticosteroid treatment, chemotherapy, or transplant. Patients with obstinate strongyloidiasis or albendazole resistance can be treated with ivermectin. [13] Controversy exists in the treatment of strongyloidiasis in immunocompromised and critically ill patients who have reduced intestinal absorption of the oral antiparasitic drugs. Hence, parenteral route is the most feasible and promising route for treatment in these patients. Ivermectin is highly bound to human serum albumin, reduces the distribution of drug to tissues, and contributes to poor therapeutic outcome. Hypoalbuminemia is common in HS; the free drug concentration is elevated and hence, the tissue level of ivermectin should be monitored daily, as the drug can be toxic to the central nervous system producing emesis, mydriasis, and ataxia. [14],[15] Uncomplicated strongyloidiasis requires a 2- or 3-day regimen with follow-up stool specimens to ensure the complete eradication of larvae. For DS/HS, therapy is extended to at least 1 week or until the parasites are no longer detectable. Since filariform larvae of Strongyloides are highly resistant to chemical agents, treatment requires complete elimination of the parasite rather than a simple decrease in the worm burden. [8] Treatment is not always effective and some patients may continue to harbor the parasite even after drug therapy. [4] In this patient, a 2-day regimen of ivermectin given along with withdrawal of methotrexate led to clearance of larvae from stools.


  Conclusion Top


Diagnosis and treatment of strongyloidiasis remain challenging. Screening for this infection should be considered in every person who has compatible symptoms, history of travel to residence in endemic areas, and risk factors for disseminated disease. The outcome of strongyloidiasis depends largely on timely diagnosis and therapy, which will reduce morbidity and mortality.

Acknowledgement

The author thank the treating dermatologist for her suggestion and support.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Chordia P, Christopher S, Abraham OC, Muliyil J, Kang G, Ajjampur SS. Risk factors for acquiring Strongloides stercoralis infection among patients attending a tertiary hospital in South India. Indian J Med Microbiol 2011;29:147-51.   Back to cited text no. 1
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Keiser PB, Nutman TB. Strongyloides stercoralis in the immunocompromised population. Clin Microbiol Rev 2004;17:208-17.   Back to cited text no. 2
    
3.
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Biggs BA, Caruana S, Mihrshahi S, Jolley D, Leydon J, Chea L, et al. Short report: Management of chronic strongyloidiasis in immigrants and refugees; Is serologic testing useful? Am J Trop Med Hyg 2009;80:788-91.   Back to cited text no. 4
    
5.
Smallman LA, Young JA, Shortland-Webb WR, Carey MP, Michael J. Stongyloides stercoralis hyperinfestation syndrome with Escherichia coli meningitis: Report of two cases. J Clin Pathol 1986;39:366-70.  Back to cited text no. 5
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Genta RM. Dysregulation of strongyloidiasis: A new hypothesis. Clin Microbiol Rev 1992;5:345-55.  Back to cited text no. 6
    
7.
Repetto SA, Durán PA, Lasala MB, González-Cappa SM. High rate of strongyloidosis infection, out of endemic area, in patients with eosinophilia and without risk of exogenous reinfections. Am J Trop Med Hyg 2010;82:1088-93.   Back to cited text no. 7
    
8.
Siddiqui AA, Berk SL. Diagnosis of strongyloides stercoralis infection. Can Infect Dis 2001;33:1040-7.  Back to cited text no. 8
    
9.
Uparanukraw P, Phongsri S, Morakote N. Fluctuations of larval excretion in strongyloides stercoralis infection. Am J Trop Med Hyg 1999;60:967-73.  Back to cited text no. 9
    
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Kitchen LW. Case studies in international medicine. Am Fam Physician 1999;59:3040-4.  Back to cited text no. 10
    
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Kim J, Joo HS, Kim DH, Lim H, Kang YH, Kim MS. A case of gastric strongyloiasis in a Korean patient. Korean J Parasitol 2003;41:63-7.   Back to cited text no. 11
    
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Buonfrate D, Requena-Mendez A, Angheben A, Muñoz J, Gobbi F, Van Den Ende J, et al. Severe strongyloidiasis: A systematic review of case reports. BMC Infect Dis 2013;13:78.   Back to cited text no. 12
    
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Hunter CJ, Petrosyan M, Asch M. Dissemination of Strongyloides stercoralis in a patient with systemic lupus erythematosus after initiation of albendazole: A case report. J Med Case Rep 2008;2:156-8.  Back to cited text no. 13
    
14.
Guzzo CA, Furtek CI, Porras AG, Chen C, Tipping R, Clineschmidt CM, et al. Safety, tolerability and pharmacokinetics of escalating high doses of ivermectin in healthy adult subjects. J Clin Pharmacol 2002;42: 1122-33.  Back to cited text no. 14
    
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Leung V, Al-Rawahi GN, Grant J, Fleckenstein L, Bowie W. Case report: Failure of subcutaneous ivermectin in treating Strongyloides hyperinfection. Am J Trop Med Hyg 2008;79:853-5.  Back to cited text no. 15
    


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