|Year : 2019 | Volume
| Issue : 2 | Page : 143-146
Strongyloides stercoralis hyperinfection masquerading as chronic obstructive pulmonary disease: A case report
Narasimhulu Koyalagundla, Vidyasagar Kekathi, Syfulla Shariff, Sharfraz Ahamed Mohammed, Rajendra Naik Banavath
Department of Medicine, Kurnool Medical College, Kurnool, Andhra Pradesh, India
|Date of Submission||25-Feb-2019|
|Date of Acceptance||26-Mar-2019|
|Date of Web Publication||30-Jul-2019|
Dr. Vidyasagar Kekathi
Flat No: 207, Dheeraj Enclave, Sapthagiri Nagar, Kurnool - 518002, Andhra Pradesh
Source of Support: None, Conflict of Interest: None
Strongyloides stercoralis is a soil-transmitted helminth. Infection in human beings may be asymptomatic in immunocompetent individuals or cause life-threatening symptoms in immunocompromised individuals. We present a case of S. stercoralis in an immunocompetent individual who was misdiagnosed as obstructive airway disease.
Keywords: COPD, corticosteroids, hyperinfection, Strongyloides, strongyloidiasis
|How to cite this article:|
Koyalagundla N, Kekathi V, Shariff S, Mohammed SA, Banavath RN. Strongyloides stercoralis hyperinfection masquerading as chronic obstructive pulmonary disease: A case report. J NTR Univ Health Sci 2019;8:143-6
|How to cite this URL:|
Koyalagundla N, Kekathi V, Shariff S, Mohammed SA, Banavath RN. Strongyloides stercoralis hyperinfection masquerading as chronic obstructive pulmonary disease: A case report. J NTR Univ Health Sci [serial online] 2019 [cited 2019 Aug 25];8:143-6. Available from: http://www.jdrntruhs.org/text.asp?2019/8/2/143/263635
| Introduction|| |
Strongyloides stercoralis is a geohelminth nematode worm with worldwide distribution, especially prevalent in tropical climates such as South America, Africa, and Southeast Asia. Estimates are unreliable due to difficulties in diagnosing infection. In recent years, its incidence is increasing and has become a major problem in immunosuppressive individuals.
Larval forms enter the human body through skin, reach the lungs via systemic circulation, from where they ascend airways, and are swallowed finally settling in the small intestine. Strongyloides usually cause asymptomatic infection in immunocompetent individuals.
| Case Report|| |
A 55-year-old male presented with complaints of high-grade fever, cough, and breathlessness for 3 days, and vomiting since 3 days. He had similar complaints for around 1 year for which he used to take over-the-counter drugs for his symptoms and frequent hospitalizations.
He was diagnosed as having chronic obstructive pulmonary disease (COPD) about a year back before the presenting complaints and was on increasing doses of oral bronchodilator therapy and oral corticosteroids but not as a smoker and alcoholic. Family history is not significant.
On examination, he had herpes labialis and cushingoid appearance [Figure 1]. Respiratory system revealed bilateral fine crepitations with occasional wheeze. Other systems were normal.
His blood investigations revealed Hb – 12.8 g/dl, WBC – 15,700, and platelet count of 2.2 lakhs/mm 3. His total eosinophil count was 760 and total Immunoglobulin E was 394 IU/ml, both of which were significantly elevated. Total serum protein was 5.8 g/dl, serum albumin was 3.5 g/dl, and globulin was 2.3 g/dl. His renal and hepatic functions were within normal limits.
Chest X-ray was normal. High Resolution Computerised Tomography chest showed COPD changes in both lungs with hyperinflation. Subsegmental collapse of both middle lobes and bilateral pleural thickening were other findings noted in CT. Pulmonary Function Test revealed obstructive pattern. 2D ECHO was normal. Ultrasound abdomen revealed no major pathology.
Upper GastroIntestinal Endoscopy was done in view of prolonged history of vomiting, which revealed multiple scattered white spots with diffuse prominent villi in duodenum [Figure 2]. Histopathological examination [Figure 3] and [Figure 4] showed focal cryptitis with the increase in intraepithelial lymphocytes. Crypts and surface lining epithelium show filariform larva and eggs. Lamina propria shows lymphoplasmacytic cell, neutrophilic infiltrate, and markedly increased eosinophils. These histological features were in favor of strongloidiasis.
|Figure 3: Low-power view of biopsied material from duodenum showing cryptitis and crypt infiltration with eosinophils and lymphoplasmacytic cells|
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|Figure 4: High-power microscopy showing larval form embedded within small bowel villi|
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Bronchoscopy was done for obtaining bronchoalveolar lavage (BAL) samples and to look for lung lesions. Sputum sample was examined for Strongyloides and Acid Fast Bacilli, which was negative. BAL fluid was sent for examination, which was normal. Multiple stool samples were sent for examination, which revealed a normal study. Colonoscopy was done to rule out ileocecal junction lesion common in reinfection, which was normal.
| Discussion|| |
Strongyloidiasis is a disease mostly caused by nematode worm S. stercoralis and to a lesser extent by Strongyloides fulleborni kellyi. The clinical consequences of infection range from asymptomatic disease to life-threatening disseminated disease. It has a worldwide distribution, especially prevalent tropics. Estimates of global prevalence are probably unreliable due to difficulties in diagnosing infection. In recent years, it has become a serious problem in individuals who are on suppressive treatment. It has two forms: one parasitic and the other free living. There are three developmental forms: adult, rhabditiform larva, and filariform (infective) larva. The life cycle is complex  and involves two stages in which reproduction takes place: an internal sexual cycle involving parasitic worms and the external sexual cycle involving free-living worms.
Under unsuitable environmental conditions, the external sexual cycle may be omitted and autoinfection may occur. In the external sexual cycle, the free-living rhabditiform larvae develop into free-living adults, which copulate in the soil and produce eggs.
Infection, acquired originally from contaminated soil via free-living filariform infective larvae, begins with the entry of the infective larvae into the skin. The larvae migrate into cutaneous blood vessels and are carried to the lungs. In the lungs, they enter the alveoli and pass up the respiratory tree, where they may be delayed by the host response, become adults, and invade the bronchial epithelium. At times, filariform larvae fail to break out of the alveoli, gain access to the general circulation, and can invade the brain, intestine, lymph glands, liver, lungs, and, rarely, myocardium.
Autoinfection can arise in one of two ways: in the first way, the filariform larvae do not pass out in the stools but reinvade the bowel or skin (external autoinfection); the other way is when the filariform larvae lodge in the bronchial epithelium and produce further progeny (internal autoinfection). It results in the intermittent recurrence of symptomatic episodes. In the case of any breakdown in the immune defenses, a rapid increase in the worm burden results in hyperinfection.
Immunity is both antibody- and cell-mediated. Humoral antibody-mediated immunity is elicited by the secretions of infective larvae with a Type I response, an eosinophilic tissue response, and a peripheral eosinophilia – often with urticarial rashes. Antibodies are produced which cross-react with many other helminths, including filariae. Cell-mediated immunity is elicited by an adult and larval worms in the tissues, which are localized and destroyed by a cell-mediated granulomatous reaction. If cell-mediated immunity is depressed for any reason, such as immunodepressive states of steroids, then a generalized hyperinfection results, causing massive strongyloidiasis. Among persons coinfected with human T-cell lymphotropic virus type 1, production of IFN-γ may decrease the production of antibodies that participate in the host immune response defense mechanism against infection.
The prepatent period from infection to the appearance of rhabditiform larvae in the stools is 1 month. The vast majority of infections in endemic areas are symptomless. Larvae are first detected in the stools 27 days after infection.
Most of the patients who develop hyperinfection syndrome are receiving corticosteroids often for COPD. Pulmonary strongyloidiasis may mimic COPD exacerbation. Hyperinfection may develop as early as 20 days after the onset of corticosteroid therapy and as late as several years.,,
Definitive diagnosis of strongyloidiasis is usually made on the basis of detection of larvae in stool or sputum. However, relying on stool studies alone for screening is inadequate. A single stool exam is said to be approximately 50% sensitive for making the diagnosis. The blood agar plate culture method, in which the serpiginous tracks of bacterial growth along the paths of motile larvae become apparent after 1 or 2 days of incubation at room temperature, is a preferred method because of its high sensitivity and ease of implementation in standard microbiology laboratories., Serologic testing is now widely available and is sensitive but not specific. A single test does not reliably distinguish past from current infection., Monitoring the response to treatment could be very difficult with detection of strongyloid larvae in the stool specimen because of the inconsistent shedding of the larvae.,,
We treated our patient with ivermectin two doses 1 week apart, antibiotics and tapered steroids, and bronchodilators were given for symptomatic relief. Ivermectin is preferred over albendazole for treatment because of rapid clearance rates of parasite. Patient symptoms subsided and general condition improved along with clearance of duodenal lesions [Figure 5].
| Conclusion|| |
The purpose of presenting this case is to report an underreported common geohelminthic hyper infection masquerading as COPD and gastroenteritis. The authors would like to recommend work up for Strongyloides infection if patients present with steroid-resistant COPD or worsening of symptoms with steroids.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
The authors thank Department of Gastroenterology and Department of Pulmonary Medicine, Kurnool Medical College for their kind support.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]