A 53-year-old male from Kerala, South India presented with loose stools, which were watery in nature and without blood, three-four episodes per day for 3 weeks. He complained of vague abdominal pain on and off, decreased appetite and weight loss of 3-4 kg over 1 month. He gave no history of associated fever, vomiting, urticarial rashes, or any respiratory symptoms.
In addition to having alcohol use disorder, he was a known case of type II diabetes mellitus, hypertension and hyperlipidaemia and was on regular oral medications for the previous 2 years. He also experienced recurrent episodes of stroke, which resulted in a left-sided hemiparesis 2 years previously. He was also diagnosed as having pulmonary tuberculosis (sputum-positive), for which he had been on anti-tubercular therapy (ATT) for the previous 6 months. He denied intravenous (IV) drug abuse or any high-risk sexual behaviour. He was not on steroids or immunosuppressive drugs and gave no history of travel outside the state. He reported consumption of only cooked food and there was no food intolerance. All his family members were reported to be healthy.
He was a cattle farmer and worked barefoot on his cattle farm; he also had a shallow pond near to his home where he used to grow freshwater fish for consumption. To his knowledge there was no practice of open field human defecation in the farm area.
He was treated symptomatically at primary health care facilities and since there was no relief, he was referred to this tertiary care centre.
On clinical examination, he was not febrile and vitals were within normal limits. He had bilateral pitting pedal oedema and macular erythematous rashes over the anterior aspect of both the legs for 2 weeks, which were non-migratory in nature. Systemic examination was normal.
Routine blood investigations showed decreased haemoglobin (Hb) 9.6 %, elevated total count (TC) 13 600 cells cumm-1 with differential count (DC), polymorphs 90 %, lymphocyte 6 %, eosinophil 2 % and monocytes 2 %, an erythrocyte sedimentation rate (ESR) of 78 mm h-1, and serum electrolytes showed hypokalaemia (potassium - 2.6 meq l-1). His random blood sugar on admission was elevated (274 mg dl-1). He tested negative for viral markers of human immunodeficiency virus (HIV), hepatitis C virus (HCV) and hepatitis B virus (HBV). Ultrasonography (USG) of the abdomen showed fatty hepatomegaly with focal lesions in the liver, for which computed tomography (CT) of the abdomen and pelvis with contrast was performed. This showed several hypodense lesions involving segment 5 of the liver with mild hepatomegaly. CT of the lungs showed cavitation in the upper lobes of both lungs. Upper gastrointestinal endoscopy was performed, which was normal. Stool was sent for microscopy and bacteriological culture.
Macroscopically, the stool was watery, yellowish coloured, with no mucus or blood. Wet preparation revealed numerous motile larvae in the rhabditiform stage, which measured 100-400 microm in lengthx15-20 microm in width and had a short buccal cavity. There were a few oval shaped eggs, ~50-60x30-35 microm in size, with larvae, suggestive of S. stercoralis. There were no pus cells or red blood cells. (Fig. 1) Stool microscopy following the formal ether concentration technique did not show any additional findings. Stool microscopy was repeated with freshly collected stool samples on three separate occasions, which also demonstrated motile rhabditiform larvae of S. stercoralis (Fig. 2). In addition, agar culture method was performed to visualize the positive trail sign. Nearly 2 g of freshly passed stool was placed on an agar plate. The plate was sealed with tape and then incubated at room temperature for 2 days. The plate was later examined and showed a 'positive trail sign', that is, there were tracks present as the bacteria were carried over the agar by the migrating larvae. The agar culture method was to be repeated after therapy, if microscopy of stool did not reveal larvae, as it is a more sensitive test for assessing the elimination of the parasite.
The bacteriological culture of stool yielded Aeromonas sobria, which was sensitive to ciprofloxacin, chloramphenicol, tetracycline and cotrimoxazole. Stool occult blood (Hemospot kit, standard guaiac method, Tulip Diagnostics, Goa, India) and Clostridium difficile toxin (VIDAS difficile toxin A and B, bioMerieux SA) were negative.
Hyperinfection syndrome with disseminated strongyloidiasis, alcoholic liver disease, type 2 diabetes mellitus, hypertension, dyslipidaemia and pulmonary tuberculosis.
Therapy included blood sugar and electrolyte correction and the patient was empirically started on ciprofloxacin intravenously (IV) along with parenteral fluids and other supportive measures.
Following the stool microscopy report, a stat oral dose of a combination of albendazole 400 mg and ivermectin 6 mg, followed by once daily for 2 days, was given. The patient was continued on ciprofloxacin IV for 4 days. He showed symptomatic improvement by the second day of treatment, his stool became semisolid in consistency and the number of motile larvae in fresh stool showed an appreciable reduction. He was discharged after 4 days on mixtard insulin and oral ciprofloxacin 500 mg twice daily for 3 days.
The patient was readmitted on the third day of discharge with complaints of fever and recurrence of diarrhoea. His blood sugar value at the time of readmission was again elevated (210 mg dl-1). His total leucocyte count (TLC) was 12 000 cumm-1, with polymorphs 60 %. His blood was sent for culture and empirical therapy was initiated with injected piperacillin/tazobactam and mixtard insulin. Unfortunately, on day 2 of readmission he expired. Escherichia coli was isolated from his blood culture 3 days after his readmission, sensitive to cephalosporins, carbapenems, piperacillin/tazobactam and aminoglycosides, but resistant to ciprofloxacin, which he was discharged on for the Aeromonas infection.