|Year : 2012 | Volume
| Issue : 2 | Page : 236-239
Human intestinal capillariasis: A rare case report from non-endemic area (Andhra Pradesh, India)
PL Vasantha, N Girish, K Sai Leela
Department of Microbiology, Kamineni Institute of Medical Sciences, Narketpally, Nalgonda dt; Andhra Pradesh 508 254, India
|Date of Submission||29-Dec-2011|
|Date of Acceptance||26-Feb-2012|
|Date of Web Publication||28-May-2012|
P L Vasantha
Department of Microbiology, Kamineni Institute of Medical Sciences, Narketpally, Nalgonda dt; Andhra Pradesh 508 254
Source of Support: None, Conflict of Interest: None
Human intestinal capillariasis is caused by Capillaria philippinensis. This disease is endemic in Philippines and Thailand. To the best of our knowledge, we report the third case of human intestinal capillariasis from India and the first case from Andhra Pradesh, which is a non-endemic area. A 40-year-old female presented with diarrhoea, vomiting, decreased urinary output, ascitis, pedal oedema, hypoalbuminemia, and electrolyte imbalance. Microscopic examination of stool sample revealed the presence of ova, larvae, and adult worms of C. philippinensis. Patient recovered from the disease after taking albendazole 400 mg daily for 1 month along with supportive treatment.
Keywords: Human intestinal capillariasis, India, non-endemic area
|How to cite this article:|
Vasantha P L, Girish N, Leela K S. Human intestinal capillariasis: A rare case report from non-endemic area (Andhra Pradesh, India). Indian J Med Microbiol 2012;30:236-9
|How to cite this URL:|
Vasantha P L, Girish N, Leela K S. Human intestinal capillariasis: A rare case report from non-endemic area (Andhra Pradesh, India). Indian J Med Microbiol [serial online] 2012 [cited 2016 Jul 23];30:236-9. Available from: http://www.ijmm.org/text.asp?2012/30/2/236/96708
| ~ Introduction|| |
Human intestinal capillariasis caused by Capillaria philippinensis is an endemic disease in Philippines  and Thailand.  C. philippinensis infection is mainly acquired by ingestion of raw, undercooked, small fresh water or brackish water fish, in which larval forms of the parasite develop. This infection mainly involves small intestine (jejunum) and patients suffer from chronic diarrhoea, protein losing enteropathy, borborygmus and electrolyte loss.  If early diagnosis and treatment is not given, it can be fatal. Diagnosis is often missed in non-endemic areas because of lack of knowledge about existence of this disease. Even though sporadic cases were reported from non-endemic countries like Iran, Egypt,  Taiwan,  Japan, Indonesia, Korea, Spain  and Italy, only two cases have been reported from India. , No case was reported from Andhra Pradesh. This case of human intestinal capillariasis is the third case from India and the first case from Andhra Pradesh state.
| ~ Case Report|| |
A 40-year-old woman was admitted in the hospital with the complaints of diarrhoea (10 episodes per day) for the past 1 month and vomiting since 15 days. There was distension of abdomen and decreased urinary output, and she was having shortness of breath since 15 days. There was no clinical history of diabetes mellitus and hypertension. There was also no history of TB, epilepsy or asthma.
She was emaciated and on physical examination there was pedal oedema, ascites and puffiness of the face. BP was 90/60. Chest X-ray and ultrasonography abdomen were normal. Patient was treated with antibiotics and intravenous fluids for 2 days.
Laboratory tests revealed the following: Total protein 3.7 g/dl, albumin 0.7 g/dl, A/G ratio 0.2, total bilirubin 0.37 mg/dl, direct bilirubin 0.08 mg/dl, serum glutamic oxaloacetic transaminase (SGOT) 37 IU/l, serum glutamic pyruvic transaminase (SGPT) 45 IU/l, alkaline phosphatase 110 IU/l, serum creatinine 0.6 mg/dl, blood urea 26 mg/dl, random blood sugar 91 mg/dl, serum sodium 121 mmol/l, serum potassium 2.4 mmol/l, and serum chloride 79 mmol/l.
Complete blood picture (CBP) showed the following: Total count 6600/mm 3 , neutrophils 53%, lymphocytes 42%, eosinophils 3%, monocytes 2%, basophils 0, platelets adequate, Hb 13.2 g%, RBCs were normocytic and normochromic, erythrocyte sedimentation rate (ESR) 10 mm in the first hour, adenosine deaminase (ADA) 47.62 units/l. HIV test was nonreactive and HBsAg was negative. Ascitic fluid analysis showed the following results: Total count 40 cells/mm 3 , neutrophils 10%, lymphocytes 90%, RBC occasional, sugar 105 mg/dl, protein 0.2 g/dl and stool for occult blood was positive.
Microscopic examination of the stool sample revealed the presence of bile-stained, peanut-shaped ova, sized approximately 45 × 21 μm with flat mucous plugs at both poles [Figure 1]. Ova showed thick egg shells with radial striations [Figure 2]. They were identified as ova of C. philippinensis. Adult worms and larval forms were observed in the stool sample during treatment. Larval forms were sized approximately 250-300 μm [Figure 3] and adult worms were having sizes varying from 2 to 5 mm. Female adult worm was identified by its characteristic stichosome, which is muscular oesophagus surrounded by rows of secretory cells called stichocytes and uterus filled with eggs [Figure 4] and [Figure 5].
|Figure 1: Saline wet mount preparation of stool sample showing ovum of C. philippinensis (×1600)|
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Treatment was started with albendazole 200 mg twice daily along with fluid and electrolyte replacement, protein and multivitamin supplementation.
Microscopic examination of the stool sample after taking albendazole for 4 days revealed drastic reduction in number of ova along with appearance of dead larvae. Patient rapidly recovered from diarrhoea on the third day of treatment itself. She was treated with albendazole for 1 month. The stool sample sent on 19 th day of treatment revealed the presence of adult worms, but no ova and larvae. The stool microscopy examination done on 25 th day revealed no ova, larvae or adult worms. The patient recovered from all symptoms except pedal oedema which is due to hypoalbuminemia, requiring protein supplementation for prolonged period. The patient was discharged with advice for frequent follow-up.
|Figure 2: Ovum of C. philippinensis showing radial striations in the wall (×2400)|
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|Figure 3: Saline wet mount preparation of stool sample showing larva of C. philippinensis (×400)|
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|Figure 4: Saline wet mount preparation of stool sample showing adult female C. philippinensis (×100)|
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| ~ Discussion|| |
Human intestinal capillariasis is an endemic disease in Philippines and Thailand. Only two cases have been reported from India. No case was reported from Andhra Pradesh. The first case from India was reported by Kang et al. in 1994 from Vellore  and the second case by Rana et al. in 2009 from Chandigarh.  This is the third case report from India and the first case from Andhra Pradesh to the best of our knowledge. The first case of human intestinal capillariasis occurred in 1962 in a healthy young man from Luzon (Philippines), who subsequently died. This was first reported by Chitwood et al. in 1964 as an autopsy finding.  Sporadic cases were reported from non-endemic areas like Iran, Egypt, Taiwan, Japan, Indonesia, Korea, Spain and Italy. Epidemics occurred in Philippines during 1967 - 1968 involving 1300 persons with 90 deaths and another occurred in late 1978 and early 1979 involving 50 persons. 
C. philippinensis is a nematode belonging to class Adenophorea, subclass Enoplia, order Trichurida and family Trichinellidae.  In the life cycle of C. philippinensis, fish eating birds are natural definite hosts. Adult worms present in the intestine of birds release ova. Bird droppings along the flyways disperse these eggs into water bodies, where fish become infected. Larval forms develop in fish and it is the source of infection to man and bird. In Philippines, it is mainly Ixobrychus sinensis which is the naturally infected bird and Hypseleotris bipartite is the naturally infected fish. 
C. philippinensis infection is mainly acquired by ingestion of raw, undercooked, small fresh water or brackish water fish.  In Philippines, the traditional dish "Kilawin", which is raw fish soaked in vinegar, is the main source of infection.
The source of infection in the present case can be the fish which the patient used to eat, as there was no history of patient's travel to endemic areas. The fish could have been infected by the droppings of migratory birds from endemic areas.
The present case was having hypoalbuminemia, severe electrolyte loss, diarrhoea, ascitis and pedal oedema. This can be explained by the presence of all stages of parasite in the mucosa of intestine causing inflammation with mixed population of mononuclear and polynuclear cells and flattening of villi. This leads to severe chronic diarrhoea, protein losing enteropathy, fat malabsorption, hypoalbuminemia and loss of electrolytes. 
The severity of symptoms in this intestinal nematode infection can be explained by the autoinfection and hyperinfection, which is evident from the experimental studies done by Cross et al. in monkeys and Mongolian gerbils. In their studies, they observed that the larval forms which were introduced into the animals developed into adult male and female worms. The female worm produced first stage larvae in 13 - 14 days. These larvae developed into adult males and females in 22 - 24 days, and the second-generation female began to release thick-shelled unembryonated eggs, which passed in the faeces in 25 - 35 days post infection. Most female worms at this time were oviparous, but a few female worms always produced larvae, an event that led to autoinfection and hyperinfection. 
Simple wet mount examination of stool sample and identification of ova, larvae and adult worm in the stool sample can clinch the diagnosis. But ova of C. philippinensis need to be differentiated from those of Trichuris trichura. Ova of C. philippinensis can be identified by their peanut shape, flattened mucous plugs and striations in the wall. Adult worms vary in sizes from 2 to 5 mm. Male worms are shorter (1.5 - 3.9 mm) compared to female worms (2.3 - 5.3 mm). They are identified by their characteristic stichosome, a muscular oesophagus surrounded by rows of stichocytes. Male worms have single sheathed spicule. Female uterus contains numerous thick-shelled eggs and thin-shelled eggs with or without embryos or larvae. Larvae found in stool sample in different stages of development and hence are difficult to identify as C. philippinensis larvae. 
In this case, the patient was treated with albendazole which can act upon adult worms, larval forms and ova. Treatment was given for 1 month as prolonged treatment is necessary to cure the disease.Because of high mortality associated with the disease, early diagnosis and treatment is essential, and diagnosis is often delayed or missed due to lack of awareness of existence of this infection in non-endemic areas.
Though it is an uncommon infection in our country, there is always a chance of import of parasite through the migration of birds from endemic countries and physician should consider C. philippinensis as the aetiological agent in diagnosing diarrhoea in non-endemic areas like India. There is a need to do the epidemiological investigation or studies to know the source, transmission and prevalence of this infection in India.
| ~ Acknowledgement|| |
We thank Dr. Subhash Chandra Parija, Professor and Head of Dept. of Microbiology, JIPMER, Puducherry, India, for confirming Capillaria philippinensis
| ~ References|| |
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|5.||Dronda F, Chaves F, Sanz A, Lopez-velez R. Human intestinal capillariasis in an area of non endemicity: Case report and review. Clin Infect Dis 1993;17:909-12. |
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|8.||Chitwood MB, Valasquez C, Salazar NG. Capillaria philippinensis sp.N. (Nematoda: Trichinellida) from the intestine of man in the Phillippines. J Parasitol 1968;54:368-71. |
|9.||Cross JH, Singson CN, Battad S, Basaca-Sevilla V. Intestinal capillariasis: Epidemiology, parasitology and treatment. Proc R Soc Med Int Cong Symp Ser 1979;24:81-6. |
|10.||Cross JH, Basaca Sevilla V. Intestinal capillariasis, In: Pawalowski ZS, ed. Bailliere's clinical tropical medicine and communicable diseases. Intestinal helminthic infections. London: Bailliere Tindall; 1987. P. 735-46. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
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