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|Year : 2012 | Volume
| Issue : 2 | Page : 160
A case of Cryptosporidium infection in a child of celiac disease
N Pal, R Sharma, B Sharma, R Suman
Department of Microbiology, SMS Medical College, Jaipur, Rajasthan, India
|Date of Web Publication||14-Jun-2012|
Department of Microbiology, SMS Medical College, Jaipur, Rajasthan
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Pal N, Sharma R, Sharma B, Suman R. A case of Cryptosporidium infection in a child of celiac disease. J Postgrad Med 2012;58:160
We report an unusual case of Cryptosporidium infection in a child of celiac disease.
A two-year-old male child was admitted with complaints of diarrhea off and on, vomiting, abdominal distension and weight loss since four months. Patient was treated symptomatically by local physicians and was relieved of symptoms temporarily.
There was no history of antenatal, intranatal and postnatal complications. There was no family history of similar disease.
The weight of child was 8 kg (below 3 rd percentile as per NCHS standards).  Vital parameters were normal. Respiratory, cardiovascular, nervous system and per abdominal examination was normal.
Laboratory investigations revealed: lymphocytosis (52.1%); hemoglobin 8 g/dl; low serum iron (43.0 g/dl); intermediate serum folic acid (4.63 ng/ml); decreased serum vitamin B12 (127 pg/ml); increased tissue transglutaminase IgA -120.8 U/ml (cutoff > 100 U). Serum electrolytes were within normal limits. Non-reactive for HIV 1 and 2 antibodies. Sonography of abdomen revealed distended bowel. Duodenal biopsy showed partial villous atrophy, increased number of lymphocytes, plasma cells and few neutrophils in lamina propria.
Patient's stool sample on gross examination was yellowish, frothy, semisolid and with mucous. Microscopic examination of stool showed: WBC - 2-3/HPF, presence of mucous with no RBC, and fat globules. Stool smear was prepared by formalin-ether concentration method and stained by modified Ziehl Neelsen method. Smear showed 2-6 μm oval acid-fast oocysts of Cryptosporidium.  No pathogenic bacteria were isolated on culture of stool.
Reports of tTGA and duodenal biopsy confirmed diagnosis of celiac disease and that of stool examination for cryptosporidiosis.
Nitazoxanide 100 mg was given for three days, there was symptomatic relief after which the patient was discharged and repeat stool examination for Cryptosporidium was negative.
Celiac disease is predominantly a disease affecting the European population (1case in every1000 live births).  In India, the true prevalence is still not known, possibly because the diagnosis is being delayed or missed. A significant increase of 15.5 cases per year from a North Indian tertiary hospital establishes that celiac disease is increasingly being recognized.  Investigations in a case study of a young child with diarrhea by Carroccio et al., showed intestinal mucosa atrophy and positive serum anti-endomysial and anti-tissue transglutaminase (anti-tTG) antibodies during intestinal giardiasis infection. After giardiasis was cured, he showed normal intestinal architecture and negative serum anti-endomysial and anti-tTG antibodies although he continued to assume a normal diet. Similarly, in our case regression of symptoms was seen after treatment of cryptosporidiosis with Nitazoxanide indicating the possibility of conversion of active celiac disease to latent disease, however, follow-up study could not be done in our case as the patient was discharged.
Cryptosporidiosis and celiac disease, both are causes of chronic diarrhea so we recommend that all patients of malabsorption should be adequately investigated for multiple etiologies, especially parasitic infections which are common in developing countries. Multicentric studies should be conducted to find out the possibility of regression of active celiac disease status to a latent celiac disease status after removal of environmental factors (like associated parasitic infections).
| :: References|| |
|1.||Ghai OP, Jain V, Sankhyan N, Agarwal R. Normal Growth and its Disorders. In: Ghai OP, Paul VK, Bagga A, editors. Ghai Essential Pediatrics. 7 th ed. New Delhi: CBS Publishers; 2009. p. 1-21. |
|2.||Laboratory methods for diagnosis of parasitic infections. In: Forbes BA, Sahm DF, Weissfeld AS, editors. Bailey and Scott's diagnostic Microbiology. 12 th ed. Missouri: Mosby, Inc.; 2007. p. 543-62. |
|3.||Sood MR. Disorders of Malabsorption. In: Behrman RE, Kliegman RM, Jenson HB, Stanton BF, editors: Nelson's Text book of Pediatrics. 18 th ed. Philadelphia: Saunders; 2008. p. 1587-602. |
|4.||Sood A, Midha V, Sood N, Kaushal V, Puri H. Increasing incidence of celiac disease in India. Am J Gastroenterol 2001;96:2804-5. |
|5.||Carroccio A, Cavataio F, Montalto G, Paparo F, Troncone R, Iacono G. Treatment of giardiasis reverses "active" celiac disease to "latent" celiac disease. Eur J Gatroenterol Hepatol 2001;13:1101-5. |