Trichuris trichiura: an unusual cause of chronic diarrhoea in a renal transplant patient

Neng-Chyan Huang, Hua-Chang Fang, Kang-Ju Chou and Hsiao-Min Chung

Division of Nephrology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung and National Yang-Min University, School of Medicine, Taipei, Taiwan

Correspondence and offprint requests to: Hsiao-Min Chung, MD, Division of Nephrology, Kaohsiung Veterans General Hospital, 386 Ta-Chung 1st Rd, Kaohsiung, Taiwan 813. Email: hmchung{at}isca.vghks.gov.tw

Keywords: renal transplant; trichuriasis; watery diarrhoea



   Introduction
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 Introduction
 Case
 Discussion
 References
 
Trichuriasis is a worldwide parasitic infection most prevalent in tropical and subtropical areas [1,2]. It is the third most common roundworm parasite in humans [1,2]. Trichuriasis is usually clinically asymptomatic. However, heavy infection, especially in small children, can cause gastrointestinal symptoms, such as abdominal pain, diarrhoea, nausea, vomiting, anorexia, constipation and chronic appendiceal syndrome [1,2]. In a cross-sectional study, the prevalence of Trichuris trichiura was 39.7% in schoolchildren in tropical areas [3]. Despite the high prevalence, it has rarely been reported as a cause of severe diarrhoea in renal allograft recipients.

In this report, we are presenting a 43-year-old renal allograft recipient who suffered from intractable watery diarrhoea and a weight loss of 17 kg over 2 months. To our knowledge, this is the first reported case of severe chronic diarrhoea caused by trichuriasis in an adult renal allograft recipient.



   Case
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 Introduction
 Case
 Discussion
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A 43-year-old renal allograft recipient was admitted to the hospital with intractable watery diarrhoea and weight loss of 17 kg in 2 months. He had received continuous ambulatory peritoneal dialysis 10 years ago due to end-stage renal disease caused by chronic glomerulonephritis. One year later, he received a renal allograft. Initially, steroids and cyclosporin were prescribed for immunosuppression. Chronic rejection was confirmed 5 years later by the examination of a graft biopsy. In the meantime, azathioprine was added to his drug regimen and substituted by mycophenolate mofetil 2 years later. His lowest serum creatinine was 2 mg/dl after transplantation. During the follow-up period, his serum creatinine increased gradually to 5 mg/dl. In addition to immunosuppressives, he was on colchicine for the treatment of gouty arthritis.

Recently, he reported having watery diarrhoea and progressive weight loss. Our initial course of action was to withdraw colchicine and to examine his stool, which was negative for occult blood. His symptoms, however, waxed and waned for 2 months and his weight declined by 17 kg. A differential count of the white blood cells showed 84% segmental neurtophils, 10% lymphocytes and 6% monocytes of but no eosinophilia. In the meantime, anaemia inappropriate for his present renal function (serum creatinine 5 mg/dl) was noted. His haemoglobulin was of 6 g/dl, the mean corpuscular volume of red blood cells was 70 fl. His serum iron was 11 mg/dl, total iron binding capacity 249 mg/dl and serum ferritin 317 ng/ml, indices that pointed to iron deficiency anaemia. Tracing back the red cell indices to before the detection of anaemia revealed that microcytosis had been present. Therefore, electrophoresis of haemoglobin was performed, and showed haemoglobin A2 at 6.3% (normal range 1.5–3.5%), indicating the presence of ß-thalassemia trait. Repeated direct wet mount examinations of stool for ova and parasites as well as routine bacterial cultures, including for Salmonella and Shigella, and an immunoassay for Clostridium difficile toxin A, all were negative. A colonoscopy revealed diffuse hyperaemic changes grossly, and the biopsy specimen showed non-specific colitis. In the absence of a recognizable pathogen, mycophenolate mofetil was discontinued. Because of persistent symptoms and a declining renal function, with an elevation of serum creatinine to 8.8 mg/dl, he had a renal biopsy, which on microscopic examination showed an acute ischaemic tubular necrosis superimposed on a chronic rejection background. The patient was given supportive treatment including i.v. fluid administration. Although the serum creatinine increased further, to 11.2 mg/dl, he responded well to volume replacement and the serum creatinine declined gradually to 6 mg/dl in 2 weeks. On the fourth direct wet mount stool examination, eggs of T.trichiura were found. Based on this finding, mebendazole was prescribed for 3 days 100 mg twice daily. The diarrhoea improved drastically; he gained appetite and his weight gradually increased over 2 months to the level normal for him. In the interval, the serum creatinine decreased to 5.7 mg/dl.



   Discussion
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 Introduction
 Case
 Discussion
 References
 
Gastrointestinal complications are common in recipients of allograft renal transplants who are on immunosuppressive therapy [4]. Diarrhoea is the most common gastrointestinal complication in the setting of renal transplantation [4]. With respect to the causes of diarrhoea, parasites are reported to be its second predominant aetiology in renal allograft recipients [4]. However, trichuriasis had not been reported before in this population.

The diagnosis delay in this patient might be due to the following causes. First, the use of colchicine and mycophenolate mofetil obviated further investigations of the causes of diarrhoea [5]. Secondly, a definite diagnosis of trichuriasis depends on the identification of barrel-shape eggs in stool [1]. They may be overlooked, however, if one does not specifically search for them; hence a thorough examination of the stool is necessary for definite diagnosis. Finally, the typical eosinophilia that accompanies parasitic infections was absent in our patient, because T.trichiura lies free in the intestinal lumen and does not penetrate into the mucosa to trigger eosinophilia [1]. Even with trichuriasis with severe bloody diarrhoea, the rectal biopsy only showed mast cells without eosinophilia [1,6]. Therefore, even in the absence of eosinophilia, some parasitic infections, like trichuriasis, should be kept in mind when dealing with patients with chronic diarrhoea.

The life cycle of T.trichiura includes maturation of eggs in the soil, and there is no autoinfection as with Strongylus stercolis [1]. People living under poor hygienic conditions are at greater risk of developing trichuriasis—including institutionalized or mentally retarded persons and children of the primary school age. In more than half the cases of severe trichuriasis, there is a history of ingestion of non-food substances such as soil and wood [1]. However, our patient had no evident predisposing conditions such as poor hygiene, a habit of eating raw or underdone food, or a history of travel to underdeveloped countries. An interesting question to be answered is whether or not immunocompromised hosts, such as renal transplant recipients, are at a greater risk of trichuriasis. Based on the life cycle of T.trichiura, renal transplant patients are not expected to be at greater risk [7]. Trichuriasis usually is asymptomatic, but may be severe in small children with heavy infections. In our patient, the ova of T.trichiura were found only on the fourth examination of stool samples. These facts in combination with the absence of poor hygiene were against the possibility of the heavy infection that could explain the severe symptoms. Side effects from colchicine and mycophenolate mofetil were logically suspected, but could not account for all the facts.

In conclusion, in renal transplant patients with chronic diarrhoea, parasitic infections should be considered in the differential diagnosis, incuding trichuriasis. Trichuriasis may cause or exacerbate microcytic anaemia especially when the parasitic burden is heavy. Based on what is known of the life cycle of T.trichiura, an immunocompromised condition is not expected to increase the risk; poor hygiene is the most important predisposing factor.

Conflict of interest statement. None declared.



   References
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 Introduction
 Case
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 References
 

  1. Tsieh Sun. Trichuriasis in Parasitic Disorders: Pathology, Diagnosis, and Management, 2nd Edn. Lippincott, Williams & Wilkins, Baltimore, MD: 1999; 185–189
  2. Wolfe MS. Oxyuris, trichostrongylus and trichuris. Clin Gastroenterol 1978; 7:201–217[ISI][Medline]
  3. Albonico M, Ramsan M, Wright V et al. Soil-transmitted nematode infections and Mebendazole treatment in Mafia Island schoolchildren. Ann Trop Med Parasitol 2002; 96:717–726[CrossRef][ISI][Medline]
  4. Kathuria P, Sakhuja V, Gupta KL et al. Gastrointestinal complications after renal transplantation. 10 year data from a North Indian Transplant Center. ASAIO J 1995; 41: M698–703[Medline]
  5. Gonwa TA. Mycophenolate mofetil for maintenance therapy in kidney transplantation. Clin Transplant 1996; 10:128–130[ISI][Medline]
  6. Liu LX, Weller PF. Intestinal nematodes. In: Fauci AS, Braunwald E, Isselbacher KJ et al. (eds), Harrion’s Principles of Internal Medicine, 14th edn. McGraw-Hill, New York, NY: 1998; 1208–1212
  7. Fontanet AL, Sahlu T, Rinke de Wit T et al. Epidemiology of infection with intestinal parasites and human immunodeficiency virus (HIV) among sugar-estate residents in Ethiopia. Ann Trop Med Parasitol 2000; 94:269–278[CrossRef][ISI][Medline]
Received for publication: 3. 1.03
Accepted in revised form: 9. 4.03





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