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 Table of Contents  
CASE REPORT
Year : 2016  |  Volume : 3  |  Issue : 4  |  Page : 295-297

Atypical fulminant presentation of amebiasis in chronic kidney disease patient on maintenance hemodialysis


1 Department of Nephrology, Christian Medical College and Hospital, Ludhiana, Punjab, India
2 Department of Pathology, Christian Medical College and Hospital, Ludhiana, Punjab, India

Date of Web Publication14-Sep-2016

Correspondence Address:
Dr. Manmeet Singh Jhawar
Department of Nephrology, Christian Medical College and Hospital, Ludhiana, Punjab
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2348-3334.190583

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  Abstract 

Amebiasis is a common cause of dysentery in India and can have an atypical fulminant course with negative serological tests in immunosuppressed individuals such as chronic kidney disease (CKD). We present a patient of CKD on dialysis who presented with features of dysentery with negative blood and serology workup. The diagnosis of amebic colitis was made after colonoscopy and histopathology which revealed amebic trophozoites and her symptoms abated after appropriate therapy. This case report illustrates the need for colonoscopy and histopathology for definite diagnosis of fulminant presentation of amebic colitis in an immunosuppressed individual such as CKD.

Keywords: Amebiasis, atypical fulminant colitis, chronic kidney disease


How to cite this article:
Jhawar MS, Das J, George P, Kwatra KS. Atypical fulminant presentation of amebiasis in chronic kidney disease patient on maintenance hemodialysis. CHRISMED J Health Res 2016;3:295-7

How to cite this URL:
Jhawar MS, Das J, George P, Kwatra KS. Atypical fulminant presentation of amebiasis in chronic kidney disease patient on maintenance hemodialysis. CHRISMED J Health Res [serial online] 2016 [cited 2019 Nov 20];3:295-7. Available from: http://www.cjhr.org/text.asp?2016/3/4/295/190583


  Introduction Top


Amebiasis is a common cause of dysentery in India. Chronic kidney disease (CKD) patients due to their inherent immunosuppressed state do not mount a good immune response, and thus, may present as fulminant disease with atypical presentation with negative serological tests. Colonoscopy with histopathology is important to establish a diagnosis of amebiasis in this setting so as to institute appropriate therapy.


  Case Report Top


A 63-year-old female, CKD on maintenance hemodialysis developed diffuse abdominal pain with fresh bleeding in stools, hemoglobin dropped from 10.9 g/dl to 6.4 g/dl, and coagulation profile was normal (platelets – 1.51 lac, prothrombin time-international normalized ratio – 1.16, activated partial thromboplastin time - 27.3/27.9–32.7). Stool culture, clostridium deficile toxin, amebic serology, and blood culture were negative. Ultrasound abdomen showed thickened bowel loops. Colonoscopy [Figure 1] revealed discrete medium to a large ulcer in the entire colon, normal intervening mucosa, and bulky ileocecal valve with ulcerations. A differential diagnosis of inflammatory bowel disease versus amebic colitis was kept and she was empirically started on metronidazole and mesalamine. Histopathology [Figure 2] and [Figure 3] revealed extensive areas of ulceration with acute inflammatory exudates and amebic trophozoites embedded within necrotic tissue suggestive of amebic colitis. Mesalamine was stopped; metronidazole was continued followed by luminal agents. She improved clinically with complete resolution of signs and symptoms.
Figure 1: Discrete ulcers, intervening normal mucosa, bulky ileo-cecal valve with ulcerations

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Figure 2: Amebic trophozoites (black arrows) within necrotic tissue surrounded by a clear halo. Some of them show ingested RBCæs (H and E, ×400)

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Figure 3: Periodic acid-Schiff stain highlights the trophozoites of amoeba (black arrows)

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  Discussion Top


Entamoeba histolytica is the cause of amebiasis (amebic colitis), a protozoan disease, affecting large intestine, 40–50 million symptomatic cases reported annually worldwide.[1] Poor sanitation leads to transmission of protozoan to humans through water contaminated with feces.[2]

Amebic colitis presents typically with weight loss, cramping abdominal pain, and bloody diarrhea for the duration of up to several weeks. Penetration of intestinal mucous layer by trophozoites results in colitis.[3]

Differential diagnosis of dysentery in this setting includes Shigella,  Salmonella More Details, Campylobacter,  Escherichia More Details coli, inflammatory bowel disease, ischemic colitis, diverticulitis, and arteriovenous malformation.[4] Antigen detection and polymerase chain reaction are specific and sensitive means to detect E. histolytica in stool.[5] In cases where stool tests for E. histolytica are negative or unavailable, colonoscopy may be helpful for diagnosis of amebic colitis.[6]

Our patient had features of dysentery with abdominal pain, stool analysis, serology was negative, and cultures were sterile. In view of negative stool tests, colonoscopy was done which revealed multiple ulcers with intervening normal mucosa.

Histopathological findings of amebic colitis range from diffuse nonspecific mucosal thickening with or without ulcerations, focal ulcerations, classic flask-shaped lesions with ulceration extending through mucosa and muscularis into submucosa and necrosis and perforation of the intestine; with or without visualization of amebae.[7] Visualization of amebae is aided by periodic acid-Schiff or immunoperoxidase and antilectin antibodies.[8]

In this patient, biopsy was diagnostic with finding of amebic trophozoites. She improved following intravenous metronidazole therapy and luminal agents. CKD patients due to their inherent immunosuppressed state do not mount a good immune response and thus, may present as a fulminant disease with atypical presentation with negative serological tests. In these settings, colonoscopy and biopsy are important for definitive diagnosis so as to institute appropriate therapy.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Petri WA Jr., Haque R, Lyerly D, Vines RR. Estimating the impact of amebiasis on health. Parasitol Today 2000;16:320-1.  Back to cited text no. 1
    
2.
Schuster FL, Visvesvara GS. Amebae and ciliated protozoa as causal agents of waterborne zoonotic disease. Vet Parasitol 2004;126:91-120.  Back to cited text no. 2
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3.
Yi D, Lee RT, Longo P, Boger ET, Lee YC, Petri WA Jr., et al. Substructural specificity and polyvalent carbohydrate recognition by the Entamoeba histolytica and rat hepatic N-acetylgalactosamine/galactose lectins. Glycobiology 1998;8:1037-43.  Back to cited text no. 3
    
4.
Haque R, Huston CD, Hughes M, Houpt E, Petri WA Jr. Amebiasis. N Engl J Med 2003;348:1565-73.  Back to cited text no. 4
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5.
Haque R, Mollah NU, Ali IK, Alam K, Eubanks A, Lyerly D, et al. Diagnosis of amebic liver abscess and intestinal infection with the TechLab Entamoeba histolytica II antigen detection and antibody tests. J Clin Microbiol 2000;38:3235-9.  Back to cited text no. 5
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6.
Stanley SL Jr. Amoebiasis. Lancet 2003;361:1025-34.  Back to cited text no. 6
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7.
Prathap K, Gilman R. The histopathology of acute intestinal amebiasis. A rectal biopsy study. Am J Pathol 1970;60:229-46.  Back to cited text no. 7
[PUBMED]    
8.
McCarthy JS, Peacock D, Trown KP, Bade P, Petri WA Jr., Currie BJ. Endemic invasive amoebiasis in Northern Australia. Med J Aust 2002;177:570.  Back to cited text no. 8
    


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  [Figure 1], [Figure 2], [Figure 3]



 

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