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Varicella-associated Colitis in a 6-Month-Old Infant

Eren, Makbule*; Eren, Serdar; Aydýn, Özgür; Arýkan, Serap§

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Journal of Pediatric Gastroenterology and Nutrition: November 2006 - Volume 43 - Issue 5 - p 688-690
doi: 10.1097/01.mpg.0000228108.75993.60
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Chickenpox, the primary infection of varicella zoster virus, is a common and highly contagious childhood illness among immunocompetent children. Although generally self-limited, the infection usually presents with generalized, pruritic, vesicular rash over the trunk and face, fever and systemic symptoms. Sometimes mucosal and conjunctival vesicles may exist. The disease can be more severe in adolescents, adults and immunocompromised patients. Typically, the infection remains cutaneous, although visceral involvement has been described especially in immunocompromised patients.

So far, varicella has been associated with colitis in a few situations: as a triggering infection of ulcerative colitis, while on immunosuppressive therapy with steroids and azathioprine in ulcerative colitis, and during zona zoster on the corresponding dermatome (1–5). However, to our best knowledge, colonic involvement has not been documented during primary infection.

Here we report varicella-associated colitis in an immunocompetent 6-month-old infant without oral mucosal involvement and treated successfully with oral acyclovir.


A well-developed and previously healthy 6-month-old male infant was brought to the hospital with a complaint of bloody diarrhea. He was term delivered on cesarean section weighing 3100 g. A typical vesicular rash had spread across the patient's whole body. His oral mucosa was free of these vesicular lesions. Laboratory tests revealed hemoglobin of 9.7 g/dL; white blood cell count, 7700/μL; platelet count, 267,000/μL; increased erythrocyte sedimentation rate, 46 mm/h and C-reactive protein level, 10.8 mg/mL. Lymphocytes and erythrocytes were noticed on direct microscopic fecal examination. With typical vesicular rash, the patient was diagnosed with chickenpox, although there was no history of household contacts. The diagnosis was further confirmed with positive results of varicella-specific immunoglobulin (Ig) G and IgM. His mother did not have any varicella contact during pregnancy, and her serological investigation for varicella revealed previous infection (positive for varicella-specific IgG but negative for IgM).

Colonoscopy was performed to evaluate bloody diarrhea, and several vesicular eruptions and nodular structures were noted on the colonic mucosa until the splenic flexure (Fig. 1A, B). Histopathological evaluation of these eruptions and nodular structures revealed colitis with lymphoplasmocyte and neutrophil infiltration in the lamina propria and crypt epithelium, respectively. After acyclovir treatment, orally 30 mg/kg/day, 3 times per day, for 10 days, skin lesions crusted over, and control colonoscopy revealed obvious regression of the previously detected blisters and nodules (Fig. 2). Also histopathologically, regression of the colitis was observed.

FIG. 1
FIG. 1:
Vesicular eruptions (A) and nodular structures (B) on the colonic mucosa at splenic flexura before acyclovir treatment.
FIG. 2
FIG. 2:
Regression of the previously detected blisters and nodules after acyclovir treatment.


Although most healthy children have self-limited primary varicella infection, immunocompromised patients with either primary or recurrent infection, infants, adolescents and patients receiving systemic corticosteroids may experience more severe and complicated disease. Gastric and esophageal involvement has been described in an immunocompromised patient (6). Here we reported a case of colitis during primary varicella infection, in an immunocompetent infant, presenting with bloody diarrhea in the early stage of cutaneous vesicular rash without oral mucosal involvement. Chickenpox is a clinical diagnosis based on the typical morphology and distribution of the skin lesion. Confirmation can be obtained by culture or immunofluorescence staining of the vesicular scrapings, polymerase chain reaction and serology. Detection of the virus DNA by polymerase chain reaction has been reported to be superior to other methods (7). Serology supports the diagnosis only in 48% of cases. Histopathologically, varicella infection is characterized with acidophilic inclusion bodies in the nuclei (6). Although we could demonstrate neither these inclusion bodies nor the virus DNA, regression of visible colonic blisters and histopathological findings with acyclovir treatment parallel to the regression of skin eruptions may confirm the varicella association of colitis.

To date, varicella colitis has been described in patients on immunosuppressive therapy for various reasons (1–5). Okimura et al. (4) reported zona zoster and colitis on related dermatome in a 58-year-old adult, but colitis during primary infection was not described.

On the other hand, varicella has been reported to be one of the triggering infectious agents of inflammatory bowel disease (IBD) (5). Thus, the colitis of our patient could be directly caused by the virus or a new appearing IBD. However, because it resolved while the vesicules crusted over, it is unlikely that the patient had IBD.

Neonates, immunocompromised adults and children with complicated disease are recommended to be treated with intravenous acyclovir, 10-mg/kg dose, every 8 hours for 5 to 10 days (8–10). To date, there has been no report on the treatment of varicella-induced colitis in an immunocompetent child. Because the patient was a well infant, we preferred oral acyclovir and succeeded.

In conclusion, colitis can be one of the presenting signs during primary infection of varicella, and treatment with oral acyclovir seems to be enough in such an immunocompetent well infant.


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© 2006 Lippincott Williams & Wilkins, Inc.