Published online January 4, 2006
PEDIATRICS
Vol. 117
No. 1
January 2006, pp.
224-226
(doi:10.1542/peds.2005-0177)
Secondary Bacteremia After Rotavirus Gastroenteritis in Infancy
Alexander Lowenthal, MD, MSca,
Gilat Livni, MDa,b,c,
Jacob Amir, MDb,d,
Zmira Samra, PhDe and
Shai Ashkenazi, MD, MSca,b,c
a Departments of Pediatrics A
d C
b Unit of Infectious Diseases, Schneider Children’s Medical Center of Israel, Petach Tikva, Israel
e Department of Clinical Microbiology, Rabin Medical Center, Petach Tikva, Israel
c Felsenstein Medical Research Center, Petach Tikva, Israel
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ABSTRACT
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We describe 1 neonate and 3 infants with bacteremia secondary to rotavirus gastroenteritis. All had a typical course of an increase in temperature several days after admission. The causative organisms were Enterobacter cloacae and Klebsiella pneumoniae, both normal commensals of the small intestine. Pediatricians should be aware of this complication.
Key Words: diarrhea • neonates • infants • Klebsiella spp • Enterobacter spp
Rotavirus is a major cause of infantile gastroenteritis, with an annual incidence of 
130 million cases and 440000 deaths.1 The disease is usually self-limited in otherwise healthy infants. Damage to the small intestine during rotavirus gastroenteritis is well documented. In humans, this includes columnar-to-cuboidal epithelial metaplasia, resulting in shortening and stunting of the villi, and denudation of the enterocytes in the villous tips.2 In animals, villous ischemia has been observed also, presumably because of virus-induced release of a vasoactive agent from infected epithelium, resulting in functional enterocyte damage.3 Despite these changes and the abundant endogenous bacterial flora in the small intestine,4 secondary bacteremia caused by enteric organisms after rotavirus gastroenteritis has not been reported.
Here we describe 4 cases of bacteremia secondary to rotavirus gastroenteritis diagnosed over a 2-year period. Our objectives are to alert physicians to this complication and to infer that damage to the gut mucosa occurring during rotavirus gastroenteritis enables enteric bacteria to invade the bloodstream, especially in neonates and infants.
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PATIENTS AND METHODS
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Inclusion Criteria
Our stringent inclusion criteria for these cases were (1) previously healthy state without underlying immunodeficiency or bowel disorder, (2) either absence of fever or presence of fever with a negative blood culture, negative stool culture, and positive fecal rotavirus antigen assay at admission, and (3) no evidence of phlebitis or other source of fever, negative urine culture, and positive blood culture for an enteric nondiarrheogenic bacterium at occurrence of bacteremia.
Microbiologic Examinations
Organism identification and antibiotic susceptibility by the disk-diffusion method were performed according to the National Committee for Clinical Laboratory Standards5 with the appropriate media and control strains. Stool specimens were cultured on Salmonella-Shigella agar, Campylobacter agar, and selenite broth and examined for rotavirus and adenovirus antigens by Rota/Adeno Combistick (Novamed, Jerusalem, Israel). For culture, venous blood was inoculated into pediatric bottles (Soybean Casein Digest Broth, Johnson Laboratory, Towson, MD) and processed with Bactec-9240 (BD, Franklin Lakes, NJ).
Patients
Patient 1 was referred because of vomiting, diarrhea, and fever for 4 days (Table 1). Physical examination disclosed a febrile infant with moderate dehydration. Stool was free of blood and mucus. Blood count, blood chemistry, and venous blood gases were within normal ranges except for mild metabolic acidosis. Three days after admission, fever rose to 40°C and blood culture yielded Enterobacter cloacae. Treatment with ceftriaxone (50 mg/kg) was initiated, and the child recovered quickly.
Patient 2 was referred because of vomiting, diarrhea, and fever starting 1 day before admission. Physical examination disclosed a febrile infant with moderate dehydration. Neither blood nor mucus was observed in the stool. Initial laboratory data revealed no leukocytosis, mild hyponatremia, and mildly elevated liver transaminases. Two days later, after initial improvement, fever rose to 39.5°C. Two blood cultures grew E cloacae within 36 to 44 hours, rendering the possibility of contamination unlikely. When culture results were received, the child was afebrile and recovered without antibiotic therapy.
Patient 3 was referred because of loss of appetite and diarrhea. Physical examination disclosed mild dehydration and mild jaundice. Stool was negative for blood or mucus and positive for rotavirus antigen. Initial laboratory data revealed no leukocytosis, normal electrolytes, elevated bilirubin (12 mg/dL, all indirect), and normal venous blood gases. Three days after admission, fever rose to 38.2°C. Blood, cerebrospinal fluid, and urine cultures were obtained, and only the blood culture yielded Klebsiella pneumoniae. Gentamicin (5 mg/kg) was administered for 7 days followed by cefixime (8 mg/kg) for another 3 days, with complete recovery.
Patient 4 was admitted for vomiting and apathy. Physical examination was unremarkable. Intussusception was initially suspected and excluded by abdominal ultrasound. The following day, diarrhea appeared with positive fecal rotavirus antigen. Two days later, fever rose to 39.3°C and blood culture grew E cloacae. Ceftazidime was administered with uneventful recovery.
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DISCUSSION
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We describe 1 neonate and 3 infants with confirmed rotavirus gastroenteritis complicated by secondary bacteremia. The hallmark of these events was an increase in body temperature (either recrudescence of fever or new-onset fever in previously afebrile infants) several days after admission for rotavirus gastroenteritis. This clinical course, with no apparent source of the fever, prompted us to obtain blood cultures, leading to the diagnoses. This clinical course is typical of secondary bacterial complications of other viral infections such as varicella or viral respiratory infections.
To our knowledge, these are the first descriptions of secondary bacteremia complicating rotavirus gastroenteritis. Although this complication is apparently rare, the lack of descriptions is probably also related to unawareness of this complication and failure to obtain blood cultures later in the course of rotavirus gastroenteritis.
E cloacae and K pneumoniae, members of the Enterobacteriaceae family, are normal commensals of the human intestine.4 These facultative anaerobes are distributed ubiquitously throughout most of the gut, including the small intestine, as opposed to obligatory anaerobes, which usually are confined to the colon.4 It therefore is conceivable that the mucosal damage during rotavirus infection2,3 may be sufficient to allow bacterial translocation, leading to secondary bacteremia, notably in the relatively vulnerable intestinal wall of young infants.
Bacteremia following bacterial gastroenteritis is well documented. Shigella and nontyphoidal Salmonella bacteremia were detected in 1% to 5% and 6%, respectively, of patients with the corresponding gastroenteritis in whom blood cultures were taken systematically.6,7 Bacteremia occurred more commonly in malnourished or immunocompromised patients and in neonates and young infants.6–8 Moreover, secondary bacteremia by organisms of the normal intestinal flora, such as coliforms9 and Klebsiella species,10 has been described following shigellosis. In these cases, as in ours, initial blood cultures were sterile, indicating that the bacterial translocation induced by the damage to intestinal mucosa occurred later in the course of the disease.
Pediatricians should be alert to this rare but potentially serious complication of rotavirus gastroenteritis. Thus, when a second peak of fever with no obvious source occurs in infants with rotavirus gastroenteritis, blood cultures should be obtained and empiric antibiotic therapy should be considered pending the culture results. We hope that this routine of obtaining blood cultures will lead to similar experience and reports from other locations.
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FOOTNOTES
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Accepted Apr 8, 2005.
Address correspondence to Shai Ashkenazi, MD, MSc, Department of Pediatrics A, Schneider Children’s Medical Center of Israel, 14 Kaplan St, Petach Tikva 49202, Israel. E-mail: sashkenazi{at}clalit.org.il or ashai{at}post.tau.ac.il
The authors have indicated they have no financial relationships relevant to this article to disclose.
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