An adenovirus type F41 outbreak in a pediatric bone marrow transplant unit: analysis of clinical impact and preventive strategies.
BACKGROUND
Adenovirus (HAdV) was identified in blood and stool specimens from 6 children on a pediatric bone marrow transplant (BMT) unit within 2 weeks. Two further adenovirus positive patients were identified in other areas of the childrens' hospital. The study aimed to determine the clinical course of different HAdV subtypes and to investigate whether the cluster was caused by nosocomial transmission or by endogenous reactivation.


METHODS
Descriptive epidemiologic investigation was performed reviewing patients' charts. Molecular typing of identified adenovirus-DNA was performed by partial sequencing of the hexon gene.


RESULTS
In 6 of 8 patients, HAdV-F41 was detected in feces. All but 1 patient presented with vomiting or diarrhea and all were treated with cidofovir. In 4 patients transmissions of HAdV-F41 within the hematological department were probable whereas 2 children on the BMT ward reactivated HAdV-C1 and -C2, respectively. HAdV-F41 was shed in feces for up to 64 days after onset of clinical symptoms. HAdV-F41 DNA in blood reached a maximum of 2 x 10(5) copies/mL. One patient harbored two HAdV types simultaneously, HAdV-F41 in feces and HAdV-C2 in blood samples. HAdV-C2 reached high virus concentrations in blood (4 x 10(9) copies/mL) and led to the only fatal case. Although the HAdV-F41 outbreak involving 6 children led to gastroenteritis and may also have been associated with mild hepatitis, coincidental, endogeneous reactivations of other HAdV types (C1 and C2) led to a more severe course.


CONCLUSIONS
HAdV typing is essential both for the prognosis and for distinguishing between transmission or endogenous reactivation. Applying HAdV-specific infection control measures is crucial to prevent transmission.
Mattner
Frauke
F
Medizinische Mikrobiologie und Hygiene, Universitätsklinikum Schleswig-Holstein, Campus Lübeck, Lübeck, Germany. frauke.mattner@uk-sh.de
Sykora
Karl-Walter
KW
Meissner
Barbara
B
Heim
Albert
A
D000256:Adenoviridae / Q000145:classification / Q000235:genetics / Q000302:isolation & purification*; D000257:Adenoviridae Infections / Q000453:epidemiology* / Q000503:physiopathology / Q000517:prevention & control / Q000821:virology*; D000293:Adolescent; D000998:Antiviral Agents / Q000627:therapeutic use; D001769:Blood / Q000821:virology; D016026:Bone Marrow Transplantation / Q000009:adverse effects; D036022:Capsid Proteins / Q000235:genetics; D002648:Child; D002675:Child, Preschool; D000077404:Cidofovir; D003428:Cross Infection / Q000453:epidemiology* / Q000503:physiopathology / Q000517:prevention & control / Q000821:virology*; D003596:Cytosine / Q000031:analogs & derivatives / Q000627:therapeutic use; D004279:DNA, Viral / Q000737:chemistry / Q000235:genetics; D004196:Disease Outbreaks; D005243:Feces / Q000821:virology; D005759:Gastroenteritis / Q000821:virology; D005838:Genotype; D005858:Germany / Q000453:epidemiology; D006525:Hepatitis, Viral, Human / Q000821:virology; D006801:Humans; D007223:Infant; D063065:Organophosphonates / Q000627:therapeutic use; D017422:Sequence Analysis, DNA; D019562:Viral Load; D014766:Viremia; D017201:Virus Shedding
D000998:Antiviral Agents; D036022:Capsid Proteins; D004279:DNA, Viral; D063065:Organophosphonates; C018315:hexon capsid protein, Adenovirus; D003596:Cytosine; D000077404:Cidofovir