Citrobacter koseri_B

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Record number: 
Adverse Occurrence type: 
MPHO Type: 
Estimated frequency: 
Rare. Risk of transfusion-transmitted bacterial infection (TTBI) is 0.19 per 100,000 blood products transfused with around one fatal event each year.
Time to detection: 
Thirty minutes after transfusion.
Alerting signals, symptoms, evidence of occurrence: 
Thirty minutes after the start of the platelet concentrate transfusion, bradycardia and dyspnea appeared, quickly followed by chills, nausea, vomiting, headache, and hyperthermia. TTBI was suspected and the patient was immediately treated with intravascular antibiotics. On Day 1, 20 hours after transfusion, the patient displayed acute desaturation and chest x-rays revealed pulmonary interstitial syndrome. Patient was intubated and ventilated on day 2. On Day 3, the patient developed severe acute respiratory distress syndrome leading to death on Day 7. Cultures of the patient blood sampled on days 0, 1, and 2 were all positive for Citrobacter koseri. Typically symptoms of septic tranfusion reaction can manifest during the tranfusion, or within 24 hours afterward. Septic reaction due to PCs' transfusion is presented by clinical symptoms such as fever, shaking chills, tachycardia, hypotension, disseminated intravascular coagulation (DIC), rash, generalized pain, multiorgan failure, and finally shock and death. Furthermore, the aforementioned clinical symptoms occur not necessarily due to septic reactions; it could be caused by other diseases or noninfectious transfusion adverse reactions such as transfusion related acute lung injury (TRALI), allergic/anaphylactic reactions, hemolytic transfusion, and nosocomial infections.
Demonstration of imputability or root cause: 
C. koseri was isolated from APC culture 12 hours after the event from the few milliliters of APC remaining in the platelet bag and from patient blood cultures on days 0, 1, and 2. Cultures of samples of donor blood, stool, urine, the skin of the inside of the elbow at the point of needle insertion and ear were all negative for C. koseri, but a nasal sample was positive for C. koseri. All C. koseri isolates had the same antimicrobial susceptibility pattern as wild-type strains, had identical patterns on pulsed-field gel-electrophoresis, and had more than 95% of similarity by repetitive sequence-based polymerase chain reaction (rep-PCR).
Imputability grade: 
3 Definite/Certain/Proven
Suggest new keywords: 
TTBI, Citrobacter koseri, apheresis PLT concentrate (APC)
Suggest references: 
1) Hauser,L et al. Fatal transfusion-transmitted infection due to Citrobacter koseri. Transfusion. 2016 Jun;56(6):1311-1313. 2) Fernandes C, Oliveira MC, Jorge MT. A case report of Citrobacter koseri bacteraemia after transfusion of contaminated red cells. Transfus Med. 2012 Dec;22(6):450-1. doi: 10.1111/j.1365-3148.2012.01186.x. Epub 2012 Oct 5. PMID: 23035958. 3) Emery, A., Marpaux, N., Naegelen, C., Valot, B., Morel, P. and Hocquet, D. (2020), Genotypic study of Citrobacter koseri, an emergent platelet contaminant since 2012 in France. Transfusion, 60: 245-249. 4) Tichit R, Saumet L, Marchandin H, Haouy S, Latry P, Sirvent N. Choc septique après transfusion d'un concentré plaquettaire contaminé par Citrobacter koseri chez une patiente en aplasie fébrile post-chimiothérapie [Septic shock following platelet transfusion contaminated with Citrobacter koseri in a child with postchemotherapy febrile neutropenia]. Arch Pediatr. 2016 Jan;23(1):86-9. French. doi: 10.1016/j.arcped.2015.09.030. Epub 2015 Nov 6. PMID: 26552624. 5) Razjou F, Dabir Moghaddam A, Karimi G, Zadsar M. Platelet Septic Transfusion Reactions in Patients With Hemato-Oncological Diseases. Iran J Pathol. 2017 Spring;12(2):112-118. Epub 2017 Apr 1. PMID: 29515632; PMCID: PMC5831066.
Please note that your link to this article does NOT work, so I attached the PDF The Fernandes article is Record 998 in NOTIFY. I don't have the PDF for it. One of the references is in French only - keep it or not.
Expert comments for publication: 
C. koseri is one of many possible TTI from platelet concentrates. Emery and colleagues investigated 5 C. koseri transmissions that occurred in France between 2012-2017 and determined that there was not a particular clone of C. koseri causing the outbreak, and the reason for the presence of this organism was not able to be determined. Razjou and colleagues reported in 2017 an incidence of 0.4% of tranfusion reactions among patients with leukemia or lymphoma receiving donor platelet concentrates. Platelet concentrates are more susceptible to bacterial contamination than other blood products, thought to be largely due to storage conditions (22 degrees C), and is the greatest transfusion transmitted infectious disease risk in the United States. According to CDC, transfusion-transmitted sepsis has been recognized and culture-confirmed in at least 1 of 100,000 recipients and has led to immediate fatal outcome in 1 in 500,000 recipients. The actual risk of transfusion-associated sepsis is likely higher, as infections due to contaminated blood products are under-reported. It is critical for clinicians to be aware of the problem of bacterial contamination of blood products, particularly platelets, and to consider the possibility of bacterial contamination when investigating febrile transfusion reactions. Bacterial contamination of a blood component is not typically considered in the differential diagnosis of a transfusion-related illness because signs and symptoms (including fever, rigors, and change in blood pressure) resemble those expected from either a transfusion reaction or sepsis due to any cause. Gram-positive organisms found on skin (e.g. Staphylococcus epidermidis) are the most frequent contaminants of platelet units. Although less commonly recognized as contaminants, gram-negative bacteria (e.g., Serratia, Enterobacter, Salmonella spp.) cause more severe and often fatal infections.