Skip directly to site content Skip directly to page options Skip directly to A-Z link Skip directly to A-Z link Skip directly to A-Z link
Volume 20, Number 11—November 2014

Helicobacter cinaedi Infection of Abdominal Aortic Aneurysm, Japan

On This Page
Article Metrics
citations of this article
EID Journal Metrics on Scopus

Cite This Article

To the Editor: Infected abdominal aortic aneurysm (IAAA) is uncommon, but life-threatening; the mortality rate ranges from 25% to30% (1,2). Identification of the pathogen is essential for diagnosis and treatment. Previous studies have shown that species of the genera Salmonella, Staphylococcus, and Streptococcus are the most common pathogens associated with IAAA, but a causative organism is not identified in 14%–40% of patients (1,2). Helicobacter cinaedi has mainly been isolated from immunocompromised patients with bacteremia, cellulitis, and septic arthritis (3,4). Here, we report 3 cases of IAAA caused by H. cinaedi detected by 16S ribosomal RNA (16S rRNA) gene analysis.

The 3 patients (case-patients 1–3) were referred to Tohoku University Hospital, Sendai, Japan, for surgical treatment of IAAA in 2013. None had a history of disease known to cause immunodeficiency. Because their abdominal aneurysms enlarged rapidly, all 3 patients underwent resection of the aneurysm and extensive local debridement and irrigation. Histopathologic examination of the surgical specimens revealed severe atherosclerosis and inflammation, consistent with a diagnosis of IAAA. For each case-patient, blood culture (BacT/ALERT; bioMérieux Industry, Tokyo, Japan) was negative, as was culture of surgically removed tissue on HK semisolid agar (Kyokuto Pharmaceutical Industrial Co., Ltd., Tokyo, Japan) at 35°C under aerobic conditions for 7 days for enrichment of microorganisms, and on chocolate agar at 35°C under 5% CO2 for 48 h. We then used 16S rRNA gene analysis to identify a pathogen. We extracted DNA from resected tissues using a QIAamp DNA Mini kit (QIAGEN K.K., Tokyo, Japan), amplified it using PCR, and sequenced it using universal primers for 16S rRNA (5). We used the EzTaxon-e Database for sequence analysis (, which revealed that the 16S rRNA gene sequence of bacteria in the aneurysmal tissues was identical to that of H. cinaedi.

For case-patient 3, we cultured microaerophilic tissue at 35°C using Trypticase Soy Agar II with 5% sheep blood (Kyokuto Pharmaceutical Industrial Co.) and an Anaero Pouch-MicroAero (Mitsubishi Gas Chemical Co., Inc., Tokyo, Japan) to detect H. cinaedi. We observed bacterial colonies, after Gram staining, which showed gram-negative spiral rods. By 16S rRNA gene analysis, we confirmed that the isolate was H. cinaedi.

For each of the 3 case-patients, species identification was further confirmed by sequence analysis of 23S ribosomal RNA (23S rRNA) (DNA Data Bank of Japan: = ja) and amplification of the gyrB gene region that is specific to H. cinaedi (6,7). In samples from the 3 patients, there were mutations of the 23S rRNA gene and amino acid substitutions in GyrA related to macrolide and fluoroquinolone resistance, respectively (6,8). After identifying the pathogen, we selected antimicrobial agents based on the reported drug susceptibility profile of H. cinaedi (6,8). The patients survived and are being followed up as outpatients. Clinical and molecular characteristics of the 3 cases of IAAA with H. cinaedi infection are shown in the Table.

Although the high negative culture rate for pathogens causing IAAA had been explained by prolonged preoperative antimicrobial drug therapy (2), another possibility is that H. cinaedi may be a causative organism. Earlier research has suggested that H. cinaedi infections can remain undiagnosed or be incorrectly diagnosed because of difficulty in isolating this microorganism (9). H. cinaedi grows slowly under microaerophilic conditions, but no current standard laboratory methods result in a diagnosis of this pathogen (6,7,9). We isolated H. cinaedi from surgically removed tissue from case-patient 3 by microaerophilic culture after taking this pathogen into consideration. For diagnosis of H. cinaedi infections, methods leading to accurate identification by clinical microbiological laboratories are needed. Currently, H. cinaedi is identified by molecular analysis of the 16S rRNA gene (6,7,10). In addition, matrix-assisted laser desorption/ionization–time-of-flight mass spectrometry (MALDI-TOF MS) (10), may become a useful tool for this purpose.

Standard breakpoints of antimicrobial drugs for H. cinaedi have not been defined, but all isolates in this study had mutations that indicated resistance to macrolides and fluoroquinolones. For adequate treatment for H. cinaedi infections, guidelines for selection of antimicrobial drugs and surveillance of its antimicrobial susceptibility profile are required.

During November 2012–November 2013, 8 patients underwent their first operation for IAAA at the university hospital. We used 16S rRNA gene analysis of surgical tissues and culture of blood and tissue specimens to detect pathogens (data not shown). Identification of H. cinaedi in 3 of 8 patients suggests that it could be a prevalent pathogen related to IAAA. Taking such information into consideration could affect the prognosis of many patients. Accordingly, tissue should be cultured while considering H. cinaedi infection in patients with IAAA. H. cinaedi colonizes the gastrointestinal tract, and bacterial translocation may lead to bacteremia associated with mucosal damage (4). However, the route of transmission and reason most H. cinaedi infections have been reported in Japan are unclear. To clarify the relationship between H. cinaedi and IAAA, further clinical and epidemiologic studies are needed. Meanwhile, we recommend clinical consideration of H. cinaedi infection, use of appropriate laboratory procedures to identify cases, and development of treatment guidelines.

Dr Kakuta is an infectious disease and infection control doctor at Tohoku University Hospital, Sendai, Japan. Her research interests are clinical infectious diseases, infection control, and antimicrobial resistance.


Risako KakutaComments to Author , Hisakazu Yano, Hajime Kanamori, Takuya Shimizu, Yoshiaki Gu, Masumitsu Hatta, Tetsuji Aoyagi, Shiro Endo, Shinya Inomata, Chihiro Oe, Koichi Tokuda, Daiki Ozawa, Hitoshi Goto, Yukio Katori, and Mitsuo Kaku
Author affiliations: Tohoku University Graduate School of Medicine, Sendai, Japan



  1. Miller  DV, Oderich  GS, Aubry  MC, Panneton  JM, Edwards  WD. Surgical pathology of infected aneurysms of the descending thoracic and abdominal aorta: clinicopathologic correlations in 29 cases (1976 to 1999). Hum Pathol. 2004;35:111220. DOIPubMedGoogle Scholar
  2. Laohapensang  K, Aworn  S, Orrapi  S, Rutherford  RB. Management of the infected aortoiliac aneurysms. Ann Vasc Dis. 2012;5:334–41.
  3. Lasry  S, Simon  J, Marais  A, Pouchot  J, Vinceneux  P, Boussougant  Y. Helicobacter cinaedi septic arthritis and bacteremia in an immunocompetent patient. Clin Infect Dis. 2000;31:2012. DOIPubMedGoogle Scholar
  4. Araoka  H, Baba  M, Kimura  M, Abe  M, Inagawa  H, Yoneyama  A. Clinical characteristics of bacteremia caused by Helicobacter cinaedi and time required for blood cultures to become positive. J Clin Microbiol. 2014;52:151922. DOIPubMedGoogle Scholar
  5. Zhang  J, van Hung  P, Hayashi  M, Yoshida  S, Ohkusu  K, Ezaki  T. DnaJ sequences of Bacillus cereus strains isolated from outbreaks of hospital infection are highly similar to Bacillus anthracis. Diagn Microbiol Infect Dis. 2011;70:30715. DOIPubMedGoogle Scholar
  6. Rimbara  E, Mori  S, Matsui  M, Suzuki  S, Wachino  J, Kawamura  Y, Molecular epidemiologic analysis and antimicrobial resistance of Helicobacter cinaedi isolated from seven hospitals in Japan. J Clin Microbiol. 2012;50:255360. DOIPubMedGoogle Scholar
  7. Minauchi  K, Takahashi  S, Sakai  T, Kondo  M, Shibayama  K, Arakawa  Y, The nosocomial transmission of Helicobacter cinaedi infections in immunocompromised patients. Intern Med. 2010;49:17339. DOIPubMedGoogle Scholar
  8. Tomida  J, Oumi  A, Okamoto  T, Morita  Y, Okayama  A, Misawa  N, Comparative evaluation of agar dilution and broth microdilution methods for antibiotic susceptibility testing of Helicobacter cinaedi. Microbiol Immunol. 2013;57:3538. DOIPubMedGoogle Scholar
  9. Oyama  K, Khan  S, Okamoto  T, Fujii  S, Ono  K, Matsunaga  T, Identification of and screening for human Helicobacter cinaedi infections and carriers via nested PCR. J Clin Microbiol. 2012;50:3893900 . DOIPubMedGoogle Scholar
  10. Taniguchi  T, Sekiya  A, Higa  M, Saeki  Y, Umeki  K, Okayama  A, Rapid identification and subtyping of Helicobacter cinaedi strains by intact-cell mass spectrometry profiling with the use of matrix-assisted laser desorption ionization-time of flight mass spectrometry. J Clin Microbiol. 2014;52:95102. DOIPubMedGoogle Scholar




Cite This Article

DOI: 10.3201/eid2011.140440

Related Links


Table of Contents – Volume 20, Number 11—November 2014

EID Search Options
presentation_01 Advanced Article Search – Search articles by author and/or keyword.
presentation_01 Articles by Country Search – Search articles by the topic country.
presentation_01 Article Type Search – Search articles by article type and issue.



Please use the form below to submit correspondence to the authors or contact them at the following address:

Risako Kakuta, Department of Infection Control and Laboratory Diagnostics, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aoba-ku, Sendai 980-8574, Japan

Send To

10000 character(s) remaining.


Page created: October 20, 2014
Page updated: October 20, 2014
Page reviewed: October 20, 2014
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.