• Users Online: 222
  • Print this page
  • Email this page


 
 Table of Contents  
CASE REPORT
Year : 2020  |  Volume : 4  |  Issue : 1  |  Page : 32-34

Postendoscopic variceal sclerotherapy campylobacter jejuni bacteremia


Department of Internal Medicine, Hamad Medical Corporation, Doha, Qatar

Date of Submission25-Dec-2019
Date of Acceptance31-Jan-2020
Date of Web Publication12-Mar-2020

Correspondence Address:
Dr. Deema Hussam Al Soub
Department of Internal Medicine, Hamad Medical Corporation, P.O. Box 3050, Doha
Qatar
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/LJMS.LJMS_70_19

Rights and Permissions
  Abstract 


Campylobacter jejuni bacteremia is rare. We herein report a case of C. jejuni bacteremia in a patient with multiple risk factors, including diabetes mellitus, liver cirrhosis, and hepatocellular carcinoma. The presentation was nonspecific. Diagnosis was made only after positive blood culture which took 5 days. The organism was resistant to several antibiotics; however, treatment with azithromycin was associated with successful outcome.

Keywords: Bacteremia, Campylobacter jejuni, endoscopic sclerotherapy


How to cite this article:
Al Soub DH, Uddin M, Bakhsh NK. Postendoscopic variceal sclerotherapy campylobacter jejuni bacteremia. Libyan J Med Sci 2020;4:32-4

How to cite this URL:
Al Soub DH, Uddin M, Bakhsh NK. Postendoscopic variceal sclerotherapy campylobacter jejuni bacteremia. Libyan J Med Sci [serial online] 2020 [cited 2020 May 29];4:32-4. Available from: http://www.ljmsonline.com/text.asp?2020/4/1/32/280569




  Introduction Top


Endoscopic variceal ligation (EVL) and endoscopic variceal sclerotherapy (EVS) are the main therapeutic procedures for the emergency treatment and secondary prophylaxis of esophageal varices in cirrhosis. Postendoscopic bacteremia has been reported after EVS and EVL.[1] Camara et al. were the first to report early postsclerotherapy bacteremia.[2] Other reports on the incidence of early bacteremia postinjection sclerotherapy have varied widely from 5% to 50%.[3],[4] In a meta-analysis of 19 studies, it was found that the frequency of bacteremia after EVS was 17%, which was higher than the frequency of bacteremia after EVL, which was 6%.[5] One study found that all postendoscopic-positive blood cultures emerged following emergency sessions but not elective procedures.[6] It is believed that the bacteremia is the result of bacterial translocation of endogenous microbial flora into the bloodstream.[7] The most common organisms causing bacteremia post-EVL and EVS are Streptococci, coagulase-negative Staphylococci (CNS),  Escherichia More Details coli, and Klebsiella spp.[6] Literature search did not reveal any case of Campylobacter jejuni bacteremia following variceal sclerotherapy.

C. jejuni is a common cause of bacterial enteritis in developed countries. Campylobacter bacteremia is rare accounting for <1% of the total incidence of all Campylobacter infections.[8],[9] Underlying conditions known to predispose for Campylobacter bacteremia include HIV infection, liver diseases, transplant recipients, and malignancies.[10],[11] We herein describe a case of C. jejuni bacteremia following EVS in a patient with liver cirrhosis and hepatocellular carcinoma and review pertinent literature.


  Case Report Top


A 61-year-old male, known to have diabetes mellitus, hepatitis C-related cirrhosis, portal vein thrombosis, presented with a previous history of schistosomiasis and Hassab's operation done in Egypt in 1991. He is also known to have hepatocellular carcinoma diagnosed 5 months before admission for only palliative treatment. He was admitted to the hospital on October 23, 2017, with upper gastrointestinal bleeding, for which he had undergone endoscopy, and was found to suffer from bleeding gastric varices, for which he had sclerotherapy. He was discharged home on October 26, 2017; however, he was readmitted on November 3, 2017, with the complaints of decreased food intake, dizziness, easy fatigability, nausea but no vomiting, abdominal pain, or change in bowel habit and no fever. On examination, he was jaundiced, drowsy, with evidence bilateral flapping tremors (asterisks). Temperature was 39.6°C, blood pressure 131/74 mmHg, pulse rate 90/min, and respiratory rate 18/min. Laboratory investigation revealed: WBC 9900/mm3, Hb 12.1 g/dL, platelets 157,000/mm3, C-reactive protein 17 mg/dL, procalcitonin 0.11 ng/mL, aspartate aminotransferase 89 U/L, alanine aminotransferase 42 U/L, creatinine 108 μmol/L, and lactic acid 4.6 mmol/L. Chest X-ray showed increased bronchovascular markings. He was diagnosed as chest infection and was given ceftriaxone. Blood culture collected on November 3, 2017, was reported negative after 48 h. Two days after admission, the patient felt better and was discharged home on oral cefuroxime to be continued for 7 days. However, 3 days after discharge, the microbiology laboratory reported a growth of C. jejuni in the initial blood culture that was sensitive to erythromycin but resistant to ciprofloxacin and tetracycline. The patient was called for admission and was given intravenous azithromycin for a total of 14 days. He improved and was discharged home.


  Discussion Top


Campylobacter, particularly C.jejuni, has been established as the most common cause of bacterial gastroenteritis worldwide,[8],[9] with an estimated prevalence of 2–20 million cases annually in the states of the European Union alone. In the US and Europe, bacteremia has been reported to occur in 0.1%–1% of Campylobacter cases.[12],[13] Bacteremia appears to occur more frequently among immunosuppressed patients or those with other comorbidities,[10],[11] although a surveillance study in Finland noted that 53 of 76 cases of bacteremia (70%) occurred in patients without any underlying disease.[14] Fernández-Cruz et al. reported in a recent overview of Campylobacter bacteremia that only 0.24% of all hospitalized patients with bloodstream infections could be associated with Campylobacter spp. and that these bacteremias were community-acquired in 81% of cases.[10]C.jejuni was the most often isolated bacterium next to Campylobacter fetus and Campylobacter coli. One of the possible reasons for the low incidence of bacteremia is the poor performance of automated blood culture systems for the detection of Campylobacter spp.[15] Another cited explanation is that in modern clinical microbiology laboratories, the incubation period for blood culture bottles is usually limited to 4–5 days. As the detection of Campylobacter-related bacteremia requires a median growth rate exceeding 5 days for a substantial proportion of isolates, it is therefore conceivable that many episodes of Campylobacter-related bacteremia may go unnoticed. It has been therefore recommended by some authors that the contents of blood culture bottles should be subcultured onto solid media at the end of the standard 5-day incubation period.[16]

Post-EVS bacteremia is not uncommon with an incidence of 17% reported in one meta-analysis.[5] The most common organisms causing bacteremia following endoscopic sclerotherapy of esophageal varices are Streptococci, CNS, E. coli, and Klebsiella spp.[6] and are believed to result of bacterial translocation of endogenous microbial flora into the bloodstream.[7] Review of the literature revealed no case of C. jejuni bacteremia post-EVS.

Our patient had several risk factors for C. jejuni bacteremia, including hepatitis C-related liver cirrhosis and hepatocellular carcinoma. These two risk factors have been cited as the most common risk factors for C. jejuni bacteremia.[9] We believe that the organism was introduced in our patient during EVS because of the temporal relation to the procedure since it developed few days after the procedure.

An important finding in our patient is the delayed isolation of the organism which took 5 days of incubation to become positive. This finding coincides with the findings in the literature and emphasizes the importance of alerting the microbiology laboratory protocols to prolong the incubation of the blood cultures, when there is a strong suspicion of C. jejuni bacteremia. The isolate was resistant to ciprofloxacin and tetracycline which are usually active against C. jejuni. Fluoroquinolones are usually considered the first-line agents for the treatment of C. jejuni infections; however, the prevalence of fluoroquinolone-resistant Campylobacter is rising. Resistance rates of greater than 50% have been reported in Spain, Hungary, and several developing countries.[17] Fortunately, resistance to macrolides among Campylobacter has remained stable at <5% in most parts of the world, making it the first choice for empiric therapy for patients with C. jejuni infections.[18]


  Conclusion Top


C. jejuni bacteremia remains rare. Important risk factors include liver cirrhosis, immunosuppression, and cancer. Identification of the organism requires prolonged blood incubation. Resistance to many antibiotics, especially for fluoroquinolones, is rising; however, it remains low for macrolides making it the best choice for empiric therapy.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Tseng CC, Green RM, Burke SK, Connors PJ, Carr-Locke DL. Bacteremia after endoscopic band ligation of esophageal varices. Gastrointest Endosc 1992;38:336-7.  Back to cited text no. 1
    
2.
Camara DS, Gruber M, Barde CJ, Montes M, Caruana JA Jr., Chung RS. Transient bacteremia following endoscopic injection sclerotherapy of esophageal varices. Arch Intern Med 1983;143:1350-2.  Back to cited text no. 2
    
3.
Brayko CM, Kozarek RA, Sanowski RA, Testa AW. Bacteremia during esophageal variceal sclerotherapy: Its cause and prevention. Gastrointest Endosc 1985;31:10-2.  Back to cited text no. 3
    
4.
Ayrs SJ, Goff JS, Warren GH. Endoscopy sclerotherapy for bleeding oesophageal varices: Effects and complications. Ann Intern Med 1983;98:900-3.  Back to cited text no. 4
    
5.
Jia Y, Dwivedi A, Elhanafi S, Ortiz A, Othman M, Zuckerman M. Low risk of bacteremia after endoscopic variceal therapy for esophageal varices: A systematic review and meta-analysis. Endosc Int Open 2015;3:E409-17.  Back to cited text no. 5
    
6.
Zuckerman MJ, Jia Y, Hernandez JA, Kolli VR, Norte A, Amin H, et al. A Prospective randomized study on the risk of bacteremia in banding versus sclerotherapy of esophageal varices. Front Med (Lausanne) 2016;3:16.  Back to cited text no. 6
    
7.
Wahl P, Lammer F, Conen D, Schlumpf R, Bock A. Septic complications after injection of N-butyl-2-cyanoacrylate: Report of two cases and review. Gastrointest Endosc 2004;59:911-6.  Back to cited text no. 7
    
8.
Blaser MJ. Epidemiologic and clinical features of Campylobacter jejuni infections. J Infect Dis 1997;176 Suppl 2:S103-5.  Back to cited text no. 8
    
9.
Nielsen H, Hansen KK, Gradel KO, Kristensen B, Ejlertsen T, Østergaard C, et al. Bacteraemia as a result of Campylobacter species: A population-based study of epidemiology and clinical risk factors. Clin Microbiol Infect 2010;16:57-61.  Back to cited text no. 9
    
10.
Fernández-Cruz A, Muñoz P, Mohedano R, Valerio M, Marín M, Alcalá L, et al.Campylobacter bacteremia: Clinical characteristics, incidence, and outcome over 23 years. Medicine (Baltimore) 2010;89:319-30.  Back to cited text no. 10
    
11.
Reed RP, Friedland IR, Wegerhoff FO, Khoosal M. Campylobacter bacteremia in children. Pediatr Infect Dis J 1996;15:345-8.  Back to cited text no. 11
    
12.
Skirrow MB, Jones DM, Sutcliffe E, Benjamin J. Campylobacter bacteraemia in England and Wales, 1981-91. Epidemiol Infect 1993;110:567-73.  Back to cited text no. 12
    
13.
Samuel MC, Vugia DJ, Shallow S, Marcus R, Segler S, McGivern T, et al. Epidemiology of sporadic Campylobacter infection in the United States and declining trend in incidence, FoodNet 1996-1999. Clin Infect Dis 2004;38 Suppl 3:S165-74.  Back to cited text no. 13
    
14.
Feodoroff B, Lauhio A, Ellström P, Rautelin H. A nationwide study of Campylobacter jejuni and Campylobacter coli bacteremia in Finland over a 10-year period, 1998-2007, with special reference to clinical characteristics and antimicrobial susceptibility. Clin Infect Dis 2011;53:e99-106.  Back to cited text no. 14
    
15.
Wang WL, Blaser MJ. Detection of pathogenic Campylobacter species in blood culture systems. J Clin Microbiol 1986;23:709-14.  Back to cited text no. 15
    
16.
Louwen R, van Baarlen P, van Vliet AH, van Belkum A, Hays JP, Endtz HP. Campylobacter bacteremia: A rare and under-reported event? Eur J Microbiol Immunol (Bp) 2012;2:76-87.  Back to cited text no. 16
    
17.
Gaunt PN, Piddock LJ. Ciprofloxacin resistant Campylobacter spp. in humans: An epidemiological and laboratory study. J Antimicrob Chemother 1996;37:747-57.  Back to cited text no. 17
    
18.
Gupta A, Nelson JM, Barrett TJ, Tauxe RV, Rossiter SP, Friedman CR, et al. Antimicrobial resistance among Campylobacter strains, United States, 1997-2001. Emerg Infect Dis 2004;10:1102-9.  Back to cited text no. 18
    




 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Case Report
Discussion
Conclusion
References

 Article Access Statistics
    Viewed164    
    Printed10    
    Emailed0    
    PDF Downloaded21    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]