Excerpt
A 76-year-old male patient with malaise, inflammatory disease, and clinical suspicion of pneumonia was admitted to the pneumology department. Chest radiograph showed right perihilar, and upper lobe consolidation with patchy infiltrates, attributed to tuberculosis incurred at a young age. Antibiotic treatment with piperacillin–tazobactam 4.5 g t.i.d. iv was initiated. The patient presented with pronounced cachexia and marasmus due to persistent diarrhea lasting at least a year, decreased food intake following a gastric bypass in September 2014, and chronic alcohol abuse. In the past 2 years he lost 60 kg. Furthermore, he has MGUS and was treated for mitral valve endocarditis in June 2014. A molecular assay detected Campylobacter non-coli and non-jejuni in the feces, but culture remained negative. Intravenous fluid resuscitation and erythromycin 500 mg t.i.d. iv was started. Abdomen CT scan with contrast disclosed a whirlpool sign of the inferior mesenteric vein, suggestive of internal duodenal loops herniation, yet, without obstruction symptoms. Intraperitoneal fluid stagnation and substantial rectal distention were present. Laparoscopic exploration revealed neither internal herniation nor obstruction. However, anterior to the promontory a mass was seen which spilled puss when punctured. Conversion to laparotomy confirmed the presence of a (probably) mycotic aneurysm of both internal and external iliac artery bifurcation. Iliac bifurcation resection followed by vascular reconstruction achieved with femoro-femoral crossover with a 6-mm armed prosthesis was carried out. Due to the emergency setting the use of auto- or allograft was ruled out. After 5 days of incubation,
Campylobacter fetus was cultured from the mycotic aneurysm, and meropenem 1 g t.i.d iv was added. The blood cultures though remained sterile. The isolate was susceptible to erythromycin, ciprofloxacin, tetracycline, amoxicillin–clavulanate, meropenem and resistant to ceftriaxone, performed according to Eucast guidelines, with minimum inhibitory concentrations of 0.75, 0.5, 1, 0.5, 0.047 and 8 µg/ml, respectively. After 6 weeks, therapy was switched to oral ciprofloxacin 750 mg b.i.d. However, due to the frail general condition resulting in little hope for successful treatment, all treatments were stopped. The patient died.
Campylobacter is mainly known as a gastro-intestinal disease following ingestion of contaminated food products. Over 90% of the cases are due to
C. jejuni or
coli [
1]. In contrast to the latter species,
C. fetus causes more often bacteremia (19–53%), and is seldom cultured in feces, even with optimal growth conditions [
1,
2]. Furthermore,
C. fetus has a tropism for vascular endothelium, with local production of pro-coagulant, and subsequent thrombus formation [
3]. This sequence is associated with the development of secondary invasive infections, mostly mycotic aneurysms. The majority of patients with a
C. fetus bacteremia are older males with an underlying disease. Patients with hematological malignancies, cardiovascular diseases, immunosuppressive therapy, diabetes, liver diseases, solid organ cancers, and medical devices are at risk [
2,
4]. Our patient had a combination of intra-abdominal problems promoting local intravascular invasion, accounting for the sterile blood cultures. Up to 15% fatality rates are reported, mainly in patients with an asymptomatic infection, receiving no or inappropriate empiric antibiotic treatment with fluoroquinolones and third-generation cephalosporins [
2,
4].
C. fetus is considered more susceptible to antibiotics compared to
C. coli and
C. jejuni. However, 13–60% resistance rates of
C. fetus isolates to cefotaxime are reported [
4,
5]. The resistance of the
Campylobacter species to fluoroquinolones is high (> 30%), and resistance to macrolides is increasing, more in
C. coli compared to
C. jejuni, 11 and 3% respectively [
6]. Therefore, neither quinolones, macrolides, nor third-generation cephalosporins should be prescribed as empirical therapy of
Campylobacter bacteremia or presumptive invasive disease [
3,
4]. So far, there is no consensus regarding the empirical treatment of
Campylobacter bacteremia. Antibiotics such as tigecycline, gentamicin, amoxicillin–clavulanate, and carbapenems are among the most active antibiotics [
3]. Although tigecycline is probably not an option when treating
Campylobacter bacteremia, it is a possible addition when dealing with soft tissue infections. A carbapenem or amoxicillin–clavulanate in monotherapy, or in combination with gentamicin, is the current practice as first-line therapy. However, in contrast to imipenem, therapy failure is reported with amoxicillin–clavulanate [
3].
C. fetus bacteremia in immunocompetent patients may be transient and resolve without antibiotic coverage. Even so, patients at risk certainly benefit from timely and appropriate antibiotic therapy [
2,
3]. …
