Management of an Abdominal Aortic Aneurysm Infected with Campylobacter Fetus: A Case Report
Article Outline
We present a rare case of an abdominal aortic aneurysm (AAA) infected with Campylobacter fetus. The patient presented with abdominal pain and leukocytosis, without a palpable AAA. Computed tomography (CT) of the abdomen showed a 3.1 × 3.0 cm infrarenal abdominal aneurysm with an extra-aortic fluid collection. At surgery, an in situ graft was placed. Intraoperative aortic wall cultures grew pansensitive C. fetus, and blood cultures remained negative. At 9-month follow-up, the patient was doing well without complaints. To our knowledge, this represents only the ninth reported case of an AAA with an aortic wall culture positive for C. fetus.
Campylobacter fetus–associated infections are a rare occurrence. They are known to cause septic abortions in sheep as well as cattle.1, 2 In humans, C. fetus has been associated with infections such as meningoencephalitis, septic arthritis, peritonitis, salpingitis, lung abscess, empyema, cellulitis, urinary tract infection, vertebral osteomyelitis, suppurative thrombophlebitis, and cholecystitis.1, 3, 4 The first ever reported case of a mycotic aneurysm associated with sepsis due to C. fetus was in 1971 by Dolev et al.2 The patient was treated with an initial course of intravenous antibiotics but died due to aneurysm rupture prior to attempted repair. A culture of the aortic wall specimen was negative. The first successful repair was reported in 1983 by Marty et al.5 Since then, aortic infections due to C. fetus have remained rare. We report the ninth case of an abdominal aortic aneurysm (AAA) in which the aortic wall culture was positive for C. fetus.
Case Report
The patient was a 78-year-old African American male with a history of hyperlipidemia and chronic prostatitis who presented to the emergency department complaining of 5 days of abdominal pain associated with episodes of nonbilious, nonbloody emesis. The pain was described as a nonradiating, pressure-like sensation in the mid-abdomen. Of note, the patient had been seen 2 days prior in the emergency department for prostatitis and a urethral stricture with a urinary tract infection. At that time, the stricture was dilated and the patient was sent home on tamsulosin and ciprofloxacin. His past medical history was remarkable for multiple emergency room visits for urinary tract infections. The patient was a nonsmoker and had no documented history of atherosclerotic vascular disease. Upon arrival to the emergency room, the patient was afebrile, was tachycardic to 106, and had a blood pressure of 160/90. His abdomen was soft, with mild tenderness to palpation in the periumbilical area. No masses were palpated. He had a white blood cell count elevated to 16,500/μL. Computed tomography (CT) of the abdomen showed a 3.1 × 3.0 cm infrarenal abdominal aneurysm with an extra-aortic fluid collection, which was read by radiology as consistent with an inflammatory aneurysm. The patient was initially admitted to the intensive care unit for tight blood pressure control and conservative management of an inflammatory AAA. However, upon review of the CT scan with the vascular attending, there appeared to be an area of disrupted calcific plaque protruding into the fluid collection, which raised the concern for a possible contained rupture. The patient was taken emergently to the operating room.
At surgery, the retroperitoneal tissue was found to be edematous and hyperemic. The tissue overlying the aneurysm was not thickened or fibrosed and did not have the appearance of an inflammatory aneurysm. Since there was no evidence of purulence, repair of the infrarenal AAA was carried out using a Dacron® (DuPont, Wilmington, DE) graft. An intraoperative specimen of the aortic wall was sent off for histological examination and culture. The microscopic diagnosis revealed severe atherosclerosis with calcification, ossification, and mural thrombus. The adventitia had a zone of intense acute and chronic inflammation, which was consistent with an infected aneurysm. Intraoperative cultures eventually grew C. fetus subspecies fetus. Blood cultures were negative. The patient remained afebrile, had an uneventful hospital stay, and was discharged on postoperative day 12 on lifelong levofloxacin. At 9-month follow-up, the patient was symptom-free and a repeat CT scan was negative.
Discussion
The term mycotic aneurysm was first coined by William Osler in 1885, who described a 30-year-old man who died after developing four aortic arch aneurysms secondary to endocarditis.6, 7 The term is misleading since the majority of mycotic aneurysms are due to bacterial infection and are not fungal in nature.8 In most cases, culture of the arterial wall is positive for bacterial organisms. This is in contrast to inflammatory aneurysms, which are culture-negative.9
The most commonly cultured organisms in mycotic aneurysms include Staphylococcus (30%), Streptococcus (10%), and Salmonella (10%),10, 11 with Staphylococcus epidermidis as the single most common isolate.6 C. fetus is a very rare cause of mycotic aneurysms. To our knowledge, the present case is only the ninth in which an aortic wall culture from an AAA has grown C. fetus. There have been an additional five cases with a positive C. fetus blood culture in association with an AAA where aortic wall cultures were either negative or unavailable. C. fetus is a curved, microaerophilic, gram-negative rod and has a propensity for vascular endothelium.12 It occurs as two subspecies, including C. fetus fetus (also known as Vibrio fetus, or subspecies intestinalis) which is a known pathogen in the causation of sporadic abortion in cattle. In humans, C. fetus fetus infections are rare but, when present, usually manifest as septicemia or meningitis. It has also been associated with puerperal and neonatal sepsis.3 The other subspecies is C. fetus venerealis and is not significant in humans.
The diagnosis of a mycotic aneurysm, which accounts for 0.7-3% of AAAs, can be problematic. They are more likely to cause symptoms than noninfected AAAs.7, 13, 14 However, the classic triad of fever, pain, and a pulsatile mass is found in <50% of patients.15, 16 Of the 14 reported cases of Campylobacter-associated AAA, only 29% (4/14) had the classic triad. The present case highlights the difficulty of diagnosis as there was no pulsatile mass on exam and the patient was afebrile. The likely etiology of the AAA infection was the patient's urinary tract infection. Dilation of his urethral stricture served as a conduit for hematogenous dissemination of the bacterium, which seeded a preexisting atherosclerotic aneurysm. In other cases, it has been postulated that a preceding gastrointestinal infection is the precipitant event in the AAA infected with C. fetus since many of the affected patients had gastrointestinal symptoms.1, 2, 4, 6, 12, 17, 18, 19, 20, 21 Of the documented cases, 71% (10/14) of the patients reported having either nausea or vomiting as a presenting symptom. Nine (64%) reported having either abdominal or back pain, and 10 (71%) were febrile (Table I). Other clues to the presence of a mycotic aneurysm include leukocytosis or an elevated erythrocyte sedimention rate; however, these are not always present.13 Hence, when symptoms are nonspecific and physical exam and laboratory data are inconclusive, a diagnosis of infected aortic aneurysm is often not suspected during clinical evaluation.
Table 1. Abdominal aortic aneurysms associated with Campylobacter fetus infection
| Author | Year | Abd/BackPain | GI Sx's | Febrile | Pulsatile mass | Blood Cx | Specimen Cx | Antibiotic therapy | Species | CT scan | In-situ Graft | Extra-anatomic Bypass | Outcome |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Dolev et al. | 1971 | + | + | + | + | + | − | Chloramphenicol × 6 days | C. fetus subsp. fetus | Ø | + | Ø | Rupture, death |
| File et al. | 1979 | − | − | + | − | + | − | Gentamicin × 5 days; ampicillin × 14 days | C. fetus subsp. intestinalis | Ø | Ø | Ø | Rupture, death |
| Taylor et al. | 1979 | − | + | + | − | + | Ø | Gentamicin & Cefazolin × 9days; then tetracycline × 10 days | C. fetus subsp. Intestinalis | Ø | Ø | Ø | Rupture, death |
| Marty et al. | 1983 | + | − | + | + | + | + | Cefamandole × 2 days postop, then gentamicin × 14 days then trimethoprim/sulfamethoxazole × 3 wks, then tetracycline × 6 months | C. fetus subsp. fetus | 5.3 cm AAA, density interpreted as extravasated blood | + | − | Alive; 2 year f/u |
| Anolik et al. | 1983 | − | − | + | − | + | + | IV tetracycline & chloramphenicol × 16 days; dc'd on continuous oral erythromycin | C. fetus | Large distal aortic and left common iliac aneurysm | − | + | Alive; 45 month f/u |
| Blabey et al. | 1983 | + | + | + | − | + | − | Gentamicin × 28 days; Cefotaxime × 21 days | C. fetus | 4 cm infrarenal AAA, 4 days later 2 cm expansion | − | + | Alive; 18 month f/u |
| Perry | 1985 | − | + | + | − | + | − | Erythromycin & Gentamicin × 8 weeks | C. fetus subsp. fetus | 5 cm AAA suspect for infection at distal aorta, possible disruption of anterior wall | + | − | Alive; 6 month f/u |
| Righter & Woods | 1985 | + | + | − | + | Ø | + | Erythromycin × 7 days | C. fetus subsp. fetus | Ø | + | − | Alive; 3 years f/u |
| Rutherford et al. | 1989 | − | + | − | − | − | + | Cefazolin × 2 days postop; then cefotaxime & gentamicin × 19 days; d'c on gentamicin × 6 wks, then amoxicillin × 3 months | C. fetus subsp. fetus | 4 × 5 cm AAA w/ large thrombus anterior and soft tissue density along outside of aortic wall anteriorly and laterally | + | − | Alive; 2 years f/u |
| Kato et al. | 1990 | + | + | + | + | − | + | Fosfomycin & γ globulin × 5 days; then gentamicin & minocycline × 10 days postop, then miconazol × 5 days | C. fetus subsp. fetus | 8 × 10 cm AAA w/ fibrous adhesions to mesentery, desmoplastic reaction w/ duodenum, edema with hyperemia of retroperit. | − | + | Alive; 36 month f/u |
| Allerberger et al. | 1991 | + | + | + | Ø | + | + | Not reported | C. fetus subsp. fetus | Ø | Ø | Ø | Rupture, death |
| Grollier et al. | 1993 | + | − | − | Ø | Ø | + | Not reported | C. fetus subsp. fetus | Ø | + | − | Alive; 12 month f/u |
| Mii et al. | 1998 | + | + | + | + | − | + | IV cefodizime & clindamycin × 1 wk; then IV cefoperazon/sul-bactam & cephotiam × 3 wks; d/c on oral minocycline & levofloxacin × 1 mo | C. fetus | Saccular, eccentric aneurysm located in distal abdominal aorta | + | − | Alive; 1 year f/u |
| Tran et al. | 2005 | + | + | − | − | − | + | Cipro po on admission, IV cipro × 1 day; cefotetan × 2 days; metronidazole × 5 days; cefepime × 2 days; imipenem × 18 days; d/c continuous levofloxacin | C. fetus subsp. fetus, C. hyointestinalis | 3.1 × 3 cm infrarenal AAA with periaortic fluid and stranding consistent with an inflammatory aneurysm | + | − | Alive; 9 month f/u |
CT offers great assistance in the diagnosis of mycotic aneurysms, although the findings on CT scan are inconsistent and variable. Macedo et al.13 observed that the majority of mycotic aneurysms are saccular in shape with a lobulated contour and 70% of the time are located at or above the renal arteries. An increase in fat density around the aorta, representing retroperitoneal response to the infection, is an important finding.13, 22 Periaortic edema is also common but can be overlooked if not searched for carefully. Other, more uncommon findings on CT of mycotic aneurysms include periaortic gas or the presence of multiple aneurysms.13 CT scan findings in mycotic aneurysms can be confused with inflammatory aneurysms, as in the present case. The classic findings with inflammatory aneurysms are periaortic fibrosis with marked anterolateral wall thickening.23 In the present case, the CT scan findings demonstrated periaortic fluid and inflammation. Contrary to the diagnosis of an inflammatory aneurysm, however, there also appeared to be disruption of the aortic wall calcification, suggesting a possible contained rupture.
Several approaches have been advocated in the management of mycotic aneurysms. The gold standard is to perform an extra-anatomic bypass followed by aortic resection, oversewing of the aortic stump, and coverage with omentum, as was successfully done by Anolik et al.24 for an AAA infected with C. fetus. Another method is to place the graft in situ, as was done with the first successful repair of an AAA infected with C. fetus by Marty et al. in 1983.5 However, the in situ approach remains controversial due to the risk of recurrent graft infection. Of the 10 cases where an operative procedure was performed, three underwent extra-anatomic bypass and seven had an in situ graft reconstruction. Of those that received the in situ graft, one patient had the procedure done after rupture and expired soon after the operation. Of the remaining six cases with in situ grafting, all did well on long-term follow-up, suggesting that the in situ technique is an acceptable alternative.3, 12, 18, 19, 24 The endovascular approach to the repair of mycotic aneurysms has recently yielded successful results. Koeppel et al.25 reported successful endovascular repair of an AAA infected with Salmonella enteritidis with 1-year follow-up. However, since experience with this specific procedure in the setting of an infected AAA is limited, it is still unclear if endovascular repair provides the best long-term results. Theoretical advantages to the endovascular approach include less operative risk, particularly in patients who are critically ill and who may not tolerate an open repair. Following repair, most authors recommend a 3- to 6-month course of postoperative antibiotic therapy,7 although treatment has ranged from as short as 7 days to lifelong antibiotics.
Overall mortality for mycotic aneurysms has ranged 5-44%.15, 26 The risk of rupture is as high as 50-85%,16 and if rupture occurs, mortality exceeds 75%.27 Of the four patients reported with aortic rupture associated with Campylobacter, all died, whereas all who had surgical intervention prior to rupture survived, including the present case.
In conclusion, mycotic aneurysms caused by C. fetus are very rare. Because the classic triad of fever, abdominal pain, and a pulsatile mass are not always present, the diagnosis of a mycotic aneurysm can be challenging. In the present case, the diagnosis was made by the combination of symptoms, leukocytosis, and the finding of a disrupted calcific plaque and periaortic fluid on CT scan. Although extra-anatomic bypass has been advocated as the gold standard of treatment for mycotic aneurysms, in situ graft reconstruction, as evidenced in this case, can also be an effective surgical option in AAAs infected with C. fetus. Endovascular repair remains a potential, less invasive surgical option for the future. The duration of postoperative antibiotic treatment remains controversial.
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Presented at the 23rd Annual Meeting of the Southern California Vascular Surgical Society, La Quinta, California, May 13-15, 2005.
PII: S0890-5096(07)00066-0
doi:10.1016/j.avsg.2007.01.002
© 2007 Annals of Vascular Surgery Inc. Published by Elsevier Inc All rights reserved.
