Aortic Homograft Endocarditis Caused by Campylobacter jejuni

Abstract

We report the first case of homograft endocarditis caused by Campylobacter jejuni, which was treated successfully with antibiotic therapy and valve replacement. To our knowledge, only two other cases of C. jejuni endocarditis, involving native valves, have been reported in the medical literature. CASE REPORTIn May 2009, a 46-year-old male born in Morocco and living in The Netherlands for the past 22 years was admitted to the hospital with a 3-month history of recurrent fever and general weakness. The patient also reported night sweats, weight loss, and a dry cough. The symptoms developed after travel to Morocco, where he had experienced an episode of headache, shaking, vomiting, sweating, dizziness, and myalgia but no diarrhea. His past medical history was significant for symptomatic aortic valve stenosis, for which his aortic valve was replaced with a homograft in 2000; grade 2/4 mitral valve insufficiency; and chronic hepatitis C nonresponsive to treatment with (peg)interferon and ribavirin in 1998 and 2002 to 2003. His further medical history included chronic alcohol abuse, depression, and chronic tension headache. A routine transthoracic echocardiogram performed in the outpatient clinic a week before admission showed severe aortic homograft and mitral valve insufficiency.On physical examination on admission, the patient's temperature was 37.9°C and later that day it climbed to 40.0°C; his pulse was 100 beats per min, and his blood pressure was 116/58 mm Hg. Cardiac examination revealed a grade 3/6 systolic souffle and a grade 4/6 diastolic souffle, with no clear increase in intensity compared to that heard in earlier auscultations. There were no Janeway lesions, Osler's nodes, conjunctival hemorrhages, or signs of arterial emboli or septic pulmonary emboli. Laboratory tests showed a C-reactive protein level of 149 mg/liter, a leukocyte count of 7.2 ϫ 10 9 /liter with normal differentiation and a hemoglobin level of 7.1 mmol/liter. His chest X-ray was normal, and auramine staining of his stomach fluid and a test for antibodies to HIV were negative. On transesophageal echocardiography, new severe aortic homograft insufficiency was found, together with partial aortic valve destruction and dehiscence and mitral valve insufficiency. Artificial valve vegetation could not be ruled out. Blood cultures were taken, and empirical intravenous treatment with vancomycin, gentamicin, and rifampin for homograft endocarditis was started. Blood cultures taken on the day of admission became positive after 4 days. The Gram stain showed slightly curved Gram-negative rods which were oxidase, catalase, hippurate, and indoxyl acetate positive, corresponding to Campylobacter jejuni. The isolate was sensitive to clarithromycin, ciprofloxacin, and tetracycline by the disk diffusion method (Oxoid, Basingstoke, United Kingdom). The MIC of imipenem was 0.125 mg/liter, as determined by Etest (bioMérieux, Marcy l'Etoile, France) on Mueller-Hinton agar (Becton Dickinson, Heidelberg, Germany) with 5% sheep blood. Vancomycin, gentamicin, and ...

Global Epidemiology of Campylobacter Infection

“…Campylobacter-associated endocarditis is an infrequent condition in which both native and prosthetic valves can be affected. Previous studies have shown that individuals with Campylobacterassociated endocarditis have either C. jejuni or C. fetus infection and that one-third of these patients suffer from concurrent chronic diseases, including hepatic cirrhosis, connective tissue disease, tuberculosis, or cancer (233)(234)(235)(236)(237)(238)(239). Furthermore, four cases of atrial fibrillation associated with C. jejuni infection have been reported in the literature (230,240), and both C. jejuni and C. fetus infections have been associated with Campylobacter-associated aortitis (241)(242)(243)(244).…”

Pathobiont release from dysbiotic gut microbiota biofilms in intestinal inflammatory diseases: a role for iron?

“…Consistent with an enteropathogen-induced dispersion of pathobionts, the transient infection promoted the translocation of commensal bacteria to the spleen and liver, depolarized epithelial TLR9, and worsened post-infectious DSS colitis [65]. These observations shed light on how infections with C. jejuni , and other enteropathogens, including parasites and viruses, may exacerbate inflammation in patients with IBD, lead to post-infectious Irritable Bowel Syndrome, and perhaps contribute to extra-intestinal complications, such as haemolytic-uremic syndrome, endocarditis, and a variety of others [52, 66–71]. Recent studies found that human microbiota rendered dysbiotic by exposure to enteropathogens, of when obtained from patients with IBD, in association with their elevated content of activated virulence genes, cause lethal toxicity in the nematode Caenorhabditis elegans [26, 72].…”

Campylobacterbacteremia: A rare and under-reported event?

“…Such complications have also been reported in patients hospitalized with Campylobacter-related bacteremia and underlying health problems such as Campylobacterrelated meningitis [80,81], hepatitis [82], arthritis [83], abdominal septic aortic pseudoaneurysm [84], peritonitis [85,86], acute pancreatitis [87,88], cellulitis [89,90], pericarditis [91], endocarditis [92] and hemolytic uremic syndrome (HUS) [93]. Again, these reports indicate that Campylobacter is able to efficiently travel through the blood stream in gastroenteritis patients, specifically to tissues or organs that can only be reached via the circulating blood stream.…”