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Pseudomonas mendocina native valve infective endocarditis: a case report
© The Author(s). 2016
Received: 15 March 2016
Accepted: 7 September 2016
Published: 4 October 2016
Gram-negative microorganisms are uncommon pathogens responsible for infective endocarditis. Pseudomonas mendocina, a Gram-negative water-borne and soil-borne bacterium, was first reported to cause human infection in 1992. Since then, it has rarely been reported as a human pathogen in the literature. We describe the first case of native valve infective endocarditis due to P. mendocina in the USA.
A 57-year-old white man presented with bilateral large leg ulcers, fever, and marked leukocytosis. His past medical history included gout and chronic alcohol use. P. mendocina was isolated from his blood cultures. A comprehensive review of P. mendocina infection in the literature was performed. A total of eight cases of P. mendocina infection were reported in the literature. More than two-thirds of the cases of P. mendocina septicemia were associated with native valve infective endocarditis. Thus, an echocardiogram was performed and demonstrated mitral valve endocarditis with mild mitral insufficiency. His leg wounds were debrided and were probably the source of P. mendocina bacteremia. Unlike Pseudomonas aeruginosa, P. mendocina is susceptible to third-generation cephalosporins. Our patient received a 6-week course of antimicrobial therapy with a favorable clinical outcome.
Our reported case and literature review illuminates a rare bacterial cause of infective endocarditis secondary to P. mendocina pathogen. Native cardiac valves were affected in all reported cases of infective endocarditis, and a majority of affected heart valves were left-sided. The antibiotics active against P. mendocina are different from those that are active against P. aeruginosa, and they notably include third-generation cephalosporins. The outcome of all reported cases of P. mendocina was favorable and no mortality was described.
KeywordsPseudomonas mendocina infection Pseudomonas mendocina septicemia Endocarditis
Infective endocarditis is a life-threatening infection of the endocardial surfaces of the cardiac valves. Gram-positive cocci, mainly Staphylococcus aureus and Streptococci, are the leading causes of infective endocarditis. Gram-negative rods and fungi are not common pathogens of infective endocarditis . Pseudomonas mendocina causing infective endocarditis has rarely been reported in the literature. P. mendocina is a ubiquitous soil and water dwelling Gram-negative non-fermentative rod discovered in 1970 in Mendoza, Argentina . For the first 22 years after its discovery, it was presumed to be non-pathogenic in humans. As a soil and water organism, the primary research into this organism looked at its abilities to remediate oils and organic chemicals. Little to no research was done into its pathogenicity or virulence factors. In 1992, the first case of infection in humans by P. mendocina was reported in Argentina in a 63-year-old man with infective endocarditis .
Here we present the first case of infective endocarditis from P. mendocina reported in the USA and perform a comprehensive review of the published literature of the infection.
On physical examination, he was awake and oriented to time, place, and self. He was, however, in distress from his leg pain. His vital signs revealed a temperature of 36.6 °C (97.9 °F), heart rate of 90/minute, blood pressure of 172/96 mmHg, and respiratory rate of 16/minute with an oxygen saturation of 100 % on room air. The other remarkable physical findings included a gallop heart rhythm without heart murmurs, and jugular venous distention. There were two large cutaneous ulcerations over both his lower legs. On his right shin, the lesion measured approximately 25×8 cm. The wound on his left ankle was oval in shape and measured 8 cm in diameter (Figs. 1 and 2). Foul-smelling purulent drainage was noted on his right shin ulcer. Laboratory studies showed a marked leukocytosis of 24,000/mm3. X-rays of his tibia and fibula showed soft tissue edema, but no discreet osseous abnormalities. Blood cultures were drawn on admission due to leukocytosis and the extensive nature of the leg ulcerations. It was followed by empiric therapy with intravenous vancomycin and piperacillin-tazobactam.
Antibiotic susceptibility profile of Pseudomonas mendocina isolated from our patient
Minimal inhibitory concentration, susceptibility (μg/ml)
The genus Pseudomonas comprises at least 140 species . Among them, Pseudomonas aeruginosa possesses an abundance of virulence factors and is regarded as the most important pathogen responsible for serious life-threatening infections in humans . P. mendocina, a non-aeruginosa Pseudomonas species, rarely causes human infection.
Published reports of Pseudomonas mendocina infection
Age (in years)/Gender
Past medical history
Aragone et al., 1992 
Poliomyelitis, diabetes mellitus, aortic valve replacement, pacemaker
Fever and chills
Native mitral valve endocarditis
IV ceftriaxone + IV gentamicin (6 weeks), then po ciprofloxacin (2 weeks)
Johansen et al., 2001 
Situs inversus, tetralogy of Fallot, ventricular septal defect closure, resection of pulmonary valve cusps
Abdominal pain, dyspnea, flu-like symptoms
Native tricuspid valve endocarditis
IV gentamicin + IV penicillin, then IV gentamicin + IV ampicillin, followed by po ofloxacin (7 weeks)
Tricuspid valve repair
Chi et al., 2005 
Alcoholism, renal disease
Lower back pain
Deep spinal tissue
IV cefepime × 2 weeks, followed by po ciprofloxacin × 4 weeks
Mert et al., 2007 
Weight loss and fever
Native mitral valve endocarditis
IV ceftazidime + IV amikacin × 6 weeks
Mitral valve replacement
Suel et al., 2011 
Atrial fibrillation, transient ischemic attack, hypertension
Native aortic valve endocarditis
IV piperacillin + IV gentamicin × 6 weeks
Nseir et al., 2011 
Fever and chills
Bacteremia (no vegetation on transthoracic echocardiogram)
IV gentamicin × 4 days + po ofloxacin × 2 weeks
Howe et al., 2013 
Atraumatic left thigh pain
Chiu and Wang, 2013 
Foot wound infection (polymicrobial pathogens)
IV cefazolin + IV gentamicin, then po ciprofloxacin × 2 weeks, followed by po trimethoprim-sulfamethoxazole × 16 days
Native mitral valve endocarditis
IV piperacillin-tazobactam × 6 weeks
The source of P. mendocina infection was not identified in most reported cases. Nseir and colleague’s speculation on the source of infection is fascinating . They found that the patient had a peculiar habit of allowing a bird to drink water from his mouth. P. mendocina was isolated both from the tap water and the bird’s drinking water. In our case, our patient had already received intravenous antibiotics for 3 days when his leg wound cultures were obtained. His skin tissue cultures failed to grow P. mendocina because of the inhibitory effect of antibiotics on the bacterial growth. Thus, we postulated that the leg wound ulcers were the likely nidus of the infection.
Because P. mendocina is not a common human pathogen, little knowledge exists about the antimicrobial resistance patterns of this organism. This pathogen was reportedly susceptible to ampicillin in some reported cases [5, 7]. However, ampicillin or ampicillin-sulbactam is not tested in the antibiotic susceptibility of non-aeruginosa Pseudomonas species by the US Clinical and Laboratory Standards Institute (CLSI) . The third-generation cephalosporins (cefotaxime, ceftriaxone, cefoperazone, ceftizoxime) are included in the susceptibility testing and recommended as a treatment of choice if susceptible [4, 12]. Other traditional “anti-Pseudomonas aeruginosa” antibiotics, including ceftazidime, cefepime, piperacillin-tazobactam, aminoglycosides, carbapenems, and ciprofloxacin, show an excellent activity against most strains of P. mendocina [4, 12]. In one case report, Mert et al. reported that their isolate of P. mendocina was susceptible to all tested antibiotics (ampicillin, ceftazidime, cefepime, piperacillin-tazobactam, imipenem, and gentamicin) . Aragone et al. found ampicillin and cephalothin resistance in their isolate . Resistance to ampicillin and ampicillin-sulbactam was demonstrated in the isolates from a foot wound by Chiu and Wang . In a case of spondylodiscitis, the isolated P. mendocina pathogen from deep spinal tissue was only resistant to trimethoprim-sulfamethoxazole . Nseir et al. identified ceftriaxone and aztreonam resistance in their isolate . The other cases in Table 2 failed to report antibiotic resistances of their P. mendocina isolate. The present isolate in our patient was resistant to ampicillin-sulbactam and first-generation cephalosporins. While these isolates indicate a low level of antibiotic resistance in this organism, the minimal numbers of cases preclude an in-depth analysis of antibiotic resistance trends in this organism.
In summary, there were only eight cases of P. mendocina human infections reported in the literature. Thus, there is a limitation to draw major conclusions from these cases. The actual incidence of P. mendocina infection is likely to be underestimated as well as underreported. All patients with P. mendocina infection survived. Most cases were noticeably associated with native valve infective endocarditis. The preponderance of P. mendocina for causing endocarditis warrants a discussion of echocardiography for patients with P. mendocina septicemia. Further research and clinical studies are required to identify the underlying mechanism and pathogenicity of this association. Although it is a relatively susceptible pathogen, we would not advocate using ampicillin, ampicillin-sulbactam, or the first- and second-generation cephalosporins as first-line therapy in a serious infection even if reported to be susceptible. The third-generation cephalosporins are acceptable and recommended in the treatment of P. mendocina infection. Guidance from antimicrobial susceptibility profiles in accordance with CLSI standards is always helpful for the optimal therapy with favorable clinical outcome.
We, the authors, would like to extend our thanks to all the medical and surgical teams who participated in our patient’s care.
GR, JM, and ZM participated in the patient’s care, literature search, and manuscript drafting. NB and ZM were involved in a comprehensive literature review and editorial review of the manuscript. All authors read and approved the final version of the manuscript.
Dr Bhanot received an honorarium from the Speaker’s Bureau of Astellas and he reviewed an article for the Postgraduate Institute for Medicine, USA. All other authors declare no competing interests.
Consent for publication
Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
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