Abstract

Introduction

Staphylococcus lugdunensis, a coagulase negative species, has been recently recognized (1988) and described as a rare cause of endocarditis.

Endocarditis due to this organism has been reported to have a high mortality rate in most published cases, and involves native valves more frequently than other coagulase negative staphylococci 1,2. In contrast to the few embolic phenomena associated with other coagulase negative staphylococcal endocarditis, S. Lugdun is reported to have a higher incidence of embolic phenomena 3. There are few data concerning the epidemiology and ecology of S. Lug, but we believe as many others do, that this organism is similar to other coag. neg. species in that it is ubiquitary, found on the skin andmucous membranes. However, in most reported cases, the portal of entry has not been identified.

In this paper we report a case of a young patient who underwent a conservative surgical treatment with favorable outcome for an infective endocarditis due to Staphylococcus Lugdunensis.

Case

A 20-year-old white male patient, with no significant past medical history, was admitted to our hospital in March 1997 with a history of exertion dyspnea, extreme fatigue, fever, night sweats, abdominal pain and vomiting. There was no history of dental extraction or upper respiratory tract infection before the onset of present illness. Laboratory tests were performed and showed a severe hypoxia: PO2 61 mmHg: PCO2 30 mmHg, and the other following values: WBC 12800/mm3, ESR 30, Hb 13.8, Na 132, K 3.24, Cl 92, creat 113.

Chest X- Ray showed a diffuse bilateral interstitial infiltrative process predominating mostly on the right lung. On physical exam, the patient was pale and extremely tired, the heart rate was 90 per minute. Diminished breath sounds were noted at both bases of the lungs with crepitations of the right lung. A loud pansystolic cardiac murmur of grade 2/6 was heard at the apex without irradiation, this was considered to be partially attributable to high fever. However we decided at that time to postpone any exploration of this murmur after total recovery of the patient.

The initial interpretation of these data was suggestive of an interstitial acute lung infection, and the patient was started on a 4 week course of empirical antibiotherapy initially including Erythromycin and Ceftriaxone with adequate doses of methylprednisolone succinate. (Solumedrol). Shortly after, Erythromycin was replaced by Ofloxacine because we have detected biologic signs of hepatic cytolysis. After the patient was discharged home with resolution of pain and temperature, blood cultures were proved to be positive for coagulase negative staphylococcus that was subsequently identified as Staphylococcus Lugdunensis.

Five days after the last dose of antibiotics, the patient has presented again to the emergency room for recurrence of fever with obvious change in his previously noted systolic ejection murmur on physical exam, there was no evidence of hepatosplenomegaly or other peripheral manifestations of endocarditis.

An intensive work up was carried out including laboratory tests (WBC 9000, ESR 26), a bone scan which revealed a homogeneous fixation without any infectious bony localization, a two dimensional echocardiography identified a mild mitral valve regurgitation, and demonstrated the existence of large vegetations at the anterior and posterior leaflets of the mitral valve, which was confirmed by trans-oesophageal echography. A specialized stomatology consultation was significant for severe dental caries.

On the basis of susceptibility testing results, cefazolin (6 g daily) and netilmicin (300 mg daily) and rifampin (1.2 g daily) were started. Despite its susceptibility, penicillin was excluded from the regimen because allergic problem. Dose adaptation was made according to serum bactericidal activity. Hyperoxemia has been induced to increase aminoglycosides activity in poorly oxygenated vegetation tissue. A clear improvement of the clinical and biologic status was noted, with CRP falling into normal range. Valvular vegetations were shown to be stable on echocardiography follow-up. After few days of apyrexia, recurring low-grade fever was attributed to a deep venous thrombosis localized at the left peroneal vein. We did not anticoagulate, but followed-up the patient closely with duplex scan. After reviewing numerous reports by many authors highlighting the aggressive nature and virulence of S. Lugdunensis, and once the patient has been stable on medical treatment, he was taken to surgery and underwent a mitral valvuloplasty. Before the Cardio- Pulmonary Bypass was established we identified an important mitral regurgitation in contrast to what was demonstrated on preoperative echocardiography. We did a transseptal approach and found huge vegetation localized at the anterior leaflet of the mitral valve, the posterior leaflet was almost non-existent. Finally, in order to reduce the risk of infection, we abstained from introducing any synthetic material. We simply resected the pathologic area of the anterior leaflet and performed an annuloplasty by placing stitches at the antero-external commissure thus minimizing the mitral regurgitation without creating any iatrogenic stenosis. The competence of the valve was then interrogated and a minimal residual regurgitation was detected. The postoperative recovery was satisfying with no misfortunate events noted. An intraoperative Gram stain of the mitral vegetations was negative for bacteria; as were blood cultures. Repeated transoesophageal echocardiography showed a non-significant mitral incompetence with no evidence of residual vegetations. Postoperatively the patient was maintained on intravenous antibiotics for 10 days and discharged home on a 3-week course of oral antibiotics (Pefloxacine, Fucidine and Rifadine). A 6-month follow-up postoperatively has been gratifying.

Discussion

Trying to explain the increasing incidence of native valve endocarditis caused by coag. neg. staphylococci, the increased use of indwelling intravascular catheters and the increased recognition of the coag neg staphylococci as pathogens are the most accepted reason. 3 to 5% of cases of native valve endocarditis are due to these pathogens 4, Staph epidermidis being the most common species involved in native valve endocarditisThe predilection of Staph. Lug for native valves was evident in the literature where 67% of reported cases involved native valves (the mitral valve in 67% and the aortic valve in 33% of cases. We didn’t find in our patient any previous history of valvular disease and no obvious portal of entry for bacteremia, except for the dental caries. The same pathogen is a rare cause of endocarditis and is characterized by it’s highly pathogenic potential 5. This aggressive natural history is due to the acute hemodynamic compromise frequently encountered with this particular pathogen and can be explained by the ability of this organism to destroy the native valve. This particular pathogen behaves like S. aureus, which is a coagulase positive organism. According to Lambe et al. 6, it seems that S.lug is able to bind vitronectin and fibrinogen to extracellular matrix protein similar to S. aureus. In his review of the literature, Koh 7 concluded that the use of commercial identification systems can lead to misidentification of S. lug with other staphylococci and consequently delay appropriate treatment. 1,2,8. Isolates of coag neg should undergo detailed identification, and the detection of coagulase fibrinogen affinity factor and ornithine decarboxylase are substantial in the diagnosis of S. lug. 1.

Based on our own experience and supported by the world wide literature, we believe that embolic complications are rarely seen in cases of infective endocarditis caused by coagulase negative staphylococci compared to other organisms. Such recognition isn’t the rule in the case of S. Lugdun which, to the contrary, is more frequently emboligenic 3. With our particular patient we suspected an embolic infarction of the spleen on an abdominal ultrasound basis, but serial abdominal echography failed to demonstrate any detectable lesion.

Conclusion

In this paper we presented a case of a staphylococcus lugdunensis endocarditis affecting the native mitral valve, upon which we performed a mitral valvuloplasty, thus avoiding valve replacement with all it’s complications as a foreign body. In conclusion, one should always be aware that this particular form of endocarditis is different from other coagulase negative staphylococci endocarditis, since it involves predominately native valves, and it has a destructive and aggressive course with a high mortality rate in contrary to other coag neg species. However we are convinced that medical treatment should seek use of synergic antibiotics carefully monitored on detailed in vitro data for each patient, and early diagnosis and tailored surgery are crucial for a better outcome.

References