A Rare Presentation of Erysipelothrix rhusiopathiae Endocarditis with Acute Heart Failure

Abstract

Erysipelothrix rhusiopathiae is an occupation-related infection that can be found in farm animals or marine life. This infection can present with a spectrum of infection ranging from local cellulitis to aortic endocarditis. Developing endocarditis is rare from this organism with only a few case reports in the literature. We presented a case of E. rhusiopathiae bacteremia that led to aortic valve endocarditis with a Gerbode defect within the mitral valve complicated with an acute exacerbation of congestive heart failure, necessitating emergent valve replacement surgery, with eventual permanent pacemaker due to complete heart block. We intend to highlight some unusual characteristics of this infection including thrombocytopenia and hyponatremia. It is important to identify this infection in early stages to prevent the late disseminating complications including endocarditis.

1. Introduction

Erysipelothrix rhusiopathiae (E. rhusiopathiae) is an encapsulated, non-spore forming, facultative aerobic, catalase-negative, oxidase negative, Gram-positive bacillus.1,2 Most human infections arise from environmental or occupational exposure, most commonly associated with marine, livestock, avian handling, and dog bites/scratches 3,4,5. E. rhusiopathiae infection in humans, closely follows swine infection. It has three presentations described here from most localized to most diffuse. Most locally, erysipeloid is a mild local cutaneous infection. More diffusely is a diffuse generalized cutaneous infection. And lastly, an invasive septic form most often associated with endocarditis 4. Despite the ubiquitous habitat in the environment, this organism remains a relatively rare cause for infective endocarditis.6 E. rhusiopathiae endocarditis is associated with poor outcomes with a nearly 38 % mortality rate.7 The invasive septic form is uncommon, with only 60-some case reports in the literature. 8 Herein, we present a case of a 57-year old woman with E. rhusiopathiae infective Aortic valve endocarditis who developed a Gerbode defect.

2. Case presentation

A 57 year old woman with no past medical history presented to the hospital for 3 weeks of weakness and fatigue. She developed progressively worsening dyspnea on exertion where she now had trouble walking up one flight of stairs without taking a break. She also noted decreased appetite, nausea, and a 12 pound weight loss over this period. She described history of an insect bite on her left thigh which presented as an erythematous plaque and a black center scar, approximately one month prior to admission. A few days after the insect bite, she had subjective fevers and non-bloody, non-bilious vomiting for two days and was treated with a course of unknown oral antibiotics from her primary physician. Her job involved working on her computer from home, owned a cat and dog, had a garden, and did not fish or noted any other injuries other than the insect bite.

On physical examination, she was tachycardic and afebrile. She was noted to have jugular venous distention, a large diastolic murmur heard best at the right upper sternal border, bilateral crackles on lung auscultation, and bilateral lower extremity edema. She had Leukocytosis of 11.6×10³/uL (4.8–10.8×10³/ uL), hemoglobin of 10.6 g/dL(12–16 g/dL), thrombocytopenia at 36,000/uL (150,000–450,000/uL). She had electrolyte abnormalities with hyponatremia of 119 mmol/L (136–145 mmol/L) and serum osmolality of 260mOsm/L (280–295mOsm/L), and hypokalemia of 3.1 mmol/L (3.5–5.1 mmol/L). Other lab abnormalities included an elevated BNP at 2563 pg/mL (<100 pg/ml), C-reactive protein at 30.10mg/L (<1mg/ L), an erythrocyte sedimentation rate of 83 mm/h (0–30 mm/h). Chest x -ray revealed bilateral pleural effusions and interstitial edema. An initial transthoracic echocardiogram(TTE) revealed severe aortic regurgitation with vegetations on the aortic leaflets and a left ventricular ejection fraction (LVEF) of 60 % with grade III diastolic dysfunction (Fig. 1). She was started on IV broad spectrum antibiotics with vancomycin and piperacillin-tazobactam.

Fig. 1.

Presentation of vegetation on aortic valve.

Initial gram stains of her blood cultures showed gram positive rods that were not identified via rapid multiplex PCR (biofire). Subsequently, the cultures were identified as Erysipelothrix rhusipathiae. Her antibiotics were changed to Penicillin G, and the patient was transferred to a higher level facility with cardiothoracic surgery capabilities. Her dyspnea did not improve from admission despite appropriate antibiotics, and she subsequently develop atrial fibrillation with rapid ventricular response (RVR). Pre-operative transesophageal echocardiogram (TEE) showed vegetations on all three aortic valve leaflets. The patient underwent a planned aortic valve replacement (AVR) which was complicated with incidental intraoperative finding of an aortic valve to right atrium fistula (Gerbode defect). During surgical repair of the Gerbode defect, tissue samples from pathology revealed a valvular abscess. Intraoperative photos were shown in Fig. 2.

Fig. 2.

(left) Left ventricular outflow tract to right atrium fistula (right) right and non-coronary cusp of aortic valve perforation with multiple vegetation on aortic valve.

Thrombocytopenia was resolved within the 10 days after initiation of appropriate antibiotic and prior to surgery. After the surgery, hospital course was further complicated by a new onset complete heart block with severe heart failure with reduced ejection fraction (HFrEF) of 25%–30 %.This necessitated placement of a permanent pacemaker. Hospital course was complicated by brief ventricular fibrillation with 30 s of cardiopulmonary resuscitation which later automatic implantable cardioverter defibrillator (AICD) was placed. Following up the patient 6 months after discharge, minimal improvement in ejection fraction noted despite compliance with goal directed medical therapy (GDMT).

3. Discussion

Our case highlights a rare case of E. rhusiopathiae infection that led to aortic valve endocarditis and congestive heart failure that required valve replacement which concomitantly had electrolyte imbalance and thrombocytopenia. Erysipelothrix is commonly an occupation-related infection that can be associated with farm animals or marine life,2 and it can also be found in domesticated animals such as dogs and pigs.9 Transmission of E. rhusiopathiae has also been seen from insects who collect a blood meal from mice and birds.10 Although the source of transmission could not be confirmed for our patient, it can be inferred from the history that the vector may have been an insect which caused an erythematous plaque.

Infection with E. rhusiopathiae can have three stages; acute septic form, subacute urticarial form and chronic endocarditis. Acute form can present as cellulitis 7–14 days following the infiltration of the bacterium into the skin. Other manifestations include fever, arthralgia, diffuse cutaneous bullas. Endocarditis is a rare presentation which develops from local infection.11 Our patient presented with a local papule which progressed to bacteremia then ultimately infective endocarditis. The similarity of our case can be the presentation of the patient’s symptoms such as skin lesions and valvular heart involvement which are the classic presentations of E. rhusiopathiae cardiac involvement.12 As presented in prior case reports, infective endocarditis in E. rhusiopathiae infection can involve the aortic valve,13,14 which is similar to our case.

There were no reported data for accompanied hyponatremia and hypokalemia with this infection, therefore, it can represent the rarity of our case, revealing some unusual manifestations with E. rhusiopathiae. Although these electrolyte abnormalities may not directly be attributable to this organism, these manifestations have been presented in our case. For instance, Legionella pneumoniphila is one of the morst common causes of infection-induced hyponatremia, despite the mechanism of this phenomenon being poorly understood. Additionally, other infectious organisms such as Mycobacterium tuberculosis, Rickettsia typhi, HIV, Cryptococcus neoformans, and Malaria spp. can cause hyponatremia via additional unknown mechanisms.15 Thrombocytopenia and arteritis possibly due to neuraminidase inhibitors having been found in the rats infected with E. rhusiopathiae, likewise in our case.16

Besides endocarditis, during the surgery, our patient was found to have a Gerbode defect which is a fistula between the left ventricle and right atrium. Gerbode defect is mainly caused by surgery, however, the degree of Gerbode defect that is caused by non-iatrogenesis can be due to Myocardial infarction (MI), blunt cardiac trauma, and endocarditis. The rationale behind the endocarditis-induced Gerbode defect is the reopening of the congenital defect in the membranous atrio-ventricular septum due to inflammation.17 Ramirez et al. showed a case report of Gerbode defect with E. rhusiopathiae in a dog,18 however, we could not find any reports of Gerode defect due to E. rhusiopathiae infection in humans. In this case, we provided some unusual manifestations of E. rhusiopathiae infection including electrolyte imbalance and Gerbode defect, that previously were not reported in the literature, it is important to lighten up these new findings for future consideration of this disease management.