Case Reports in Infectious Diseases

Volume 2013 (2013), Article ID 923034, 4 pages

http://dx.doi.org/10.1155/2013/923034

Case Report

Septicemia and Aortic Valve Endocarditis due to Erysipelothrix rhusiopathiae in a Homeless Man

Dean Campbell and Mark Cowan

University of Maryland School of Medicine, Baltimore, MD 21201, USA

Received 11 February 2013; Accepted 19 March 2013

Academic Editors: L. M. Bush, S. Dogra, and P. O. Sumba

Copyright © 2013 Dean Campbell and Mark Cowan. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract.

We report a case of bacterial endocarditis due to Erysipelothrix rhusiopathiae in a homeless man with no animal exposure. His course was complicated by an allergic reaction to ampicillin, urinary bladder infection, respiratory failure, and acute kidney injury. He recovered completely after aortic valve replacement and a 6-week course of intravenous ceftriaxone.

1. Background

Erysipelothrix rhusiopathiae is a gram-positive rod causing swine erysipelas. It is a zoonotic infection in humans, with meat (swine) and fish handlers being at greatest risk. It most commonly causes erysipeloid, a localized cellulitis caused by direct bacterial invasion of cuts or abrasions in the skin. However, the skin infection can become generalized, and the organism can produce acute systemic septicemia. We report the case of a patient with E. rhusiopathiae bacteremia complicated by renal failure, respiratory failure, and aortic valve endocarditis.

2. Case Presentation

A 51-year-old Caucasian man without significant past medical history presented to a community hospital with a two-week history of shortness of breath and new onset chest pain. These symptoms were accompanied by the appearance of a rash on his fingers that spread up to his hands and wrists, but which had resolved before presentation to health care. Physical exam was significant for fever to 38.1°C, but otherwise normal vital signs. There was diffuse rhonchi heard bilaterally and a diastolic murmur heard best at the heart base. Significant laboratory values included: WBC count 14,500/mm³ with 40% segmental neutrophils and 44% bands, hematocrit 25.4%, blood urea nitrogen 96 mg/dL, and serum creatinine 2.4 mg/dL. The liver function tests were normal, as was the coagulation profile. Urinalysis was significant for hematuria with >100 white blood cells. Leukocyte esterase was positive. Electrocardiogram showed a normal sinus rhythm without conduction abnormalities, and his initial chest X-ray was normal.

The patient had a history of moderate alcohol use. He had a remote history of intravenous heroin abuse, although he had not used in 20 years. He was homeless, lived in his car, and worked as a mechanic. He denied any exposures to pigs or fish, although he occasionally encountered deer and rabbits in the woods where he lived. He denied eating any undercooked meat.

The patient was pancultured, and intravenous ampicillin-sulbactam was initiated. On the fourth hospital day, the lab reported that the blood cultures were growing a gram-positive rod they could not identify, and the cultures were sent to a reference laboratory for analysis. A transthoracic echocardiogram revealed a thickened aortic valve with a possible vegetation, and moderate aortic insufficiency. The patient’s respiratory status declined over the next 2 days, and he required intubation and mechanical ventilation. Chest X-ray demonstrated evolving pulmonary edema. He was then transferred to our academic medical center for further workup and management.

On transfer the patient remained febrile. HEENT exam was significant for poor dentition and a normal fundus. Neck exam revealed elevated jugular venous pressure while lying flat and on positive pressure ventilation. Lung sounds were coarse bilaterally. Cardiac exam revealed a III/IV diastolic murmur heard best at the left lower sternal border. There were no splinter hemorrhages, Osler’s nodes, or Janeway lesions. Electrocardiogram was normal. Computed tomography of the chest revealed large bilateral pleural effusions and pulmonary edema consistent with pulmonary edema, without evidence of septic emboli. A transesophageal echocardiogram showed multiple aortic valve vegetations with severe aortic regurgitation. The reference laboratory identified the gram-positive rod as Erysipelothrix rhusiopathiae. The patient developed an allergic reaction to ampicillin manifested as a maculopapular rash across his chest and was switched to intravenous ceftriaxone. He underwent an uncomplicated aortic valve replacement with a bioprosthetic valve. Surgical cultures were sent and were negative. The patient was sent to a long-term care facility to finish a six-week course of intravenous antibiotics and for rehabilitation. He made a full recovery and was in good health on followup visit 8 months later.

3. Discussion

Rhusiopathiae (formerly insidiosa) is the sole pathogenic member of the genus Erysipelothrix, which also includes the species tonsillarum and a third as yet unnamed species [1, 2]. It was first isolated by Koch in 1880 [3] and was described as the causative agent in swine erysipelas in 1886 [4, 5]. It was recognized as a pathogenic microorganism in humans in 1909 when Rosenbach described its isolation from the cutaneous lesions of erysipeloid [6]. It is the causative agent in a number of agriculturally important diseases in pigs, turkeys, chickens, ducks, shellfish, emus, and sheep. In humans, several distinct clinical syndromes have been described, and the organism is generally considered an occupational disease resulting from contact with infected animals or their waste products [2].

3.1. Epidemiology

The most important reservoir of E. rhusiopathiae in human infection is thought to be swine, although birds and rodents are frequently infected, and many different types of animal may carry the organism, including insects. It has a worldwide distribution with isolates detected in culture from Africa, Asia, Australia, the Americas, and Europe. The organism is shed by diseased swine in all bodily fluids, even if the animal is clinically well, with an average of 20–40% of healthy swine harboring the organism, usually detected in the tonsils (oropharynx) or the feces [2]. In the environment, the organism can remain viable for up to two weeks in water, several months in picked bacon or smoked ham [7], and long periods of time in exterior fish slime [8], contaminated soil, or animal carcasses [9]. The most important risk factor is occupational exposure to animals likely to harbor the organism, as seen in farmers, butchers, veterinarians, fishermen, slaughterhouse workers, abattoir workers, and housewives [1, 7]. Other less common affected occupations include meat inspectors, knackers, animal caretakers, lobstermen, bone button makers, game handlers, fertilizer workers, cooks, seal and whale hunters, crabbers, bakers, furriers, leather makers, soap makers, and stockyard workers [8]. Seafood workers appear to be especially at risk [9]. Infection is usually through scratches or puncture wounds in the skin, although penetration through intact skin has been reported [10]. Additionally, infection by E. rhsiopathiae may be underdiagnosed due to the resemblance it bears to other infections, as well as the difficulty in isolating or identifying the pathogen [11]. Human-to-human transmission has not been documented.

3.2. Bacteriology

Morphologically, E. rhusiopathiae is a thin, pleomorphic, nonsporulating gram-positive rod [3]. It is nonmotile, cannot ferment sucrose, and forms clear colonies [2]. It is mildy α-hemolytic, and a facultative anaerobe [12]. It requires various amino acid additives, as well as riboflavin and small amounts of oleic acid to grow [13]. The organism is negative for catalase, oxidase, methyl red, indole, and Voges-Proskauer reactions [14]. More recent detection methods have used an API Coryne system strip [15] or PCR-based techniques [16]. These studies are generally performed only at a reference laboratory and on specific request by the referring hospital or physician. Immune evasion by E. rhusiopathiae can take two distinct forms. In the absence of specific host antibodies (i.e., de novo infection), the organism is able to evade phagocytosis by immune cells. This may be due to formation of a heat labile capsule by the organism, which has been implicated as a virulence factor in mice [17]. In the presence of specific antibodies, the organism can continue to replicate intracellularly, despite having undergone phagocytosis by immune cells [18]. It has been shown that neuraminidase plays a significant role in bacterial attachment and subsequent invasion into host cells [11]. The mechanism for this is not known. Sensitivity testing of strains of E. rhusiopathiae from nine pigs and one human were performed by Venditti et al. [19], and Fidalgo et al. [20]. They demonstrated good susceptibility of the organism to penicillin, imipenem, cefotaxime, ceftriaxone, piperacillin, clindamycin, and fluoroquinolones. 6/10 isolates were highly resistant to vancomycin; 4/10 were intermediate. Teicoplanin and daptomycin were somewhat better than vancomycin but were judged by the authors to be unsatisfactory. 60–80% were inhibited by erythromycin, tetracycline, and chloramphenicol. There was no activity with trimethoprim-sulfamethoxazole or aminoglycoside antibiotics. These studies imply that β-lactam antibiotics are the drugs of choice for the organism, with fluoroquinolones as an acceptable alternative in lactamase allergic or intolerant patients. The resistance of the organism to vancomycin occurs via intrinsic resistance rather than acquired resistance and relies on the vanC gene [21]. This has potentially important clinical consequences. The Gram stain, appearance, and catalase negativity may initially suggest Lactobacillus, Actinomyces, Corynebacterium (Diphtheroids), Streptococcus, or even Enterococcus species. Not all of these species are fully characterized in all labs, and therefore E. rhusiopathiae may be missed. Since the Gram stain shows a gram-positive rod, clinicians may be led to choose vancomycin empirically, and unless the organism is identified, they may inadequately treat the infection [22].

3.3. Clinical Characteristics

E. rhusiopathiae infection in humans takes three common forms [1, 2]. Most commonly, a mild, cutaneous infection termed erysipeloid forms in the area of the inoculation. It is seen after an incubation period of ~4 days (range 1–7 d). Most cases occur in the summer and early fall and affect men more often than women. Reported ages range from 10 to 72 years old (mean 45). The lesion lasts from 2 to 4 weeks and is self-limiting. A more severe cutaneous form can occur, associated with a diffuse, purpuric rash, which is blue or purple and has well-defined, raised borders. There is pain and pruritis, and the rash has a predominantly peripheral distribution. The most severe form of the disease occurs typically with a subacute onset. Preceding rash is often reported, and pharyngitis may be associated with the prodrome if consumption of infected material was the mechanism of transmission [23]. Blood cultures are generally positive for the organism, and characteristically there is concomitant endocarditis [7, 24], although this is not universal [25, 26]. 60% of the cases involve the aortic valve. Valve replacement is necessary in 35%, and mortality is 40% despite early recognition and appropriate antibiotics [27]. There can be perivalvular and myocardial abscesses [28, 29]. Physicians must have a high index of suspicion for Erysipelothrix to avoid empirically prescribing ineffective agents such as vancomycin and aminoglycosides [30]. It has been associated with acute leukemia in a child [31], and septicemia in a neonate [32]. There are accounts of occurrence in adults with lupus [33, 34], HIV [35], oropharyngeal cancer [36], necrotizing fasciitis [37], colon perforation [38], and several reports of association with septic arthritis [39–41]. Demonstrated consequences of septicemia include acute renal failure [42] and multiple brain infarctions [43]. Recently, there has also been a reported case of Erysipelothrix pneumonia in an immunocompetent patient, who likely contracted the illness from feeding his cow in a barn while smoking. The authors of the study suggested that although there have not yet been reports of Erysipelothrix entering the body via inhalation, the pneumonia likely developed via inhalational transmission of the organism [44].

4. Conclusion

Erysipelothrix rhusiopathiae is an uncommon cause of septicemia and endocarditis. Awareness of this organism is imperative, as proper microbiologic testing is essential in the diagnosis, and appropriate antibiotic choices can only be made through identification of the organism. It most commonly causes a self-limited skin infection, but as seen in our case, can cause life-threatening illness.

References

A. C. Reboli and W. E. Farrar, “Erysipelothrix rhusiopathiae: an occupational pathogen,” Clinical Microbiology Reviews, vol. 2, no. 4, pp. 354–359, 1989.

C. J. Brooke and T. V. Riley, “Erysipelothrix rhusiopathiae: bacteriology, epidemiology and clinical manifestations of an occupational pathogen,” Journal of Medical Microbiology, vol. 48, no. 9, pp. 789–799, 1999.

R. Koch, Investigations into the Etiology of Traumatic Infectious Diseases, New Sydenham Society, London, UK, 1880.

J. M. Robson, R. Mcdougall, S. Van Der Valk, S. D. Waite, and J. J. Sullivan, “Erysipelothrix rhusiopathiae: an uncommon but ever present zoonosis,” Pathology, vol. 30, no. 4, pp. 391–394, 1998.

F. A. Loeffler, “Experimentalle Untersuchungen uber Schweinerotlauf,” Arbeiten Aus Der Kaiserlichen Gesundheitsamte, vol. 1, pp. 46–55, 1886.

F. J. Rosenbach, “Experimentelle, morphologische und klinische Studie über die krankheitserregenden Mikroorganismen des Schweinerotlaufs, des Erysipeloids und der Mäusesepsis,” Zeitschrift für Hygiene und Infektionskrankheiten, vol. 63, no. 1, pp. 343–369, 1909.

D. C. Hill and J. N. Ghassemian, “Erysipelothrix rhusiopathiae endocarditis: clinical features of an occupational disease,” Southern Medical Journal, vol. 90, no. 11, pp. 1147–1148, 1997.

R. L. Wood, “Erysipelothrix infection,” in Diseases Transmitted From Animals to Man, W. T. Hubbert, W. F. McCullough, P. R. Schnurrenberger, and C. C. Thomas, Eds., pp. 271–281, Springfield, Ill, USA, 6th edition, 1975.

T. C. Gilchrist, “Erysipeloid, with a record of 329 cases, of which 323 were caused by crab bites, or lesions produced by crabs,” Journal of Cutaneous Diseases, vol. 22, pp. 507–519, 1904.

G. F. McGinnes and F. Spindle, “Erysipeloid condition among workers in a bone button factory due to the bacillus of swine erysipelas,” American Journal of Public Health, vol. 24, pp. 32–35, 1934.

Q. Wang, B. J. Chang, and T. V. Riley, “Erysipelothrix rhusiopathiae,” Veterinary Microbiology, vol. 140, no. 3-4, pp. 405–417, 2010.

A. C. Reboli and W. E. Farrar, “The genus Erysipelothrix,” in The Prokaryotes: A Handbook on the Biology of Bacteria: Ecophysiology, Isolation, Identification, Applications, A. Balows, H. G. Truper, M. Dworkin, W. Harder, and K. Schleifer, Eds., pp. 1629–1642, Springer, New York, NY, USA, 2nd edition, 1992.

R. L. Wood, “Erysipelas,” in Diseases of Swine, A. D. Leman, B. E. Straw, W. L. Mengeling, S. D’Allaire, and D. J. Taylor, Eds., pp. 475–486, Iowa State University Press, Ames, Iowa, USA, 7th edition, 1992.

G. E. Cottral, Manual of Standardized Methods for Veterinary Microbiology, Cornell University Press, Ithaca, NY, USA, 1978.

A. Soto, J. Zapardiel, and F. Soriano, “Evaluation of API Coryne system for identifying coryneform bacteria,” Journal of Clinical Pathology, vol. 47, no. 8, pp. 756–759, 1994.

C. J. Brooke, V. McLaughlin, B. J. Mee, and T. V. Riley, “An investigation of “crayfish poisoning” in Western Australia,” Medical Journal of Australia, vol. 170, no. 6, p. 288, 1999.

Y. Shimoji, Y. Yokomizo, T. Sekizaki, Y. Mori, and M. Kubo, “Presence of a capsule in Erysipelothrix rhusiopathiae and its relationship to virulence for mice,” Infection and Immunity, vol. 62, no. 7, pp. 2806–2810, 1994.

Y. Shimoji, “Pathogenicity of Erysipelothrix rhusiopathiae: virulence factors and protective immunity,” Microbes and Infection, vol. 2, no. 8, pp. 965–972, 2000.

M. Venditti, V. Gelfusa, A. Tarasi, C. Brandimarte, and P. Serra, “Antimicrobial susceptibilities of Erysipelothrix rhusiopathiae,” Antimicrobial Agents and Chemotherapy, vol. 34, no. 10, pp. 2038–2040, 1990.

S. G. Fidalgo, C. J. Longbottom, and T. V. Riley, “Susceptibility of Erysipelothrix rhusiopathiae to antimicrobial agents and home disinfectants,” Pathology, vol. 34, no. 5, pp. 462–465, 2002.

R. R. S. Nelson, “Intrinsically vancomycin-resistant Gram-positive organisms: clinical relevance and implications for infection control,” Journal of Hospital Infection, vol. 42, no. 4, pp. 275–282, 1999.

S. A. Dunbar and J. E. Clarridge, “Potential errors in recognition of Erysipelothrix rhusiopathiae,” Journal of Clinical Microbiology, vol. 38, no. 3, pp. 1302–1304, 2000.

J. B. McClain, “Erysipelothrix rhusiopathiae,” in Principles and Practice of Infectious Diseases, G. L. Mandell, R. G. Douglas, and J. E. Bennett, Eds., pp. 1599–1600, Churchill-Livingstone, New York, NY, USA, 3rd edition, 1990.

J. P. Heidrich, M. Stahl, R. Dittmann, M. Maass, and W. Solbach, “Mitral valve endocarditis caused by Erysipelothrix rhusiopathiae,” Deutsche Medizinische Wochenschrift, vol. 126, no. 15, pp. 431–433, 2001.

S. Abedini and A. Lester, “Erysipelothrix rhusiopathiae bacteremia after a dog bite,” Ugeskrift for Laeger, vol. 159, no. 28, pp. 4400–4401, 1997.

M. G. Schuster, P. J. Brennan, and P. Edelstein, “Persistent bacteremia with Erysipelothrix rhusiopathiae in a hospitalized patient,” Clinical Infectious Diseases, vol. 17, no. 4, pp. 783–784, 1993.

J. L. Nerad and D. R. Snydman, “Erysipelothrix rhusiopathiae,” in Infectious Diseases, S. L. Gorbach, J. G. Bartlett, and N. R. Blacklow, Eds., pp. 1440–1442, W. B. Saunders, Philadelphia, Pa, USA, 1992.

S. Nandish and N. Khardori, “Valvular and myocardial abscesses due to Erysipelothrix rhusiopathiae,” Clinical Infectious Diseases, vol. 29, no. 5, pp. 1351–1352, 1999.

A. Artz, S. Szabo, L. Zabel, and H. Hoffmeister, “Aortic valve endocarditis with paravalvular abscesses caused by Erysipelothrix rhusiopathiae,” European Journal of Clinical Microbiology and Infectious Diseases, vol. 20, no. 8, pp. 587–588, 2001.

T. Miura, K. Hashizume, T. Ariyoshi et al., “Active infective endocarditis due to Erysipelothrix rhusiopathiae: zoonosis caused by vancomycin-resistant gram-positive rod,” General Thoracic and Cardiovascular Surgery, vol. 61, no. 2, pp. 96–99, 2013.

G. Coman, I. Miron, C. Pânzaru, M. Cârlan, and E. Petraru, “Erysipelothrix rhusiopathiae bacteremia in a child with acute leukemia,” Revista medico-chirurgicala a Societatii de Medici si Naturalisti din Iasi, vol. 101, no. 1-2, pp. 218–221, 1997.

N. Jones and M. Khoosal, “Erysipelothrix rhusiopathiae septicemia in a neonate,” Clinical Infectious Diseases, vol. 24, no. 3, p. 511, 1997.

N. Thomas, M. Jesudason, U. Mukundan, T. J. John, M. S. Seshadri, and A. M. Cherian, “Infective endocarditis caused by Erysipelothrix rhusiopathiae in a patient with systemic lupus erythematosus,” Journal of Association of Physicians of India, vol. 44, no. 3, p. 223, 1996.

K. Totemchokchyakarn, S. Janwityanujit, B. Sathapatayavongs, and S. Puavilai, “Erysipelothrix rhusiopathiae septicemia in systemic lupus erythematosus,” International Journal of Dermatology, vol. 35, no. 11, pp. 818–820, 1996.

C. Marne, Lopéz de Juan, J. F. Lorenzo, and M. Galdós, “Bacteremia caused by Erysipelothrix rhusiopathiae in an HIV-positive patient,” Enfermedades Infecciosas y Microbiología Clínica, vol. 14, no. 6, pp. 403–404, 1996.

W. H. Sheng, P. R. Hsueh, C. C. Hung, C. T. Fang, S. C. Chang, and K. T. Luh, “Fatal outcome of Erysipelothrix rhusiopathiae bacteremia in a patient with oropharyngeal cancer,” Journal of the Formosan Medical Association, vol. 99, no. 5, pp. 431–434, 2000.

R. Simionescu, S. Grover, R. Shekar, and B. C. West, “Necrotizing fasciitis caused by Erysipelothrix rhusiopathiae,” Southern Medical Journal, vol. 96, no. 9, pp. 937–939, 2003.

R. A. Callon Jr. and P. G. Brady, “Toothpick perforation of the sigmoid colon: an unusual case associated with Erysipelothrix rhusiopathiae septicemia,” Gastrointestinal Endoscopy, vol. 36, no. 2, pp. 141–143, 1990.

M. E. Ruiz, J. S. Richards, G. S. Kerr, and V. L. Kan, “Erysipelothrix rhusiopathiae septic arthritis,” Arthritis and Rheumatism, vol. 48, no. 4, pp. 1156–1157, 2003.

J. L. . Bianchi-Llave, M. P. Perez-Barrio, F. J. Borrego-Utiel, and A. Liebana-Canada, “Septic arthritis caused by Erysipelothrix rhusiopathiae,” Enfermedades Infecciosas Y Microbiologia Clinica, vol. 14, no. 7, pp. 452–453, 1996.

P. G. Vallianatos, A. C. Tilentzoglou, and A. D. Koutsoukou, “Septic arthritis caused by Erysipelothrix rhusiopathiae infection after arthroscopically assisted anterior cruciate ligament reconstruction,” Arthroscopy, vol. 19, no. 3, p. 26, 2003.

A. Fernandez-Crespo, A. Serra, J. Bonet, and M. Giminez, “Acute oliguric renal failure in a patient with an Erysipelothrix rhusiopathiae bacteremia and endocarditis,” Nephron, vol. 74, no. 1, p. 231, 1996.

S. B. Ko, D. E. Kim, H. M. Kwon, and J. K. Roh, “A case of multiple brain infarctions associated with Erysipelothrix rhusiopathiae endocarditis,” Archives of Neurology, vol. 60, no. 3, pp. 434–436, 2003.

M. Meric and S. Ozcan, “Erysipelothrix rhusipathiae pneumonia in an immunocompetent patient,” Journal of Medical Microbiology, vol. 61, no. 3, pp. 450–451, 2012.