Case Report Native Pulmonic Valve Endocarditis due to … · 2019. 7. 31. · Case Report Native...

Case ReportNative Pulmonic Valve Endocarditis due to Mycobacteriumfortuitum: A Case Report and Literature Review

Aaron M. Mulhall1 and Renee S. Hebbeler-Clark1,2

1Division of Pulmonary, Critical Care, and Sleep Medicine, University of Cincinnati Medical Center, 231 Albert Sabin Way,Cincinnati, OH 45267, USA2Division of Infectious Diseases, University of Cincinnati Medical Center, 231 Albert Sabin Way, Cincinnati, OH 45267, USA

Correspondence should be addressed to Aaron M. Mulhall; [email protected]

Received 8 May 2015; Revised 1 June 2015; Accepted 2 June 2015

Academic Editor: Daniela M. Cirillo

Copyright © 2015 A. M. Mulhall and R. S. Hebbeler-Clark. This is an open access article distributed under the Creative CommonsAttribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work isproperly cited.

Endocarditis secondary to Mycobacterium fortuitum is a rare entity often involving prosthetic valves and rarely native valves.Pulmonic valve endocarditis secondary to any organism is rare. We report the first case of native pulmonic valve endocarditissecondary toM. fortuitum and a literature review of native valveM. fortuitum endocarditis.

1. Introduction

Mycobacterium fortuitum, a member of rapidly growing non-tuberculous mycobacteria, is a well-known cause of skin andsoft tissue infections and postsurgical wound infections [1].Sporadic cases of endocarditis associated with this organismhave been reported, mostly involving prosthetic valves. Iso-lated pulmonic valve endocarditis caused by any organism israre, making up about 2% of all cases of infective endocarditis[2]. Nontuberculous mycobacteria pulmonic valve endo-carditis has never been reported in the literature. Here, wedescribe a case of native pulmonic valve endocarditis second-ary toM. fortuitum as well as a review of the literature.

2. Case Presentation

A 64-year-old female with a history of ventilator dependentrespiratory failure secondary to end-stage chronic obstructivepulmonary disease (COPD) and bioprosthetic mitral valvereplacement 8 years agowas admitted to themedical intensivecare unit (MICU) for worsening respiratory failure frompulmonary edema and multifocal pneumonia secondary toEscherichia coli. She was diuresed and completed a course of

antibiotics with ceftriaxone. A transesophageal echocardio-gram (TEE) was performed during this admission revealingsevere prosthetic mitral valve stenosis, mildly elevated pul-monary artery pressures, a normal tricuspid valve, and novegetation on any valve. She was ultimately transferred to along term postacute care hospital. Over the following month,the patient continued to decline in clinical status, and fur-ther investigation was undertaken. Rapid-growing mycobac-terium was isolated from three cultures for mycobacteriafrom a tracheal aspirate. Interferon Gamma Release Assay(IGRA) andM. tuberculosis complex polymerase chain reac-tion (PCR) of a tracheal aspirate were negative. Rapid-growing mycobacterium was isolated from multiple bloodcultures from a peripherally inserted central catheter (PICC)and from peripheral venipuncture. M. fortuitum was theorganism identified in all cultures. Empiric antibiotic therapywas initiated with amikacin, imipenem, and clarithromycin;and the PICC line was removed. The resistance-pattern con-firmed that the isolate was sensitive to amikacin and imipe-nem, but resistant to clarithromycin. The patient was ulti-mately readmitted to the MICU for hypotension and con-cerns for overdiuresis and volume depletion. A transthoracicechocardiogram (TTE) was performed (40 days after the pre-vious TTE and 12 days after initiation of antibiotics) revealing

Hindawi Publishing CorporationCase Reports in Infectious DiseasesVolume 2015, Article ID 274819, 4 pageshttp://dx.doi.org/10.1155/2015/274819

2 Case Reports in Infectious Diseases

Figure 1: Transthoracic echocardiogram showing a 10mm × 11mmvegetation (arrow) on the ventricular aspect of the pulmonic valve.

a new 10mm × 11mm vegetation on the ventricular aspect ofthe pulmonic valve, severe tricuspid regurgitation, and severeprosthetic valve mitral stenosis (Figure 1). The patient wasnot a candidate for pulmonic valve replacement and medicalmanagement was continued. Given the grim prognosis, thepatient ultimately decided to stop antibiotic therapy andentered hospicewhere she ultimately passed away.Thepatientcompleted 16 days of antibiotics at the time she was dis-charged to hospice.

3. Discussion

Mycobacterium fortuitum is a ubiquitous organism that canbe found in soil, dust, and tap water and is well known forcausing skin infections and postsurgical wound infections[1]. It belongs to the family of rapid-growing nontuberculousmycobacteria, meaning that it grows in culture within oneweek. Infections with this organism are often a result of directinoculation, usually as a result of posttraumatic infections,postsurgical wound infections, and catheter-associated infec-tions. Disseminated infections mostly occur in immunodefi-cient patients [3].

Endocarditis caused by this organism is uncommon,mostly affecting patients with prosthetic valves [4–6]. Endo-carditis of native cardiac valves due to M. fortuitum is a rareoccurrence, with only a small number of cases being reported[7–12] (Table 1). Upon review of the nine cases of native valveM. fortuitum endocarditis (including our own) the mean agewas 24.4 years old (range 0.5–64 years); the population was66% female; valves infected were 44% aortic, 44% tricuspid(one patient with both aortic and tricuspid vegetation), 22%mitral (one patient with both aortic and mitral vegetation),and 11% pulmonic; 56% had either an open or percutaneouscardiac procedure as the inciting event inoculating the patientand 22% were infected secondary to intravenous drug use;22% received a valve replacement or removal of implantedcardiac hardware; and 44% of patients were alive at the timeof their respective case report publication (in our case, thepatient entered hospice).

There is only anecdotal evidence for the recommendedtreatment of severe disseminatedM. fortuitum infections. All

reviewed cases of native valve endocarditis secondary to thisorganism were treated with parenteral amikacin plus two ofthe following: fluoroquinolone, cefoxitin, TMP/SMX, or amacrolide. These agents should be initiated and continuedfor several weeks (most cases were treated for 6 weeks) untilclinical improvement was identified and then transitioned tooral therapy with two effective agents for 6–12 months.

Our patient’s isolate was sensitive to amikacin and imipe-nem, but resistant to clarithromycin. It is difficult to deter-mine if the vegetation arose during antibiotic therapy, as shewas only treated for 12 days prior to finding this vegetation.Antibiotic resistance and bacterial control were not majorconcerns based on the isolate resistance-pattern. We believethat she likely developed this vegetation in the previousmonth when she was clinically declining from an unclearetiology. Unfortunately, in this case, we could not confirm, bytissue diagnosis, that the vegetation was due toM. fortuitum.This is because the patient was not a surgical candidate forpulmonic valve replacement and the family declined a post-mortem examination. While it is possible that the vegetationwas not due toM. fortuitum, it is highly unlikely in the settingof new cardiac valve vegetation and persistently positiveblood cultures forM. fortuitum.

There are a couple of potential mechanisms to explainhow our patient became infected. One possibility is that ourpatient had airway colonization with M. fortuitum relatedto her end-stage COPD and the organism entered herbloodstream, subsequently seeding her pulmonic valve. M.fortuitum is commonly isolated from respiratory cultures inpatients with underlying lung disease including COPD, pul-monary fibrosis, bronchiectasis, and prior pulmonary tuber-culosis infection [13].

It is thought that the mycobacteria in the lungs gainsaccess to the bloodstream via translocation. Previous studiesof M. tuberculosis suggest that the organism is ingestedby alveolar macrophages and then is transported by thesemacrophages and peripheral blood monocytes across thealveolar wall into the bloodstream. More recent evidencesuggests that mycobacteria can also invade type II alveolarepithelial cells and translocate across the epithelial wall intothe bloodstream [14]. Another potential mechanism is thatour patient acquired M. fortuitum by a catheter-associatedbloodstream infection that subsequently seeded her lungsand pulmonic valve. The propensity of M. fortuitum tocause catheter-related infections, its resistance to a numberof antibiotics, and its association with tap water and waterdistribution centers have some relationwith its ability to formbiofilms [15].

Our case is the first reported case of M. fortuitum nativevalve endocarditis affecting the pulmonic valve. It is alsothe first reported case to have the organism isolated from apulmonary source (tracheal aspirate) as well as the blood-stream. Even with antibiotics this disease is highly fatal andsource control with valve replacement/removal of infectioushardware greatly improves survival [12]. The extremely poorprognosis associated with this disease reinforces the needto consider endocarditis in any patient with Mycobacteriumbacteremia, regardless of species.

Case Reports in Infectious Diseases 3

Table1:Re

ported

caseso

fnativev

alve

endo

carditisc

ausedby

Mycobacteriu

mfortuitum.

Reference

Age

Gender

Valves

affected

Associated

procedures

Com

orbiditie

sOrganism

isolated

from

othersou

rces

Surgicaltherapy

Antibiotic

therapy

Survival

Our

patie

nt(2015)

64Female

Pulm

onic

Non

eEn

d-stageC

OPD

,biop

rosth

eticMVR,

mitralste

nosis

Trachealaspirate,

PICC

No

Amikacin,imipenem

,cla

rithrom

ycin

No

Vukovice

tal.[7]

12Female

Tricuspid

Bovine

patch

VSDrepair

Non

eNo

No

Not

repo

rted

Alivea

t12mon

ths

after

diagno

sis

2Female

Tricuspid

Bovine

patch

VSDrepair

Dow

nsynd

rome

No

No

Not

repo

rted

Alivea

t12mon

ths

after

diagno

sis

0.5

Male

Tricuspid

Bovine

patch

VSDrepair

Non

eVe

getatio

n,VS

Dpatch

VSDpatchremoval,

VSDrepair

Not

repo

rted

Alivea

t12mon

ths

after

diagno

sis

Natsagetal.[8]

49Female

Aortic,

tricuspid

IVDU

Skin

abscesses,

hepatitisC

No

No

TMP/SM

X,lin

ezolid,

ciprofl

oxacin

Alivea

t6weeks

after

diagno

sis

Collison

andTrehan

[9]

50Male

Mitral,

aortic

PCIand

stent

placem

ent

Coron

aryartery

disease,congestiv

eheartfailure

Not

repo

rted

AVR,

MVR,

coronary

artery

bypassgraft

Clarith

romycin,

imipenem

,moxifloxacin,

amikacin

No

Sing

hetal.[10]

54Female

Aortic

Hem

odialysis

Aorticste

nosis,m

itral

regurgitatio

n,ES

RDNo

No

TMP/SM

X,ciprofl

oxacin,

amikacin,clofazimine

No

Spelletal.[11]

47Male

Aortic

IVDU

Hum

anim

mun

odeficiency

virus

No

AVRoff

ered

(patient

declined)

Amikacin,

ciprofl

oxacin,

cefoxitin

No

Kuruvilaetal.[12]

20Female

Mitral

Ballo

onmitral

valvulotom

y

Rheumaticheart

disease

Cerebrospinalflu

idNo

Amikacin,

azith

romycin,

rifam

pin

No

VSD:ventricular

septaldefect;P

CI:p

ercutaneou

scoron

aryinterventio

n;IV

DU:intraveno

usdrug

use;CO

PD:chron

icob

structiv

epulmon

arydisease;ES

RD:end

-stage

renald

isease;PICC

:peripherally

inserted

centralcatheter;MVR:

mitralvalver

eplacement.

4 Case Reports in Infectious Diseases

Conflict of Interests

The authors declare that there is no conflict of interestsregarding the publication of this paper.

References

[1] D. E. Griffith, T. Aksamit, B. A. Brown-Elliott et al., “An officialATS/IDSA statement: diagnosis, treatment, and prevention ofnontuberculous mycobacterial diseases,” American Journal ofRespiratory and Critical Care Medicine, vol. 175, no. 4, pp. 367–416, 2007.

[2] K. Nishida, O. Fukuyama, and D. S. Nakamura, “Pulmonaryvalve endocarditis caused by right ventricular outflow obstruc-tion in association with sinus of valsalva aneurysm: a casereport,” Journal of Cardiothoracic Surgery, vol. 3, article 46,2008.

[3] B. A. Brown-Elliott and R. J. Wallace Jr., “Infections causedby nontuberculous mycobacteria,” in Principles and Practiceof Infectious Diseases, Elsevier Churchill Livingstone, Philadel-phia, Pa, USA, 7th edition, 2010.

[4] S. L. Narasimhan and T. W. Austin, “Prosthetic valve endo-carditis due to Mycobacterium fortuitum,” Canadian MedicalAssociation Journal, vol. 119, no. 2, pp. 154–155, 1978.

[5] R.G.Norenberg, G. K. Sethi, S.M. Scott, andT. Takaro, “Oppor-tunistic endocarditis following open-heart surgery,” Annals ofThoracic Surgery, vol. 19, no. 5, pp. 592–604, 1975.

[6] J. Olalla, M. Pombo, J. M. Aguado et al., “Mycobacteriumfortuitum complex endocarditis—case report and literaturereview,”ClinicalMicrobiology and Infection, vol. 8, no. 2, pp. 125–129, 2002.

[7] D. Vukovic, V. Parezanovic, B. Savic et al., “Mycobacteriumfortuitum endocarditis associated with cardiac surgery, Serbia,”Emerging Infectious Diseases, vol. 19, no. 3, pp. 517–519, 2013.

[8] J. Natsag, Z. Min, Y. Hamad, B. Alkhalil, A. Rahman, and R.Williams, “A mysterious gram-positive rods,” Case Reports inInfectious Diseases, vol. 2012, Article ID 841834, 4 pages, 2012.

[9] S. P. Collison and N. Trehan, “Native double-valve endocarditisby Mycobacterium fortuitum following percutaneous coronaryintervention,” Journal of Heart Valve Disease, vol. 15, no. 6, pp.836–838, 2006.

[10] M. Singh, A. Bofinger, G. Cave, and P. Boyle, “Mycobacteriumfortuitum endocarditis in a patient with chronic renal failure onhemodialysis,” Pathology, vol. 24, no. 3, pp. 197–200, 1992.

[11] D. W. Spell, J. G. Szurgot, R. W. Greer, and J. W. Brown III,“Native valve endocarditis due to Mycobacterium fortuitumbiovar fortuitum: case report and review,” Clinical InfectiousDiseases, vol. 30, no. 3, pp. 605–606, 2000.

[12] M. T. Kuruvila, P. Mathews, M. Jesudason, and A. Ganesh,“Mycobacterium fortuitum endocarditis and meningitis afterballoon mitral valvotomy,” Journal of Association of Physiciansof India, vol. 47, no. 10, pp. 1022–1023, 1999.

[13] W.-J. Koh, O. J. Kwon, K. Jeon et al., “Clinical significance ofnontuberculous mycobacteria isolated from respiratory speci-mens in Korea,” Chest, vol. 129, no. 2, pp. 341–348, 2006.

[14] L. E. Bermudez, F. J. Sangari, P. Kolonoski, M. Petrofsky, andJ. Goodman, “The efficiency of the translocation of Mycobac-terium tuberculosis across a bilayer of epithelial and endothelialcells as a model of the alveolar wall is a consequence of trans-port within mononuclear phagocytes and invasion of alveolar

epithelial cells,” Infection and Immunity, vol. 70, no. 1, pp. 140–146, 2002.

[15] L. Hall-Stoodley and H. Lappin-Scott, “Biofilm formation bythe rapidly growing mycobacterial species Mycobacterium for-tuitum,” FEMS Microbiology Letters, vol. 168, no. 1, pp. 77–84,1998.

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