1145
Infective Endocarditis of a Native Valve Due to Acinetobacter : Case Report and Review Jeremy D. Gradon, Edward K. Chapnick, and Larry I. Lutwick
From the Division of Infectious Diseases, Maimonides Medical Center, Brooklyn, New York
A case of community-acquired infective endocarditis of a native valve that was caused by
Acinetobacter calcoaceticus subspecies anitratus is presented. The previously reported cases are
Infective endocarditis (IE) of a native valve that is caused by Acinetobacter organisms is rare. To date, 15 cases have been reported in the English-language literature [1-12]. We present a case of community-acquired native valve IE caused by Acinetobacter calcoaceticus subspecies anitratus and review the previously reported cases. A previously healthy 48-year-old woman was admitted to the hospital with a 4-week history of intermittent fever, chills, malaise, and weight loss. She had no history of valvular heart disease, recent dental work, penetrating wounds, hospitalizations, or intravenous drug abuse. She had seen a private physician during the first week of her illness. He prescribed an empirical 10-day course of oral amoxicillin, which lowered her temperature; however, upon cessation of the therapy, the fever recurred. She was found to be anemic, and hospitalization was advised. Upon admission to the hospital, she appeared to be chronically ill and was not experiencing acute distress. Her temperature was 101°F. The oral cavity was intact with no obvious dental lesions. There were no cutaneous signs indicative of trauma or drug abuse. Cardiac examination revealed a 1/6 systolic murmur in the mitral area. Abdominal examination was remarkable for a nontender spleen that was 4 cm in diameter. The remainder of the physical examination was unremarkable. She had no evidence of splinter hemorrhages, Osler's nodes, Janeway lesions, Roth's spots, or other peripheral stigmata of IE. On admission the white blood cell count was 14,000/mm 3 (85% polymorphonuclear leukocytes and
Received 22 October 1991; revised 24 January 1992. Reprints or correspondence (present address): Jeremy D. Gradon, Medical Branch, Division of AIDS, National Institute of Allergy and Infectious Diseases, 6003 Executive Boulevard, Rockville, Maryland 20892. Clinical Infectious Diseases 1992;14:1145-8 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1405-0020$02.00
10% band forms), and the hematocrit was 27%. Results of the remainder of the routine laboratory tests were normal. Echocardiography showed thickening of the mitral and aortic valve leaflets and mild mitral regurgitation but no definite vegetations. Five blood specimens from five separate sites were drawn within 24 hours of admission. Antibiotic therapy was withheld, pending culture results. On the second hospital day, a diffuse maculopapular rash involving the trunk, extremities, palms, and soles developed; it faded spontaneously within 24 hours. The lesions were dusky red and varied in size (from 3 to 6 mm in diameter). On the third day of hospitalization, the patient developed nausea, abdominal pain, and a fever (temperature, 104°F). Emergency computed tomography of the abdomen showed splenomegaly with large areas of mixed attenuation consistent with abscess formation. Therapy with intravenous imipenem (500 mg every 6 hours) was started, and an emergency laparotomy was performed. At operation, an enlarged spleen (19 X 12 X 7 cm; weight, 470 g) was found and removed. Pathological examination of the spleen revealed multiple abscesses and areas of infarction. The next day, cultures of all five blood specimens were reported to be positive for a small gram-negative coccobacillus, which was subsequently identified as A. anitratus sensitive only to gentamicin, imipenem, and cefotaxime. The same organism was subsequently isolated from the abscess in the spleen. The patient was treated with intravenous imipenem for 4 weeks and was discharged in good health. She remains well on follow-up. A summary of data on the previously reported cases of native valve IE ,is listed in table 1. The characteristics of the six reported cases of prosthetic valve endocarditis due to Acinetobacter species are listed in table 2. The genus Acinetobacter consists of one species—cakoaceticus. Two subspecies, anitratus and /woffi, are recognized. This taxonomic classification was introduced in 1968. Until then various genera had been described, and confusion over
Downloaded from http://cid.oxfordjournals.org/ at University of Sussex on August 21, 2015
reviewed, and therapy for this disorder is discussed. The presence of a transient maculopapular rash involving the palms and soles but sparing the face is suggested as a possible early clinical clue to the diagnosis. Native valve endocarditis caused by Acinetobacter species is an acute, aggressive illness that is more likely to be fatal than the prosthetic valve form; of the previously described patients, five of 15 with native valve endocarditis and one of six with prosthetic valve endocarditis died. In the appropriate clinical setting, we recommend therapy with an antimicrobial agent known to be active against Acinetobacter organisms when blood cultures are reported to yield oxidase-negative, gram-negative coccobacilli until the final identification of the microorganism is known.
1146
Acinetobacter Endocarditis
CID 1992;14 (May)
Table 1. Summary of data on native valve endocarditis due to Acinetobacter species. Underlying cardiac disease
Affected valve
Factors predisposing to IE Splenomegaly
Duration of illness
[1] [2]
8/M 19/M
18 d 4d
CHD ?RHD
Aortic
[3]
23/M
6w
? RHD
Aortic
[4]
52/M
4w
Aortic
[5]
31/M
3d
Bicuspid and aortic valves None
Aortic
[6] [7]
18/F 32/F
2w 1d
RHD None
Mitral Aortic
? iv drug abuse
[8]
13/F
14 d
None
Aortic
? Septic abortion
—
[9] [10] [10] [10] [11]
46/M 11/F 22/F 26/M 27/M
26 d ? 4w 2d 4d
None CHD CHD RHD None
Stab wounds Middle ear infection Dental work ? Burns, iv catheters
_ _
[PR]
48/F
28 d
None
[Reference]
Maculopapular rash _
Mitral Mitral and aortic ? Mitral
Dental work
?
+
+
+
—
+
?
+
Oxytetracycline Erythromycin, tetracycline streptomycin Chloramphenicol, penicillin None
Outcome Lived Lived
Died Died
—
Chloramphenicol, ampicillin, tetracycline Penicillin Ampicillin, chloramphenicol Penicillin, gentamicin, isoniazid Gentamicin/cephapirin ? ? Chloramphenicol Imipenem
Lived Lived Lived Lived Died
+
Imipenem
Lived
— —
_
+
Antibiotic therapy
Lived
Lived Died Died
NOTE. IE = infective endocarditis; CHD = congenital heart disease; ? = unknown; — = absent; RHD = rheumatic heart disease; + = present; and PR = present report.
taxonomy existed; Acinetobacter was classified as Mima and Herellea. In 1968 oxidase-negative, non-nitrate-reducing, catalase-positive, gram-negative bacteria were placed in the genus Acinetobacter [17]. Acinetobacter species are ubiquitous in the environment. These organisms can be isolated from virtually 100% of soil and water samples, which may account for up to 50% of the organisms present. The skin of as many as 25% of healthy, nonhospitalized adults is colonized with Acinetobacter species [18], and up to 7% of these individuals have transient pharyngeal colonization [19]. Of the two subspecies ofAcinetobacter, A. calcoaceticus variety /woffi has a predilection for the genitourinary tract, while A. calcoaceticus variety anitratus is found at other body sites [20]. These two subspecies have accounted for 0.6%-2% of cases of nosocomial gram-negative bacteremia in different series [21, 22]. Acinetobacter organisms do not possess any formal virulence factors and therefore are, in general, opportunistic pathogens. However, these organisms are often resistant to multiple antimicrobial agents [23]. The resistance that is demonstrated results from aminoglycoside-modifying enzyme or /3-lactamase production and other plasmid-mediated mechanisms [24-26]. Since Acinetobacter organisms are ubiquitous in the envi-
ronment and are part of the indigenous flora of humans, many potential primary sources of infection exist. Eight of the 20 cases reviewed above had no identifiable inciting event leading to endocarditis. The 12 identified events leading to IE with Acinetobacter species are dental work (three patients), open heart surgery (two), and intravenous drug abuse, septic abortion, stab wounds, burns with intravenous catheters in place, upper respiratory tract infection with epistaxis, chronic otitis media, and motor vehicle accident (one each). Thus, any breach of the integument can result in seeding of a heart valve by Acinetobacter organisms. Recently, community-acquired acinetobacter pneumonia among Australian Aborigines has been reported [27], as has an outbreak among foundry workers [28]. In 1966 Shea and Phillips [5] proposed that mima endocarditis be recognized as a distinct clinical syndrome (which has subsequently been shown not to be the case). Of interest, however, is the mention made of a maculopapular rash involving the palms and soles. This occurrence has been reported in two of the previous cases [3, 5] and was also present transiently in our patient on day 2 of hospitalization. Acinetobacter organisms do not possess any virulence factors and therefore do not invade tissues once their source of
Downloaded from http://cid.oxfordjournals.org/ at University of Sussex on August 21, 2015
Age (y)/sex
Gradon, Chapnick, and Lutwick
CID 1992;14 (May)
Table 2. Summary of data on prosthetic valve endocarditis due to Prosthetic valve affected
Onset of prosthetic valve endocarditis after valve replacement
Acinetobacter
Predisposing factor
Age (y)/sex
A. calcoaceticus subspecies
[13]
40/?
anitratus
Mitral
3d
OHS
[13]
38/?
anitratus
Mitral
1d
OHS
[14]
56/?
/woffi
Mitral
[15]
48/M
/woffi
Mitral and aortic
31 mo
URI, epistaxis
[16]
47/M
/woffi
Aortic
14 y
MVA
[16]
52/M
/woffi
Aortic
2 mo
species.
Splenomegaly
Rash —
—
Dental work
+
Antibiotic therapy
Chloramphenicol, penicillin, erythromycin — Penicillin, streptomycin, methicillin ? Methicillin, chloramphenicol, colistin, nitrofurazone Petechiae Ampicillin, kanamycin, penicillin — Cefotaxime, gentamicin — Cefotaxime, gentamicin
Outcome Lived
Lived
Died
Lived
Lived Lived
NOTE. ? = information not available; OHS = open heart surgery; — = not present; URI = upper respiratory infection; MVA = motor vehicle accident; and + = present.
introduction has been removed. However, because of the presence of multiple antibiotic resistance mechanisms, bacteremia due to these organisms requires broad-spectrum antibiotic therapy. Most strains are now resistant to many antibiotics, including ampicillin, carbenicillin, cefotaxime, geritamicin, and chloramphenicol. Therapy should be based on the sensitivities of the specific strain isolated. Imipenem, to date, is uniformly effective against Acinetobacter organisms. An alternative therapeutic option is a combination of a 13-lactam agent and an aminoglycoside [23]. The patient that we have described had evidence of splenic embolization with abscess formation and splenic infarction. Splenic involvement in patients with IE is common and has been reported in 20%-57% of cases of IE [29]. It is more common with prolonged illness. Four of 11 reported cases of native valve IE due to Acinetobacter species and two of six cases of prosthetic valve endocarditis due to Acinetobacter species were noted to have splenomegaly. Splenomegaly would thus appear to be a common but not dominant feature of acinetobacter IE. In summary, it is difficult to make any firm statements regarding IE caused by Acinetobacter species. There are wide variations in the presentations and clinical course of the disease. Patients with rheumatic or congenital heart disease tend to have an acute onset of illness with a significant incidence of heart failure and peripheral embolization; death occurred in two of nine reported cases [3, 4]. Among patients with normal heart valves, disease onset is acute with a high incidence of visceral embolization, and the mortality rate is
higher (three of five patients died [7, 8, 12]). Among patients with prosthetic heart valves, disease appears to be less aggressive than the native valve form; five of six patients survived. None of these patients required surgical intervention. Treatment of IE should be based on the sensitivity of the individual isolate. Empirical broad-spectrum therapy for acinetobacter infections (e.g., imipenem/cilastatin) should be considered for any patient with IE for whom oxidasenegative, gram-negative coccobacilli are isolated from blood cultures. The therapy can be adjusted when the identity and antimicrobial susceptibilities of the infecting organism are known.
Acknowledgment
The authors thank Ann Borlo for expert secretarial assistance in the preparation of the manuscript.
References 1. Pike RM, Schulze ML, McCullough M. Isolation of Mima polymorpha from a patient with subacute bacterial endocarditis. Am J Clin Pathol 1951;21:1094-6. 2. Minzter A. Human infection caused by the Mimeae organisms. Report of a case of presumably healed bacterial endocarditis due to Herellea vaginicola. Arch Intern Med 1956;98:352-5. 3. King OH, Copeland GD, Berton WM. Cardiovascular lesions of the Mimeae organisms. Am J Med 1963;35:241-50. 4. Hirsch SR, Koch ML. Herellea (Bacterium anitratum) endocarditisreport of case. JAMA 1964;187:148-50.
Downloaded from http://cid.oxfordjournals.org/ at University of Sussex on August 21, 2015
[Reference]
1147
1148
Acinetobacter Endocarditis
19. Rosenthal S, Tager IB. Prevalence of gram negative rods in the normal pharyngeal flora. Ann Intern Med 1975;83:355-7. 20. Hoffman S, Mabeck CE, Vejlsgaard R. Bacteriuria caused by Acinetobacter calcoaceticus biovars in a normal population and in general practice. J Clin Microbiol 1982;16:443-51. 21. Weinstein MP, Reller LB, Murphy JR, Lichtenstein KA. The clinical significance of positive blood cultures: a comprehensive analysis of 500 episodes of bacteremia and fungemia in adults. I. Laboratory and epidemiologic observations. Rev Infect Dis 1983;5:35-53. 22. Centers for Disease Control. Nosocomial infection surveillance, 1984. MMWR CDC Surveill Summ 1986;35:17SS-29SS. 23. Allen DM, Hartman BJ. Acinetobacter species. In: Mandell GL, Douglas RG Jr, Bennett JE, eds. Principles and practice of infectious diseases. 3rd ed. New York: Churchill Livingstone, 1990:1696-700. 24. Murray BE, Moellering RC Jr. Aminoglycoside-modifying enzymes among clinical isolates ofAcinetobacter calcoaceticus subsp. anitratus (Herellea vaginicola): explanation for high-level aminoglycoside resistance. Antimicrob Agents Chemother 1979;15:190-9. 25. Rolston KVI, Bodey GP. In vitro susceptibility ofAcinetobacter species to various antimicrobial agents. Antimicrob Agents Chemother 1986;30:769-70. 26. Hinchcliffe E, Vivian A. Naturally occuring plasmids in Acinetobacter calcoaceticus: a P class R factor of restricted host range. J Gen Microbiol 1980;116:75-80. 27. Anstey NM, Currie BJ, Withnall KM. Community-acquired acinetobacter pneumonia in the Northern Territory of Australia. Clin Infect Dis 1992;14:83-91. 28. Cordes LG, Brink EW, Checko PJ, et al. A cluster of Acinetobacter pneumonia in foundry workers. Ann Intern Med 1981;95:688-93. 29. Scheid WM, Sande MA. Endocarditis and intravascular infections. In: Mandell GL, Douglas RG Jr, Bennett JE, eds. Principles and practice of infectious diseases. 3rd ed. New York: Churchill Livingstone, 1990:670-706.
Downloaded from http://cid.oxfordjournals.org/ at University of Sussex on August 21, 2015
5. Shea DW, Phillips JH. Mimeae endocarditis: a clinical syndrome? Am J Med Sci 1966;252:201-5. 6. Almog C, Sompolinsky D, Itzchak I, Nahum A. Bacterial endocarditis due to Minna polymorpha. Isr J Med Sci 1967;3:875-9. 7. Thompson WR. H. vaginicola endocarditis in a heroin addict [letter]. JAMA 1971;215:982. 8. Clinicopathologic Conference: Fever, friction rub and pulmonary edema in a 13-year-old girl. J Tenn Med Assoc 1972;65:1108-4. 9. Altman KA, Sacks F. Bronchopneumonia and endocarditis caused by Acinetobacter anitratun (HereIlea vaginicola). N Y State J Med 1979;79:1434-5. 10. Rao KNA, Kotian M, Prabhu SGS. Infective endocarditis due to Acinetobacter calcoaceticus. ' J Postgrad Med 1980;26:186-91. 11. Pal RB, Sujatha V, Kale VV. Acinetobacter calcoaceticus causing subacute bacterial endocarditis [letter]. Lancet 1981;2:313. 12. Cumberland NS, Jones KP. Hospital acquired native valve endocarditis caused by Acinetobacter calcoaceticus and treated with imipenem/ cilastin. J R Army Med Corps 1987;133:156-8. 13. Stein PD, Harken DE, Dexter L. The nature and prevention of prosthetic valve endocarditis. Am Heart J 1966;71:393-407. 14. Yeh TJ, Anabtawi IN, Cornett VE, White A, Stem WH, Ellison RG. Bacterial endocarditis following open heart surgery. Ann Thorac Surg 1967;3:29-36. 15. Block PC, DeSanctis RW, Weinberg AN, Austen WG. Prosthetic valve endoc a rditis. J Thorac Cardiovasc Surg 1970;60:540-8. 16. Weinberger I, Davidson E, Rotenberg Z, Fuchs J, Agmon J. Prosthetic valve endocarditis caused by Acinetobacter calcoaceticus subsp. /woffi. J Clin Microbiol 1987;25:955-7. 17. Henriksen SD. Moraxella, Acinetobacter and the Mimeae. Bacteriol Rev 1973;37:522-61. 18. Al-Khoja MS, Darrell JH. The skin as a source of Acinetobacter and Moraxella species occurring in blood cultures. J Clin Pathol 1979;32:497-9.
CID 1992;14 (May)
Infective Endocarditis of a Native Valve Due to Acinetobacter : Case Report and Review Jeremy D. Gradon, Edward K. Chapnick, and Larry I. Lutwick
From the Division of Infectious Diseases, Maimonides Medical Center, Brooklyn, New York
A case of community-acquired infective endocarditis of a native valve that was caused by
Acinetobacter calcoaceticus subspecies anitratus is presented. The previously reported cases are
Infective endocarditis (IE) of a native valve that is caused by Acinetobacter organisms is rare. To date, 15 cases have been reported in the English-language literature [1-12]. We present a case of community-acquired native valve IE caused by Acinetobacter calcoaceticus subspecies anitratus and review the previously reported cases. A previously healthy 48-year-old woman was admitted to the hospital with a 4-week history of intermittent fever, chills, malaise, and weight loss. She had no history of valvular heart disease, recent dental work, penetrating wounds, hospitalizations, or intravenous drug abuse. She had seen a private physician during the first week of her illness. He prescribed an empirical 10-day course of oral amoxicillin, which lowered her temperature; however, upon cessation of the therapy, the fever recurred. She was found to be anemic, and hospitalization was advised. Upon admission to the hospital, she appeared to be chronically ill and was not experiencing acute distress. Her temperature was 101°F. The oral cavity was intact with no obvious dental lesions. There were no cutaneous signs indicative of trauma or drug abuse. Cardiac examination revealed a 1/6 systolic murmur in the mitral area. Abdominal examination was remarkable for a nontender spleen that was 4 cm in diameter. The remainder of the physical examination was unremarkable. She had no evidence of splinter hemorrhages, Osler's nodes, Janeway lesions, Roth's spots, or other peripheral stigmata of IE. On admission the white blood cell count was 14,000/mm 3 (85% polymorphonuclear leukocytes and
Received 22 October 1991; revised 24 January 1992. Reprints or correspondence (present address): Jeremy D. Gradon, Medical Branch, Division of AIDS, National Institute of Allergy and Infectious Diseases, 6003 Executive Boulevard, Rockville, Maryland 20892. Clinical Infectious Diseases 1992;14:1145-8 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1405-0020$02.00
10% band forms), and the hematocrit was 27%. Results of the remainder of the routine laboratory tests were normal. Echocardiography showed thickening of the mitral and aortic valve leaflets and mild mitral regurgitation but no definite vegetations. Five blood specimens from five separate sites were drawn within 24 hours of admission. Antibiotic therapy was withheld, pending culture results. On the second hospital day, a diffuse maculopapular rash involving the trunk, extremities, palms, and soles developed; it faded spontaneously within 24 hours. The lesions were dusky red and varied in size (from 3 to 6 mm in diameter). On the third day of hospitalization, the patient developed nausea, abdominal pain, and a fever (temperature, 104°F). Emergency computed tomography of the abdomen showed splenomegaly with large areas of mixed attenuation consistent with abscess formation. Therapy with intravenous imipenem (500 mg every 6 hours) was started, and an emergency laparotomy was performed. At operation, an enlarged spleen (19 X 12 X 7 cm; weight, 470 g) was found and removed. Pathological examination of the spleen revealed multiple abscesses and areas of infarction. The next day, cultures of all five blood specimens were reported to be positive for a small gram-negative coccobacillus, which was subsequently identified as A. anitratus sensitive only to gentamicin, imipenem, and cefotaxime. The same organism was subsequently isolated from the abscess in the spleen. The patient was treated with intravenous imipenem for 4 weeks and was discharged in good health. She remains well on follow-up. A summary of data on the previously reported cases of native valve IE ,is listed in table 1. The characteristics of the six reported cases of prosthetic valve endocarditis due to Acinetobacter species are listed in table 2. The genus Acinetobacter consists of one species—cakoaceticus. Two subspecies, anitratus and /woffi, are recognized. This taxonomic classification was introduced in 1968. Until then various genera had been described, and confusion over
Downloaded from http://cid.oxfordjournals.org/ at University of Sussex on August 21, 2015
reviewed, and therapy for this disorder is discussed. The presence of a transient maculopapular rash involving the palms and soles but sparing the face is suggested as a possible early clinical clue to the diagnosis. Native valve endocarditis caused by Acinetobacter species is an acute, aggressive illness that is more likely to be fatal than the prosthetic valve form; of the previously described patients, five of 15 with native valve endocarditis and one of six with prosthetic valve endocarditis died. In the appropriate clinical setting, we recommend therapy with an antimicrobial agent known to be active against Acinetobacter organisms when blood cultures are reported to yield oxidase-negative, gram-negative coccobacilli until the final identification of the microorganism is known.
1146
Acinetobacter Endocarditis
CID 1992;14 (May)
Table 1. Summary of data on native valve endocarditis due to Acinetobacter species. Underlying cardiac disease
Affected valve
Factors predisposing to IE Splenomegaly
Duration of illness
[1] [2]
8/M 19/M
18 d 4d
CHD ?RHD
Aortic
[3]
23/M
6w
? RHD
Aortic
[4]
52/M
4w
Aortic
[5]
31/M
3d
Bicuspid and aortic valves None
Aortic
[6] [7]
18/F 32/F
2w 1d
RHD None
Mitral Aortic
? iv drug abuse
[8]
13/F
14 d
None
Aortic
? Septic abortion
—
[9] [10] [10] [10] [11]
46/M 11/F 22/F 26/M 27/M
26 d ? 4w 2d 4d
None CHD CHD RHD None
Stab wounds Middle ear infection Dental work ? Burns, iv catheters
_ _
[PR]
48/F
28 d
None
[Reference]
Maculopapular rash _
Mitral Mitral and aortic ? Mitral
Dental work
?
+
+
+
—
+
?
+
Oxytetracycline Erythromycin, tetracycline streptomycin Chloramphenicol, penicillin None
Outcome Lived Lived
Died Died
—
Chloramphenicol, ampicillin, tetracycline Penicillin Ampicillin, chloramphenicol Penicillin, gentamicin, isoniazid Gentamicin/cephapirin ? ? Chloramphenicol Imipenem
Lived Lived Lived Lived Died
+
Imipenem
Lived
— —
_
+
Antibiotic therapy
Lived
Lived Died Died
NOTE. IE = infective endocarditis; CHD = congenital heart disease; ? = unknown; — = absent; RHD = rheumatic heart disease; + = present; and PR = present report.
taxonomy existed; Acinetobacter was classified as Mima and Herellea. In 1968 oxidase-negative, non-nitrate-reducing, catalase-positive, gram-negative bacteria were placed in the genus Acinetobacter [17]. Acinetobacter species are ubiquitous in the environment. These organisms can be isolated from virtually 100% of soil and water samples, which may account for up to 50% of the organisms present. The skin of as many as 25% of healthy, nonhospitalized adults is colonized with Acinetobacter species [18], and up to 7% of these individuals have transient pharyngeal colonization [19]. Of the two subspecies ofAcinetobacter, A. calcoaceticus variety /woffi has a predilection for the genitourinary tract, while A. calcoaceticus variety anitratus is found at other body sites [20]. These two subspecies have accounted for 0.6%-2% of cases of nosocomial gram-negative bacteremia in different series [21, 22]. Acinetobacter organisms do not possess any formal virulence factors and therefore are, in general, opportunistic pathogens. However, these organisms are often resistant to multiple antimicrobial agents [23]. The resistance that is demonstrated results from aminoglycoside-modifying enzyme or /3-lactamase production and other plasmid-mediated mechanisms [24-26]. Since Acinetobacter organisms are ubiquitous in the envi-
ronment and are part of the indigenous flora of humans, many potential primary sources of infection exist. Eight of the 20 cases reviewed above had no identifiable inciting event leading to endocarditis. The 12 identified events leading to IE with Acinetobacter species are dental work (three patients), open heart surgery (two), and intravenous drug abuse, septic abortion, stab wounds, burns with intravenous catheters in place, upper respiratory tract infection with epistaxis, chronic otitis media, and motor vehicle accident (one each). Thus, any breach of the integument can result in seeding of a heart valve by Acinetobacter organisms. Recently, community-acquired acinetobacter pneumonia among Australian Aborigines has been reported [27], as has an outbreak among foundry workers [28]. In 1966 Shea and Phillips [5] proposed that mima endocarditis be recognized as a distinct clinical syndrome (which has subsequently been shown not to be the case). Of interest, however, is the mention made of a maculopapular rash involving the palms and soles. This occurrence has been reported in two of the previous cases [3, 5] and was also present transiently in our patient on day 2 of hospitalization. Acinetobacter organisms do not possess any virulence factors and therefore do not invade tissues once their source of
Downloaded from http://cid.oxfordjournals.org/ at University of Sussex on August 21, 2015
Age (y)/sex
Gradon, Chapnick, and Lutwick
CID 1992;14 (May)
Table 2. Summary of data on prosthetic valve endocarditis due to Prosthetic valve affected
Onset of prosthetic valve endocarditis after valve replacement
Acinetobacter
Predisposing factor
Age (y)/sex
A. calcoaceticus subspecies
[13]
40/?
anitratus
Mitral
3d
OHS
[13]
38/?
anitratus
Mitral
1d
OHS
[14]
56/?
/woffi
Mitral
[15]
48/M
/woffi
Mitral and aortic
31 mo
URI, epistaxis
[16]
47/M
/woffi
Aortic
14 y
MVA
[16]
52/M
/woffi
Aortic
2 mo
species.
Splenomegaly
Rash —
—
Dental work
+
Antibiotic therapy
Chloramphenicol, penicillin, erythromycin — Penicillin, streptomycin, methicillin ? Methicillin, chloramphenicol, colistin, nitrofurazone Petechiae Ampicillin, kanamycin, penicillin — Cefotaxime, gentamicin — Cefotaxime, gentamicin
Outcome Lived
Lived
Died
Lived
Lived Lived
NOTE. ? = information not available; OHS = open heart surgery; — = not present; URI = upper respiratory infection; MVA = motor vehicle accident; and + = present.
introduction has been removed. However, because of the presence of multiple antibiotic resistance mechanisms, bacteremia due to these organisms requires broad-spectrum antibiotic therapy. Most strains are now resistant to many antibiotics, including ampicillin, carbenicillin, cefotaxime, geritamicin, and chloramphenicol. Therapy should be based on the sensitivities of the specific strain isolated. Imipenem, to date, is uniformly effective against Acinetobacter organisms. An alternative therapeutic option is a combination of a 13-lactam agent and an aminoglycoside [23]. The patient that we have described had evidence of splenic embolization with abscess formation and splenic infarction. Splenic involvement in patients with IE is common and has been reported in 20%-57% of cases of IE [29]. It is more common with prolonged illness. Four of 11 reported cases of native valve IE due to Acinetobacter species and two of six cases of prosthetic valve endocarditis due to Acinetobacter species were noted to have splenomegaly. Splenomegaly would thus appear to be a common but not dominant feature of acinetobacter IE. In summary, it is difficult to make any firm statements regarding IE caused by Acinetobacter species. There are wide variations in the presentations and clinical course of the disease. Patients with rheumatic or congenital heart disease tend to have an acute onset of illness with a significant incidence of heart failure and peripheral embolization; death occurred in two of nine reported cases [3, 4]. Among patients with normal heart valves, disease onset is acute with a high incidence of visceral embolization, and the mortality rate is
higher (three of five patients died [7, 8, 12]). Among patients with prosthetic heart valves, disease appears to be less aggressive than the native valve form; five of six patients survived. None of these patients required surgical intervention. Treatment of IE should be based on the sensitivity of the individual isolate. Empirical broad-spectrum therapy for acinetobacter infections (e.g., imipenem/cilastatin) should be considered for any patient with IE for whom oxidasenegative, gram-negative coccobacilli are isolated from blood cultures. The therapy can be adjusted when the identity and antimicrobial susceptibilities of the infecting organism are known.
Acknowledgment
The authors thank Ann Borlo for expert secretarial assistance in the preparation of the manuscript.
References 1. Pike RM, Schulze ML, McCullough M. Isolation of Mima polymorpha from a patient with subacute bacterial endocarditis. Am J Clin Pathol 1951;21:1094-6. 2. Minzter A. Human infection caused by the Mimeae organisms. Report of a case of presumably healed bacterial endocarditis due to Herellea vaginicola. Arch Intern Med 1956;98:352-5. 3. King OH, Copeland GD, Berton WM. Cardiovascular lesions of the Mimeae organisms. Am J Med 1963;35:241-50. 4. Hirsch SR, Koch ML. Herellea (Bacterium anitratum) endocarditisreport of case. JAMA 1964;187:148-50.
Downloaded from http://cid.oxfordjournals.org/ at University of Sussex on August 21, 2015
[Reference]
1147
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