HACEK organism: Difference between revisions

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==Pathophysiology==
==Pathophysiology==
All of these organisms are part of the normal oropharyngeal flora which grow slowly, prefer a carbon dioxide–enriched atmosphere and share an enhanced capacity to produce [[endocardial]] infections, especially in young children.
The pathogenesis of HACEK endocarditis is presumed to be related to colonization of the oropharynx with bacteria that gain access to the vascular space following either trauma or local infection. In addition to valvular infections in the heart, these organisms can also produce other infections such as [[bacteremia]], [[abscess|abscesses]], [[peritonitis]], [[otitis media]], [[conjunctivitis]], [[pneumonia]], [[peritonitis]], [[arthritis]] and [[osteomyelitis]], and [[periodontal infections]].
 
In addition to valvular infections in the heart, these organisms can also produce other infections such as [[bacteremia]], [[abscess]]es, [[peritonitis]], [[otitis media]], [[conjunctivitis]], [[pneumonia]], [[peritonitis]], [[arthritis]] and [[osteomyelitis]], and [[periodontal infections]].


==Epidemiology and Demographics==
==Epidemiology and Demographics==

Revision as of 15:52, 1 May 2013

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Template:GCC

Overview

HACEK organisms is a group of fastidious, slow growing, pleomorphic Gram negative bacilli which form part of the oropharynx commensals and require enhanced carbon dioxide tension for recovery in culture. HACEK refers to the initials of organisms including:

Pathophysiology

The pathogenesis of HACEK endocarditis is presumed to be related to colonization of the oropharynx with bacteria that gain access to the vascular space following either trauma or local infection. In addition to valvular infections in the heart, these organisms can also produce other infections such as bacteremia, abscesses, peritonitis, otitis media, conjunctivitis, pneumonia, peritonitis, arthritis and osteomyelitis, and periodontal infections.

Epidemiology and Demographics

HACEK organisms account for about 3% of cases of endocarditis,[2] with an insidious onset and subacute course. They are the most common Gram negative casue of endocarditis among patients who do not use intravenous drugs. Most patients with HACEK endocarditis have preexisting cardiac defects or prior dental manipulations. The duration of symptoms prior to diagnosis is reported to be longer than 2 weeks but shorter than 6 months.[3]

Diagnosis

Laboratory Studies

Given the fastidious growth requirements, HACEK bacteria are a recognized cause of culture-negative endocarditis. The organisms can be identified after subculture on 5 to 8% sheep blood and chocolate agar at 35 to 37°C for 48 to 72 hours in an aerobic atmosphere containing 5 to 10% CO2.[4] Although the mean duration for incubation of blood cultures until detection of growth is 3 to 5 days, up to 30 days may be required. Biochemical properties are used to differentiate members of the HACEK group. However, biopatterns may be varied by inoculum volume and growth conditions, which prompts the utilization of molecular techniques such as 16S rRNA sequencing.[5][6][7]

Treatment

The treatment of endocarditis caused by HACEK organisms should be based on antimicrobial susceptibility tests, including tests for β-lactamase ctivity. Since many of these organisms are slow growing, such tests can be problematic. Although there are limited published clinical data demonstrating the efficacy of ceftriaxone or ampicillin-sulbactam therapy, these drugs should be considered the regimens of choice for the treatment of patients with HACEK endocarditis.[8] Fluoroquinolones should be considered as an alternative agent for patients unable to tolerate β-lactam therapy. The American Heart Association recommends that native-valve and prosthetic-valve endocarditis be treated for 4 weeks and 6 weeks, respectively.[9] HACEK endocarditis is associated with a favorable prognosis, with a cure rate of 82 to 87% of patients with medical treatment alone or associated with surgery.[10]

References

  1. 1.0 1.1 Nørskov-Lauritsen N, Kilian M (2006). "Reclassification of Actinobacillus actinomycetemcomitans, Haemophilus aphrophilus, Haemophilus paraphrophilus and Haemophilus segnis as Aggregatibacter actinomycetemcomitans gen. nov., comb. nov., Aggregatibacter aphrophilus comb. nov. and Aggregatibacter segnis comb. nov., and emended description of Aggregatibacter aphrophilus to include V factor-dependent and V factor-independent isolates". Int. J. Syst. Evol. Microbiol. 56 (Pt 9): 2135–46. doi:10.1099/ijs.0.64207-0. PMID 16957111. Unknown parameter |month= ignored (help)
  2. Steckelberg JM, Melton LJ, Ilstrup DM, Rouse MS, Wilson WR (1990). "Influence of referral bias on the apparent clinical spectrum of infective endocarditis". Am. J. Med. 88 (6): 582–8. PMID 2346159. Unknown parameter |month= ignored (help)
  3. Das M, Badley AD, Cockerill FR, Steckelberg JM, Wilson WR (1997). "Infective endocarditis caused by HACEK microorganisms". Annu. Rev. Med. 48: 25–33. doi:10.1146/annurev.med.48.1.25. PMID 9046942.
  4. Brouqui P, Raoult D (2001). "Endocarditis due to rare and fastidious bacteria". Clin. Microbiol. Rev. 14 (1): 177–207. doi:10.1128/CMR.14.1.177-207.2001. PMC 88969. PMID 11148009. Unknown parameter |month= ignored (help)
  5. Das I, DeGiovanni JV, Gray J (1997). "Endocarditis caused by Haemophilus parainfluenzae identified by 16S ribosomal RNA sequencing". J. Clin. Pathol. 50 (1): 72–4. PMC 499719. PMID 9059363. Unknown parameter |month= ignored (help)
  6. Hamed KA, Dormitzer PR, Su CK, Relman DA (1994). "Haemophilus parainfluenzae endocarditis: application of a molecular approach for identification of pathogenic bacterial species". Clin. Infect. Dis. 19 (4): 677–83. PMID 7528552. Unknown parameter |month= ignored (help)
  7. Wormser GP, Bottone EJ, Tudy J, Hirschman SZ (1978). "Case report. Cardiobacterium hominis: review of prior infections and report of endocarditis on a fascia lata prosthetic heart valve". Am. J. Med. Sci. 276 (1): 117–26. PMID 727215.
  8. Francioli PB (1993). "Ceftriaxone and outpatient treatment of infective endocarditis". Infect. Dis. Clin. North Am. 7 (1): 97–115. PMID 8463657. Unknown parameter |month= ignored (help)
  9. Baddour LM, Wilson WR, Bayer AS; et al. (2005). "Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications: a statement for healthcare professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: endorsed by the Infectious Diseases Society of America". Circulation. 111 (23): e394–434. doi:10.1161/CIRCULATIONAHA.105.165564. PMID 15956145. Unknown parameter |month= ignored (help)
  10. Berbari EF, Cockerill FR, Steckelberg JM (1997). "Infective endocarditis due to unusual or fastidious microorganisms". Mayo Clin. Proc. 72 (6): 532–42. doi:10.1016/S0025-6196(11)63302-8. PMID 9179137. Unknown parameter |month= ignored (help)

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