This document discusses infective endocarditis (IE), including: - IE is caused by microbial infection of the heart endothelium or foreign bodies like prosthetic valves. It is life-threatening but uncommon. Morbidity and mortality remain high despite advances. - Incidence is estimated at 1.7-6.2 per 100,000 patient-years in Western countries and 17,000 cases per year in India, often affecting younger patients with rheumatic or congenital heart disease. - Staphylococcus aureus is the most common cause in developed nations while viridans group streptococci are common in developing countries. Multidrug resistance is a growing problem. - Diagnosis

1. DR. SUBODH KUMAR MAHTO
PGIMER,DR.RML HOSPITAL
NEW Delhi

2.  Microbial infection of the endothelial surface of the
heart or iatrogenic foreign bodies like prosthetic valves
or other intracardiac devices.
 Uncommon but life threatening infection
 Despite advances in diagnosis ,anti microbial therapy
and management of complication-high morbidity and
mortality

3.  Estimated incidence in Western population- 1.7 - 6.2
cases per 100,000 patient years,
 India- 17,000 episodes of IE per year
 In relatively young patients with underlying rheumatic
and congenital heart diseases.
Int J Cardiol 2005; 98: 253–260

5.  Local inflammation triggers endothelial cells to express
integrins of β1 family
 S. aureus and other pathogens carry fibronectin-binding
proteins on their surface.
 When activated, endothelial cells bind fibronectin via integrin
and provide an adhesive surface to circulating staphylococci.
 Internalization of S. aureus into valve endothelial cells (persist
and escape host defences and antibiotics, or multiply and
spread to distant organs).

6.  Also occur as a consequence of chewing and tooth brushing.
 Such spontaneous bacteraemia - low grade and short duration
[1– 100 cfu/ml of blood for 10 min]
 Both magnitude of bacteraemia and ability of the pathogen to
attach to damaged valves are important
 Its high incidence explain why most cases of IE are unrelated
to invasive procedures.
Ann Intern Med 1998;129: 761–769.

8. 1. IE with positive blood culture (85%)
- IE due to streptococci and enterococci
- IE due to staphylococci (aureus and CONS)
2. IE with negative blood cultures because of prior
antibiotic treatment
3. IE frequently a/w negative blood cultures
4. IE associated with constantly negative blood culture

9.  Viridans streptococci- S sanguis, S oralis (mitis), S
salivarius, S mutans, Gemella morbillorum.
 S milleri and S anginosus group (S intermedius,
anginosus, and constellatus)
 Abiotrophia defectiva and Granulicatella species/
nutritionally variant streptococci)- require broth
supplemented with pyridoxal hydrochloride or
cysteine.

10.  Enterococcus faecalis (90% )
 Rarely, by E. faecium and E. durans
 Highly tolerant to antibiotic-induced killing
 Eradication requires prolonged administration (up to
6 weeks) of synergistic bactericidal combinations of
cell wall inhibitors with aminoglycosides

11.  S aureus -most common cause of IE in developed world.
 Increase incidence due to- healthcare contact (eg,
intravascular catheters, surgical wounds, indwelling
prosthetic devices).
 Nonaddicts S aureus -left side of heart
 Mortality rates -25% to 40%.
 IDUs- tricuspid valve.
 Cure rates- high (85%)

12.  NVE- estimated incidence ~ 5% of all cases of
endocarditis.
 PVE- up to 52% of early onset PVE attributed to
CoNS.

14.  Fastidious Gram-negative bacilli
 Haemophilus parainfluenzae,
 H aphrophilus, H paraphrophilus, H influenzae,
 Actinobacillus actinomycetemcomitans,
 Cardiobacterium hominis,
 Eikenella corrodens,
 Kingella kingae, and K denitrificans

15.  Among Enterobacteriaceae- Salmonella most common
cause.
 Most cases - caused by S choleraesuis, S typhimurium,
and S enteritidis.
 Common features-Left-sided disease, large vegetations,
and involvement of architecturally normal valves
 Mortality rates -70%

16.  Male:female ratio -2.5:1
 Mean age -30 years.
 Affects normal valves in most cases.
 Left-sided endocarditis-early surgery with valve
replacement.
 Isolated right-sided IE-medical therapy may be curative.

17.  Mostly by Candida and Aspergillus
 Survival rate <20%
 Blood culture –positive in Candida ,negative in
Aspergiillus

18. Exp Clin Cardiol. 2012 Winter; 17(4): 175–178.

20.  Multidrug resistance- Viridans group streptococci.
 Oxacillin resistance- S. aureus (ORSA)
 Development of intermediate and highlevel resistance to
vancomycin - S. aureus & Vancomycin resistance- Enterococci
 S aureus surpassed Viridans group streptococci as leading
cause of IE.
 Overall worsening of average clinical course of patients with
endocarditis
Arch Intern Med. 2002;162:90 –94.

22.  Approximate incidence-1.5 to 3.3 cases per 1000
person years.
 Two thirds of these patients-no clinical evidence of
underlying heart disease
 Only 35% of IDUs with IE demonstrate heart
murmurs on admission.

23.  S. aureus -most common cause of right-sided IE in IDUs
 Left sided IE - caused equally by viridans group
streptococci and S aureus.
 Distribution –
◦ Tricuspid alone or in combination with others-73 %
◦ Aortic alone – 7 %;
◦ Mitral alone – 6 %;
◦ Aortic plus mitral - 1.5 %

24.  5-10% cases of IE
 Most frequently in IVDAs
 Mainly involve tricuspid valve
 Staph.aureus- 60-90%
 Prognosis good- in hospital mortality rate <10%

26. Symptoms % of Pts Signs % of Pts
Fever 80-85 Fever 80-90
Chills 42-75 Murmur 80-95
Sweats 25 Changing M 10-40
Anorexia 25-55 Neuro abn 30-40
Wt loss 25-35 Emboli 20-40
Malaise 25-40 Splenomegaly 15-50
Dyspnea 20-40 Clubbing 10-20
Cough 25 Peripheral manifestations
Stroke 13-20 Osler nodes 7-10
Myalgia/Arthral. 15-30 Splinters 5-15
Chest pain 8-35 Petechiae 10-40
Janeway lesion 6-10
Roth spots 4-10
Braunwald 8th Edition

28. 1. Nonspecific
2. Nonblanching
3. Linear reddish-brown lesions found under the nail bed
4. Usually do NOT extend the entire length of the nail

29. 1. More specific
2. Painful and erythematous nodules
3. Located on pulp of fingers and toes

30. 1. More specific
2. Erythematous, blanching macules
3. Nonpainful
4. Located on palms and soles

32.  New regurgitant heart murmur
 Embolic event of unknown etiology
 Sepsis of unknown origin
 Fever ( associated with intracardiac device, prosthetic valve,
CHD, previous h/o IE, IVU, any intervention, new
conduction disturbance, CHF, positive blood cultures,
vascular/ immunologic/neurologic signs and symptoms,
pulmonary embolism and peripheral abscess)

34. 1. According to Location
◦ Left sided native wall IE
◦ Left sided Prosthetic wall IE (PVE)
 Early PVE: < 1 year after surgery
 Late PVE: > 1 year after surgery
◦ Right sided IE
◦ Device related IE

35. 2. According to mode of Acquisition
 Health Care Associated
oNosocomial ( >48 hour after hospitalization)
oNon-Nosocomial ( <48 hour after hospitalization)
Home based nursing, IV therapy/ chemotherapy,
hemodialysis < 30 days before onset of IE
Hospitalized in acute care facility < 90 before onset of IE
Resident in nursing home/ long term care facility
 Community Acquired ( <48 hour after hospitalization)
 Intravenous drug abuse associated

36. 3. According to time of developememt
 Acute
◦ Toxic presentation
◦ Progressive valve destruction & metastatic infection
developing in days to weeks
◦ Most commonly caused by S. aureus
 Sub acute
◦ Mild toxicity
◦ Presentation over weeks to months
◦ Rarely leads to metastatic infection
◦ Most commonly S. viridans or enterococcus

37.  Relapse:
repeat episodes of IE caused by the same organism
<6 month after the initial episode
 Reinfection:
infection with different microorganism
or
Repeat episode of infection caused by the same
organism >6 month after initial episode

39.  Definite IE - Pathological confirmation from surgical
autopsy specimen.
 Probable IE - Persistant bacteremia and evidence of
either new valvular regurgitation or vascular
phenomena in face of underlying valvular heart
disease

40.  Only minority of patient with bonafied IE could be
classified as definite cases.
 IVU was not recognised as an important predisposing
condition.
 ECHO finding were not included.

41. 1. Definite infective endocarditis
 Pathological criteria
◦ Microorganisms demonstrated by culture or histological
examination of a vegetation, a vegetation that has
embolized, or an intracardiac abscess specimen; or
◦ Pathological lesions; vegetation or intracardiac abscess
confirmed by histological examination showing active
endocarditis
 Clinical criteria
◦ 2 major criteria; or
◦ 1 major criterion and 3 minor criteria; or
◦ 5 minor criteria

42. 2. Possible IE
◦ 1 major criterion and 1 minor criterion; or
◦ 3 minor criteria
3. Rejected IE
◦ Firm alternative diagnosis explaining evidence of IE; or
◦ Resolution of IE with antibiotic therapy for 4 days; or
◦ No pathological evidence of IE at surgery or autopsy, with
antibiotic therapy for 4 days; or
◦ Does not meet criteria for possible IE as above

43. 1. Blood culture positive for IE
 Typical microorganisms consistent with IE from 2 separate blood
cultures: Viridans streptococci, S. bovis, HACEK, S. aureus; or
community-acquired enterococci in the absence of a primary focus;
or
 Microorganisms consistent with IE from persistently positive blood
cultures : At least 2 positive cultures of blood samples drawn 12 h
apart; or all of 3 or a majority of 4 separate cultures of blood (with
first and last sample drawn at least 1 h apart)
or
 Single positive blood culture for Coxiella burnetii or anti–phase 1
IgG antibody titer >1:800

44. 2. Evidence of Endocardial involvement
Echocardiogram positive for IE defined as follows:
 Oscillating intracardiac mass on valve or supporting
structures, in the path of regurgitant jets, or on implanted
material inabsence of an alternative anatomic explanation;
 Abscess;
 New partial dehiscence of prosthetic valve;
 New valvular regurgitation (worsening or changing of
preexisting murmur not sufficient)

45.  Predisposition- predisposing heart condition, or IDU
 Fever- temperature 38°C
 Vascular- major arterial emboli, septic pulmonary infarcts,
mycotic aneurysm, ICH, conjunctival hemorrhages, and
Janeway’s lesions
 Immunologic - GN, Osler’s nodes, Roth’s spots, and RF
 Microbiological evidence- positive blood culture but does
not meet a major criterion or serological evidence of active
infection with organism consistent with IE

46. Microbiological
Diagnosis

47.  Positive blood cultures - cornerstones of diagnosis.
 Three sets taken including at least one aerobic and one
anaerobic each containing 10 mL of blood
 Prolonged culture- associated with rising likelihood of
contamination

48. 1. Inadequate microbiological techniques,
2. Infection with highly fastidious bacteria or nonbacterial
pathogens,
3. Previous administration of antimicrobial agents before
blood cultures were obtained
 Blood cultures - negative in up to 31 % of patients
Int J Cardiol 2005; 98: 253–260

50.  Electron microscopy -high sensitivity but time
consuming and expensive.
 Coxiella burnetii and Bartonella species -easily
detected by serological testing using indirect
immunofluorescence or ELISA
 Legionella -Immunological analysis of urine

51.  PCR - rapid and reliable detection of fastidious and non-
culturable agents in patients with IE.
Limitations
1. Lack of reliable application to whole blood samples,
2. Risk of contamination,
3. False negatives due to the presence of PCR inhibitors,
4. Inability to provide information concerning bacterial
sensitivity to antimicrobial agents
5. Persistent positivity despite clinical remission.

52. Microbiological diagnosis in culture-positive and culture-negative
infective endocarditis. IE = infective endocarditis; PCR =
polymerase chain reaction. *If the organism remains unidentified and the
patient is stable, consider antibiotic withdrawal and repeat blood
cultures.

54.  Sensitivity of TTE - 40 to 63%
 Sensitivity of TEE - 90 to 100%.
 Echo features suggestive of IE-
1. Vegetation
2. Abscess
3. Psuedoaneurysm
4. Perforation
5. Fistula
6. Valve aneurysm
7. Dehiscence of prosthetic valve

55.  False negative
1. Presence of preexisting severe lesions (MVP, degenerative
calcified lesions, prosthetic valves),
2. Vegetations are very small <2 mm,
3. Not yet present or already embolized.
 False positive-
Degenerative /myxomatous valve, SLE, advanced
malignancy (marantic endocarditis), chordal rupture.

59. Penicillin Sensitive Relative Penicillin Resistant
1. Cryst Penicillin G or
Ceftriaxone X 4 weeks
2. Cryst Penicillin G
or X 2 weeks
Ceftriaxone
plus
Gentamicin X 2 weeks
3. Vancomycin X 4 weeks
1. Cryst Penicillin G
or X 4 weeks
Ceftriaxone
plus
Gentamicin X 2 weeks
2. Vancomycin X 4 weeks

60. Penicillin Sensitive Penicillin Resistant
1. Cryst Penicillin G
or X 6 weeks
Ceftriaxone
with/without
Gentamicin X 2 weeks
2. Vancomycin X 6 weeks
1. Cryst Penicillin G
or X 6 weeks
Ceftriaxone
plus
Gentamicin X 6 weeks
2. Vancomycin X 6 weeks

61. Oxacillin Susceptible Oxacillin Resistant
1. Oxacillin/Nafcillin
or X 6 weeks
Cefazolin (penicillin allergic)
with/without
Gentamicin X 3-5 days
1. Vancomycin X 6 weeks

62. Oxacillin Susceptible Oxacillin Resistant
1. Oxacillin/Nafcillin X ≥ 6 weeks
plus
Rifampicin X ≥ 6 weeks
plus
Gentamicin X 2 weeks
1.Vancomycin X ≥ 6 weeks
plus
Rifampicin X ≥ 6 weeks
plus
Gentamicin X 2 weeks

63. Penicillin/Gentamicin/
Vancomycin Sensitive
Penicillin/Streptomycin/
Vancomycin Sensitive
1. Cryst Penicillin G or
Ampicillin X 4 - 6 weeks
plus
Gentamicin X 4 - 6 weeks
2. Vancomycin X 6 weeks
plus
Gentamicin X 6 weeks
1. Cryst Penicillin G or
Ampicillin X 4 - 6 weeks
plus
Streptomycin X 4 - 6 weeks
2. Vancomycin X 6 weeks
plus
Streptomycin X 6 weeks

64. Penicillin Resistant
Aminoglyco/Vanco Sensitive
Penicillin Aminoglycoside
Vancomycin Resistant
1. Ampicillin-Sulbactam
plus X 6 weeks
Gentamicin
(only for β Lactamase producing)
2. Vancomycin
plus X 6 weeks
Gentamicin
1. E faecium:
Linezolid or ≥ 8 weeks
Quinupristin-dafopristin
2. E faecalis:
 Imipenem/Cilastatin + Ampicillin
or ≥ 8 weeks
 Ceftriaxone* + Ampicillin
(dose is 4g/24hr)

65. 1. Ceftriaxone
or
2. Ampicillin – Sulbactam
or
3. Ciprofloxacin

66. Native valve Prosthetic Valve
1. Ampicillin-Sulbactam
plus X 4 - 6 weeks
Gentamicin
2. Vancomycin
plus
Gentamicin X 4 - 6 weeks
plus
Ciprofloxacin
1. Early (< 1 year)
Vancomycin + Cefepime +
Rifampicin X 6 weeks
plus
Gentamicin X 2 weeks
2. Late ( > 1 year)
Same as native valve
plus X 6 weeks
Rifampicin

67. Culture Negative Culture Positive
1. Ceftriaxone X 6 weeks
plus
Gentamicin X 2 weeks
With/without
Doxycycline X 6 weeks
1. Doxycycline X 6 weeks
plus
Gentamicin X 2 weeks

68.  Valve replacement after 7 to 10 days of antibiotic
therapy.
 Antibiotic-third generation cepahlosporin with
Gentamycin.
Arch Intern Med. 1980;140:199 –202.

69.  Left-sided - early surgery with valve replacement.
 Isolated right-sided - medical therapy may be
curative [preferred regimen –high dose Tobramycin
(8 mg/kg per day IV or IM OD) with either extended-
spectrum penicillin or ceftazidime or cefepime for 6
weeks.
Infection. 2004;32: 163–169.

70. 2 Phase therapy-
 Induction therapy– valve replacement and parental
Amphotericin B continued for 6 weeks.
 Suppressive therapy -with oral azoles lifelong
thereafter.
Clin Infect Dis. 2001;32:50–62.

71.  2 weeks therapy with oxacillin with/without gentamycin:
1. Methicillin susceptible S. aureus.
2. Absence of metastatic site of infection.
3. Absence of cardiac and extra cardiac complication.
4. < 20 mm vegetation
5. Absence of immunosuppresion CD4 (>200cells/mm)
with or without HIV
6. Absence of left sided valve infection

72.  Standard 4-6 weeks therapy for
1. Rt. HF, vegetation >20mm, acute respiratory failure,
acute renal failure, empyema
2. Associated left sided IE
3. IVU with severe immunosuppression with or
without HIV

74.  Proportion of CHD in patients with IE- varies
between 2-18%
 More frequently affect the right heart
 Prognosis better – mortality rate 10%

80.  Most frequent complication (50-60%)
 Most frequent indication for surgery
 Affects aortic (29%) and mitral valve (20%) mainly

81. CHF may develop acutely from-
1. Perforation of a native or bio prosthetic valve leaflet,
2. Rupture of infected mitral chordae,
3. Valve obstruction by bulky vegetations,
4. Sudden intracardiac shunts from fistulous tracts or
prosthetic dehiscence.
Circulation 2005 e394-e434

82. Persisting fever due to
 Inadequate antibiotic therapy
 Resistant organism
 Infected lines
 Locally uncontrolled infection
 Embolic complication
 Extra cardiac site of infection
 Adverse reaction to antibiotics.

83. Perivalvular abcess:
 Frequent in PVE (56-100%).
 In NVE more common in aortic valve (10-40%)
Fistula formation:
 1.6 % in IE.
 S.Aureus- most common organism (46%)
Peri valvular extension:
 Suspected in persisting high grade unexplained fever and A-V
block in ECG.
 TEE is modality of choice for diagnosis.

84.  Left sided IE: spleen and brain
 65% of embolic events involve CNS
 Right sided NVE / Pacemaker IE: Pulmonary embolism
 Overall embolic risk: 20-50%
 90% of CNS emboli lodge in the distribution of MCA.
 Risk reduces to 6-21% 2 weeks after therapy.

85.  In 20-40% of IE patients.
 Include: ischemic or hemorrhagic stroke, TIA, silent
cerebral embolism, infectious aneurysm, brain abscess,
meningitis , toxic encephalopathy and seizures.
 Most common organism: S. Aureus

86.  Overall mortality rate among IE patients with
ICMAs is 60%.
 Occurrence of ICMAs : 1.2% to 5% of cases,
underestimated because some ICMAs remain
asymptomatic and resolve with antimicrobial
therapy.

87.  Imaging procedures indicated in patients with-
1. Localized or severe headaches;
2. “Sterile” meningitis, especially if erythrocytes or
xanthochromia is present;
3. Focal neurological signs.
 Treatment- neurosurgery or endovascular therapy.

88.  Tender, pulsatile mass in a patient with IE
 Hematemesis, hematobilia, and jaundice- rupture of a
hepatic artery MA;
 Arterial HTN and hematuria- rupture of a renal MA;
 Massive bloody diarrhoea -rupture of an ECMA into
the small or large bowel.
Treatment- Long term suppressive antibiotic therapy
with Autologous venous grafts

89.  Acute renal failure: In 30% of patients
◦ Causes: immune complexes, renal infarction, nephrotoxic
drugs, contrast agents, HF, sepsis
◦ Hemodialysis may be required
 Rheumatic: Peripheral arthritis in 14%,
Spondylodiscitis in 3-15%

90.  Splenic abscess: splenic infarction common complication
of left-sided IE (40% of cases)
◦ Only 5% with splenic infarction develop splenic abscess.
◦ Viridans streptococci and S aureus each account for 40%
◦ Definitive treatment: splenectomy with appropriate
antibiotics
◦ If possible, splenectomy should be performed before
valve replacement surgery

91.  Myocarditis :
◦ Can cause cardiac failure
◦ Ventricular arrhythmia imply a poor prognosis
◦ Best assessed using TTE
 Pericarditis:
◦ Purulent pericarditis rare
◦ Ruptured psuedoaneurysm & fistula may communicate
with pericardium causing fatal consequenses

93.  IE is much more likely to result from frequent
exposure to random bacteremia associated with daily
activities than from bacteremia caused by a dental,
GI tract, or GU tract procedure.
 Prophylaxis may prevent an exceedingly small
number of cases of IE, if any, in individuals who
undergo a dental, GI tract, or GU tract procedure.

94.  The risk of antibiotic-associated adverse events
exceeds the benefit, if any, from prophylactic
antibiotic therapy.
 Maintenance of optimal oral health and hygiene may
reduce the incidence of bacteremia from daily
activities and is more important than prophylactic
antibiotics for a dental procedure to reduce the risk
of IE.

96. High-risk category
 Prosthetic cardiac valves, including bioprosthetic and
homograft valves
 Previous bacterial endocarditis
 Complex cyanotic congenital heart disease (e.g., single
ventricle states, TGA, TOF)
 Surgically constructed systemic-pulmonary shunts or
conduits

97. Moderate-risk category
 Congenital cardiac malformations other than those
listed in the high-risk and negligible-risk categories
 Acquired valvular dysfunction (e.g. RHD)
 Hypertrophic cardiomyopathy
 Mitral valve prolapse with valvular regurgitation
and/or thickened leaflets

98. Negligible-risk (no greater risk than general population)
 Isolated secundum ASD.
 Surgical repair of ASD, VSD, PDA (without residua > 6 mnth)
 Previous CABG.
 Mitral valve prolapse without valvular regurgitation
 Physiologic, functional or innocent heart murmur
 Previous Kawasaki disease without valvular dysfunction
 Previous rheumatic fever without valvular dysfunction
 Cardiac pacemakers and ICD.

99.  Dental extractions
 Periodontal procedures, including surgery, scaling, root planning,
probing and recall maintenance
 Dental implant placement and reimplantation of avulsed teeth
 Endodontic (root canal) instrumentation or surgery only beyond the
apex
 Subgingival placement of antibiotic fibers or strips
 Initial placement of orthodontic bands (but not brackets)
 Intraligamentary local anesthetic injections
 Prophylactic cleaning of teeth or implants, where bleeding is
anticipated

100.  Restorative dentistry (operative and prosthodontic) with or
without retraction cord
 Local anesthetic injections (non intraligamentary)
 Intracanal endodontic treatment (post-placement and build-up)
 Placement of rubber dams
 Postoperative suture removal
 Placement of removable prosthodontic or orthodontic devices
 Oral impressions
 Fluoride treatments
 Oral radiographs
 Orthodontic appliance adjustment
 Shedding of primary teeth

101.  Respiratory tract
◦ Tonsillectomy and/or adenoidectomy
◦ Surgical procedures that involve respiratory mucosa
◦ Bronchoscopy with a rigid bronchoscope
 Gastrointestinal tract
◦ Sclerotherapy for esophageal varices
◦ Esophageal stricture dilation
◦ ERCP with biliary obstruction
◦ Biliary tract surgery
◦ Surgical procedures that involve intestinal mucosa
 Genitourinary tract
◦ Prostatic surgery
◦ Cystoscopy
◦ Urethral dilation

102.  Genitourinary tract
◦ Vaginal hysterectomy†
◦ Vaginal delivery†
◦ Cesarean section
◦ In uninfected tissue:
◦ Urethral catheterization
◦ Uterine dilatation and curettage
◦ Therapeutic abortion
◦ Sterilization procedures
◦ Insertion or removal of intrauterine devices

103.  Gastrointestinal tract
◦ Transesophageal echocardiography
◦ Endoscopy with or without gastrointestinal biopsy
 Respiratory tract
◦ Endotracheal intubation
◦ Bronchoscopy using a flexible bronchoscope, with or
without biopsy
◦ Tympanostomy tube insertion
 Other procedures
◦ Cardiac catheterization, including balloon angioplasty
◦ Coronary stents and implanted cardiac pacemakers and
defibrillators
◦ Incision or biopsy of surgically scrubbed skin
◦ Circumcision

105.  Mean patient age - 49.3 ± 13.7 years.
 M : F - 3.3:1.
 Rheumatic heart disease- 37.7% patients.
 Patients already received antibiotic therapy before
presentation- 54.1%.
 Blood cultures positive - 67.2% patients.
 Commonest microbial isolates:
Streptococci and Staphylococci 21.4% patients each.
Indian Journal of Critical Care Medicine:2013;140-47

106.  Emergence of antimicrobial resistance in classic IE microflora,
namely, the gram-positive cocci.
 Existence of antimicrobial resistance in complex ecologic biofilms.
 Changing pattern of causal agents now regarded as important
pathogens of IE e.g., Bartonella spp., T. whippeli, and fungi;
 Changing epidemiologic trends of persons who acquire IE,
including injection drug users, persons with HIV/AIDS, children
with CHD, and persons undergoing body piercing.