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1

Protection against infection of the epidermis depends on the mechanical barrier afforded by the

stratum corneum, since the epidermis
itself is devoid of blood vessels

2

beneath the dermal papillae provides nutrition to the stratum germinativum, and physiologic responses of this plexus produce important clinical signs and symptoms.

Rich plexus of capillaries

3

Vesicle formation due to infection is caused by

viral
proliferation within the epidermis.

4

varicella and variola, viremia
precedes the onset of a diffuse

centripetal rash that progresses from
macules to vesicles, then to pustules, and finally to scabs over the
course of 1–2 weeks.

5

Hand-foot-and-mouth disease

Coxsackievirus A16

6

begins after mite-bite inoculation of Rickettsia akari
into the skin. A papule with a central vesicle evolves to form a 1- to
2.5-cm painless crusted black eschar with an erythematous halo
and proximal adenopathy

Rickettsialpox

7

Staphylococcal scalded-skin syndrome (SSSS) in neonates is caused by a toxin (exfoliatin) from phage group II S. aureus.
SSSS must be distinguished from

toxic epidermal necrolysis (TEN),
which occurs primarily in adults, is drug-induced, and is associated
with a higher mortality rate.

8

cleavage plane is the stratum
corneum in SSSS

and the stratum germinativum in TEN


Intravenous γ-globulin is a promising treatment for TEN.

9

Impetigo contagiosa is caused by

S. pyogenes,

10

and bullous
impetigo is due to

S. aureus.

11

It is important to recognize impetigo contagiosa because of its relationship to poststreptococcal glomerulonephritis.

Rheumatic fever is not a complication of skin infection caused by S. pyogenes

12

is the most common cause of localized folliculitis.

S. aureus

13

Hot-tub folliculitis is caused
by

Pseudomonas aeruginosa in waters that are insufficiently chlorinated
and maintained at temperatures of 37–40°C. Infection is usually selflimited,
although bacteremia and shock have been reported.

14

Swimmer’s
itch occurs when a skin surface is exposed to water infested with freshwater
.

avian schistosomes

15

Mycobacterium marinum infections of the skin may present as

cellulitis or as raised erythematous nodules. Similar lesions caused by
Mycobacterium abscessus and M. chelonei have been described among
patients undergoing cosmetic laser surgery and tattooing, respectively.

16

Erythematous papules are early manifestations of cat-scratchdisease (with lesions developing at the primary site of inoculation

of Bartonella henselae) and bacillary angiomatosis (also caused by B.
henselae)

17

Raised serpiginous or linear eruptions are characteristic
of cutaneous larva migrans, which is caused by burrowing larvae of

dog or cat hookworms (Ancylostoma braziliense) and which humans
acquire through contact with soil that has been contaminated with dog
or cat feces.

18

Similar burrowing raised lesions are present in dracunculiasis caused by migration of the adult female nematode

Dracunculus medinensis.

19

Nodules caused by Onchocerca volvulus measure 1–10 cm
in diameter and occur mostly in persons bitten by

Simulium flies in
Africa. The nodules contain the adult worm encased in fibrous tissue.
Migration of microfilariae into the eyes may result in blindness.

20

Verruga peruana is caused by

Bartonella bacilliformis, which is transmitted
to humans by the sandfly Phlebotomus. This condition can take
the form of single gigantic lesions (several centimeters in diameter)
or multiple small lesions (several millimeters in diameter

21

Human papillomavirus may cause singular warts
(verruca vulgaris)

or multiple warts in the anogenital area (condylomata
acuminata).

22

begins as a pruritic papule, which
develops within days into an ulcer with surrounding vesicles and
edema and then into an enlarging ulcer with a black eschar.

Cutaneous anthrax

23

may have associated ulcerated
skin lesions with painful regional adenopathy. Although buboes are
the major cutaneous manifestation of plague, ulcers with eschars, papules,
or pustules are also present in 25% of cases.

Ulceroglandular tularemia

24

typically causes chronic skin ulcers on the
extremities of individuals living in the tropics.

Mycobacterium ulcerans

25

may be associated with cutaneous ulcerations in patients with lepromatous leprosy related to Lucio’s phenomenon, in which immunemediated
destruction of tissue bearing high concentrations of M.
leprae bacilli occurs, usually several months after initiation of effective
therapy.

Mycobacterium leprae

26

also may cause ulcerations, papules,
or erythematous macular lesions of the skin in both immunocompetent
and immunocompromised patients.

Mycobacterium tuberculosis

27

is due to S. pyogenes and is characterized by
an abrupt onset of fiery-red swelling of the face or extremities.

Erysipelas

The
distinctive features of erysipelas are well-defined indurated margins,
particularly along the nasolabial fold; rapid progression; and intense
pain. Flaccid bullae may develop during the second or third day of
illness, but extension to deeper soft tissues is rare. Treatment with
penicillin is effective; swelling may progress despite appropriate
treatment, although fever, pain, and the intense red color diminish.
Desquamation of the involved skin occurs 5–10 days into the illness.

28

is an acute inflammatory condition of the skin
that is characterized by localized pain, erythema, swelling, and heat.
It may be caused by indigenous flora colonizing the skin and appendages
(e.g., S. aureus and S. pyogenes) or by a wide variety of exogenous
bacteria.

Cellulitis

29

Even with needle aspiration of the leading edge or a punch biopsy of
the cellulitis tissue itself, cultures are positive in only

20% of cases.

This observation suggests that relatively low numbers of bacteria may cause cellulitis and that the expanding area of erythema within the skin may be a direct effect of extracellular toxins or of the soluble mediators of
inflammation elicited by the host.

30

spreads from a central localized
infection, such as an abscess, folliculitis, or an infected foreign
body (e.g., a splinter, a prosthetic device, or an IV catheter).

Cellulitis caused by S. aureus

31

is a
more rapidly spreading, diffuse process that is frequently associated
with lymphangitis and fever and should be referred to as nonpurulent
cellulitis.

cellulitis due to S. pyogenes

32

Recurrent streptococcal cellulitis of the lower extremities may
be caused by organisms of

group A, C, or G in association with chronic
venous stasis or with saphenous venectomy for coronary artery bypass
surgery.

33

Recurrent staphylococcal cutaneous infections
are more common among individuals who have

eosinophilia and elevated serum levels of IgE (Job’s syndrome) and among nasal carriers
of staphylococci.

34

occurs primarily in elderly patients and those with diabetes
mellitus or peripheral vascular disease

Cellulitis caused by Streptococcus agalactiae (group B
Streptococcus)

35

dog bites is commonly caused by

Pasteurella multocida

Pasteurella is notoriously resistant to dicloxacillin
and nafcillin but is sensitive to all other β-lactam antimicrobial
agents as well as to quinolones, tetracycline, and erythromycin.
Ampicillin/clavulanate, ampicillin/sulbactam, and cefoxitin are
good choices for the treatment of animal or human bite infections.

36

causes aggressive cellulitis in tissues surrounding
lacerations sustained in freshwater (lakes, rivers, and streams). This
organism remains sensitive to aminoglycosides, fluoroquinolones,
chloramphenicol, trimethoprim-sulfamethoxazole, and third-generation
cephalosporins; it is resistant to ampicillin, however.

Aeromonas hydrophila

37

P. aeruginosa causes three types of soft tissue infection:

ecthyma gangrenosum in neutropenic patients, hot-tub folliculitis, and cellulitis
following penetrating injury.

38

Most commonly, P. aeruginosa is introduced
into the deep tissues when a person steps on a nail.

Treatment
includes surgical inspection and drainage, particularly if the injury also
involves bone or joint capsule.

Choices for empirical treatment while
antimicrobial susceptibility data are awaited include an aminoglycoside,
a third-generation cephalosporin (ceftazidime, cefoperazone,
or cefotaxime), a semisynthetic penicillin (ticarcillin, mezlocillin, or
piperacillin), or a fluoroquinolone (although drugs of the last class are
not indicated for the treatment of children < 13

39

is most
often associated with fish and domestic swine and causes cellulitis primarily
in bone renderers and fishmongers

The gram-positive aerobic rod Erysipelothrix rhusiopathiae

. E. rhusiopathiae remains
susceptible to most β-lactam antibiotics (including penicillin), erythromycin,
clindamycin, tetracycline, and cephalosporins but is resistant
to sulfonamides, chloramphenicol, and vancomycin

Its resistance to
vancomycin, which is unusual among gram-positive bacteria, is of
potential clinical significance since this agent is sometimes used in
empirical therapy for skin infection.

40

Fish food containing the water
flea Daphnia is sometimes contaminated with

M. marinum, which can
cause cellulitis or granulomas on skin surfaces exposed to the water
in aquariums or injured in swimming pools. Rifampin plus ethambutol
has been an effective therapeutic combination in some cases,
although no comprehensive studies have been undertaken In addition,
some strains of M. marinum are susceptible to tetracycline or to
trimethoprim-sulfamethoxazole.

41

Strains of MRSA that produce the

Panton-Valentine leukocidin (PVL) toxin have been reported to cause
necrotizing fasciitis.

42

formerly called streptococcal gangrene,
may be associated with group A Streptococcus or mixed aerobic–anaerobic bacteria or may occur as a component of gas gangrene
caused by Clostridium perfringens

Necrotizing fasciitis


Swelling then
develops and is followed by brawny edema and tenderness. With progression,
dark-red induration of the epidermis appears, along with bullae
filled with blue or purple fluid. Later the skin becomes friable and
takes on a bluish, maroon, or black color. By this stage, thrombosis of
blood vessels in the dermal papillae (Fig. 156-1) is extensive

Extension
of infection to the level of the deep fascia causes this tissue to take on
a brownish-gray appearance. Rapid spread occurs along fascial planes,
through venous channels and lymphatics. Patients in the later stages
are toxic and frequently manifest shock and multiorgan failure

43

Leakage into the perineal area results in a syndrome
called characterized by massive swelling of the
scrotum and penis with extension into the perineum or the abdominal
wall and the legs.

Fournier’s gangrene,

44

Late in the course, the classic signs of
necrotizing fasciitis,

such as purple (violaceous) bullae, skin sloughing, and progressive toxicity, develop.

45

severe muscle pain is the hallmark
of

pleurodynia (coxsackievirus B), trichinellosis, and bacterial infection.

46

S. pyogenes may induce primary myositis (referred to as streptococcal
necrotizing myositis) in association with severe systemic toxicity.

Myonecrosis occurs concomitantly with necrotizing fasciitis in ~50%
of cases. Both are part of the streptococcal toxic shock syndrome

47

usually follows severe penetrating injuries that result
in interruption of the blood supply and introduction of soil into
wounds. Such cases of traumatic gangrene are usually caused by the
clostridial species C. perfringens, C. septicum, and C. histolyticum

Gas gangrene

48

Gas gangrene of the uterus, especially that due to
historically occurred as a consequence of illegal or self-induced
abortion and nowadays also follows spontaneous abortion, vaginal
delivery, and cesarean section

Clostridium sordellii,

Postpartum C. sordellii infections in
young, previously healthy women present as a unique clinical picture:
little or no fever, lack of a purulent discharge, refractory hypotension,
extensive peripheral edema and effusions, hemoconcentration, and
a markedly elevated white blood cell count. The infection is almost
uniformly fatal, with death ensuing rapidly. C. sordellii and C. novyi
have also been associated with cutaneous injection of black tar heroin;
mortality rates are lower among the affected individuals, probably
because their aggressive injection-site infections are readily apparent
and diagnosis is therefore promp

49

Furuncles <2.5 cm in diameter are usually treated with moist heat.

Those that are larger (4.5 cm of erythema and induration) require surgical drainage, and the occurrence of these larger lesions in association with fever, chills, or leukocytosis requires both drainage
and antibiotic treatment

50

Appropriate empirical
antibiotic treatment for mixed aerobic–anaerobic infections
could consist of ampicillin/sulbactam, cefoxitin, or the following
combination:

clindamycin (600–900 mg IV every 8 h) or metronidazole(500 mg every 6 h)

plus (2) ampicillin or ampicillin/sulbactam

(1.5–3 g IV every 6 h) plus (3) gentamicin (1–1.5 mg/kg every 8 h).

51

Herpes zoster (immunocompetent host
>50 years of age)

Acyclovir, 800 mg PO 5 times daily for 7–10 days

Valacyclovir, 1000 mg PO tid for 7 days

52

Cellulitis (staphylococcal or streptococcal

Nafcillin or oxacillin, 2 g IV q4–6h

Cefazolin, 1–2 g q8h

Ampicillin/sulbactam, 1.5–3 g IV q6h

Clindamycin, 600–900 mg IV q8h

53

MRSA skin infection

Vancomycin, 1 g IV q12h
or

Linezolid, 600 mg IV q12h

54

Necrotizing fasciitis (group A streptococcal

Clindamycin, 600–900 mg IV q6–8h
+
Penicillin G, 4 million units IV q4h

55

Gas gangrene

Clindamycin, 600–900 mg IV q6–8h,
+
Penicillin G, 4 million units IV q4–6h

56

The prototypic lesion of infective endocarditis,

the vegetation
(Fig. 155-1), is a mass of platelets, fibrin, microcolonies of microorganisms,
and scant inflammatory cells

Infection most commonly
involves heart valves but may also occur on the low-pressure side
of a ventricular septal defect, on mural endocardium damaged by
aberrant jets of blood or foreign bodies, or on intracardiac devices

57

The analogous process involving arteriovenous shunts,
arterio-arterial shunts (patent ductus arteriosus), or a coarctation of
the aorta is called

infective endarteritis.

58

is a hectically febrile illness that rapidly
damages cardiac structures, seeds extracardiac sites, and, if untreated,
progresses to death within weeks.

Acute endocarditis

59

follows an
indolent course; causes structural cardiac damage only slowly, if at all;
rarely metastasizes; and is gradually progressive unless complicated by
a major embolic event or a ruptured mycotic aneurysm.

Subacute endocarditis

60

The incidence of endocarditis is notably increased among the elderly.

in developed
countries, 25–35% of cases of native valve endocarditis (NVE) are
associated with health care, and 16–30% of all cases of endocarditis involve prosthetic valves.

61

The risk of prosthesis infection is greatest
during the

first 6–12 months after valve replacement

62

Prosthetic valve endocarditis (PVE) arising within 2 months of valve
surgery is generally nosocomial, the result of intraoperative contamination
of the prosthesis or a bacteremic postoperative complication.


This nosocomial origin is reflected in the primary microbial causes:
S. aureus, CoNS, facultative gram-negative bacilli, diphtheroids, and
fungi.

63

The portals of entry and organisms causing cases beginning
>12 months after surgery are similar to those in community-acquired
NVE.

PVE due to CoNS that presents 2–12 months after surgery often
represents delayed-onset nosocomial infection. Regardless of the time
of onset after surgery, at least 68–85% of CoNS strains that cause PVE
are resistant to methicillin.

64

Injection drug use–associated endocarditis, especially that involving
the tricuspid valve, is commonly caused by

S. aureus

65

Health care–associated NVE, most commonly caused by
may have either a nosocomial onset (55%) or a community
onset (45%); community-onset cases develop in patients who have
had extensive contact with the health care system over the preceding
90 days

Staphylococcus aureus, coagulase-negative staphylococci (CoNS), and
enterococci,

66

arising within 2 months of valve
surgery is generally nosocomial, the result of intraoperative contamination
of the prosthesis or a bacteremic postoperative complication.

Prosthetic valve endocarditis (PVE)

This nosocomial origin is reflected in the primary microbial causes:
S. aureus, CoNS, facultative gram-negative bacilli, diphtheroids, and
fungi.

67

Occasionally, there is concurrent aortic or
mitral valve infection. One-third of cases of CIED cardiovascular
implantable electronic devices endocarditis present
within

3 months after device implantation or manipulation, one-third
present at 4–12 months, and one-third present at >1 year. S. aureus
and CoNS, both of which are commonly resistant to methicillin, cause
the majority of cases.

68

in addicts
have a more varied etiology. In addition to the usual causes of endocarditis,
these cases can be due to Pseudomonas aeruginosa and Candida
species, and sporadic cases can be caused by unusual organisms such
as Bacillus, Lactobacillus, and Corynebacterium species. Polymicrobial
endocarditis occurs among injection drug users. HIV infection in drug
users does not significantly influence the causes of endocarditis

Left-sided valve infections

69

From 5% to 15% of patients with endocarditis have negative blood
cultures; in one-third to one-half of these cases, cultures are negative
because of prior antibiotic exposure.

The remainder of these patients
are infected by fastidious organisms, such as nutritionally variant
bacteria (now designated Granulicatella and Abiotrophia species),
HACEK organisms, Coxiella burnetii, and Bartonella species.

70

The undamaged endothelium is resistant to infection by most bacteria
and to thrombus formation. Endothelial injury (e.g., at the site
of impact of high-velocity blood jets or on the low-pressure side of
a cardiac structural lesion) allows either direct infection by virulent
organisms or the development of a platelet-fibrin thrombus—a
condition called

nonbacterial thrombotic endocarditis (NBTE).

71

This
thrombus serves as a site of bacterial attachment during transient
bacteremia. The cardiac conditions most commonly resulting in
NBTE are

mitral regurgitation, aortic stenosis, aortic regurgitation,
ventricular septal defects, and complex congenital heart disease

72

NBTE also arises as a result of a hypercoagulable state; this gives
rise to

marantic endocarditis (uninfected vegetations seen in patients
with malignancy and chronic diseases) and to bland vegetations

73

The organisms that commonly
cause endocarditis have surface adhesin molecules, collectively called

microbial surface components recognizing adhesin matrix molecules
(MSCRAMMs), that mediate adherence to NBTE sites or injured
endothelium.

74

Adherence is facilitated

by fibronectin-binding proteins
present on many gram-positive bacteria; by clumping factor
(a fibrinogen- and fibrin-binding surface protein) on S. aureus; by
fibrinogen-binding surface proteins (Fss2), collagen-binding surface
protein (Ace), and Ebp pili (the latter mediating platelet adherence)
in Enterococcus faecalis; and by glucans or FimA (a member of the
family of oral mucosal adhesins) on streptococci.

75

are required for S. aureus invasion of intact endothelium; thus
these surface proteins may facilitate infection of previously normal
valves.

Fibronectin-binding
proteins

76

β-Hemolytic
streptococci, S. aureus, and pneumococci typically result in an acute
course,

although S. aureus occasionally causes subacute disease.
Endocarditis caused by Staphylococcus lugdunensis (a coagulasenegative
species) or by enterococci may present acutely.

77

Subacute endocarditis is typically caused by viridans streptococci, enterococci, CoNS, and the HACEK group.

Endocarditis caused by Bartonella
species, T. whipplei, or C. burnetii is exceptionally indolent

78

In patients with subacute presentations, fever is typically lowgrade
and rarely exceeds 39.4°C (103°F); in contrast, temperatures of

39.4°–40°C (103°–104°F) are often noted in acute endocarditis

79

In acute endocarditis involving a normal valve, murmurs
may be absent initially but ultimately are detected in

85% of cases.

80

Congestive heart failure (CHF) develops in

30–40% of patients as a
consequence of valvular dysfunction.

Occasionally, CHF is due to
endocarditis-associated myocarditis or an intracardiac fistula. Heart
failure due to aortic valve dysfunction progresses more rapidly than
does that due to mitral valve dysfunction

81

The classic nonsuppurative peripheral
manifestations of subacute endocarditis (e.g., Janeway lesions;
Fig. 155-2A) are related to

prolonged infection; with early diagnosis
and treatment, these have become infrequent

82

Septic embolization
mimicking some of these lesions (subungual hemorrhage,
Osler’s nodes) is common in patients with

acute S. aureus endocarditis

Hematogenously seeded focal infection occurs most often in the skin,
spleen, kidneys, skeletal system, and meninges. Arterial emboli, onehalf
of which precede the diagnosis, are clinically apparent in up to 50%
of patients.

83

are independently associated
with an increased risk of embolization

Endocarditis caused by S. aureus, vegetations >10 mm in
diameter (as measured by echocardiography), and infection involving
the mitral valve, especially the anterior leaflet,

Cerebrovascular
emboli presenting as strokes or occasionally as encephalopathy complicate
15–35% of cases of endocarditis. Again, one-half of these events
precede the diagnosis of endocarditis.

84

The frequency of stroke is 8 per
1000 patient-days during the week prior to diagnosis; the figure falls to

4.8 and 1.7 per 1000 patient-days during the first and second weeks of
effective antimicrobial therapy, respectively. This decline exceeds that
which can be attributed to change in vegetation size. Only 3% of strokes
occur after 1 week of effective therapy.

85

(Mycotic aneurysms are focal dilations
of arteries occurring at points in the artery wall that have been weakened by infection in the vasa vasorum or where septic emboli have lodged.)

Microabscesses in brain and meninges occur commonly
in S. aureus endocarditis; surgically drainable intracerebral abscesses
are infrequent.

86

Almost 50% of endocarditis
associated with injection drug use is limited to the

tricuspid
valve and presents with fever but with faint or no murmur and no
peripheral manifestations.

87

which are common
with tricuspid endocarditis, cause cough, pleuritic chest pain,
nodular pulmonary infiltrates, or occasionally pyopneumothorax

Septic pulmonary emboli,

88

Infection of the aortic or mitral valves presents with the

typical clinical
features of endocarditis, including peripheral manifestations.

89

allows a clinical diagnosis
of definite endocarditis

Documentation of two major criteria, of one major criterion and three minor criteria, or of five minor criteria

90

The diagnosis of endocarditis is rejected
if

an alternative diagnosis is established, if symptoms resolve and do
not recur with ≤4 days of antibiotic therapy, or if surgery or autopsy
after ≤4 days of antimicrobial therapy yields no histologic evidence of
endocarditis.

91

Major Criteria of Modified Duke

Positive blood culture

Typical microorganism for infective endocarditis from two separate blood cultures

Viridans streptococci, Streptococcus gallolyticus, HACEK group organisms, Staphylococcus aureus, or Community-acquired enterococci in the absence of a primary focus,

or

Persistently positive blood culture, defined as recovery of a microorganism consistent with infective endocarditis from: Blood cultures drawn >12 h apart; or All of 3 or a majority of ≥4 separate blood cultures, with first and last
drawn at least 1 h apart
or

Single positive blood culture for Coxiella burnetii or phase I IgG antibody titer of >1:800

2. Evidence of endocardial involvement Positive echocardiogram

Oscillating intracardiac mass on valve or supporting structures or in the path of regurgitant jets or in implanted material, in the absence of an alternative anatomic explanation
or
Abscess, or New partial dehiscence of prosthetic valve,
or New valvular regurgitation (increase or change in preexisting murmur not sufficient)

92

Minor Criteria of IE

1. Predisposition: predisposing heart conditionsc or injection drug use
2. Fever ≥38.0°C (≥100.4°F)
3. Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages,
Janeway lesions
4. Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factor
5. Microbiologic evidence: positive blood culture but not meeting major criterion, as noted previously,d or serologic evidence of active infection with an organism consistent with infective endocarditis

93

Definite endocarditis is defined by

documentation of two major criteria, of one major criterion and three minor criteria, or of five minor criteria. See text for further details.

Transesophageal echocardiography is required for optimal assessment of possible prosthetic
valve endocarditis or complicated endocarditis.

Valvular disease with stenosis or regurgitation,
presence of a prosthetic valve, congenital heart disease including corrected or partially corrected conditions (except isolated atrial septal defect, repaired ventricular
septal defect, or closed patent ductus arteriosus), prior endocarditis, or hypertrophic
cardiomyopathy

Excluding single positive cultures for coagulase-negative staphylococci and diphtheroids, which are common culture contaminants, or for organisms that do not cause endocarditis frequently, such as gram-negative bacilli.

94

Among patients with
untreated endocarditis who ultimately have a positive blood culture,
95% of all blood cultures are positive.

The diagnostic criteria attach
significance to the species of organism isolated from blood cultures.
To fulfill a major criterion, the isolation of an organism that causes
both endocarditis and bacteremia in the absence of endocarditis
(e.g., S. aureus, enterococci) must take place repeatedly (i.e., persistent
bacteremia) and in the absence of a primary focus of infection

Organisms that rarely cause endocarditis but commonly contaminate
blood cultures (e.g., diphtheroids, CoNS) must be isolated repeatedly
if their isolation is to serve as a major criterion.

95

In patients with suspected NVE, PVE, or CIED endocarditis who have
not received antibiotics during the prior 2 weeks,

three 2-bottle blood culture sets, separated from one another by at least 2 h, should be
obtained from different venipuncture sites over 24 h. If the cultures
remain negative after 48–72 h, two or three additional blood culture
sets should be obtained, and the laboratory should be consulted for
advice regarding optimal culture techniques

96

Pending culture results,
empirical antimicrobial therapy should be withheld initially from

hemodynamically stable patients with suspected subacute endocarditis,
especially those who have received antibiotics within the preceding
2 weeks.

97

Serologic tests can be used to implicate
organisms that are difficult to recover by blood culture:

Brucella,
Bartonella, Legionella, Chlamydia psittaci, and C. burnetii

98

Transthoracic echocardiography
(TTE) is noninvasive and exceptionally specific; however, it
cannot image

vegetations <2 mm in diameter, and in 20% of patients
it is technically inadequate because of emphysema or body habitus.
TTE detects vegetations in 65–80% of patients with definite clinical
endocarditis but is not optimal for evaluating prosthetic valves or
detecting intracardiac complications.

99

When endocarditis is likely, a negative TEE result does not
exclude the diagnosis but rather warrants repetition of the study once
or twice in 7–10 days.

TEE is the optimal method for the diagnosis
of PVE, the detection of myocardial abscess, valve perforation, or
intracardiac fistulae and for the detection of vegetations in patients
with CIED. In patients with CIED and negative blood cultures, a
mass adherent to the lead is likely to be a bland thrombosis rather
than an infected vegetation.

100

Because S. aureus bacteremia is associated with a high prevalence
of endocarditis,

routine echocardiographic evaluation (TTE or preferably
TEE) is recommended in these patients

101

Patients with nosocomial
S. aureus bacteremia are at increased risk of endocarditis if one or
more of the following are present:

positive blood cultures for 2–4 days,
hemodialysis dependency, a permanent intracardiac device, spine
infection, nonvertebral osteomyelitis, or an endocarditis-predisposing
valve abnormality.

102

are
commonly increased in endocarditis (Table 155-2).

The erythrocyte sedimentation rate,
C-reactive protein level, and circulating immune complex titer

Cardiac catheterization
is useful primarily to assess coronary artery patency in older
individuals who are to undergo surgery for endocarditis.

103

IE suspected

Low initial patient risk
and low clinical suspicion

Initial TTE

104

IE suspected

High initial patient risk†;
moderate to high clinical
suspicion or difficult imaging
candidate

Initial TEE

High initial patient risk for infective endocarditis (IE), as listed in Table 155-8, or evidence of intracardiac complications (new regurgitant murmur, new electrocardiographic conduction changes, or congestive heart failure).

High-risk echocardiographic features include large vegetations, valve insufficiency, paravalvular infection, or ventricular dysfunction. Rx indicates initiation of antibiotic therapy. (Reproduced with permission from

105

2-week penicillin/gentamicin or ceftriaxone/gentamicin regimens
should not be used to

treat PVE or complicated NVE.

106

Clinical and Laborat ory Feat ures of Infecti ve Endocarditis

Fever 80–90
Chills and sweats 40–75
Anorexia, weight loss, malaise 25–50

107

An isolate’s resistance
to cell wall–active agents or its ability to replicate in the presence of
gentamicin at ≥500 μg/mL or streptomycin at 1000–2000 μg/mL—a
phenomenon called

high-level aminoglycoside resistance

In the absence
of high-level resistance, gentamicin or streptomycin should be used
as the aminoglycoside

108

if the penicillin/ampicillin MIC is ≥8
μg/mL, vancomycin can be considered;

and if the vancomycin MIC is
≥8 μg/mL, penicillin or ampicillin can be considered.

109

If there is high-level resistance to both gentamicin and streptomycin,
a synergistic bactericidal effect cannot be achieved by the
addition of an aminoglycoside; thus no aminoglycoside should be
given.

Instead, an 8- to 12-week course of a single cell wall–active
agent can be considered; for E. faecalis endocarditis, high doses
of ampicillin combined with ceftriaxone or cefotaxime are suggested

Nonrandomized comparative studies suggest
that ampicillin-ceftriaxone may be as effective as (and less nephrotoxic than) penicillin or ampicillin plus an aminoglycoside in the treatment of E. faecalis endocarditis.

110

Penicillin-susceptibleb streptococci,
S. gallolyticus

Penicillin G (2–3 mU IV q4h for 4 weeks)
Ceftriaxone (2 g/d IV as a single dose for 4 weeks)

plus

Gentamicind (3 mg/kg qd IV or IM, as a single dosee
or divided into equal doses q8h for 2 weeks)

111

Relatively penicillin-resistantce Strep

Penicillin G (4 mU IV q4h) or ceftriaxone (2 g IV qd) for
4 weeks
plus
Gentamicind (3 mg/kg qd IV or IM, as a single dosee
or divided into equal doses q8h for 2 weeks)

112

Moderately penicillin-resistantg
streptococci, nutritionally
variant organisms, or Gemella
species

IE

Penicillin G (4–5 mU IV q4h) or ceftriaxone (2 g IV qd)
for 6 weeks
plus
Gentamicind (3 mg/kg qd IV or IM as a single dosee or
divided into equal doses q8h for 6 weeks)

113

IE Enterococci

Penicillin G (4–5 mU IV q4h) plus gentamicind (1 mg/kg
IV q8h), both for 4–6 weeks

Ampicillin (2 g IV q4h) plus gentamicind (1 mg/kg IV
q8h), both for 4–6 weeks

Ampicillin (2 g IV q4h) plus ceftriaxone (2 g IV q12h),
both for 6 weeks

114

IE

MSSA infecting native valves
(no foreign devices

Nafcillin, oxacillin, or flucloxacillin (2 g IV q4h for
4–6 weeks)

115

IE

MRSA infecting native valves
(no foreign devices

Vancomycinc (15 mg/kg IV q8–12h for 4–6 weeks)

For treatment of endocarditis caused by methicillin-resistant
S. aureus (MRSA), vancomycin, dosed to achieve trough concentrations
of 15–20 μg/mL, is recommended

116

IE

MRSA infecting prosthetic
valves

Vancomycinc (15 mg/kg IV q12h for 6–8 weeks)

plus

Gentamicind (1 mg/kg IM or IV q8h for 2 weeks)

plus

Rifampini (300 mg PO q8h for 6–8 weeks)

117

IE

MSSA infecting prosthetic
valves

Nafcillin, oxacillin, or flucloxacillin (2 g IV q4h for 6–8
weeks)

plus

Gentamicind (1 mg/kg IM or IV q8h for 2 weeks)
plus

Rifampini (300 mg PO q8h for 6–8 weeks)

118

HACEK Organisms

Ceftriaxone (2 g/d IV as a single dose for 4 weeks) Can use another third-generation cephalosporin at comparable dosage

Ampicillin/sulbactam (3 g IV q6h for 4 weeks)

119

Coxiella burnetii

Doxycycline (100 mg PO q12h) plus hydroxychloroquine
(200 mg PO q8h), both for 18 (native valve) or
24 (prosthetic valve) months

120

Staphylococcal PVE is treated for

6–8 weeks with a multidrug
regimen. Rifampin is an essential component because it kills staphylococci
that are adherent to foreign material in a biofilm.

121

In the absence of meningitis, endocarditis caused
by Streptococcus pneumoniae isolates with a penicillin MIC of ≤1
μg/mL can be treated with

IV penicillin (4 million units every 4 h),
ceftriaxone (2 g/d as a single dose), or cefotaxime (at a comparable dosage)

Infection caused by pneumococcal strains with a penicillin MIC of ≥2 μg/mL should be treated with vancomycin. If meningitis is suspected or present, treatment with vancomycin plus ceftriaxone—
at the doses advised for meningitis—should be initiated until susceptibility results are known

Definitive therapy should then be
selected on the basis of meningitis breakpoints (penicillin MIC, 0.06
μg/mL; or ceftriaxone MIC, 0.5 μg/mL).

122

Therapy for
Candida endocarditis consists of

amphotericin B plus flucytosine
and early surgery; long-term (if not indefinite) suppression with an
oral azole is advised. Echinocandin treatment of Candida endocarditis
has been effective in sporadic cases; nevertheless, the role of
echinocandins in this setting has not been established

123

Empirical therapy for
acute endocarditis in an injection drug user should cover MRSA and
gram-negative bacilli.

Treatment with vancomycin plus gentamicin,
initiated immediately after blood samples are obtained for culture,
covers these organisms as well as many other potential causes

Similarly, treatment of health care–associated endocarditis must
cover MRSA

124

Antimicrobial therapy for CIED endocarditis is
adjunctive to complete device removal.

The antimicrobial selected
is based on the causative organism and should be used as recommended for NVE

125

IE
Blood cultures should be repeated daily until sterile in patients with endocarditis due to S. aureus or difficult-to-treat organisms, rechecked if there is recrudescent fever, and performed again 4–6
weeks after therapy to document cure.

Blood cultures become sterile within 2 days after the start of appropriate therapy when infection is caused by viridans streptococci, enterococci, or HACEK
organisms.

In S. aureus endocarditis, β-lactam therapy results in
sterile cultures in 3–5 days

MRSA endocarditis, positive cultures may persist for 7–9 days with vancomycin or daptomycin treatment

126

IE
When fever persists for 7 days despite appropriate
antibiotic therapy,

Patients should be evaluated for paravalvular
abscess, extracardiac abscesses

Vegetations become smaller with effective therapy;
however, 3 months after cure, 50% are unchanged and 25% are slightly larger.

127

From 25% to 40% of patients with
left-sided endocarditis undergo cardiac surgery during active infection,
with slightly higher surgery rates for PVE than NVE.

Intracardiac
complications (which are most reliably detected by TEE) and CHF
are the most commonly cited indications for surgery.

128

IE
Surgery Required for Optimal Outcome

Moderate to severe congestive heart failure due to valve dysfunction

Partially dehisced unstable prosthetic valve

Persistent bacteremia despite optimal antimicrobial therapy

Lack of effective microbicidal therapy (e.g., fungal or Brucella endocarditis)

S. aureus prosthetic valve endocarditis with an intracardiac complication

Relapse of prosthetic valve endocarditis after optimal antimicrobial therapy

129

IE
Surgery to Be Strongly Considered for Improved Outcomea

Perivalvular extension of infection

Poorly responsive S. aureus endocarditis involving the aortic or mitral valve

Large (>10 mm in diameter) hypermobile vegetations with increased risk of embolism, particularly with prior embolic event or with significant valve dysfunction

Persistent unexplained fever (≥10 days) in culture-negative native valve endocarditis

Poorly responsive or relapsed endocarditis due to highly antibiotic-resistant enterococci or gram-negative bacill

130

Timing of Cardiac Surgical Intervention in Patie nts with Endocarditis

Emergent (same day)

Acute aortic regurgitation plus preclosure of mitral valve

Sinus of Valsalva abscess ruptured into right heart

Rupture into pericardial sac

131

Timing of Cardiac Surgical Intervention in Patie nts with Endocarditis

Urgent (within 1–2 days)

Valve obstruction by vegetation

Unstable (dehisced) prosthesis

Acute aortic or mitral regurgitation with heart failure (New York Heart Association class III or IV)

Septal perforation

Perivalvular extension of infection with or without new electrocardiographic

conduction system changes

Lack of effective antibiotic therapy

132

Elective (earlier usually
preferred)

Vegetation diameter >10 mm plus severe aortic or mitral valve dysfunctiona

Progressive paravalvular prosthetic regurgitation

Valve dysfunction plus persisting infection after ≥7–10 days of antimicrobial therapy

Fungal (mold) endocarditis

133

Moderate to severe refractory
CHF caused by new or worsening valve dysfunction is the major indication for cardiac surgery.

At 6 months of follow-up, patients
with left-sided endocarditis and moderate to severe heart failure
due to valve dysfunction who are treated medically have a 50%
mortality rate, while among matched patients who undergo surgery
the mortality rate is 15%.

134

This complication, which is most common
with aortic valve infection, occurs in 10–15% of native valve and 45–60% of prosthetic valve infection

Perivalvular Infection

135

is the test of choice to detect perivalvular abscesses (sensitivity,
≥85%).

TEE with color
Doppler

136

Removal of all hardware is recommended for
patients with established CIED infection (pocket or intracardiac lead)
or erosion of the device through the skin.

Percutaneous lead extraction
is preferred. With lead vegetations of >3 cm and the resulting
risk of a pulmonary embolus or with retained hardware after
attempted percutaneous extraction, surgical removal should be
considered.

the CIED can be reimplanted percutaneously or surgically
(epicardial leads) at a new site after at least 10–14 days of effective
antimicrobial therapy.

137

Whenever feasible,
cardiac surgery should be delayed for 2–3 weeks after a nonhemorrhagic embolic infarction and for

4 weeks after a cerebral hemorrhage.
A ruptured mycotic aneurysm should be treated before
cardiac surgery

138

Antibiotic Regimens for Prophyla xis of Endocarditis in
Adults with High-Risk Cardiac Lesions

Standard oral regimen

Amoxicillin: 2 g PO 1 h before procedure

B. Inability to take oral medication

Ampicillin: 2 g IV or IM within 1 h before procedure

C. Penicillin allergy
1. Clarithromycin or azithromycin: 500 mg PO 1 h before procedure
2. Cephalexinc: 2 g PO 1 h before procedure
3. Clindamycin: 600 mg PO 1 h before procedure

D. Penicillin allergy, inability to take oral medication
1. Cefazolinc or ceftriaxonec: 1 g IV or IM 30 min before procedure
2. Clindamycin: 600 mg IV or IM 1 h before procedure

139

High-Risk Cardiac Lesions for Which Endocarditis
Prophylaxis Is Advised before Dental Procedures

Prosthetic heart valves
Prior endocarditis
Unrepaired cyanotic congenital heart disease, including palliative shunts or
conduits
Completely repaired congenital heart defects during the 6 months after
repair
Incompletely repaired congenital heart disease with residual defects
adjacent to prosthetic material
Valvulopathy developing after cardiac transplantationa