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5.3 Bacterial Infections
surrounding erythema; affects intact skin, has more
generalized distribution
Histology: subcorneal/intragranular acantholysis,
neutrophils in blister cavity, Gram-positive cocci
■
Treatment:
Localized: topical mupirocin, retapamulin, or
fusidic acid
Widespread: oral b-lactamase–resistant PCN or rstgeneration cephalosporin (CSN; clindamycin or
clarithromycin if PCN-allergic)
■
Decolonization: used for patients w/ recurrent
infections; topical mupirocin BID to nares for 7 to 10
days 1/– skin decolonization w/ mupirocin ointment,
bleach baths or chlorhexidine washes
■
Other high-yield facts
Nonbullous impetigo caused by S. pyogenes
serotypes 1, 4, 12, 25, and 49 n poststreptococcal
glomerulonephritis in 5%; risk not altered by
antibiotics
No risk of rheumatic fever from streptococcal
impetigo (vs. streptococcal pharyngitis)
Bullous impetigo 1 renal insufciency or
immunodeciency n exfoliatoxin may disseminate
n staphylococcal scalded skin syndrome (SSSS)
ETA is chromosomally encoded; ETB is plasmid
encoded
Bullous impetigo and pemphigus foliaceus have
nearly identical histology n need DIF and culture
(positive culture in bullous impetigo)
• Bacterial folliculitis
■
S. aureus folliculitis: most common form; most
commonly on face (beard area typically)
Supercial form (Bockhart’s impetigo): small
papulopustules on erythematous background
Deep form (“sycosis barbae”): large red
papulopustules 1/– plaques with small pustules
■
Gram-negative folliculitis: seen in acne patients on
long-term antibiotics
■
Pseudomonal folliculitis: a/w poorly chlorinated hot
tubs/whirlpools
■
Treatment:
Supercial staph folliculitis: chlorhexidine washes,
topical mupirocin/clindamycin
Widespread staph folliculitis: b-lactamase–resistant
PCN or rst-generation CSN, tetracyclines
Gram-negative folliculitis: isotretinoin
Pseudomonal folliculitis: self-resolves; ciprooxacin
if severe
Decolonization of nares/skin helpful if recurrent
• Abscesses, furuncles, and carbuncles
■
All are walled off collections of pus, most commonly from
S. aureus (often methicillin-resistant S. aureus [MRSA]);
may be complicated by surrounding cellulitis/phlebitis
■
Abscess: inamed and uctuant nodule; arises on any site
■
Furuncle: only occurs in a/w hair follicles/on hair-bearing
sites (“FURuncle 5 FURry sites”); head/neck (#1 site) .
intertriginous zones, thighs, other sites of friction
■
Carbuncle: collection of furuncles, often deeper w/
multiple draining sinuses; most often affects thick
skin of posterior neck, back, and thighs; systemic
symptoms typically present
■
Treatment:
Simple abscesses/furuncles: warm compresses
Larger/deeper lesions: incision and drainage (I&D)
Complicated (sensitive locations, extensive disease,
a/w cellulitis/phlebitis, systemic symptoms,
recalcitrant, and immunosuppressed): doxycycline,
TMP-SMX, and clindamycin (depending on local
resistance patterns)
Culture necessary since frequently due to MRSA
Decolonization of nares/skin helpful if recurrent
• MRSA
■
#1 cause of purulent infections in emergency
department; usually p/w furunculosis; may be a/w
cellulitis, and necrotic plaques
■
Resistance: specic mecA genes (from SCCmec types I–VI,
mobile genetic elements) n encodes mutated penicillinbinding protein, PBP2a n g afnity for b-lactams
■
Possible resistance to macrolides (active drug efux pump
[msrA/msrB gene], inactivating enzymes, cross-resistance to
clindamycin by alteration of bacterial ribosome by
erythromycin ribosomal methylase [erm genes])
■
Community-associated MRSA (CA-MRSA; majority)
also has Panton-Valentine leukocidin (PVL) virulence
factor; a/w increased virulence, leading to more severe
necrosis of skin and other tissues
■
CA-MRSA susceptible to more antibiotics than hospitalassociated MRSA
■
Treatment:
Minor infection: TMP-SMX, minocycline/
doxycycline, or clindamycin
Severe infection: vancomycin (best choice); linezolid,
daptomycin, ceftaroline, and telavancin as second line
• Staphylococcal scalded skin syndrome (SSSS)
■
Most commonly infants/young children (low mortality,
,5%) who lack neutralizing antibodies and have g renal
clearance
■
Also seen in adults w/ chronic renal failure (high
mortality, .50%); M . F (2–4:1)
■
p/w febrile prodrome, widespread skin tenderness;
skin eruption begins on face (perioricial radial
ssuring) and intertriginous zones (Fig. 5.5) n
generalizes within 48 hours as wrinkled-appearing
Fig. 5.5 Staphylococcal scalded skin syndrome with a wrinkled appearance of
the erythematous skin in addition to peeling and denudation. (From James WD,
Elston DM, McMahon PJ. Bacterial infections. In: Andrews’ Diseases of the Skin:
Clinical Atlas. Philadelphia: Elsevier; 2018:185–202.)
305
CHAPTER 5 • Infectious Diseases
skin w/ accid bullae and positive Nikolsky sign n
desquamation continues for up to 1 week, then heals
without scarring
■
Pathogenesis: infection by phage group II (types 55
and 71) S. aureus at a different/distant site n
production of ETA and ETB) n exfoliatoxins
disseminate via bloodstream n widespread cleavage
of Dsg1 n subcorneal/intragranular acantholysis
■
Histology: resembles pemphigus foliaceus; lacks
inammatory cells and bacteria in blisters (vs. bullous
impetigo)
■
Cultures from bullae are negative; blood cultures
almost always negative in children, but often positive
in adults
■
Treatment:
Mild disease: b-lactamase–resistant PCN (dicloxacillin)
or rst-generation CSN (cephalexin)
Severe disease: hospitalization (manage fever, pain,
uids, electrolytes, skin care) 1 IV antibiotics
(nafcillin, methicillin)
■
Other high-yield facts
Same exfoliatoxins as bullous impetigo (ETA/ETB),
but hematogenously disseminated
Most common primary sites of infection in
children 5 nasopharynx or conjunctivae (vs.
pneumonia and bacteremia in adults)
• Staphylococcal toxic shock syndrome (TSS)
■
Severe multisystem disease with cutaneous and
internal involvement (renal . GI, MSK, CNS, hepatic,
hematologic, and mucosal)
Typically affects young, healthy adults; occult
primary site of infection
Two forms: “menstrual TSS” (,50% of cases; young
women w/ superabsorbent tampons; mortality rate
less than 5%) or “nonmenstrual TSS” (.50%;
M 5 F; a/w nasal packing, surgery, skin, or internal
infections; mortality rate ,20%)
♦ Both forms p/w high fever (.102°F) 1 rash 1
systemic symptoms (e.g., myalgias, headache) 1
hypotension (100%)
♦ Mucocutaneous eruption classically starts
w/ scarlatiniform eruption (initially on trunk
n becomes generalized), redness and edema
of palms/soles, “red strawberry tongue,”
conjunctival hyperemia n palmoplantar
desquamation (1–3 weeks later), Beau’s
lines, onychomadesis; usually negative blood
cultures (,15% positive); low mortality
(,5% for menstrual TSS and ,20% for
nonmenstrual TSS)
■
Pathogenesis: production of toxic shock syndrome
toxin-1 (TSST-1) by certain strains of S. aureus n
TSST-1 acts as superantigen, binding to Vb region
of TCR and class II MHC on APCs n nonspecic
activation of T cells 1 cytokine storm (h TNF-a, IL-1,
IL-6, TLR2, and TLR4)
■
Treatment:
b-lactamase–resistant antibiotics, clindamycin
(suppresses toxin production) 1/– IVIG; IV uids
for hypotension; hospitalization
■
Other high-yield facts
Compared with strep TSS, staph TSS has lower
mortality (3%–20% vs. 30%–60%), less orid
primary site infection, more frequent rash, and less
frequent blood culture positivity (,15% vs. .50%)
• Pyomyositis
■
S. aureus infection of skeletal muscle; usually have
predisposing factors (immunosuppression, diabetes,
trauma, and intravenous drug abuse [IVDA]); p/w 1- to
2-week febrile prodrome, muscle pain, and a soft tissue
mass w/ surrounding woody induration n muscle
abscess 1/– septicemia
■
Treatment: I&D 1 IV antibiotics, then long oral
antibiotic course
■
MRI is best diagnostic tool
• Botryomycosis
■
Deep granulomatous and suppurative infection most
frequently caused by S. aureus
■
May extend to skeletal muscle and bone; affects all
ages; a/w g T-cell counts and other defects in cellular
immunity
■
70% have skin-limited disease (rarely visceral in
severely immunosuppressed patients; lung most
common); p/w deep, ulcerative plaques/nodules with
multiple draining sinuses that drain yellow granules
■
Histology: large granules w/ basophilic center
(nonlamentous bacteria) and eosinophilic/hyaline
periphery (Splendore-Hoeppli phenomenon;
composed of IgG and C3 deposits), granules are
surrounded by abscess and granulomatous inammation
(Fig. 5.6); granules are PAS1, Giemsa1, and Gram(1)
■
Treatment:
Surgical debridement/excision 1 antistaphylococcal
antibiotics
Fig. 5.6 Botryomycosis: there are multiple dermal abscesses surrounding discrete bacterial colonies. (From Grayson W, Calonje E. Infectious diseases of the
skin. In: Calonje E, Brenn T, Lazar AJ, Billings SD, eds. McKee’s Pathology of the
Skin. 5th ed. Philadelphia: Elsevier; 2020:826–975.)
306
5.3 Bacterial Infections
Streptococcal skin infections
• Ecthyma
■
Deep variant of impetigo; most common in children;
caused by S. pyogenes; p/w few vesicopustules, most
commonly on legs n develop into “punched-out”
ulcers with purulent base and hemorrhagic crust n
slowly self-resolves w/ scarring
Frequently as a result of scratching bug bites
■
Diagnosis: wound culture conrmatory, blood culturenegative, biopsy 1 Gram stain in difcult cases
■
Treatment: b-lactamase–resistant PCN (dicloxacillin)
or rst-generation CSN (cephalexin)
• Erysipelas (“St. Anthony’s Fire”)
■
Supercial variant of cellulitis (upper-mid dermis vs.
deep dermis/SQ) with sharply dened (“ridge-like”)
borders, ery-red color, and pain/burning sensation;
prominent lymphatic involvement; most common
sites 5 lower extremity (#1 site) . face (Fig. 5.7)
Lymphedema is a major risk factor
■
Usually caused by group A b-hemolytic strep
■
Labs: wound/blood cultures usually negative; best
conrmatory tests 5 h DNase B and ASO titers
■
Treatment: PCN (treatment of choice) for 2 weeks;
erythromycin if PCN-allergic
• Perianal streptococcal skin infection
■
Classically boys . 4 years old; p/w sharply dened red
plaques spreading up to 3 cm from anus (girls can get
similar presentation on vagina/vulva); a/w pain upon
defecation, blood in stool, guttate psoriasis outbreak
■
Labs: skin culture conrmatory
■
Treatment: oral cefuroxime (treatment of choice) or
PCN (slightly less effective)
• Blistering distal dactylitis
■
Initially p/w darkening of skin of distal nger (.toe)
volar fat pad n progresses to purulent vesicle/bulla
on erythematous background within 1 week; affects
Fig. 5.7 Erysipelas on the malar cheek. (From Dinulos JGH. Bacterial infections.
In: Habif’s Clinical dermatology: a color guide to diagnosis and therapy. 7th ed.
Philadelphia: Elsevier; 2021:331–375.)
children; results from picking nose or local skin
trauma; S. pyogenes . S. aureus
■
Treatment: I&D 1 10-day course oral b-lactam
• Scarlet fever
■
Young children (1–10 years old); caused by
group A b-hemolytic streptococcus n produces
streptococcal pyrogenic toxins A, B, and C (SPE-A,
B, and C)
■
Most commonly in setting of streptococcal pharyngitis/
tonsillitis; p/w sore throat, high fevers, and systemic
symptoms n 1 to 2 days later, macular erythema on
upper trunk/neck n soon develop classic “sandpaper-
like” papular eruption, Pastia’s lines (linear petechiae;
favors exural sites), ushed cheeks with circumoral
pallor, and “white strawberry tongue” (white
background 1 red papillae) n later “red strawberry
tongue,” purulent exudate from throat n 1 to 2 weeks
later, palmoplantar desquamation
■
Labs: positive throat/nasal culture conrmatory;
elevated DNase B and ASO titers
■
Treatment: PCN (treatment of choice), amoxicillin, or
rst-generation CSN/erythromycin/clindamycin (if
PCN-allergic)
■
Other high-yield facts:
Notable complications: acute glomerulonephritis
and rheumatic fever
Purulent pharyngitis almost always present (helpful
clue)
10% of all patients w/strep throat develop scarlet
fever; mortality rate has dropped hugely since the
advent of antibiotics (1% currently vs. 20%
mortality in pre-antibiotic era)
• Streptococcal toxic shock syndrome
■
Similar clinical features as staph-TSS, but affects
young/healthy adults, is more severe w/ higher
mortality (30%–60%), usually a/w orid skin/
soft tissue infections (often necrotizing fasciitis
[NF] vs. occult infections in staph-TSS), much less
frequent generalized macular erythematous rash,
and far more frequent blood culture positivity
(.50%)
■
Most common primary source 5 skin infection from
skin barrier breakdown (excoriation, bug bite, and
infected surgical site)
■
Classically p/w severe localized pain in extremity w/
redness, swelling, or NFn within 24 to 48 hours,
systemic symptoms (hypotension [100%])
■
Pathogenesis: group A b-hemolytic strep (M types 1
and 3) produce various toxins:
SPE A, B, and C
Streptococcal mitogenic toxin Z (SMEZ)
Streptolysin O
■
Toxins act as superantigens, binding to Vb region of
TCR and class II MHC on APCs n nonspecic
activation of T cells 1 cytokine storm (h TNF-a, IL-1,
IL-6, TLR2, and TLR4)
■
Treatment: most cases severe, requiring hospitalization 1
surgical debridement of soft tissue infection (possibly
fasciotomy or amputation) 1 clindamycin (inhibits
toxin production) 1 PCN 1/– IVIG
307
CHAPTER 5 • Infectious Diseases
Polymicrobial Gram-positive skin
infections
• Cellulitis
■
Infection of deep dermis/SQ most commonly affecting
adults w/ skin barrier disruption; p/w tender/red/
warm, ill-dened plaques w/ fever/chills/lymphangitis
In severe cases, may see necrosis, bullae, vesicles
■
Most commonly caused by group A b-hemolytic strep
. S. aureus (most common cause in children); most
common sites: head/neck (children), lower extremities
(adults), and IV injection sites on arms (IVDA)
■
Labs: blood cx always negative in immunocompetent
patients
■
Notable variants:
Haemophilus inuenzae (discussed in Gram-negative
infection section)
Cellulitis a/w diabetic ulcers or chronic decubitus
wounds: mixed infection w/ Gram-positive cocci
and Gram-negative aerobes and anaerobes
■
Treatment:
Uncomplicated cases: oral dicloxacillin, cephalexin,
or clindamycin for 10 days (must empirically cover
for staph and strep)
Cellulitis a/w diabetic/decubitus ulcers: piperacillin/
tazobactam, or ciprooxacin 1 metronidazole
Severe cases: hospitalize and IV antibiotics
MRSA cellulitis: TMP-SMX, minocycline/doxycycline,
and clindamycin
■
Other high-yield facts
Lymphatic damage (e.g., prior cellulitis, lymph node
dissection, vein harvesting) n h risk of recurrent cellulitis
Presence of abscess or necrotizing cellulitis are clues
to MRSA
• Necrotizing fasciitis
■
Rapidly progressive, life-threatening (up to 50%
mortality) necrotizing infection of skin, SQ, and fascia
■
Most common site 5 extremities (.trunk)
■
Caused by group A b-hemolytic strep M types 1 and 3
(#1 cause in children) or polymicrobial (#1 cause in
adults; mixture of Streptococci, S. aureus, E. coli, Clostridium,
and Bacteroides)
■
Initially p/w severely painful indurated/“woody” plaque
(“pain out of proportion to visible skin changes”) n over
1 to 2 days and rapidly progresses n color changes
from erythematous n dusky purple/gray 1/–
hemorrhagic bullae/ulceration, crepitus, foul-smelling
discharge; patients always severely toxic-appearing
(fever, tachycardia, and septic shock) n late in course
and skin becomes anesthetic (nerves destroyed)
■
Imaging: MRI may demonstrate gas
■
Fournier’s gangrene: NF of genitalia/perineum/lower
abdominal wall
■
Meleney’s gangrene: polymicrobial NF arising as a
postoperative complication
■
Treatment: fasciotomy 1 IV antibiotics (piperacillin/
tazobactam 1 clindamycin 1 ciprooxacin)
■
Other high-yield facts
Risk factors: diabetes, immunosuppression,
peripheral vasular disease (PVD), CRF, trauma,
bevacizumab, IVDA, and recent surgery
Prognostic factors a/w h mortality: older age,
h time to rst debridement, h extent of infection,
females, h lactic acid, and h creatinine
Corynebacterial skin infections
• Erythrasma
■
Caused by Corynebacterium minutissimum (Gram-
positive lamentous rod)
■
Affects stratum corneum of moist, intertriginous
zones (groin and toe webs [particularly fourth] .
axillae, inframammary, umbilicus, and intergluteal)
Fluoresces “coral red” w/ Wood lamp (bacterial
coproporphyrin III production)
Groin: light red-pink (later brown) slightly scaly
patches w/ thin scale
Toe webs: chronic, asymptomatic ssuring and
maceration
Histology: lamentous Gram-positive rods within
stratum corneum
■
Treatment:
Localized: topical clindamycin/erythromycin/
mupirocin, Whiteld ointment
Widespread/recalcitrant: oral erythromycin,
clarithromycin, tetracyclines
• Pitted keratolysis
■
Caused by Kytococcus sedentarius, which digests keratin
in stratum corneum
■
Non-inammatory infection of weight-bearing areas of
plantar (.palmar) skin
■
p/w Small crateriform pits and foul odor n may
coalesce into arciform pits
Risk factors: hyperhidrosis and occlusion
■
Histology: deep pits in stratum corneum with Grampositive bacteria at base
■
Treatment: topical erythromycin (or clindamycin,
mupirocin, benzoyl peroxide) 1/– 20% aluminum
chloride, botulinum toxin
• Trichomycosis axillaris
■
Asymptomatic, adherent yellow-red concretions on
axillary hair shafts; uoresces with Wood lamp; caused
by Corynebacterium tenuis
■
Treatment: shaving of axillary hair (treatment of
choice); may use topical erythromycin/clindamycin/
benzoyl peroxide
Clostridium skin infections
• Clostridial anaerobic cellulitis and myonecrosis
■
Very rapid, potentially fatal necrotizing soft tissue
infections with localized gas production (“gas
gangrene”)
Caused by Clostridium perfringens (Gram-positive,
spore-forming rod)
♦ Obligate anaerobe (only reproduces in hypoxic
tissues)
■
Due to traumatic inoculation (surgery or crush/
penetrating injuries) of C. perfringens into oxygen-poor
deep tissues; bacteria produces two pathogenic toxins:
a-toxin (cleaves lipids) and perfringolysin O (induces
vascular clots and worsens tissue hypoxia) n bacteria
308
5.3 Bacterial Infections
proliferates freely in anaerobic environment, producing
CO
and cleaving lipids n clinically p/w crepitus,
2
foul-smelling brown exudate (“dirty dishwater”
color), w/ variable skin changes
Myonecrosis more likely to have swelling, overlying
skin changes, pain, toxemia, bacteremia, but less
likely to have crepitus than anaerobic cellulitis
Risk factors: diabetes, PVD
■
Imaging: X-ray reveals gas in soft tissues
■
Labs: blood culture usually negative
■
Treatment: immediate aggressive surgical debridement
(most important) 1 clindamycin and piperacillintazobactam 1/– hyperbaric oxygen
Filamentous bacteria
• Actinomycosis
■
Agent: Actinomyces israelii
■
Gram-positive, non-acid fast, and anaerobic/
microaerophilic lamentous bacteria
■
Actinomycetes spp. are part of normal ora of mouth,
GI/GU tracts n infection arises after trauma (dental
procedures or surgical interventions)
■
Subacute-chronic granulomatous lesions with
suppurating abscesses 1 sinus tracts
■
Forms:
Cervicofacial (most common, accounts for 70%):
“lumpy jaw disease,” red-brown nodules with
stulous abscesses draining characteristic yellow
sulfur granules (5 clumps of bacteria); a/w poor
dental hygiene and dental procedures
Pulmonary/thoracic: as a result of aspiration, p/w
pulmonary cavities at base of lungs
Pelvic: due to intrauterine devices in women
GI: as a result of trauma or inammatory disease,
p/w granulomatous lesions in bowel wall
■
Histology: dense granulomatous and suppurative
inammation with “granules” with basophilic center
(Gram-positive branching laments of Actinomyces) and
eosinophilic rim (Splendore-Hoeppli phenomenon)
■
Treatment: penicillin G or ampicillin
Chronic or deep-seated infections: 2 to 6 weeks of IV
antibiotics followed by 3 to 12 months of oral PCN
Acute infections: 2 to 3 weeks of oral PCN 1 I&D of
abscesses 1 surgical excision of sinus tracts
• Nocardiosis
■
Agent: Nocardia brasiliensis (#1 cause of actinomycotic
mycetoma), Nocardia asteroides (#1 cause of pulmonary/
systemic nocardiosis), other Nocardia spp.
■
Gram-positive, weakly acid-fast, lamentous
bacteria
■
Ubiquitous in soil (explains why foot is the most
common site of actinomycotic mycetoma!)
■
Four major forms of disease (Table 5.5), but
actinomycotic mycetoma is most testable
■
Histology: intense neutrophilic inltrate 1 sulfur
granules (only seen in actinomycotic mycetoma form);
branching laments are Gram-positive, acid-fast
bacteria (AFB)1 (Fite . Ziehl-Neelsen), and GMS1
■
Treatment: sulfonamides (treatment of choice) 1/–
surgical drainage (Box 5.1)
Table 5.5 Four Major Clinical Forms of Cutaneous Nocardiosis
Primary
Actinomycotic
mycetoma
Lymphocutaneous Occurs days to weeks after trauma
Superficial
cutaneous
Secondary
Pulmonary/systemic Subcutaneous abscesses of the chest wall
a
In Mexico and Central and South America, Nocardia brasiliensis is the
etiologic agent of 90% of actinomycotic mycetomas , whereas in the
United States, most mycetomas are caused by true fungi.
From Sommer LL, Reboli AC, Heymann WR. Bacterial diseases. In: Bolognia
JL, Shaffer JV, Cerroni L, eds. Dermatology. 4th ed. Philadelphia: Elsevier;
2018:1259–1295.
Box 5.1 “SNAP” Mnemonic
Antibiotics of choice for Nocardia versus Actinomyces 5 “SNAP”
Sulfonamides 5 Nocardia, Actinomyces 5 Penicillin
Half of all cases of actinomycotic mycetoma are
caused by the Nocardia species
Traumatic inoculation causes a painless nodule that
enlarges, suppurates, and drains via the sinus tracts
Purulent discharge contains sulfur granules
The foot is the usual site of involvement
May involve underlying muscle and bone
Appears as a crusted pustule or abscess resistant
to antibiotics
Ascending lymphatic streaks, a sporotrichoid
pattern of papulonodules, and tender palpable
lymph nodes may be seen
Traumatic implantation of foreign objects (including
soil and gravel) into the skin
The diagnosis is based on a high index of suspicion,
lack of response to routine antibiotic treatment,
and laboratory results
Pustules, nodules, and cutaneous stulae
Almost universally fatal if left untreated
Most commonly caused by Nocardia asteroids
a
Other Gram-positive infections
• Anthrax
■
Agent: Bacillus anthracis
■
Gram-positive, spore-forming rod
■
Three forms (pulmonary, GI, and cutaneous anthrax)
■
Cutaneous anthrax: most common (.95%) and least
fatal form
Arises via occupational exposure (“Woolsorter’s
disease”) from direct contact w/ infected animals/
carcasses
Presents 1 week postexposure with purpuric
papulovesicle (“malignant pustule”) that drains
serosanguinous uid n vesicle ulcerates to form
painless/black/necrotic eschar w/ satellite vesicles
and edema
20% mortality if untreated
■
Treatment:
First line (cutaneous anthrax): quinolone or
doxycycline 3 2 weeks (treat for 60 days if suspect
bioterrorism or possible inhalation exposure);
vaccine and immune globulin are available for
postexposure prophylaxis
■
Other high-yield facts:
Early treatment critical! (20% mortality if untreated
vs. 0% if treated)
309
CHAPTER 5 • Infectious Diseases
Virulence factors:
♦ Poly-D-glutamic acid capsule (resists
phagocytosis)
♦ Lethal toxin 5 protective antigen 1 lethal factor
(h TNF-a and IL-1b n septic shock, death)
♦ Edema toxin 5 protective antigen 1 edema
factor (h cAMP n edema)
• Erysipeloid
■
Acute, self-limited infection; occupational disease of
sherman or poultry/sh handlers; as a result of
traumatic inoculation of Erysipelothrix rhusiopathiae
(Gram-positive rod); most commonly p/w localized
form: red-violaceous non-suppurative cellulitis 1/–
hemorrhagic vesicles; classically affects nger web
spaces w/ sparing of terminal phalanges
■
Treatment: PCN (treatment of choice), ciprooxacin (if
PCN-allergic)
• Listeria
■
Most commonly affects pregnant women, elderly, and
the immunosuppressed as GI illness caused by the
ingestion of Listeria monocytogenes (motile Grampositive rod) n fever, bacteremia, and meningitis
■
Rarely see skin lesions—mostly occurs in setting of
neonatal septicemia (from vertical transmission), which
p/w disseminated papules/pustules/vesicles/purpura
■
Treatment:
First line: ampicillin
Second line: TMP-SMX
• Cutaneous microbiome: Most bacteria on the skin are
Actinobacteria (e.g., Propionibacterium, Corynebacterium),
Firmicutes (e.g., Staphylococcus), Proteobacteria, and
Bacteriodetes—help protect skin from pathogenic
organisms
A
II. Gram-negative skin infections
Pseudomonas
• Green nail syndrome
■
Green/blue-black nail discoloration; a/w excessive
water exposure, nail trauma; from Pseudomonas
aeruginosa pyocyanin pigment production
■
Treatment: topical quinolone, topical sodium
hypochlorite, or aminoglycoside solution
• Pseudomonal pyoderma
■
Supercial erosive infection w/ blue-green purulent
exudate, “moth-eaten” appearance to skin surface, with
“mousy” or “grape-like” odor; may arise at burn sites,
in mixed toe web infections (Fig. 5.8), and other
chronic wounds
■
Treatment: systemic antipseudomonal antibiotics,
topical antiseptics, debridement, and drying agents
• Otitis externa (“swimmer’s ear”)
■
P. aeruginosa infection of external auditory canal; p/w
edema, skin maceration, and purulent green exudate;
tympanic membrane intact; classically severe pain
upon pinna manipulation
■
Malignant otitis externa (severe variant): usually only in
diabetics or immunosuppressed; persistent drainage w/
excessive granulation tissue extending to bony portion of
ear n may result in osteomyelitis of skull base
B
Fig. 5.8 (A) and (B) Pseudomonas skin infection of the feet. Note the erosions
and blistering of the skin. (From James WD, Elston DM, McMahon PJ. Bacterial
infections. In: Andrews’ Diseases of the Skin Clinical Atlas. Philadelphia: Elsevier;
2018:185–202. B, Courtesy of Ken Greer, MD.)
■
Treatment: topical antipseudomonal agents, but
systemic for malignant otitis externa
• Pseudomonal folliculitis (“hot tub folliculitis”)
■
Self-resolving P. aeruginosa infection arising from
poorly chlorinated hot tubs/whirlpools; p/w red,
perifollicular papulopustules 1 to 2 days postexposure;
commonly affects areas covered by bathing suit
■
Treatment:
Immunocompetent: spontaneous resolution in
# 2 weeks
Widespread, immunosuppressed: oral quinolone
• Pseudomonas hot-foot syndrome
■
Self-resolving P. aeruginosa infection arising from
wading in pools w/ high concentrations of
Pseudomonas; p/w painful, red-violaceous plaques/
nodules on weight-bearing areas of plantar surface
■
Histology: perivascular/perieccrine neutrophils
■
Treatment: none required; self-resolves
310
5.3 Bacterial Infections
• Ecthyma gangrenosum
■
Cutaneous lesion indicative of P. aeruginosa septicemia;
most commonly occurs in immunosuppressed patients
w/ severe neutropenia (often bone marrow
transplantation patients); p/w a small number of
purpuric macules n progresses to hemorrhagic bullae
n bullae rupture n ulcer w/ necrotic black eschar
and tender, red skin surrounding eschar; most common
sites 5 anogenital region and extremities
■
Histology: sharply demarcated epidermal necrosis w/
hemorrhagic crust, and underlying dermal infarction w/
septic vasculitis (Gram-negative rods in vessel walls)
■
Labs: blood/wound cultures positive
■
Treatment: IV aminoglycoside 1 antipseudomonal
PCN
■
Other high-yield facts
Prognostic factors a/w poor outcomes: h # lesions,
delay in diagnosis, and prolonged neutropenia
Bartonella
• Small, facultative intracellular Gram-negative bacilli
• Three species cause human disease (Table 5.6):
■
Bartonella henselae (cat scratch disease, bacillary
angiomatosis, and peliosis hepatitis)
■
Bartonella quintana (trench fever and bacillary
angiomatosis)
■
Bartonella bacilliformis (Carrion’s disease/Oroya fever/
verruga peruana)
• Both B. henselae and B. quintana may cause: bacillary
angiomatosis, chronic afebrile bacteremia, and endocarditis
• Bacillary angiomatosis mostly occurs in HIV-positive
patients w/ CD4 count , 200; only 20% recall cat bite/
scratch (vs. 90% w/ cat scratch disease); vascular
proliferation caused by bacterial angiogenic factor
■
Can involve lymph nodes, bone, and viscera
■
Lesions are dome-shaped, vascular papulonodules
■
More developed lesions can have a friable eroded
appearance, resembling pyogenic granulomas
• Death in Oroya fever usually secondary to Salmonella
enterica superinfection; chloramphenicol 1 b-lactam is
treatment of choice (alt. is quinolone)
• Histopathology (verruga peruana and bacillary
angiomatosis): resembles pyogenic granuloma (lobular
capillary proliferation), but has dense neutrophilic
inltrate, and extra- and intracellular organisms (within
endothelial cells—Rocha-Lima inclusions) seen w/
Warthin-Starry stain (Fig. 5.9)
• Labs: B. bacilliformis—PCR, culture, immunologic testing;
B. henselae and B quintana—PCR assay (rapid, sensitive),
serologies (sensitive, specic; not for B. quintana),
chocolate agar culture (slow!)
Rickettsia
• Small, obligate intracellular Gram-negative organisms
• Transmitted by arthropod host/vector (ticks, eas, lice,
and mites)
• Target 5 endothelial cells
• Transmitted from arthropod (tick, ea, mite, and louse)
via saliva or feces n bacteria enter dermis via bite or
scratching n bacteria attach to endothelial cells n
spread hematogenously and destroy infected vessels via
reactive oxygen species formation n h vascular
permeability n vascular skin ndings (petechiae,
purpura, and vasculitis 5 “spotted fever”) and lifethreatening end organ damage (meningoencephalitis and
pulmonary edema/pneumonitis most important causes
of mortality), thrombocytopenia, hypovolemia, and
hypotension
• Three groups (Table 5.7):
■
Spotted fever group (rash in 85%–100%): R. rickettsii,
R. conorii, R. akari, R. africae, R. japonica, and R. australis
■
Typhus group (rash in 50%–80%): R. typhi and
R. prowazekii
■
Scrub typhus (rash in 50%): R. tsutsugamushi
• Eschar at inoculation site 1 week prior to illness is
constant and important feature seen in majority of
spotted fever group, and scrub typhus
■
No eschar in Rocky Mountain spotted fever (RMSF)
and typhus group
• Variable prognosis:
■
Severe: RMSF (most severe, 25% mortality if untreated,
and 4% if treated) . epidemic typhus (15% mortality
if untreated and 3% if treated)
■
Intermediate: Mediterranean spotted fever (3%–5%
mortality)
■
Benign: endemic typhus (#1% mortality) and
Rickettsialpox (0% mortality)
Other Gram-negative skin infections
• Neisseria meningitidis
■
Gram-negative diplococcus (strains A, B, C, Y, and
W-135)
■
Most commonly affects children/young adults living in
close quarters (military recruits and college students);
M . F (4: 1); humans are only reservoir; 10% to 15%
population are asymptomatic carriers (in
nasopharynx); disease transmitted via respiratory
secretions
■
Acute meningococcemia: 1 to 10 days postexposure,
p/w fever, chills, headache, petechial rash (30%–50%),
retiform purpura w/ classic “gunmetal gray” color
(Fig. 5.10), or hemorrhagic bullae on legs and trunk;
may progress to septic shock with DIC (purpura
fulminans)
Histology: LCV w/ vascular thrombosis and Gram-
negative rods in 70% biopsies
Labs: PCR assay most sensitive/specic (.blood/
tissue/CSF cultures or latex agglutination studies)
Prognosis: 10% to 15% mortality; up to 15% who
survive have hearing loss or CNS sequelae
■
Chronic meningococcemia: less common; p/w
recurrent fevers, arthralgias, and macular/papular
eruption; condition self-resolves, only to recur days to
weeks later
■
Treatment: early treatment is critical!
First line: high-dose IV PCN (treatment of choice)
Second line: quinolones or chloramphenicol (if
PCN-allergic); third-generation CSN (resistant
disease)
311
312
Table 5.6 Major Human Diseases Caused by Bartonella Species and Their Treatment
Species Disease Vector
Bartonella
bacilliformis
Bartonella
henselae
Bartonella
quintana
Fever and splenomegaly caused by bacteremia with Bartonella rochalimae (a recently recognized species) has also been described.
a
Gray baby syndrome can develop in premature neonates who receive chloramphenicol.
From Sommer LL, Reboli AC, Heymann WR. Bacterial diseases. In: Bolognia JL, Shaffer JV, Cerroni L, eds. Dermatology. 4th ed. Philadelphia: Elsevier; 2018:1259–1295.
Bartonellosis
(Carrion’s
disease, Oroya
fever, and
verruga
peruana)
Cat scratch
disease
Bacillary
angiomatosis
Bacillary peliosis
hepatis
Bacteremia
(chronic afebrile)
Endocarditis Late complication of chronic
Trench fever
“Five day fever”
“Urban trench
fever” “Quintan
fever”
Bacillary
angiomatosis
Bacteremia
(chronic afebrile)
Endocarditis Late complication of chronic
Phlebotomine sand
fly (Lutzomyia
verrucarum)
Cat flea
(Ctenocephalides
felis)
Human body
louse (Pediculosis
humanus)
Reservoir/
Host Epidemiology Clinical Presentation First Line Second Line Notes
Human Andean mountain valley
Cat Primarily seen in young
Human First reported in World War
regions of Peru, Ecuador,
and Southwestern
Columbia (altitudes of
2500–8000 feet)
More common in immuno-
logically naive tourists
and transient workers
Milder in children
people (,18 years) in the
fall and winter
Immunocompetent .
immunocompromised
Immunocompromised
(e.g., common in HIV)
Immunocompromised
Immunocompetent or
immunocompromised
bacteremia
I troops, now associated
with homelessness and
poor hygiene (“urban
trench fever”)
Immunocompromised (e.g.,
common in HIV)
Immunocompetent or
immunocompromised
bacteremia
Oroya fever (acute
phase)
Verruga peruana
(chronic phase)
Mild to moderate,
uncomplicated
Severe, complicated Doxycycline plus
Mild, uncomplicated
bacillary angiomatosis
Severe, complicated
bacillary angiomatosis
Chloramphenicol
plus b-lactam
antibiotic
Quinolone
(noroxacin and
ciprooxacin)
(.6 years of age
and not pregnant)
Azithromycin Ciprooxacin
Supportive care
(analgesics) only
Needle aspiration
of suppurative
lymph nodes
rifampin
Erythromycin Doxycycline
Erythromycin
Doxycycline plus
rifampin
Doxycycline plus
aminoglycoside
a
Trimethoprim-
sulfamethoxazole
Macrolide
Doxycycline
Rifampin 1
streptomycin
(traditional)
Azithromycin
Doxycycline plus
rifampin
Azithromycin
Clarithromycin
Successful treatment does not
eliminate risk for developing
verruga peruana
Adjunctive treatment needed with
chloramphenicol, as treatment
failures have been seen with
monotherapy
Death occurs in 40% of untreated
individuals
Only 5% of patients recall an acute
febrile illness
Disappearance of skin lesions
within 1 month with treatment
Azithromycin shown to decrease
lymph node volume, but
not effective in preventing
dissemination or complications
Severe disease includes retinitis,
encephalopathy, and visceral
spread
Jarisch–Herxheimer-like reaction
may occur
Treatment failures seen with
quinolones, trimethoprimsulfamethoxazole, and narrowspectrum cephalosporins
Use of IV antibiotics
recommended for GI intolerance
or poor absorption states
Doxycycline plus rifampin
recommended for CNS
disease, because of better CNS
penetration
CHAPTER 5 • Infectious Diseases
5.3 Bacterial Infections
B
Fig. 5.9 (A) and (B) Bacillary angiomatosis histology. Note the vascular proliferation in the dermis with plump endothelial cells, as well as clusters of neutrophils
and amphophilic collections of organisms. (From Elston DM: Vascular tumors. In: Elston DM, Ferringer T, eds. Dermatopathology. 3rd ed. Philadelphia: Elsevier,
2019:433–495.)
Table 5.7 Rickettsial Diseases
Disease (Bacterium) Vector Clinical Features Rx Other High-Yield Facts
Spotted fever group: “spotted fever” 5 high fevers (.102°F) 1 erythematous-petechial skin eruption (85%–100%) 1 constitutional symptoms
Rocky Mountain
Spotted Fever
(RMSF) (Rickettsia
rickettsii)
Mediterranean spotted
fever/“Boutonneuse
fever” (Rickettsia
conorii)
Rickettsialpox
(Rickettsia akari)
Typhus group: similar to spotted fever group in most regards; p/w erythematous macules starting around axillae; rash in only 50%–80% (vs. 85%–100% in
spotted fever group)
Endemic/murine
typhus (Rickettsia
typhi)
Cat flea typhus
(Rickettsia felis)
Epidemic typhus
(Rickettsia
prowazekii)
Dermacentor variabilis
(#1 vector, Eastern 2/3rd
and Pacic Coast of the
United States)
Dermacentor andersoni
(#2 vector, Rocky
Mountain states)
Rhipicephalus sanguineus
(Southwestern United
States)
Less commonly A. cajen-
nense, A. aureolatum, A.
imitator, and A. sculptum
Rhipicephalus
sanguineus (brown dog
tick)
Liponyssoides
sanguineus (house
mouse mite)
Xenopsylla cheopis
(Oriental rat flea)
Ctenocephalides felis
(cat flea)
Pediculus humanus var.
corporis (human body
louse)
7–14 days post-tick bite, develop
fever, headache, myalgias, and GI
symptoms n 90% develop rash
3–5 days later with faint red macules
on acral sites (wrists and ankles
are most common initial sites) n
subsequent centripetal spread
to trunk; spares face n over
time, lesions become papular and
petechial/purpuric as a result of
edema and RBC extravasation from
vessel destruction; mortality rate 5
25% if untreated (vs. ,4% if treated
early)
p/w Necrotic papule at site of tick bite
(“Tache noir”) n maculopapular
eruption favoring legs
Within 48 hours of bite p/w
papulovesicle at bite site n
progresses to eschar (.90%) n
fever and systemic symptoms w/
widespread cutaneous eruption
(face, trunk, and extremities) of
red macules and papulovesicles
w/ hemorrhagic crusts 1/–
oropharyngeal enanthem
p/w Fever 1 similar systemic
symptoms as spotted fever group 1
erythematous macules and papules
initially on axillae
Clinically identical to endemic (murine)
typhus
Epidemic typhus: a/w crowded living
conditions
Brill-Zinsser disease: recurrence of
latent infection (occurs decades later)
Flying squirrel typhus: caused by
contact w/ ying squirrels and
their eas/lice
Doxycycline is treatment
of choice in ALL patients,
even children!
Only exception: chloram-
phenicol is treatment of
choice for pregnant
patients (n risk of “gray
baby syndrome”)
First line: doxycycline
Mild disease in children:
azithromycin, clarithromycin
None required; self-
resolves within 3 weeks
May hasten resolution
w/ doxycycline
Doxycycline X. cheopis is also the vector
Doxycycline
Doxycycline
RMSF is the most severe
Rickettsial infection
40% of patients do not recall
tick bite!
Cutaneous necrosis in 4%
Lacks eschar!
The only spotted fever to be
caused by a mite
Most common in urban
areas of Northeastern
United States
Weil-Felix test does not
identify Rickettsialpox
for bubonic plague
Continued
313
CHAPTER 5 • Infectious Diseases
Table 5.7 Rickettsial Diseases—cont’d
Scrub typhus: solitary member comprising the third group of rickettsial infection; rash in only 50%
Scrub typhus (Orientia
tsutsugamushi)
Rickettsia-like bacteria
Human monocytic
ehrlichiosis (HME)
(Ehrlichia
chaffeensis)
Human granulocytic
anaplasmosis
(Anaplasma
phagocytophilum)
Q fever (Coxiella
burnetii)
GI, Gastrointestinal; LFTs, liver function tests.
Larval trombiculid mites
(“chiggers”)
Amblyomma
americanum (lone star
tick)
Ixodes scapularis and
Ixodes pacificus (same
as Lyme and Babesiosis)
Usually transmitted via
aerosols from infected
sheep and cattle
Eschar forms at bite site (60%–90%)
n fever, lymphadenopathy, and
macular rash (50%) starting initially
in axilla n subsequent centrifugal
spread; variable prognosis
Most common in Southern United
States; p/w fever, myalgias,
thrombocytopenia, leukopenia, and
maculopapular or petechial rash
(30%–40%) most commonly on trunk,
extremities; mortality rate 5 3%
Found in same geographic distribution
as Lyme disease; similar clinical
presentation as HME, but g fatality
rate, g skin findings, and h
peripheral neuropathy
Rare skin findings
Fever, pneumonia, hepatitis
First line: doxycycline
Pregnant women:
azithromycin
Doxycycline Obligate intracellular
Doxycycline Obligate intracellular
Doxycycline Rare cause of erythema
Most common in Asia;
particularly areas w/ dense
scrub vegetation
Interstitial pneumonia common
organism targets and
kills monocytes/
macrophages
Reservoir 5 white-tailed deer
No eschar seen
h LFTs
organism targets and kills
neutrophils
Coinfection w/ Lyme and
Babesiosis is common
nodosum and mixed
cryoglobulinemia vasculitis
Fig. 5.10 Stellate purpura with a central gunmetal-gray hue suggestive of
meningococcemia. (From Mishkin DR, Rosh AJ. Female infant with fever and
rash. Ann Emerg Med. 2009; 54[2]:155–180.)
Prophylactically treat all close contacts w/
ciprooxacin, rifampin, azithromycin
■
Other high-yield facts
Risk factors: asplenic patient or terminal
complement deciency (C5–C9)
Main virulence factor 5 polysaccharide capsule
Endotoxin n septic shock and purpura fulminans
In the United States, types B, C, and Y are most
common causes of acute meningococcemia
Quadrivalent vaccine protects against types A/C/
Y/W-135
• Brucellosis (Malta fever, “undulant fever”)
■
Caused by Gram-negative coccobacillus, Brucella spp.
■
Endemic in Middle East (consuming unpasteurized
goat milk/cheese)
■
In the United States, occupational disease (farmers,
butchers, and veterinarians) from direct contact or
inhalation
■
p/w Undulating fevers, arthralgias, LAD,
hepatosplenomegaly, endocarditis, foul-smelling
sweat, and rare (,10%) skin ndings (disseminated
violaceous papules, purpura, erythema nodosum-like)
• Glanders
■
Gram-negative bacillus, Burkholderia mallei
■
Caused by contact w/ infected horses, mules, or
donkeys
■
Four forms:
Localized—hemorrhagic, ulcerative papulopustule
at inoculation site
Chronic—multiple soft tissue nodules (“farcy
buds”) on skin overlying lymphatics
Septicemic form—mortality rate .95% without
treatment and 50% w/ treatment
Pulmonary form—mortality similar to septicemic
form
■
Treatment:
Localized disease: 60- to 150-day course of
amoxicillin/clavulanate, doxycycline, or TMP-SMX
Septicemic: IV carbapenems 1 ciprooxacin or
doxycycline
• Melioidosis
■
Gram-negative bacillus Burkholderia pseudomallei
■
Caused by direct contact w/ contaminated water or soil
■
Risk factors: diabetes, chronic kidney disease,
immunosuppression, and IVDA
■
Clinical presentation and mortality rates same as
glanders
■
Treatment: IV ceftazidime or a carbapenem 3 2 weeks
n 31 month TMP-SMX
• Malakoplakia (malacoplakia)
■
Chronic granulomatous infection as a result of the
inability of macrophages to kill phagocytosed E. coli
314