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Fig. 5.16 Chromoblastomycosis, facial lesions. (From Torres-Guerrero E, Isa-Isa
R, Isa R, Arenas R. Chromoblastomycosis. Clin Dermatol . 2012;30[4]:403–408.)
III. Systemic (dimorphic) mycoses
Histoplasmosis
• Species: Histoplasma capsulatum var. capsulatum
■
African: Histoplasma capsulatum var. duboisii
• Geography: Ohio and Mississippi River valley
• Microscopy (Fig. 5.17): tuberculoid granuloma with
intracellular 2 to 4 mm yeast in histiocytes (looks like
leishmaniasis, but see yeast have surrounding halo and are
more evenly distributed throughout histiocyte cytoplasm;
lacks “marquee sign” and kinetoplast) (Box 5.4)
5.4 Fungal Diseases
Box 5.4 Diseases With Parasitized Macrophages
Rhinoscleroma
Granuloma inguinale
Histoplasmosis
Leishmaniasis
Penicilliosis
Emmonsiosis
• Pathogenesis: inhalation (esp. bird and bat feces) with
hematogenous spread (can go to liver, spleen, bone
marrow, and brain; skin involvement more common in
HIV, often p/w umbilicated or “molluscoid” papules)
• Clinical presentation: primary cutaneous chancre with
lymphangitis and lymphadenitis (rare); more commonly,
secondary cutaneous molluscoid nodules, cellulitis, ulcers
(particularly oral), and panniculitis
■
Pulmonary manifestations 5 most common
presentation
• Treatment: itraconazole (mild-moderate disease), or
amphotericin B (severe disease)
Blastomycosis (“North American blastomycosis”)
• Species: Blastomyces dermatitidis
• Geography: Eastern United States (esp. SE), Great Lakes,
Ohio, and Mississippi River valleys
• Microscopy: PEH, granulomatous dermal inammation
with unipolar budding yeast (8–18 mm) (broad-based
buds)
• Pathogenesis: inhalation with subsequent hematogenous
spread to skin (.75% of cases), bones, and genitourinary
tract (e.g., prostate, spleen, liver, and brain)
• Clinical presentation: primary cutaneous form (rare)
presents with lymphangitis and lymphadenitis at injury
site; secondary cutaneous form (more common; due to
hematogenous dissemination from lungs to skin),
presents with verrucous plaques, papulopustules, and
ulcers (can occur orally as well)
■
Pulmonary manifestations 5 most common presentation
• Treatment: polyene and azole antifungals (mainly
itraconazole) and amphotericin B (severe disease)
Fig. 5.17 Histoplasmosis. Biopsy specimen shows periodic acid Schiff-positive
intracellular yeast. (From Chang P, Rodas C. Skin lesions in histoplasmosis. Clin
Dermatol. 2012;30[6]:592–598.)
Coccidioidomycosis
• Species: Coccidioides immitis and Coccidioides posadasii
• Geography: desert Southwest United States (esp. Central
Valley/San Joaquin Valley, California), Mexico, and
Central/South America
• Microscopy (Fig. 5.18): large (up to 100 mm) spherules
containing endospores; also has PEH and granulomatous
inammation
• Pathogenesis: inhalation with hematogenous spread to
skin (as well as CNS and bone); very rarely primary
cutaneous infection
• Clinical presentation: face #1 site; verrucous nodules/
papules (can be molluscum-like), pustules, abscesses, or
ulcerative lesions
■
Pulmonary manifestations 5 most common presentation
• Treatment: limited and cutaneous: itraconazole; severe:
amphotericin B; meningeal: amphotericin B and
uconazole; voriconazole also an option
325
CHAPTER 5 • Infectious Diseases
A B
Fig. 5.18 Coccidioidomycosis. Granulomas show large spherules and a giant cell containing small spherules (H&E; original magnication 400×). (From Welsh O,
Vera-Cabrera L, Rendon A, Gonzalez G, Bonifaz A. Coccidioidomycosis. Clin Dermatol. 2012;30[6]:573–591.)
■
Paracoccidioidomycosis (“South American blastomycosis”)
• Species: Paracoccidioides brasiliensis
• Geography: southern United States, Mexico, and
Central/South America
• Microscopy: PEH, granulomatous dermal inammation
with multipolar budding yeast (mariner’s wheel or
Mickey Mouse)
• Pathogenesis: inhalation of infected soil (can disseminate
to skin, liver, adrenal glands, lymph nodes,
gastrointestinal tract, and spleen); rarely may arise from
direct inoculation in skin
• Clinical presentation: granulomatous ulcerative
oropharyngeal and perioral involvement in 70% of
adults; cutaneous lesions can be contiguous,
hematogenous, or via inoculation; clinical appearance of
ulcers with inltrated borders (verrucous) and
hemorrhagic dots, and associated LAD (can be massive)
■
Men ... women
■
Pulmonary disease (granulomatous and chronic) most
common presentation
• Treatment: mild: TMP-SMX; moderate: itraconazole;
meningeal: uconazole or voriconazole; severe:
amphotericin B
IV. Opportunistic systemic mycoses
Candidiasis
• Species: C. albicans (most common in systemic and
localized infections), C. tropicalis (also very common;
in systemic infection, frequently disseminates to skin),
C. parapsilosis (commonly seen in chronic paronychia),
C. glabrata (uconazole resistance), C. krusei (uconazole
resistance), and C. dubliniensis (oropharyngeal candidiasis
in HIV patients)
• Geography: ubiquitous
• Microscopy: KOH 5 yeast and pseudohyphae
• Pathogenesis:
■
Candida species form biolm on plastic medical devices
■
SAPs (secretory aspartyl proteinases) and phospholipases
aid in fungal adhesion and tissue invasion
Chitin, mannoprotein, and glucan may function as adhesins,
which allow Candida to adhere to mucosal surfaces
■
C. albicans exists in normal ora of skin and digestive/GU
tracts with pathologic state with immunosuppression,
and debilitation and imbalances in microbiome
• Clinical presentation:
■
Mucocutaneous candidiasis: vaginal candidiasis, oral
thrush (“cottage cheese” like), median rhomboid
glossitis (central smooth erythema of tongue),
onychomycosis, chronic paronychia (not always
involved but often), candidal intertrigo (typically see
beefy red color 1 satellite pustules 1/– erosions),
angular cheilitis (perlèche; risk factors: edentulous,
elderly, atopic dermatitis, and vitamin deciencies),
and erosio interdigitalis blastomycetica (third web
space of ngers; also fourth web space of toes)
Risk factors: DM2 and corticosteroids/
immunosuppression (if chronic/severe may be sign
of HIV)
■
Deep-seated candidiasis: usually starts in GI tract; 10%
of bloodstream infections; 30% mortality in systemic
candidiasis despite antifungal therapy
Usually in immunosuppressed patients who are
neutropenic
See scattered papules/nodules, occ. hemorrhagic and
ecthyma gangrenosum-like
Also infect muscles, retina, internal organs, and
heart valves
■
Treatment:
Mucocutaneous: polyenes (e.g., nystatin) and azole
preparations (e.g., clotrimazole and uconazole)
♦ C. glabrata and C . krusei have lower sensitivity
to azole antifungals; C. albicans is developing
resistance to uconazole
Systemic: amphotericin B, azoles, and echinocandins
(rst-line in disseminated candidiasis)
Cryptococcosis
• Species: C. neoformans and C. gattii
• Geography: in bird droppings (particularly pigeons) and
bark/fruit of tropical trees; C. neoformans—ubiquitous,
C. gattii—tropical, subtropical
326
5.4 Fungal Diseases
Fig. 5.19 Cryptococcosis. Soap bubble appearance of organisms (H&E, 40x).
(Courtesy of Dr. Derek Marsee, Diagnostic Pathology Medical Group.)
• Microscopy: single-celled sphere with a double cell wall
and thick capsule (“halo” appearance), may have one or
more buds (blastoconidia); collections of organisms look
like soap bubbles (Fig. 5.19)
■
Stains: India ink, PAS, mucicarmine, GMS, and
Fontana-Masson
• Pathogenesis: inhalation n lungs (1° pulmonary infection,
usually mild) n hematogenous spread (CNS, bones, and
skin); can also arise from primary inoculation of skin (rare)
■
More common in immunosuppressed individuals (esp.
in HIV/AIDS, but also associated with sarcoidosis and
pregnancy)
■
Glucuronoxylomannan polysaccharide capsule is a
virulence factor
• Disease manifestation
■
Papules/nodules (often molluscum-like) that can be
umbilicated and/or ulcerated, and prefer head/neck,
mouth, and nose
Patients with 2° cutaneous lesions have high
mortality rate
■
Nodular lymphangitic syndrome—nodule at inoculation
site, nodular lymphangitis, and adenopathy
■
Meningoencephalitis is a serious and common
manifestation
• Treatment—mild: oral uconazole; CNS: amphotericin B
and ucytosine
Aspergillosis
• Species: Aspergillus fumigatus most common, A. avus
(second most common), and A. niger (can n otomycosis)
• Geography: ubiquitous in soil
• Microscopy (Fig. 5.20): septate hyphae with 45° angle
branching
• Pathogenesis:
■
Can be 1° cutaneous disease (most commonly A. avus)
via direct inoculation (e.g., IV catheter, trauma sites, burn
sites, and disturbed skin under dressings) versus 2°
cutaneous disease (most commonly A. fumigatus; more
common, typically in immunosuppressed, esp.
neutropenic) via inhalation n pulmonary aspergillosis n
disseminated disease
Fig. 5.20 Septated hyphae of Aspergillus spp. in the dermis. (Courtesy of Dr. Derek
Marsee, Diagnostic Pathology Medical Group.)
Both can n hematogenous spread with a tendency for
vascular invasion causing thrombus and necrosis
• Clinical presentation: six clinical forms including
erythematous edematous plaques, nodules with necrotic
centers, subcutaneous nodules (2° cutaneous)
hemorrhagic bullae, and necrotic ulcers
■
Can involve CNS, heart, kidneys, bone, and GI tract
• Treatment: azoles (e.g., voriconazole—rst line),
echinocandins, and amphotericin B
Fusarium
• Species: Fusarium solani most common
• Geography: ubiquitous in soil
• Microscopy: 45° angle branching, similar to Aspergillus
• Pathogenesis: more common in immunosuppressed;
severe burns (most common fungus cultured in burn
patients); cutaneous disease via direct inoculation and
hematogenous spread with a tendency for vascular
invasion causing thrombus/necrosis
• Clinical presentation: erythematous; edematous plaques
more common than subcutaneous nodules (purpuric or
ecthyma gangrenosum-like); panniculitis
• Treatment: no well-established treatment due to drug
resistance (cannot treat with caspofungin); localized
disease amenable to surgical debridement and systemic
antifungal therapy (e.g., voriconazole, posaconazole)
Penicilliosis
• Species: P. marneffei is only pathogenic species
• Geography: Southeast Asia
• Microscopy: intracellular parasitic phase in macrophages
• Pathogenesis: acquired by inhalation or possibly
abrasions; bamboo rat exposure may be risk factor
• Clinical presentation: similar to histoplasmosis: fever,
weight loss, LAD, cough, and hepatosplenomegaly
■
Cutaneous manifestations: papules with central
necrosis and molluscum-like lesions; face, arms, and
trunk are most common sites
• Treatment: polyenes (amphotericin B and terbinane) and
azole antifungals
327
CHAPTER 5 • Infectious Diseases
V. Uncommon fungal, protozoal, and
algae pathogens
Zygomycosis (mucormycosis)
• Species:
■
Order Mucorales, genera Rhizopus, Rhizomucor, Mucor,
Absidia, and others—systemic and cutaneous disease
■
Order Entomophthorales (e.g., Conidiobolus coronatus)—
rare, chronic, cutaneous, and subcutaneous infection
in tropics
• Geography: ubiquitous in soil and decaying vegetation
• Microscopy (Fig. 5.21): broad ribbon-like nonseptate
hyphae with 90° angle branching, angioinvasive with
thrombosis
• Pathogenesis: most commonly enter via respiratory tract
(though there are other portals of entry like skin), and
can invade blood vessels n thrombosis/infarction/
necrosis
■
More common in immunosuppressed patients, but
also nonimmunodecient (e.g., severe diabetes and
severe burns)
• Disease manifestation—subtypes include: rhinocerebral
(most common subtype; usually in diabetes patients with
DKA), pulmonary, GI, primary cutaneous (from surgery,
catheterization, or burns), and disseminated
■
All forms are rapidly progressing and commonly
fatal
■
Cutaneous lesions (can be primary or secondary)
typically indurated, necrotic black plaques/eschars
most commonly seen on face (nasal and oral in
rhinocerebral type)
■
Rhinocerebral type may have epistaxis, facial pain,
periorbital cellulitis, proptosis, and loss of extraocular
muscle movement (2° to cranial nerve palsies)
• Treatment: aggressive surgical resection of all necrotic
areas (crucial to survival of patient) and amphotericin B
(lipid formulation); posaconazole, isavuconazole may be
alternatives
Fig. 5.22
Phaeohyphomycosis. Brown hyphae (H&E, 40x). (Courtesy of Dr. Derek
Marsee, Diagnostic Pathology Medical Group.)
Phaeohyphomycosis
• Due to dematiaceous (pigmented) fungi: Exophiala
jeanselmei (#1 cause), Wangiella dermatitidis, Alternaria,
Bipolaris, Phialophora, and Curvularia
• Geography: tropics and temperate zones
• Microscopy: cyst composed of macrophages and short
hyphae, with a brous capsule
■
Hyphae are pigmented/brown, and stain positive with
Fontana-Masson (Fig. 5.22)
• Pathogenesis: immunosuppressed patients
• Clinical presentation: subcutaneous, possibly draining,
inammatory abscesses/cysts (may mimic Baker cysts)
• Treatment: excision and itraconazole
Protothecosis
• Species: Prototheca wickerhamii, not a fungus but an algae
• Geography and pathogenesis: introduced into skin via
trauma in contaminated water
• Microscopy: organisms have a morula-like appearance
on H&E
• Clinical presentation: nodules/ulcers/plaques and/or
olecranon bursitis
• Treatment: excision and systemic antifungals (e.g.,
amphotericin B)
Fig. 5.21 Zygomycosis. Nonseptate thick hyphae (H&E, 40x). (Courtesy of Dr.
Derek Marsee, Diagnostic Pathology Medical Group.)
328
Rhinosporidiosis
• Species: Rhinosporidium seeberi, not a fungus but a protozoa
• Geography: tropics (southern India and Sri Lanka)
• Pathogenesis: likely caused by contaminated water
contact as this is a sh parasite
• Microscopy: Very large (up to 300 mm sporangia
containing trophozoites in dermis
• Clinical presentation: slow-growing friable, red-purple,
soft, lobulated, mucosal polyps, particularly on nose
(associated with epistaxis), and conjunctivae; young men
most commonly
• Treatment: excision
5.5 PARASITES AND OTHER CREATURES
Parasitic infestations
Scabies
• Sarcoptes scabies var. hominis
• Most consistent factor associated with scabies is
overcrowding
• Host-species restricted (each species lives only on its
natural host)
• 30-day lifecycle within stratum corneum; 1-week survival
off human; classically affects interdigital webspaces,
postauricular, axillae, wrists, genitals (a/w chronic,
reactive inammatory nodules), feet, nipples/areolae and
umbilicus; mineral oil scraping demonstrates scabies
mite (dermoscopy can help visualize mites and burrows)
• Crusted (Norwegian) scabies in immunosuppressed/
HIV/elderly patients
■
Most common complication is secondary bacterial
infections
• Treatment of choice 5 permethrin 5% cream (two
treatments 1 week apart); other treatment options 5
ivermectin (200–400 mcg/kg 3 2 [1 week apart]), sulfur
or lindane; after treatment, postscabetic pruritus/
dermatitis up to 4 weeks
Lice
• Head louse—Pediculus humanus capitis
■
Active infection only if within 5 mm from scalp; most
commonly located in occipital and postauricular
areas
■
Mites can survive 36 hours w/o blood meal; nits are
strongly adherent to hair shaft and can survive 10 days
w/o blood meal
• Body louse—Pediculus humanus corporis
■
Larger, but similar shape to head louse
■
Not seen on skin but usually on clothing
■
Vector in epidemic typhus (R. prowazekii), louse-
borne relapsing fever (B. recurrentis), and trench
fever (B. quintana)
■
Live and lay eggs on clothing; more common in
homeless population (since unable to change/wash
clothes regularly)
• Pubic louse—Pthirus pubis
■
Identify by four frontal crab-like appendages and short/
broad body
■
Maculae ceruleae (blue-gray macules on thighs/trunk 2° to
bilirubin n biliverdin) may be seen on surrounding skin
■
Can occur on eyelashes as well as pubic hairs
• Treatment—permethrin 1%, pyrethrins, lindane 1%,
ivermectin 0.5%, spinosad 0.9%, benzyl alcohol 5%, or
malathion (ammable, only for age . 2 years old)
Tungiasis
• Burrowing ea—Tunga penetrans
■
Female burrows head-rst into skin (usually feet/toes)
and extrudes eggs from punctum before dying and
5.5 Parasites and Other Creatures
Fig. 5.23 Tungiasis—massive infestation of hand and feet in a cattle handler. (Courtesy of Dermatology Service, Santa Casa de Misericordia, Porto Alegre, Brazil.)
being sloughed with epidermis; nodules with crusts in
periungual toes (#1), soles, toe webs (Fig. 5.23); can n
gangrene
■
Most common: Caribbean, Central/South America,
and sub-Saharan Africa
■
Treatment: surgical removal or ivermectin (do tetanus
prophylaxis)
Myiasis
• Infection with dipterous larvae
■
Dermatobia hominis (human boty; most common)
Eggs can be transmitted by mosquito via exposed
skin n larval maturation (see furuncle)
■
Tumbu (Cordylobia anthropophaga)
Larva are deposited on damp clothing and penetrate
skin when clothes are worn (see on non-exposed
areas of body)
■
Wound myiasis (Cochliomyia hominivorax, Chrysomyia
bezziana)—larvae cannot penetrate intact skin; once
laid within open wound, penetrate subcutaneous
structures and can continue to penetrate through
cartilage and bone (leading to cranial penetration if
developing near nose)
• Treatment: surgical debridement of larvae 1 antibiotic for
superinfection; ivermectin; tetanus vaccination
Protozoa
Leishmaniasis
• Chronic infection due to obligate intracellular
protozoan, Leishmania spp.
■
Exist in two forms: promastigote and amastigote
■
Vector: sandies (Phlebotomus or Lutzomyia)
■
Reservoirs: mainly canines and rodents
• Pathogenesis: Within gut of sandy, organisms proliferate
into agellated promastigotes n migrate to sandy
proboscis n sandy bites human and transfers
promastigotes n histiocytes engulf promastigotes, which
then transform into amastigotes and multiply n develop
clinical manifestations within weeks (cutaneous
329
CHAPTER 5 • Infectious Diseases
leishmaniasis [CL]) or many months-years later
(mucocutaneous and visceral leishmaniasis)
■
Stronger host Th1 response (IL-2, IFN-γ) n resolution
of disease versus poor Th1 w/ development of Th2
response n progression
• Leishmaniasis may be classied by geographic region (Old
World vs. New World), or clinical presentation (cutaneous,
diffuse cutaneous, mucocutaneous, or visceral)
• Geographic classication:
■
Old World
L. major, L. tropica . L. aethiopica, L. infantum, and
others
Vector: Phlebotomus sand ies
■
New World
L. mexicana, L. braziliensis, L. amazonensis, and
others
Vector: Lutzomyia sand ies
♦ Also the vector of B. bacilliformis (n verruga
peruana, Carrion disease, bartonellosis, Oroya
fever)
• Clinical classication (four major forms):
■
Cutaneous: restricted to skin; more common in Old
World (90% occur in Middle East, Brazil and Peru;
Texas is the only endemic area in the United States)
Old World cutaneous
♦ Most common agents: L. major, L. tropica
(.L. infantum, L. aethiopica)
♦ Begins as a solitary, small, erythematous
edematous nodule at bite site (usually exposed
skin sites—arms, face, legs) that ulcerates or
becomes verrucous (Fig. 5.24) n may later
Fig. 5.24 Ulcerated nodules of Old World leishmaniasis in a sporotrichoid
pattern. (Courtesy of Dr. Anwar Qais Saadoon, Senior Dermatologist, Basra,
Iraq.)
develop sporotrichoid spread with satellite
lymphatic nodules and lymphangitis n heals
with scarring over months to years
New World cutaneous
♦ Most common agents: L. mexicana
(. L. braziliensis)
♦ More varied presentation: ulcerations (Chiclero
ulcer 5 ear lesion in workers who harvest chicle
gum in forest), impetigo-like, lichenoid, sarcoidlike, nodular, vegetating, and miliary
■
Diffuse cutaneous: more widespread cutaneous lesions;
usually arises in immunosuppressed patients
Most common agent: L. amazonensis (Americas),
L. aethiopica (Africa)
Multiple keloidal lesions of face (esp. nose) and
extremities
■
Mucocutaneous: affects skin and mucous membranes;
almost always in New World
Predominantly New World subspecies:
L. braziliensis (. L. amazonensis, L. panamensis, and
L. guyanensis)
Present with lip, nose, and oropharyngeal
inltration and ulceration
Progressive nasopharyngeal destruction n airway
obstruction, mutilation of mouth and perforation
of nasal septum (aka “tapir face” or espundia)
■
Visceral (Kala-azar, “black fever”): most severe form;
due to systemic infection of bone marrow, liver, spleen;
Old World . New World; incubation time 5 monthsyears
Most common agents: L. donovani (India, Sudan,
Bangladesh; most common cause in adults),
L. infantum (Europe; often a/w HIV), L. chagasi
Present with fever, weight loss, diarrhea, abdominal
tenderness, LAD, hepatosplenomegaly, nephritis,
intestinal hemorrhage, and death within 2 years
(if not treated)
Skin changes:
♦ Specic: papules, ulcers at bite site
♦ Non-specic: purpura, hyperpigmentation
(“black fever”), kwashiorkor changes (brittle hair
w/ discoloration), purpura
■
Post-kala-azar dermal leishmaniasis: lesions arising
up to 20 years after presumed recovery from untreated
visceral leishmaniasis (nodules, verrucous papules,
hypopigmented macules)
• Diagnosis
■
PCR is most sensitive and specic test
■
Culture: Novy-McNeal-Nicolle medium
■
Histology: amastigotes with kinetoplasts are arrayed
around periphery of parasitized histiocyte cytoplasm
(“Marquee sign”) (Fig. 5.25); organisms are best seen
on Giemsa
■
Montenegro delayed-skin reaction test is positive in
majority of CL; remains positive after cure and is
negative in febrile phase of visceral leishmaniasis
• Prognosis: most cases of Old World CL self-resolve within
15 months; New World CL due to L. Mexicana self-resolves
in 75%; mucocutaneous leishmaniasis (L. braziliensis and
L. panamensis) does NOT self-resolve and requires
treatment to prevent progressive destruction
330
Fig. 5.25 Leishmaniasis. H&E section of skin with several Leishmania organisms
inside histiocytes. (From Machado-Pinto J, Laborne L. Leishmaniasis. In: Tyring
SK, Lupi O, Hengge UR, eds. Tropical Dermatology. 2nd ed. Philadelphia: Elsevier;
2017:42–49.)
• Treatment: treat if severe/widespread, mucocutaneous, LAD,
immunocompromised host and/or to decrease scarring
■
Cutaneous and mucocutaneous leishmaniasis:
pentavalent antimony (e.g., sodium stibogluconate),
miltefosine, pentamidine, intralesional 0.2%
ciprooxacin 1 long-pulsed Nd:YAG
■
Visceral leishmaniasis: amphotericin B (ToC)
Trypanosomiasis
• African trypanosomiasis (sleeping sickness)
■
Species: T. brucei gambiense (West Africa)/T. brucei
rhodesiense (East Africa)
■
Vector: tsetse y (Glossina)
■
Clinical presentation:
Trypanosomal chancre (earliest sign: local pruritic
inammatory reaction at the site of inoculation
[48 hours]) n local LAD and ulcerates n eschar
Fever, headache, and joint pain at irregular intervals
Winterbottom’s sign (posterior cervical LAD)
(2–3 weeks) n trypanids (erythematous, urticarial
or macular diffuse eruptions [6–8 weeks]) n
neurologic changes and Kerandel’s deep delayed
hyperesthesia, daytime sleepiness (late stage)
■
Disease course: progressive over weeks to months
(East Africa), months to years (West Africa)
■
Treatment: suramin or pentamidine (early);
melarsoprol (E. African) or eornithine (W. African)
(CNS involvement)
• American trypanosomiasis (Chagas disease)
■
Species: T. cruzi
■
Vector: triatomine bug (Reduviidae)
Central/South America
■
Clinical presentation: local inammatory lesion (often
on face) at site of entry (chagoma) n Romaña sign
(Fig. 5.26) (unilateral eyelid edema and conjunctivitis
at site of inoculation) n rapid unilateral painless
bipalpebral edema n late heart, esophagus, and
intestinal enlargement (megacolon)
■
Diagnosed with PCR; Treatment: benznidazole or
nifurtimox
5.5 Parasites and Other Creatures
Fig. 5.26 Romaña sign. Acute Chagas disease in a young girl with Romaña sign
present in the left eye. (From Lupi O. Bartlett BL, Haugen RN, et al. Tropical dermatology: tropical diseases caused by protozoa. J Am Acad Dermatol. 2009;60[6]:
897–925.)
Toxoplasmosis
• Species: Toxoplasma gondii
• Geography: worldwide
• Vector: intestinal parasite of cats (human can acquire
from cat feces) and raw/undercooked meat pork/lamb/
venison meat
• Clinical presentation:
■
Acquired cutaneous disease: LAD 1 fever, but if
immunocompromised can n encephalitis, hepatitis,
pericarditis; skin: non-specic urticarial or
maculopapular eruption
■
Congenital disease (TORCH syndrome) –
hemorrhagic papules 1 possible seizures, deafness,
chorioretinitis, HSM, thrombocytopenia (see
Chapter 4, Pediatric Dermatology)
• Treatment: sulfadiazine and pyrimethamine
Helminths
Cutaneous larva migrans
• Most common tropical parasite dermatosis; found in
animal feces
• Species—Ancylostoma braziliense (most common); also
A. caninum
• Clinical presentation: erythematous serpiginous
cutaneous eruption (usually on feet) as a result of larva
penetrating intact epidermis, but unable to penetrate
human basement membrane zone (therefore unable to
cause systemic disease)
■
Moves 1 to 3 cm/day
• Treatment: albendazole, ivermectin, topical/oral
thiabendazole, and liquid nitrogen
Larva currens
• Moves faster (5–10 cm/hr)
• Strongyloides stercoralis
• Often indurated serpiginous papule on buttocks/thighs
331
CHAPTER 5 • Infectious Diseases
• If disseminated, may get periumbilical (thumbprint)
purpura and petechiae on trunk/proximal extremities
■
Loefer’s syndrome 5 chronic strongyloidiasis (affects
lungs and GI tract; eosinophilia)
• Caused by contact with contaminated soil (e.g., sitting on
beach)
• ELISA can help with diagnosis
• Treatment: ivermectin or thiabendazole
Onchocerciasis (“River blindness”)
• Species: Onchocerca volvulus
• Vector: Simulium y (black y; also vector for tularemia;
has also been implicated in Fogo selvagem form of
pemphigus; present near fast-owing rivers)
■
Geography: sub-Saharan Africa, South America, and
Yemen
• Pathogenesis: nodules of female microlariae; male
microlariae migrate between nodules to mate
• Clinical presentation: pruritic papules (can be acute,
chronic, or lichenied) n leopard skin (depigmentation
and atrophy); nodules (onchocercomas) over bony
prominences; red to purpule faces n leonine appearance;
may develop Mazzotti reaction if given
diethylcarbamazine (itchy eruption develops shortly after
giving med in infected paitent)
■
Can n blindness
• Treatment: ivermectin (treatment of choice); doxycycline
kills symbiotic Wolbachia bacteria; surgical excision of
onchocercomas
Loiasis
• Species: Loa
• Vector: Chrysops (Mango/deer ies; also transmit tularemia)
■
Geography: West and Central Africa
• Clinical presentation: calabar swellings (recurrent
migratory focal angioedema on limbs); visible migration
of adult worm across eyes
• Treatment: diethylcarbamazine
Filariasis
• Species: Brugia malayi/timori and Wuchereria bancrofti
• Vectors: multiple mosquito spp. of Culex (also West Nile
virus vector), Aedes (also vector of chikungunya fever,
Dengue fever, and yellow fever), and Anopheles (also
vector of malaria and yellow fever) mosquitoes
• Clinical presentation:
■
Acute—lymphangitis (inguinal nodes #1 site)
■
Chronic—granulomatous reaction in lymphatics n
lymphedema, elephantiasis, hydrocele
• Treatment: diethylcarbamazine (ToC) 1 doxycycline (for
Wolbachia endosymbiont)
Swimmer’s itch and seabather’s eruption
• Swimmer’s itch (“cercarial dermatitis”)
■
Species: Schistosoma, during the cercarial stage (snails
are a vector)
Northern United States and Canada fresh water
Fig. 5.27 Classic lesions of seabather’s eruption in covered areas. The disease
is caused by larvae of Linuche unguiculata. (Courtesy, Vidal Haddad Jr., MD,
PhD, São Paulo, Brazil.)
■
Clinical presentation: papules and papulovesicles on
uncovered skin 10 to 15 hours postexposure, lasts 5 to
7 days
• Seabather’s eruption (NOT a helminthic infection)
■
Species: Edwardsiella lineata (sea anemone) and Linuche
unguiculata (thimble jellysh) during larval stage
Southern United States and Caribbean salt water
■
Clinical presentation: pruritic papules and wheals in
covered areas within hours with new lesions for days
(Fig. 5.27)
Trichinosis
• Species: Trichinella spiralis
• Geography: worldwide with domestic and sylvatic
infection cycles
■
Most common reports are rural Asia and Latin America
• Vectors:
■
Domestic cycle—pigs, which are then eaten
undercooked (eating undercooked bears 5 less
common cause)
■
Sylvatic cycle—scavengers and carnivorous animals
(wild canines and felines, birds, raccoons, boars, and
walruses) eat infected rodents, and are themselves
eaten undercooked by humans
• Pathogenesis: humans eat animal meat (muscle) that
contains larval cysts n these encyst in GI tract and mature
into adults n reproduction occurs and larvae are
produced, which leaves the GI tract and encyst in skeletal
muscle
• Clinical presentation:
■
Primary dermatologic manifestation is periorbital
edema (as a result of type I allergic reaction) and
petechiae during parasite migration (esp. splinter
hemorrhages)
• Diagnosis: peripheral eosinophilia and IgE are clues;
muscle biopsy is diagnostic
■
h IgE may persist years after disease resolution
332
5.5 Parasites and Other Creatures
• Treatment: mebendazole or albendazole; may use
systemic steroids for moderate to severe hypersensitivity
reactions
Dracunculiasis (Guinea worm)
• Species: Dracunculus medinensis
• Vector: Cyclops water ea at copepod stage
• Clinical presentation: nodules and ulcers on lower
extremity (after ingestion of infected Cyclops, the organism
travels from intestines to subcutaneous tissue, where adult
worms emerge from lesion when reexposed to water)
• Prevention: drinking ltrated/boiled water prevents
ingestion of copepods that contain larva
• Treatment: removal of worm (ToC), wound care, and
metronidazole
Gnathosomiasis
• Species: Gnathostoma spinigerum
• Vector: raw freshwater sh (humans get disease by
eating—e.g., sushi)
• Clinical presentation: GI symptoms 1 fever early on;
nodular migratory panniculitis (can look like cutaneous
larva migrans or single tender nodule that moves around
skin); CNS (mortality 5 25%)
• Treatment: albendazole or ivermectin
Cysticercosis
• Species: Taenia solium (pork tapeworm), Taenia saginata
(beef tapeworm), Diphyllobothrium latum (sh tapeworm)
• Vector: poorly cooked meat (humans can be intermediate
[eggs ingested n larva/oncospheres n encyst n cysticerci]
or denitive host [ingest adult worms n travel to
intestinal mucosa])
• Clinical presentation: peripheral eosinophilia and minimal
symptoms if denitive host; in intermediate hosts, cysts can
travel n nodules in skin, and systemic symptoms (brain,
heart, etc.—may be seen on CT/MRI/X-ray)
• Treatment: albendazole, praziquantel
painful, ulcerating, ovaloid, erythematous plaque (with
a lot of necrosis) near the site of inoculation
■
ToC: metronidazole
Bites and stings
Biting and stinging insects
• Immediate reactions are as a result of histamine,
serotonin, formic acid, or kinin release
■
One fourth of cases of anaphylaxis are as a result of
stings from insects (order Hymenoptera)
■
Secondary infection of bites typically from Staphylococcus
■
Exaggerated bite reactions: CLL, chronic EBV
• Fire ants (Solenopsis): bitesn 5 mm to 1 cm sterile
pustules on lower extremities
■
Toxin 5 solenopsin D (piperidine alkaloid)
• Bees/wasps/hornets (Hymenoptera): toxin 5 phospholipase
A; can n anaphylaxis; myoglobinuria, hemoglobinuria,
acute tubular necrosis from wasps/killer bees
• Bed bugs
■
Species: Cimex lectularius (Fig. 5.28)—nocturnal
■
Nitrophorin is one of its salivary products responsible
for human immune reaction; p/w grouped “breakfast,
lunch, and dinner” urticarial papules at bite sites
• Lytta vesicatoria/Spanish y (blister beetles)
■
Cantharidin derived from heme-lymph discharge; p/w
blisters at sites of contact
• Fleas
■
Rat ea (Xenopsylla cheopis) is vector for R. typhi n
endemic typhus and Y. pestis n bubonic plague
(treatment: streptomycin and gentamicin)
■
Cat ea (Ctenocephalides felis and Ctenocephalides canis) is
vector for B. henselae (n cat scratch disease, bacillary
angiomatosis), AND B. quintana (n bacillary angiomatosis)
■
Pulex irritans is the human ea; also affects dogs
• Lepidopterism (caterpillar dermatitis)
■
Direct contact with hairs and toxin-mediated reactions
(not allergy)
Cutaneous amebiasis
Free-living amoeba
• Acanthomoeba—subacute granulomatous amebic
encephalitis; skin lesions n chronic ulcers
• Balamuthia—painless, red, and granulomatous plaque on
central face . trunk/extremities, which precedes CNS
involvement; treatment: multiagent w/ miltefosine
• Naegleria—fulminate, fatal acute necrotizing
meningoencephalitis
GI-associated amoeba
• Entamoeba histolytica
■
Usually associated with amebic colitis and/or liver/
lung involvement
■
Cutaneous lesions may spread to perianal region from
GI involvement, or be sexually transmitted with a
Fig. 5.28 Cimex spp. The bites from bedbugs are not accompanied by severe
manifestations in nonsensitized persons, but they can cause notable erythema,
edema, and itching in those persons allergic to the bites (esp. atopic
individuals). (From Haddad V. Tropical dermatology: venomous arthropods and
human skin. J Am Acad Dermatol. 2012;67[3]:e1–e14.)
333
CHAPTER 5 • Infectious Diseases
■
Train-track appearance of urticaria or hemorrhage
■
Ophthalmia nodosa are ocular reactions as hairs tend
to migrate inward
■
Specic types of caterpillars:
Puss (Megalopyge opercularis): lightly brown and
wooly appearance; results in painful, linear petechiae
Io (Automeris io): green with adjacent longitudinal
red and white stripes
Gypsy (Lymantria dispar): histamine in hair, which
can become airborne
Saddleback (Sibine stimulea): green saddle-like area
on back
• DEET (N,N-diethyl-3-methylbenzamide) is overall the
most effective insect repellant
Arachnids (ticks, mites, spiders, and scorpions)
• Ticks (Fig. 5.29)
■
Ornithodorus
Soft-bodied tick
1 inch
Identication: warty/rough, gray, and soft appearance
Transmits B. duttonii (tick-borne relapsing fever)
■
Dermacentor
Identication: alternating light and dark bands on
body with brown legs
Transmits RMSF (#1 cause), tularemia, tick
paralysis, and human granulocytic anaplasmosis/
ehrlichiosis, Q fever, Colorado tick fever
■
Ixodes pacicus, I. ricinus, I. scapularis, and I. dammini
Identication: dark legs and solid-colored body with
darker scutula
Transmits Lyme disease (#1 cause; B. burgdorferi),
acrodermatitis chronica atrophicans (B. garinii and
B. afzelli), babesiosis (#1 cause), and human
granulocytic anaplasmosis
■
Amblyomma—lone star tick
Identication: white dot on back (female)
Transmits human monocytic ehrlichiosis; tularemia;
southern tick-associated rash illness; African tickbite fever; Brazil spotted fever
Blacklegged Tick (Ixodes scapularis)
Lone Star Tick (Amblyomma americanum)
Dog Tick (Dermacentor variabilis)
334
2 inch
Adult female Adult male Nymph Larva
Fig. 5.29 Tick life cycle and size comparison. (From Centers for Disease Control and Prevention, www.cdc.gov.)