Viral infections, helminths, and arthropods

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Chapter 19

Viral infections, helminths, and arthropods

Dirk M. Elston

Viral infections

Warts

Condylomata acuminata commonly have horn cysts and resemble seborrheic keratoses. The two are differentiated by areas of compact stratum corneum, round parakeratosis, coarse hypergranulosis, and vacuolated keratinocytes with large gray nuclei. In situ hybridization can identify the human papillomavirus (HPV) type.

Bowenoid papulosis

Key features

• HPV-16 most commonly

• Atypia

Fig 19-5 Bowenoid papulosis

Bowenoid papulosis presents as discrete pink, brown, or gray lesions in the genitalia. They are typically sessile, rather than papillomatous or cauliflower-like. The histologic spectrum ranges from that of a condyloma with buckshot scatter of atypical cells to full-thickness atypia, indistinguishable from Bowen’s disease.

Heck’s disease

Key features

• Focal oral hyperplasia

• Hyperkeratosis with round parakeratosis

• Epithelial pallor

• HPV-13 and -32

Fig 19-6 Heck’s disease

Pearl

Type of wart	HPV type
Common	1, 2, 4
Flat (verruca plana)	3, 5
Plantar	1 (myrmecia), 2,4 (mosaic)
Epidermodysplasia verruciformis	5, 8, and many others
Buschke–Löwenstein tumor	6, 11
Butcher’s	7 and others
Laryngeal papillomas	6, 11
Genital dysplasia	16, 18, 31, 33, 35, and others
Heck’s focal oral hyperplasia	13, 32
Subungual squamous cell carcinoma	16

Verrucous cyst (cystic papilloma)

Key features

• Cyst with wart-like lining

Verrucous cysts may arise as a result of papillomavirus infection of a hair follicle. On plantar surfaces, they may arise from eccrine ducts and the lining is more likely to resemble myrmecia.

Herpetic infections

Herpes simplex

Key features

• Ballooning degeneration of keratinocytes

• Multinucleated keratinocytes with nuclear molding

• Herpetic cytopathic effect (basophilic eggshell of chromatin at the periphery of the nucleus)

• Mild features of leukocytoclastic vasculitis may be present

Fig 19-7 Verrucous cyst

Fig 19-8 Herpes simplex

Herpes zoster (varicella-zoster virus: VZV)

Key features

• Ballooning degeneration of keratinocytes

• Multinucleated keratinocytes with nuclear molding

• Herpetic cytopathic effect (basophilic eggshell of chromatin at the periphery of the nucleus)

• Dramatic leukocytoclastic vasculitis typical

Chicken pox (VZV)

Key features

• Ballooning degeneration of keratinocytes

• Multinucleated keratinocytes with nuclear molding

• Herpetic cytopathic effect (basophilic eggshell of chromatin at the periphery of the nucleus)

• Mild features of leukocytoclastic vasculitis may be present

Fig 19-9 Herpes zoster (shingles)

Fig 19-10 Varicella (chicken pox)

Fig 19-11 Verrucous zoster

Verrucous VZV infection

Key features

• Compact hyperkeratosis

• Variable papillomatosis

• Follicular herpetic cytopathic effect

Multinucleated giant cells with basophilic nuclear rims and nuclear molding are noted within follicular epithelium. This pattern is typically seen in immunosuppressed patients, especially in the setting of human immunodeficiency virus (HIV) infection.

Fig 19-12 Cytomegalovirus infection

Cytomegalovirus

Key features

• Large endothelial cells with owl’s-eye nuclei

• Cytoplasm may be ample or scant

In HIV patients, cytomegalovirus probably does not cause ulcers, but reactivates within ulcers. Viral cytopathic changes may be found in ulcers of various causes. This alerts the clinician to look for evidence of cytomegalovirus retinal involvement.

Fig 19-13 Smallpox

Pox and parapox infections

Smallpox (variola)

Key features

• Epidermal necrosis, often with reticular degeneration

• Eosinophilic cytoplasmic inclusions

• Nuclear inclusions may also be seen

In scrapings, Guarnieri bodies appear black with Gispen’s modified silver stain. Guarnieri bodies are aggregations of the smaller Paschen bodies.

Fig 19-14 Monkey pox (courtesy of Erik Stratman, MD)

Monkey pox

Molluscum contagiosum

Key features

• Cup-shaped lesion with scalloped border

• Henderson–Paterson bodies (molluscum bodies)

Fig 19-15 Molluscum contagiosum

Molluscum contagiosum is readily recognized by the characteristic cytoplasmic inclusions. These vary from eosinophilic to basophilic as the inclusion bodies mature.

Orf and milker’s nodules

Key features

• Epidermal necrosis

• Viral inclusion bodies (may be both cytoplasmic and intranuclear)

• Animal contact

Orf and milker’s nodules are caused by distinct viruses, but have a similar histologic appearance. Each lesion evolves through a series of clinical stages, and the histologic appearance varies by stage. During the verrucous phase, the epidermis demonstrates endophytic strand-like proliferations. The dermal papillae are edematous with dilated vessels. A dense, predominantly lymphoid infiltrate is present. Plasma cells and histiocytes are often present. Viral inclusion bodies, clumping of keratohyalin, and cytoplasmic vacuolation may still be seen.

Fig 19-16 Orf nodules

Gianotti–Crosti syndrome

Fig 19-17 Gianotti–Crosti syndrome

Hand, foot, and mouth syndrome

Key features

• Oval vesicles or ulcers on the sides of the digits, palms, soles, mouth, and buttocks

• Coxsackie A16 and others

• Reticular and ballooning degeneration of keratinocytes

Fig 19-18 Hand, foot, and mouth syndrome

Flukes, tapeworms and roundworms

Schistosomiasis

Key features

• Ova with stippled contents

• Mixed inflammatory response, commonly granulomatous

Fig 19-19 Cutaneous schistosomiasis

Schistosomes are trematodes (flukes). When cutaneous involvement occurs, it usually involves genital skin. Schistosoma haematobium is typically implicated.

Pearl

Identification of schistosome ova:

• S. haematobium – thin wall with thin vertical spine (Figure 19.20)

• S. mansoni – thick refractile wall with thick angular spine (Figure 19.21)

• S. japonicum – round with refractile wall and no visible spine (Figure 19.22)

Fig 19-20 Schistosoma hematobium

Fig 19-21 Schistosoma mansoni

Fig 19-22 Schistosoma japonicum

Flatworms

Key features

• Secretory tegument, rows of subtegumental cells

• Calcareous bodies

• Smooth muscle

• No gut

Fig 19-23 Sparganosis

Spirometra worms, the cause of sparganosis, are typical cestodes. They lack a gut, and must absorb nutrients through the tegumental cells. They cannot excrete waste, and so calcify it internally as calcareous bodies.

Sparganum proliferum

Key features

• Multilocular cyst

• High-power views show features of a flatworm

Differential Diagnosis

The features of other tapeworm cysts are similar. Some tapeworms demonstrate scolices (rings of hooks). The cysts can degenerate to little more than a rim of epithelium.

Fig 19-24 Sparganum proliferum (Courtesy of Richard Bernert, MD)

Fig 19-25 Cysticercosis for comparison

Fig 19-26 Elephantiasis (courtesy of Brooke Army Medical Center teaching file)

Fig 19-27 Onchocercoma

Elephantiasis

Key features

• Filarial roundworm within lymphatic vessel

• Inflammatory response leads to lymphedema

Onchocerciasis

Onchocerciasis is caused by Onchocerca volvulus, an obligate human pathogen spread by Simulium blackflies.

Fig 19-28 Onchocerca microfilaria

Fig 19-29 Subcutaneous dirofilariasis

Onchocercoma

Key features

• Well-defined ball of convoluted worms

• Male and female

• Females gravid

• Thin layer of striated muscle

• Corrugated cuticle

An onchocercoma represents a “mating ball” of convoluted worms. The females demonstrate microfilaria within the paired uteri. Because of their thin musculature they have been likened to married adults who no longer go to the gym and have “gone to flab.” This is in stark contrast to zoonotic dirofilarial worms that possess a thick muscular layer. In human dirofilarial infestations, a solitary “bachelor” worm is typically identified. Like other bachelors (with little to do besides work out at the gym) the musculature is well developed.

Onchocerca microfilaria

Key features

• Large microfilaria in lymphatics and free in the dermis

• Large cephalic and caudal spaces

• Paired oval terminal nuclei

Dirofilariasis

Key features

• Thick muscular layer interrupted by lateral cords

• Internal chitinous ridge

Table 19-1

Ridge patterns of Dirofilaria species

Species	Ridge pattern
D. tenuis	Wide/broken
D. repens	Narrow/sharp
D. ursi	Spaced far apart/round
D. immitis	None

Fig 19-30 Scabies

Early lesions may demonstrate abscesses with a mix of neutrophils and eosinophils. Later biopsies show a 1–3 cm granulomatous nodule surrounded by dense eosinophilic fibrin. Because humans are accidental hosts, there is only a single adult worm, and reproduction cannot occur. Microfilaria are not seen. Most human cases are associated with Dirofilaria tenuis. Aedes, Anopheles, and Culex mosquitoes act as vectors for most Dirofilaria. D. ursi is transmitted by Simulium blackflies.

All Dirofilaria demonstrate an internal lateral thickening of the cuticle in the area of the lateral cords. In D. tenuis, it appears as a prominent 10 µm pointed ridge. The cuticle is multilayered with criss-cross fibers at right angles. A gut is present, and twin non-gravid uteri are noted in females. At the ends of the worm, longitudinal ridges are absent. In this area, the uteri form loops, with four or more seen in cross-section.

Fig 19-31 Crusted (“Norwegian”) scabies

Fig 19-32 Insect bite

Arthropods

Scabies

Key features

• Mite, ova, or scybala in stratum corneum

• Chitin scrolls and pigtails

• Dermal infiltrate may resemble an insect bite

• Subepidermal bulla with eosinophils occasionally present

The dermal host response to scabies mites often resembles an insect bite reaction. There may be a wedge-shaped perivascular lymphoid infiltrate with eosinophils. The diagnosis rests on demonstration of the mite, eggs, or feces. Oval spaces in the stratum corneum should prompt deeper sections looking for an intact mite. Fragmented mites and ova curl inward, forming scrolls in the stratum corneum. Intact mites have internal striated muscle and dorsal spines. In crusted scabies, many mites are seen within a thick and crusted stratum corneum.

Fig 19-33 Tick bite

Fig 19-34 Tick

Pearl

Scabies can mimic bullous pemphigoid with eosinophil-filled bullae and positive immunofluorescence. In children, scabies can induce a Langerhans cell infiltrate and mimic Langerhans cell histiocytosis. Cases with CD30+ cells can mimic lymphomatoid papulosis.