Papules, Pustules, and Vesicles
Definition
A papule is a solid, circumscribed, elevated lesion up to 1 cm in diameter. Papules are essentially small nodules that do not extend beneath the dermis. A pustule is a fluctuant, circumscribed, elevated accumulation of pus (inflammatory cells and often necrotic debris) up to 1 cm in diameter (e.g., a small abscess).
Pustules are frequently associated with infectious diseases, although sterile pustular diseases (such as pemphigus foliaceus) exist. A vesicle is a fluid-filled, acellular, circumscribed, elevated lesion up to 1 cm in diameter. A bulla is a vesicle that is larger than 1 cm in diameter. All these lesions can be either follicular or nonfollicular in orientation, depending on the underlying cause. Pustules and vesicles are rarely seen clinically because of their fragility and hence their susceptibility to rupture. Because papules are solid lesions, they are more stable and therefore more commonly encountered.Mechanisms of Papule, Pustule, and Vesicle Formation
Papules usually form as a result of an infiltrate in the dermis, either cellular or noncellular. Cellular infiltrates may include inflammatory or neoplastic cells, although neoplastic papular lesions are relatively uncommon in large animals. Inflammatory infiltrates may be mixed, containing variable numbers of neutrophils, histiocytes, lymphocytes, plasma cells, and eosinophils, or one cell type may predominate. The composition of the inflammatory cells is influenced by the underlying cause of the papule, and the possible causes are extensive. Noncellular papular infiltrates include substances such as edema fluid, amyloid, and proliferative collagen, although these are relatively rare.
Pustules form as the result of an intraepidermal, subcorneal, or, less commonly, subepidermal accumulation of inflammatory cells. Infiltration of inflammatory cells, particularly polymorphonuclear leukocytes, leads to the release of proteolytic enzymes that liquefy tissue elements and result in the formation of a fluctuant lesion.
Eosinophils, acantholytic cells, and infectious organisms may also be noted in a pustule, depending on the underlying cause. The stimulus leading to pustule formation is most commonly infectious, although pustules can result from noninfectious causes such as hypersensitivity reactions and autoimmune disease.Vesicles form either at the dermoepidermal junction (subepidermal) or in the epidermis (intraepidermal) as a result of malformation or destruction of the basement membrane zone, or confluence of intercellular edema (spongiosis). Clinically, these types of vesicles are indistinguishable. Vesicles form as the result of certain viral diseases, during severe inflammatory reactions (allergic contact dermatitis), or with cutaneous physical damage (mechanical, chemical, or thermal). In pemphigus foliaceus or pemphigus vulgaris, autoantibodies bind to transmembrane proteins between the epidermal cells, causing disruption of epidermal intercellular attachments. The result is intraepidermal cleft formation that leads to vesiculation. In bullous pemphigoid, complement-activating antibodies bind to antigens in the basement membrane zone, causing degranulation of mast cells, chemotaxis of neutrophils and eosinophils, and release of tissue-destructive enzymes that injure the basement membrane zone. The result is loss of dermoepidermal adherence and vesicle formation.7 Vesicles are transient, fragile lesions and therefore are rarely recognized clinically. If they are not destroyed by surface trauma, rapid infiltration by inflammatory cells often transforms a vesicle into a pustule.
Approach to Diagnosis of Papules, Pustules, and Vesicles
Although papules, pustules, and vesicles may look somewhat similar on a cursory physical examination, the clinician must differentiate among the three and determine which of the lesions are present. Examination with a hand lens may help. The differential diagnoses relevant to papules, pustules, and vesicles are not necessarily the same (Box 11.4).
In all cases it is important to determine if disease is limited to the skin or if the animal's general health is compromised as well.Papular lesions have the most extensive differential diagnoses:
• Hypersensitivity reactions. Parasitic hypersensitivities are the most common (e.g., Culicoides hypersensitivity), although drug and (rarely) food hypersensitivities should also be considered. Many hypersensitivity reactions are pruritic.
• Parasites. Some species simply irritate the skin with their bites (e.g., horn fly [Haematobia irritans]) without inducing a hypersensitivity reaction.
■ BOX 11.4
Most Common Causes of Papules, Pustules, and Vesicles in Horses and Ruminants
Horses
Hypersensitivity-Usually Papules
Culicoides species
Other flying insects
Infectious-Papules or Pustules
Staphylococcal pyoderma
Dermatophilus congolensis
Immune-Mediated
Pemphigus foliaceus—papules or pustules
Bullous pemphigoid—vesicles
Ruminants
Ectoparasites-Usually Papules
Sarcoptes scabiei
Psoroptes cuniculi (goats)
Lice
Infectious
Viral diseases (e.g., vesicular stomatitis)—vesicles Staphylococcal pyoderma (goats)—pustules or papules
• Infectious diseases (bacterial, fungal, and viral). Typically papules caused by infections have a follicular orientation.
• Certain neoplastic diseases (papillomas or sarcoids).
• Uncommon causes including autoimmune diseases such as pemphigus foliaceus and diseases of uncertain cause such as equine sarcoidosis.
Pustules are most commonly associated with bacterial infections, although fungi and, in rare cases, parasites (Demodex species) can cause pustule formation. Sterile pustular diseases are less frequently seen (drug eruptions, sterile eosinophilic folliculitis of cattle)9 but should be included in the differential diagnoses. Vesicles are rapidly infiltrated by inflammatory cells and transformed into pustules. Diseases commonly associated with vesicles include viral diseases of ruminants, autoimmune diseases, contact dermatoses, and burns.
The following steps are a guide to the diagnosis of papules, pustules, and vesicles in horses and ruminants:
1. History (see Fig. 11.1)
a. In particular, determine whether the lesions are pruritic, painful, or asymptomatic.
b. Determine if contact animals of the same and/or different species are affected or unaffected. If contact animals are affected, a contagious problem should be considered: fungal (dermatophytosis), bacterial (dermatophilosis), viral (contagious ecthyma), or parasitic (Culicoides hypersensitivity).
c. Trace the temporal course of development. Rapid onset of lesions may suggest a hypersensitivity reaction.
d. Check for seasonality. A seasonal problem suggests a parasitic or hypersensitivity (pollens) cause. Lice are a problem in the winter, trombiculidiasis tends to occur in the fall, and most of the flying insects are present in the spring, summer, and early fall.
e. Determine what topical and systemic medications were given to or used on the animal before the onset of the problem. Use of certain topical agents may suggest a diagnosis of contact dermatitis, whereas administration of systemic medications may suggest drug hypersensitivity.
f. Determine if the animal has been subjected to external trauma (thermal or chemical).
2. Physical examination (see Fig. 11.2)
a. Gently palpate the lesions to determine if they are solid (papules) or fluctuant (pustules or vesicles).
b. Note if the lesions have a follicular orientation, suggesting an infectious cause.
c. Check for lesions involving the oral cavity and mucocutaneous junctions.
d. Look for evidence of excoriation, suggesting that pruritus is a feature of the disease.
e. Inspect the coat closely for small but grossly visible parasites such as lice or their eggs.
f. Inspect contact animals for evidence of disease.
3. Skin scrapings of papular lesions
4. Cytologic studies
5. Dermatophyte culture and KOH preparation
6. Dermatophilus preparation
7. Bacterial culture and sensitivity
8. Microfilarial preparation
9. Biopsy for routine histopathologic examination
10. Biopsy for direct immunofluorescence testing