Vesiculobolous lesions Flashcards
Herpes Simplex Infection
primary infection is the initial systemic infection, and secondary is the localized reactivation in a previously infected person. an immunocompromised host may develop severe secondary disease.
control of symptoms not cure is the goal, as the virus stays latent in the nerves
the virus spreads through exposure to body fluids
Herpes simplex infection progression
primary infection affects the skin, vermilion, and the oral mucous membranes, on any mucosal surface
Secondary lesions are confined to the lips, hard palate, and gingiva, healing in 1-2 weeks.
in immunodeficient patients secondary HSV1 results in significant pain and discomfort, can be chronic, destructive, and extensive.
Herpetic whitlow is an infection of the fingers through a break in the skin integrity. They form vesicles or pustules that eventually become ulcers
Herpes simplex virus Histology
intraepithelial vesicles containing exudate, inflammatory cells, and characteristic virus-infected epithelial cells are seen
Virus-infected keratinocytes contain one or more homogenous, glassy nuclear inclusions that can be found on cytologic preparations.
Herpes simplex virus differential
streptococcal pharyngitis (does not involve the lips or perioral tissues, and vessicles do not precede ulcers)
erythema multiforme (ulcers are larger, usually without a vesicular stage, and are less likely to affect the gingiva)
acute necrotizing ulcerative gingivitis (lesions are more limited to the gingiva, not preceded by vesicles)
Apthos stomatitis (usually multiple lesions, neurologic prodrome (tingling), vesicles preceding ulcers, and palatal and gingival location are indicative of HSV, and apthae are almost exclusively on nonkeratinized mucosa)
Herpes simplex diagnosis
Tzanck smear
Serology
viral culture
immunohistochemistry
PCR testing
Herpes simplex virus treatment
if no later than 48-72 hours prior to symptoms, then Acyclovir 5% ointment
5X/day topicaly
systemic acyclovir 400mg TID can be used for primary infections (usually HSV2)
for immunosupressed patients prophylactic acyclovir may be needed.
in HIV patients IV acyclovir may be needed
Varicella Zoster pathogenesis
transmitted through direct contact by contaminated droplets from skin lesions
the virus proliferates within macrophages over a 2 week incubation period
host defenses are overcome, and systemic signs and symptoms develop.
It can reside asymptomatically int eh sensory ganglia
Varicella Zoster clinical features
fever, chills, malaise, and headache accompany rash primarily in the trunk, head and neck
the rash becomes a vesicular eruption that forms pustules, and eventually ulcerates.
Secondary bacterial infections are common, and may result in scar formation.
Herpes Zoster
occurs through the branches of the nerves
can inovlve the trigeminal nerve, and resuts in unilateral oral, facial ,r occular lesions
remission usually occurs in several weeks
Varacella Zoster Histopathology
same as HSV
virus infected epithelial cells have homogenous nuclei representing viral products
multinucleation of infected cells is typical
Acantholytic vesicles break down and ulcerate
Varicella Zoster Differential
diagnosed by history of exposure, and type/distribution of lesions.
DD: primary HSV infection
hand-foot and mouth disease
Varicella Zoster treatment
Supportive therapy is indicated
for immunocompromised patients, anti-viral therapies are warranted, including systemic acyclovir, vidarabine, and interferon.
Corticosteriods are contraindicated
hand-foot-and-mouth disease etiology
Coxsacki virus
transmitted through direct contact with nasal secretions
predilection for mucous membranes of the mouth (buccal mucosa and tongue) and cutaneous regions of the hands and feet
hand-foot-and mouth clinical features
resolves spontaneously in 1-2 weeks
usually occurs in children younger than 5
The lesions progress to a vesicular state, then become ulcerated, then encrusted lesions without later scarring
hand-foot-and-mouth histopathology
the vesicles are found in the epithelium due to obligate viral replication in keratinocytes
as keratinocytes are destroyed the vesicle enlarges and becomes filled with proteinaceous debris and inflammatory cells
hand-foot-and-mouth differential
primary herpetic gingivostomatitis
varicella Zoster
hand-foot-and-mouth treatment
no specific treatment, only of symptoms
bicarbonate mouth rinses may help
measles etiology
spread by airborne droplets
rash consists of pinpoint elevations over the soft palate that coalesce with involvement of the pharynx with bright erythema
measles clinical features
the lesion spots of the buccal mucosa are known as Kiplik’s spots
complications of the virus include encephalitis and thrombocytopenic purpura
Measles Histopathology
infected epithelial cells which become necrotic, overlie an inflamed connective tissue that contains dilated vascular channels and a focal inflammatory response
measles differential diagnosis
prodromal symptoms, Koplik’s spots, and rash in unvaccinated individuals is sufficient evidence, but laboratory testing can confirm virus
Pemphigus Vulgaris etiology
mucocutaneous disease characterized by intraepihtelial blister formation from a loss of intercellular keratinocyte adhesion
Produces epithelial cell separation (acantholysis)
circulating autoantibodies of IgG reat against composnents of epithelial desmosome-tonofilament complexes
the extent of epithelial cell separation is proportional to teh titer of circulating pemphigus antibodies
pemphigus vulgaris clinical features
painful ulcers preceded by flaccid and short lived intraoral vesicles and bullae
Bullae rapidly rupture following their fomration ,eaving a red, painful ulcerated base with a friable epithelial border
lesions range from small apthos like lesions to large irregular map-like lesions
can occur with other autoimmune diseases such as myasthenia gravis, lupus erythematosus, rheumatoid arthritis, Hashimoto’s thyroiditis, thyroma, Sjogrens syndrome
pemphigus vulgaris histopathology
interepithelial clefting iwth keratinocyte acantholysis
loss of desmosomal attachment of tonofilaments, resulting in free floating Tzanck cells
the basal layer remains attached to the basement membrane
direct immunofluorescent testing can diagnose, where a sample is tested for circulating antibodies of IgG type.
