Lesi Multipel Akut (infeksi virus & bakteri)

 Disebut juga non-akantolitik, termasuk dalam lesi vesikulobulosa-erosif

intra-epitel
 Contoh :
1. Stomatitis Herpetica
2. Herpes labialis rekuren
3. Herpes zoster
4. Herpangina

A. INFEKSI VIRUS HERPES SIMPLEX

GINGIVOSTOMATITIS HERPETICA

Terdiri atas Primary dan Secondary.

Primary Gingivostomatitis Herpetica

Definition
Primary herpetic gingivostomatitis is a relatively common viral infection of the oral mucosa.

Etiology
Usually herpes simplex virus type 1 (HSV-1), and rarely type 2 (HSV-2).

Clinical features
 It is usually seen between the ages of 6 months and 6 years.
 The onset of the disease is abrupt, and is clinically characterized by high fever, headache,
malaise, anorexia, irritability, bilateral sensitive regional lymphadenopathy, and sore mouth
lesions.
- Gejala awal : demam, sakit kepala, malaise, limfadenopati, dan lesi mulut yg sakit/perih.
 The affected mucosa is red and edematous, with numerous coalescing vesicles (vesikel
mudah pecah dan bergabung menjadi vesikel yg lebih besar), which rapidly rupture, leaving
painful small, round, shallow ulcers covered by yellow fibrin (Figs.101, 102).
 The early lesions are vesicles which can affect any part of the oral mucosa, but the hard
palate and dorsum of the tongue are favored sites (Figs 12.1 and 12.2). The vesicles are
domeshaped and usually 2–3 mm in diameter. Rupture of vesicles leaves circular, sharply
defi ned, shallow ulcers with yellowish or greyish fl oors and red margins. The ulcers are
painful and may interfere with eating.
- Lesi primer : vesikel yg dapat mempengaruhi berbagai mukosa oral, tapi palatum keras
dan dorsal lingual adalah bagian yg paling sering timbul lesi. Bentuk lesi bulat dgn
 diameter 2-3mm. setelah vesikel mengalami rupture, akan terbentuk lesi sirkular, tepi
yang jelas, kedalaman dangkal dengan dasar yg kekuningan ataupun keabuan dan
eritema di pinggiran luar lesi.
 New lesions continue to develop during the first three to five days.
 The ulcers heal in 10–14 days. Both the movable and non-movable oral mucosa may be
affected. Gingival lesions are almost always present, resulting in enlargement and
edematous and painful erosions. The diagnosis is usually made on clinical grounds.

Laboratory tests
Smear, biopsy, serological tests.

Differential diagnosis
Aphthous ulcers, hand-foot-and-mouth disease, herpangina, acute necrotizing ulcerative gingivitis,
erythema multiforme, early pemphigus, desquamative gingivitis.

Treatment Symptomatic.
In severe cases, systemic aciclovir or valaciclovir.
Secondary Gingivostomatitis Herpetica

Definition and etiology

Secondary or recurrent herpetic stomatitis is a relatively common oral and perioral disease that is
due to reactivation of HSV-1. It is commonly precipitated by fever, trauma, cold, heat, sunlight,
emotional stress, and HIV infection.
Clinical features The most common sites of recurrence for HSV-1 are the lips and perioral skin, the
palate, and the attached gingiva. Clinically, the lesions present as multiple small vesicles arranged in
clusters (Fig.103). The vesicles soon rupture, leaving small ulcers that heal spontaneously within 6–10
days. Prodromal symptoms are burning, itching, tingling, and erythema. Characteristically, fever,
generalized regional lymphadenopathy, and constitutional symptoms are absent. The diagnosis is
made on clinical grounds.
Differential diagnosis
Aphthous ulcers, primary and secondary syphilis, streptococcal stomatitis, herpangina.

Treatment
Symptomatic.

Herpes Labialis Rekuren

Clinical Appearances
 Gejala awal : demam ringan, tingling/burning pada bagian yg terdapat lesi
 Terdapat vesikel pada garis tepi bibir yg akan rupture menjadi ulser dangkal
 Terbentuk krusta berwarna kekuningan
 Sembuh dalam waktu 1-2minggu tanpa bekas/jar. Parut

B. INFEKSI VIRUS VARICELLA ZOSTER

Primary varicella-zoster virus {VZV) infections in seronegative individuals are known as varicella or
chickenpox; secondary or reactivated disease is known as herpes zoster or shingles .

Varicella (Cacar Air)

Clinical features
Herpes zoster usually affects adults of middle age or over but, occasionally, attacks even children.
The fi rst signs are pain and Fig. 12.7 Herpetic whitlow. This is a characteristic non-oral site for
primary infection as a result of contact with infected vesicle fluid or saliva. The vesiculation and
crusting are identical to those seen in herpes labialis. Fig. 12.8 Herpes zoster. A severe attack in an
older person shows confl uent ulceration on the hard and soft palate on one side. Fig. 12.9 Herpes
zoster of the trigeminal nerve. There are vesicles and ulcers on one side of the tongue and facial skin
supplied by the first and second divisions. The patient complained only of toothache. irritation or
tenderness in the dermatome corresponding to the affected ganglion. Vesicles, often confl uent,
form on one side of the face and in the mouth up to the midline (Figs 12.8 and 12.9). The regional
lymph nodes are enlarged and tender. The acute phase usually lasts about a week. Pain continues
until the lesions crust over and start to heal, but secondary infection may cause suppuration and
scarring of the skin. Malaise and fever are usually associated. Patients are sometimes unable to
distinguish the pain of trigeminal zoster from severe toothache, as in the patient shown in Figure
12.9. This has sometimes led to a demand for a dental extraction. Afterwards, the rash follows as a
normal course of events and this has given rise to the myth that dental extractions can precipitate
facial zoster

Pathogenesis
Transmission of varicella is believed to be predominantly through the inhalation of contaminated
droplets. The condition is very contagious and is known to spread readily from child to child. Much
less commonly, direct contact is an alternative way of acquiring the disease. During the 2-week
incubation period, virus proliferates within macrophages, with subsequent viremia and dissemination
to the skin and other organs.
Herpes Zoster

Definition
Herpes zoster, or shingles, is an acute self-limiting viral disease.

Etiology
Reactivation of varicella-zoster virus. The most common predisposing factors for reactivation of the
virus are AIDS, leukemia, lymphoma and other malignancies, radiation, immunosuppressive and
cytotoxic drugs, and old age.

Clinical features
The thoracic, cervical, trigeminal, and lumbosacral dermatomes are most commonly affected.
Characteristically, one dermatome is usually affected. Pain and tenderness, usually associated with
headache, pulpitis, malaise, and fever, are prodromal symptoms before the appearance of oral or
skin lesions, or both. After two to four days, clusters of vesicles develop, and within two or three days
evolve into pustules and ulcers, covered by crusts (Figs.104, 105). The lesions persist for two to three
weeks. The unilateral location of the lesions is a typical pattern of herpes zoster. Oral manifestations
occur when the second and third branches of the trigeminal nerve are involved. Postherpetic
trigeminal neuralgia is a common complication, and rarely osteomyelitis, jawbone necrosis, and
tooth loss are seen. The diagnosis is made on the basis of clinical criteria.

Differential diagnosis
Varicella is clinically diagnosed by the history of exposure and by the type and distribution of lesions.
Other primary viral infections that may show some similarities include primary HSV infection and
hand-foot-and-mouth disease. Herpes zoster is most commonly confused with recurrent HSV
infections and may be indistinguishable from them on clinical grounds.Herpes simplex, erythema
multiforme.

Treatment
Analgesics and sedatives to control the pain. Aciclovir, valaciclovir, and famciclovir as antiviral drugs
may be helpful.
Histopathology.
The morphology of the VZV and the inflammatory response to its presence in both varicella and
herpes zoster are essentially the same as those with HSV. Microscopically, virus-infected epithelial
cells show homogeneous nuclei, representing viral products, with margination of chromatin along
the nuclear membrane. Multinucleation of infected cells is also typical. Acantholytic vesicles
eventually break down and ulcerate. In uncomplicated cases epithelium regenerates from the ulcer
margins with little or no scar.

Treatment.
For varicella, supportive therapy is generally indicated in normal individuals. However, in
immunocompromised patients more substantial measures are warranted. Virus-specific drugs that
are effective in treating HSV infections have also shown efficacy in Herpes the treatment of VZV
infections. These include systemically administered acyclovir, vidarabine, and human leukocyte
interferon. Corticosteroids are generally contraindicated. Patients with herpes zoster and intact
immune responses have generally been treated empirically However, it has been shown that oral
acyclovir used at high doses (800 mg five times per day for 7 to 10 days) can shorten the disease
course and reduce postherpetic pain. Analgesics provide only limited relief from pain. Topically
applied virus-specific drugs may have some benefit if used early. Topically applied substance P
inhibitor (capsaicin) may provide some relief from postherpetic pain. In patients with compromised
immune responses, systemically administered acyclovir, vidarabine, or interferon is indicated,
although success is variable.

C. INFEKSI VIRUS COXSACKIE

Hand-Foot-and-Mouth Disease

Definition
Hand-foot-and-mouth disease is an acute higly contagious viral infection transmitted from one
individual to another through either airborne spread or fecal-oral contamination.

Etiology
Coxsackievirus A16, and rarely other strains.

Clinical features
The disease usually affects children and young adults, and often occurs in epidemics. Oral
manifestations are always present, and are characterized by small vesicles (5–30 in number) that
rapidly rupture, leaving painful, shallow ulcers (2–6 mm in diameter) surrounded by a red halo
(Fig.107). The buccal mucosa, tongue, and labial mucosa are the most commonly affected sites.
Skin lesions are not constant, and present as small vesicles with a narrow red halo.
The lateral borders and the dorsal surfaces of the fingers and toes are the most common areas
involved.
Lesions may appear on the palms, soles, and buttocks.
The disease lasts five to eight days.

Differential diagnosis
Because this disease may express itself primarily within the oral cavity, a differential diagnosis should
include primary herpes gingivostomatitis and possibly varicella

Treatment
Supportive. Because of the relatively short duration, the self-limiting nature, and the general lack of
virusspecific therapy, treatment for HFM disease is usually symptomatic. Bland mouthrinses such as
sodium bicarbonate in warm water may be used to help alleviate oral discomfort.

Herpangina

Definition and etiology

Herpangina is an acute self-limiting viral infection, usually caused by coxsackievirus group A, types 1–
6, 8, 10, and 22, and less commonly by other types.

Clinical features
  The disease presents with an acute onset of fever, sore throat, dysphagia, headache, and
malaise, followed by diffuse erythema and vesicles.
 The vesicles are small and numerous, and rupture rapidly, leaving painful ulcers that heal
within 7–10 days (Fig.106).
 Characteristically, the lesions appear on the soft palate and uvula, tonsillar pillars, and
posterior pharyngeal wall. The disease has a peak incidence during summer and autumn, and
frequently affects children and young adults. The diagnosis is exclusively based on clinical
criteria.

Differential diagnosis
Herpetiform ulcers, aphthous ulcers, primary herpes simplex infection, acute lymphonodular
pharyngitis, erythema multiforme, FAPA syndrome, hand-foot-and-mouth disease.

Treatment
Supportive

Lesi Multipel Akut Non-Infeksi

 Contoh :
1. Eritema Multiforme
2. Pempigoid
3. Peny. Linear IgA

Erytema Multiforme

Definition
Erythema multiforme is an acute or subacute self-limiting disease that involves the skin and
mucous membranes.
 Etiology
The etiology is unclear. However, an immunologically mediated process triggered by herpes
simplex or Mycoplasma pneumoniae, drugs, radiation, or malignancies, is probable. (reaksi
hipersensitifitas)

Clinical features
 The disease more frequently affects young men between the ages of 20 and 30 years.
 The oral lesions present as coalescing small vesicles that rupture within two or three days,
leaving irregular, painful erosions covered by a necrotic pseudomembrane (Fig.108).
 The lips, buccal mucosa, tongue, soft palate, and floor of the mouth are most commonly
involved.
 The skin manifestations consist of erythematous, flat, round macules, papules, or plaques,
usually in a symmetrical pattern. The characteristic skin patterns are target- or iris-like lesions
(Fig.109).
 Skin bullae may occasionally be seen.
 Conjunctivitis, balanitis, vulvitis, and prodromal symptoms such as headache, malaise,
arthralgias, and fever, may also be present. Recurrences are common.
Laboratory tests
Histopathological examination

Differential diagnosis
Primary herpetic gingivostomatitis, aphthous ulcers, erosive lichen planus, pemphigus vulgaris,
pemphigoid.

Treatment
Systemic steroids. Aciclovir may be helpful in cases of recurrence

Stevens–Johnson Syndrome

Definition
Stevens–Johnson syndrome, or erythema multiforme major, is a severe form of erythema
multiforme that predominantly affects the mucous membranes. Etiology Drugs usually trigger
the disease.

Clinical features
The oral lesions are always present, and are characterized by extensive vesicle formation,
followed by painful erosions covered by grayish-white or hemorrhagic pseudomembranes
(Fig.110). The lesions may extend to the pharynx, larynx, and esophagus. The ocular lesions
consist of conjunctivitis, uveitis, symblepharon, or even panophthalmitis. The genital lesions are
balanitis or vulvovaginitis, and scrotal erosions (Fig.111). The skin manifestations may vary from
very light to severe. The diagnosis is mainly made on the basis of the clinical presentation.

Differential diagnosis
Behçet disease, pemphigus, pemphigoid, primary herpes simplex.

Treatment
Systemic steroids; antibiotics, if considered necessary in severe cases

PENYAKIT IMUNOLOGIS

Pemphigoid

Terdiri atas 2 jenis, yaitu bulosa dan sikratisial (pemfigoid membrane mukosa)

Cicatricial Pemphigoid
Definition
Cicatricial pemphigoid, or mucous membrane pemphigoid, is a chronic bullous mucocutaneous
disease that primarily affects mucous membranes, and results in atrophy or scarring.

Etiology
Autoimmunity. Bullous pemphigoid antigen (BP180), laminin 5, integrin B4, and type VII collagen
are the main target antigens.

Clinical features
The disease occurs more frequently in women than men (ratio 1.5 : 1), with a mean age at onset
of 66 years. Oral manifestations are seen in almost all patients, but other mucosae and rarely
the skin may be involved. The oral lesions are characterized by recurrent vesicles or bullae that
rupture, leaving large, superficial painful ulcerations (Fig.117). Repeated recurrences may lead
to epithelial atrophy or scarring. Usually, the lesions are limited to certain areas and they are
rarely widespread. Gingival involvement is common, producing a specific clinical pattern of
desquamative gingivitis. Ocular lesions consist of conjunctivitis, symblepharon, entropion,
trichiasis, dryness, and corneal opacity, frequently leading to blindness (Fig.118). Less
commonly, other mucosae and the skin may be involved. Laboratory tests Histopathological
examination, direct immunofluorescence.

Differential diagnosis
Bullous pemphigoid, linear IgA disease, epidermolysis bullosa acquisita, pemphigus, erosive
lichen planus, dermatitis herpetiformis, discoid lupus erythematosus, chronic ulcerative
stomatitis.

Treatment
Steroids and, rarely, immunosuppressive drugs
Bullous Pemphigoid

Definition
Bullous pemphigoid is a chronic mucocutaneous bullous disease that usually affects older
individuals.

Etiology
Autoimmunity. Bullous pemphigoid antigens (BP180, BP230) are the main target antigens.

Clinical features
The disease affects women slightly more often than men (ratio 1.7 : 1), with a mean age of 65
years at onset.
The oral mucosa is affected in about 20–40% of cases, usually after skin involvement. The oral
lesions usually follow cutaneous manifestations and begin as bullae that soon rupture, leaving
shallow ulcerations (Fig.119). Other mucous membranes may also be affected.
Skin lesions are always present, and begin as a nonspecific generalized rash followed by large,
tense bullae that rupture, leaving denuded areas without a tendency to extend peripherally
(Fig.120). The trunk, arms, and legs are the sites of predilection.

The prognosis is usually good.

Laboratory tests
Histopathological examination, direct and indirect immunofluorescence.

Differential diagnosis
Pemphigus, cicatricial pemphigoid, linear IgA disease, dermatitis herpetiformis, epidermolysis
bullosa acquisita, pemphigoid gestationis.

Treatment
Systemic steroids, immunosuppressive drugs, dapson

Penyakit Linear IgA

Linear IgA Disease

Definition
Linear immunoglobulin A (IgA) disease is a disorder that has recently been recognized in the
spectrumof chronic bullous diseases, characterized by the linear deposition of IgA along the
basement membrane zone.

Etiology
Autoimmunity.
Clinical features
The disease is more common in women than in men, and usually occurs between the ages of 40
and 50 years, although children may also be affected. Oral lesions occur in about 20–30% of
cases, and are characterized by the formation of bullae that soon rupture, leaving superficial,
nonspecific ulcerations (Figs.123, 124). The skin lesions consist of bullae that rupture, forming
ulcerations covered by crusts. Scarring conjunctivitis may also occur. The clinical features of the
disease are similar to those seen in cicatricial pemphigoid.

Laboratory tests
Histopathological examination, direct and indirect immunofluorescence.

Differential diagnosis
Cicatricial pemphigoid, bullous pemphigoid, pemphigus, dermatitis herpetiformis, pemphigoid
gestationis.

Treatment
Dapsone and steroids

Lesi Multipel Kronis

Pemphigus Vulgaris

Definition
Pemphigus is a severe chronic bullous autoimmune mucocutaneous disease.

Etiology
Autoimmunity. Desmoglein 1 and 3 are the main target antigens.

Clinical features
Four classical varieties of pemphigus are recognized: vulgaris, vegetans, foliaceus, and
erythematosus. Recently, two additional forms of the disease have been described: drug-
induced pemphigus and paraneoplastic pemphigus, which usually affect patients with
lymphoreticular malignancies. Pemphigus vulgaris is the most common variant, representing
90–95% of cases. More than 70% of pemphigus vulgaris cases begin with oral involvement. Oral
lesions are characterized by the formation of bullae, which rapidly rupture, leaving painful
erosions with a tendency to extend peripherally (Figs.113, 114). The buccal mucosa, labial
mucosa, palate, tongue, floor of the mouth, and gingiva are often involved. The skin lesions
present as flaccid bullae that rupture quickly, leaving persistent eroded areas (Fig.115).

Diagnosis
Nikolsky’s sign is positive. Any skin area may be involved, although the intertriginous regions,
umbilicus, trunk, and scalp are the most common sites affected. Lesions may develop on other
mucosae (conjunctivae, nose, larynx, pharynx, genitals, anus) (Fig.116)

Laboratory tests
Histopathological and cytological examination, direct and indirect immunofluorescence.

Differential diagnosis
Cicatricial pemphigoid, bullous pemphigoid, linear IgA disease, epidermolysis bullosa acquisita,
toxic epidermal necrolysis, primary herpetic gingivostomatitis, erythema multiforme, erosive
lichen planus, aphthous ulcers.

Treatment
Systemic steroids. Ciclosporin, azathioprine, and mycophenolate mofetil may also be used,
always in association with steroids.

The prognosis has been improving steadily during the last two decades.
Dermatitis Herpetiformis

Definition
Dermatitis herpetiformis, or Duhring–Brocq disease, is a chronic recurrent cutaneous bullous
disease, rarely with oral involvement.

Etiology
Unclear. Immunological and genetic factors, as well as gluten sensitivity, may be involved in the
pathogenesis.

Clinical features
The disease is more common in men between the ages of 20 and 50 years. The oral mucosa is
affected in 5–10% of cases.
Oral manifestations follow the skin eruption, and present as maculopapular, erythematous,
purpuric, and mainly vesicular lesions.
The vesicles appear in a cyclic pattern, and rupture rapidly, leaving shallow, painful ulcerations
(Fig.125).
The tongue, buccal mucosa, and palate are more frequently involved.
Cutaneous lesions are always present and appear as erythematous papules or plaques followed
by severe burning and pruritus and small vesicles that group in a herpeslike pattern. The lesions
exhibit exacerbations and remissions, and are commonly located symmetrically on the extensor
surfaces.

Laboratory tests
Histopathological examination, direct and indirect immunofluorescence.

Differential diagnosis
Bullous pemphigoid, cicatricial pemphigoid, linear IgA disease, pemphigus, herpetiform ulcers.

Treatment
Sulfones and sulfapyridines. A gluten-free diet may control the disease activity.

Prognosis
In most instances dermatitis herpetiformis is a lifelong condition, often exhibiting long periods of
remission. Many patients, however, maybe relegated to long-term dietary restrictions or drug
treatment or both.