the most common viral infections that affects the maxillofacial area sources( burket's oral medicine 11th ed,oral and maxillofacial pathology neville 2e )

2. HERPES SIMPLEX VIRUS (HSV) INFECTION
 The herpes viridae family of viruses contains nine
different viruses that are pathogenic in humans
 In general, infections above the waist are caused by
HSV -1 and hose below the waist by HSV -2,although
with changing sexual practices, it is not uncommon to
culture HSV -2 from oral lesions and vice versa
 The most common sites of infection are the oral and
genital mucosa and the eye. HSV infection of the
cornea(keratitis) is a major cause of blindness in the
world.

3. • HSV -1 or -2 may cause herpes whitlow,an infection of the
fingers when virus is inoculated into the fingers through a
break in the skin
• Other HSV -1 infections include herpes gladiatorum
(infections of the skin spread through the sport of
wrestling),herpes encephalitis, HSV esophagitis, and HSV
pneumonia

4. CLINICAL MANIFESTATIONS
Primary Gingivostomatitis. Most cases of
primary HSV -1 infections are subclinical and generally occur
in children and teenagers.
• There is a 1 to 3 day viral prodrome of:
Fever
Loss of appetite,
malaise,
Myalgia that may also be accompanied by headache
and nausea.
• Oral pain leads to poor oral intake, and patients may require
hospitalization for hydration.
• The disease is self-limiting in otherwise normal patients and
resolves within 10 to 14 days, typical for a viral illness.

5. ORAL FINDINGS
• Within a few days of the prodrome, erythema and
clusters of vesicles and/or ulcers appear on the
keratinizedmucosa of the hard palate, attached
gingiva and dorsum of the tongue, and the no
keratinized mucosa of the buccal and labial
mucosa, ventral tongue, and soft palate.
• Vesicles break down to form ulcers that are usually
1 to 5 mm and coalesce to form larger ulcers
with scalloped borders and marked surrounding
erythema.
• The gingiva is often fiery red, and the mouth is
extremely painful, causing difficulty with eating.
• Pharyngitis causes swallowing difficulties.
• Primary HSV infection in adults follows a similar
pattern

7. RECRUDESCENT ORAL HSV INFECTION
• Reactivation of HSV may lead to asymptomatic
shedding of HSV,in the saliva and oral secretions, an
important risk factor for transmission; it may also cause
ulcers to form.
• important triggers for reactivation of hsV:
Fever
ultraviolet radiation
Trauma
stress, and menstruation
• Recrudescent hsV on the lips is called recurrent herpes
labialis (Rhl) and occurs in 20 to 40% of the
young adult population.
• These are associated with a prodrome of itching,
tingling,or burning approximately 50% of the time,
followed in succession by the appearance of
papules,vesicles,ulcers, crusting, and then resolution of
lesions

9. • Intraoral recrudescent HSV in the
immunocompetent host occurs chiefly on the
keratinized mucosa of the hard palate, attached
gingiva, and dorsum of the tongue.
• one common presentation is the complaint of pain
in the gingiva 1 to 2 days after a scaling and
prophylaxis or other dental treatment.
• Lesions appear as 1 to 5mm painful vesicles but
more often ulcers on the marginal gingiva.

11. LABORATORY DIAGNOSIS
• HSV isolation by cell culture
• Polymerase chain reaction (PCR) from Swabs
• HSV can be identified from scrapings from the
base of lesions (especially vesicles) smeared onto
glass slides.

12. MANAGEMENT
• Primary HSV Infection:
Pain control
supportive care,
and definitive treatment.
• Acyclovir inhibits viral replication and it has little activity against non–
virally infected cells.
• The acyclovir family of drugs is inexpensive, safe, and readily
available, it is appropriate to treat even primary infections definitively
because it reduces Viral shedding and infectivity.
• the acyclovir family of drugs is inexpensive, safe, and readily
available, it is appropriate to treat even primary infections definitively
because it reduces viral shedding and infectivity.
• The use of acyclovir at 15 mg/kg five times a day in children
reduces the duration of fever, reduces hsV shedding, halts the
progress of lesions, improves oral intake, and reduces the incidence
of hospital admissions.
• Valacyclovir, the prodrug of acyclovir, has three to five times the
bioavailability of acyclovir

13. MANAGEMENT
Recurrent HSV
• RHl can often be suppressed by reducing trigger factors, such
as by using sunscreen
• RHl is self-limiting, the use of topical antiviral medications:
Reduces shedding
infectivity
pain
and the size and duration of lesions.
• Topical antiviral medications such:
5% acyclovir cream,
3% penciclovir cream,
10% docosanol cream
are efficacious if applied three to six times a day at the first
prodrome or sign of a lesion.
• Systemic therapy with valacyclovir or famciclovir (500–1,000mg
three times a day) is effective in treating active lesions or for
suppression ofhsV infection in patients who develop frequent
episodes, large lesions.

14. VARICELLA ZOSTER VIRUS (VZV) INFECTION
• Primary infection with VZV, leads to varicella(chicken pox).as
with all herpes viruses, the virus then becomes latent, usually
in the dorsal root ganglia or ganglia of the cranial nerves.
• Reactivation produces herpes zoster infection
(HZI),commonly called shingles.
• The incidence of HZVincreases with age and the degree of
immunosuppression
• As with HSV, this virus is cytopathic to the epithelial cells of
the skin and mucosa, causing blisters and ulcers.
• Transmission is usually by the respiratory route, with an
incubation period of 2 to 3 weeks

15. CLINICAL FINDINGS
• Primary VZV infection generally occurs in the first two decades of life.
• The disease begins with:
low-grade fever,
Malaise
macu-lopapular rash, followed by vesicles that have been
described as “dewdrop-like.”
• Lesions begin on the trunk and face and spread centrifugally.
• Central nervous system involvement may result in cerebellar ataxia and
encephalitis.
• Other complications of varicella include pneumonia, myocarditis, and
hepatitis.
• HZI of the skin (shingles) is more common in adults and starts with a
prodrome of deep, aching, or burning pain.

17. CLINICAL FINDINGS
• This is followed within 2 to 4 days by the appearance of crops of
vesicles in a dermatomal or “zosteriform” pattern. This pattern
describes the unilateral, linear, and clustered distribution of the
vesicles, ulcers, and scabs in a dermatome supplied by one
nerve.
• Thoracic/lumbar dermatomes are the most frequently involved,
followed by the craniofacial area.
• Lesions heal within 2 to 4 weeks, often with scarring and
hypopigmentation.
• One of the most important complications ofhZi is postherpetic
neuralgia, defined as pain that lingers for30 days or 120
days after the onset of the acute rash.
• Postherpetic neuralgia affects approximately 8 to 70% of
patients over age 50
• Predisposing factors include:
Older age
Prodromal pain
More severe clinical disease during the acute rash
phase.

19. ORAL MANIFESTATIONS
• Primary VZV infection presents as minor acute ulcerations in the
mouth that pale in clinical significance when compared with the skin
lesions.
• In recurrent VZV infection, the ophthalmic division of the trigeminal
nerve is the cranial nerve most often affected (herpes zoster
ophthalmicus); cornea involvement may lead to blindness
• Involvement of this nerve (V) leads to lesions on:
the upper eyelid, forehead, and scalp with V1
midface and upper lip with V2
and lower face and lower lips with V3

20. pain, burning, and
tenderness, usually on the palate
on one side. This is followed
several days later by the
appearance of painful, clustered1
to 5 mm ulcers(rarely vesicles,
which breakdown quickly) on the
hard palate or even buccal
gingiva, in a distinctive unilateral
distribution .These ulcers heal
within 10 to 14 days.

21. LABORATORY FINDINGS
• viral isolation using cell culture is still the best way to confirm a
diagnosis of VZV infection.
• A simple smear stained with a standard laboratory stain would reveal the
presence of multinucleated epithelial cells, but this does not distinguish
between HSV and VZV.
• PCR
• Direct fluorescent antibody testing using a smear may have greater
ensitivity.This test uses a smear obtained by scraping the lesion and staining
it with antibody against VZV conjugated to a fluorescent compound.
• VZV and H ZI are cytopathic to the epithelial cells and result in the formation
of multinucleated epithelial cells with viral inclusions, similar to HSV infection.
• Biopsy is usually not required and not the diagnostic test of choice since the
clinical presentation is usually characteristic.

22. MANAGEMENT
• As with HSV infection, management of oral lesions of
varicella and HZI is directed toward:
pain control
supportive care
and hydration
and definitive treatment to minimize the risk for
dissemination, particularly in immunocompromised patients.
• aspirin use, especially in patients with VZV infection or influenza, is
associated with the development of Reye syndrome, which is potentially fatal,
and is contraindicated; ibuprofen is the preferred analgesic.
• Treatment of primary VZV infection includes the use of acyclovir (800 mg five
times a day).
• Valacyclovir (1,000 mg three times a day) or famciclovir (500 mg three times
a day) for 7 days is effective in treating HZI and should be started within 72
hours of disease onset.

23. COXSACKIEVIRUS (CV) INFECTION
• CV, a ribonucleic acid (RNA) virus
• is a member of the genus Enterovirus
• There are 23 C V type A (CVA) and 6 C V type B (CVB) viruses
• The viruses replicate first in the mouth and then extensively in the lower
gastrointestinal tract, where they shed. Transmission is therefore primarily by
the fecal-oral route, although some shedding occurs in the upper respiratory
tract.
• In the oral cavity, C V infections lead to three disease entities:
• HFM disease
• herpangina
and lymphonodular pharyngitis.

24. HAND-FOOT-AND-MOUTH DISEASE (HFM)
• Of all the C Vs, C VA16 is the most common cause
CV infections, including herpangina, tends to be seasonal (usually summer)
Clinical Findings
• Children younger than 10 years in summer.
• Patients have a low-grade fever and sore mouth;
• 75 to 100% of patients have a skin rash especially on the hands and
feet (dorsa, palms and soles) and
30% on the buttocks.
• The rash is first red and macular and then becomes vesicular.
Oral Manifestations.
• Patients are febrile and complain of a sore mouth and throat. Lesions
begin as erythematous macules that become vesicles and quickly
break down to ulcers. Lesions are usually located on the tongue,
hard and soft palate, and buccal mucosa but can present on any
oral mucosal surface.

25. HERPANGINA
• CVA (serotypes 1–10, 16, and 22) are the most common viruses isolated from
this disease.
Clinical Findings
• As with all CV infections, children under 10 are usually IN summer. Patients
develop fever, headache, and myalgia that usually last only 1 to 3 days.
Oral Manifestations
• The first oral symptoms of herpangina are sore throat and pain on
swallowing. There may be erythema of the oropharynx, soft palate, and
tonsillar pillars.
• Small vesicles form, but these rapidly break down to 2 to 4 mm ulcers. These
persist for 5 to 10 days
• Lymphonodular pharyngitis is considered a variant of
herpangina91 and is associated with C VA10. Patients report
a sore throat, but rather than presenting with vesicles that
break down to ulcers, patients develop diffuse small nodules
in the oropharynx.

27. LABORATORY TESTS
1. CVB infections may be diagnosed by culture (usually from the throat or
feces), but only CVA9 and CVA16 grow readily and CVA is best identified by
noculation into newborn mice.
2. PCR is another sensitive and rapid way of identifying viral RNA in clinical
specimens
3. Diagnosis is usually made on clinical findings, and culture and biopsies are
rarely necessary for diagnosis.
Management
• CV infections are self-limiting (unless complications arise or the patient is
immunocompromised), and management is directed toward :
control of fever and mouth pain
supportive care
and limiting contact with others to prevent
spread of infection
• Effective antiviral gents for CV are not available.

28. MUMPS (PARAMYXOVIRUS OR EPIDEMIC
PAROTITIS )
• mumps is an acute viral infection caused by a ribonucleic acid (RNA
) paramyxovirus and is transmitted by direct contact with salivary
droplets.
• an initial vaccination measles-mumps-rubella (MMR) vaccination at
12 to 18 months of age and a second dose at 4 to 6 years of age.
• Mumps virus vaccine is not recommended for severely
immunocompromised children because the protective immune
response often does not develop, and risk of complications exists.

29. CLINICAL PRESENTATION
• mumps typically occurs in children 4 and 6 years.
• The incubation period is 2 to 3 weeks; this is followed by:
salivary gland inflammation and enlargement,
preauricular pain, fever, malaise, headache, and myalgia.
• The majority of cases involve the parotid glands, but 10% of the
cases involve the submandibular glands alone.
• The salivary gland enlargement is sudden and painful to palpation,
with edema in the skin overlying the involved glands. Salivary gland
ducts are inflamed but without purulent discharge.
• One gland can become symptomatic 24 to 48 hours before another
gland does.
• Swelling is usually bilateral and lasts approximately 7 days.
• Complications of mumps include mild meningitis and encephalitis.
Deafness, myocarditis, thyroiditis, pancreatitis. Males can
experience epididymitis and orchitis, resulting in testicular atrophy
and infertility if the disease occurs in dolescence or later.

30. Diagnosis:
The diagnosis is made by the demonstration of antibodies to the mumps S
and V antigens and to the hemagglutination antigen.
The diagnosis of mumps in adults can be more difficult. A rapid,
commercially available oral fluid assay using a mumps-specific
immunoglobulin M (IgM) capture enzyme immunoassay has
demonstrated good sensitivity and specificity as an alternative to the
conventional serologic test.
Treatment.
The treatment of mumps is symptomatic, and vaccination is important for
prevention.

32. HUMAN IMMUNODEFICIENCY VIRUS
AND ACQUIRED IMMUNODEFICIENCY
SYNDROME
• In infected individuals, the virus can be found in most bodily fluids.
HIV has been recovered from serum, blood. saliva, semen , tears,
urine, breast milk, ear secretions, and vaginal secretions.
The prime modes of transmission for HIV are:
(1) unprotected penetrative sex between men,
(2) unprotected heterosexual intercourse,
(3) injection drug use,
(4) unsanitary injections and blood transfusions,
(5) mother to child spread during pregnancy, delivery, or breast-feeding.
• Researchers have debated the infectiousness of oral fluids. HIV has
been found to be pre sent in oral fluids. but saliva appears to reduce
the ability of HIV to infect its target cells. lymphocytes. Reports of
transmission by oral fluids are rare, and it appears this is not a
significant source for the transmission of AIDS.

33. • The primary target cell of HIV is the CD4 + helper T
lymphocyte. The DNA of HIV is incorporated into the DNA of
the lymphocyte and. thus. is present for the life of the cell.
• In most viral infections. host antibodies that are protective
against the organism usually are formed. In people with HIV
infection, antibodies are developed but are not protective.
• The virus may remain silent. Cause cell death. or produce
syncytiaL fusion of the cells. Which disrupts their normal
function. A subsequent decrease in T-helper cell numbers
occurs. with a resultant loss in immune function. The normal
response to viruses, fungi, and encapsulated bacteria is
diminished.
• For untreated HIV infection, a common pattern of disease
progression has been established consisting of three
phases:
• (1) primary infection,
• (2) prolonged (median=10 years) period of clinical latency,
• (3) the appearance of clinically apparent disease.

34. CLINICAL FEATURES
• The acute viral syndrome that occurs typically develops within I to 6 weeks
after exposure in 50% to 70% of infected patients. The symptoms (e.g..
generalized lymphadenopathy. Sore throat , fever. Maculopapular rash.
headache. myalgia arthralgia. diarrhea. photophobia . peripheral
neuropathies).
• Oral changes may include mucosal erythema and focal ulcerations.
• The acute viral syndrome clears within a few weeks; during t his period, HIV
infection usually is not considered or investigated.
• The presentation of symptomatic. overt AIDS is highly variable and often is
affected by a person's prior exposure to a number of chronic infections.
• In 50% of the cases. Pneumonia caused by the protozoan Pneumocystis
cannitis the presenting feature leading to the diagnosis
• Other infections of diagnostic significance include disseminated
cytomegalovirus (CMV) infection, severe herpes simplex virus (HSV)
infection. atypical mycobacterial infection. Cryptococcal meningitis. and
central nervous system (CNS) toxoplasmosis.

36. PERSISTENT GENERALIZED
LYMPHADENOPATHY.
• HIV disease often remains silent except tor persistent
generalized lymphadenopathy (PGL).
• The prevalence of this early clinical sign varies: however, in
severalstudies it approaches 70%.
• PGL consists of Lymphadenopathy that has been present for
longer than 3 months and involves two or more sites.
• The most frequently involved sites are the posterior and
anterior cervical, submandibular, occipital. and axillary nodes.

37. CANDIDIASIS.
• Oral candidiasis is the most common intra oral manifestation
of HiV infection and often is the presenting sign that leads to
the initial diagnosis.
• Prevalence studies vary Widely, but approximately one third
of Hlv-Infectcd individuals and more than 90% of patients with
AIDS develop oral candidiasis at some time during their
disease course.
• The following four clinical pattern s are seen;
• Pseudomembranous
• Erythematous
• Hyperplastic
• Angular cheilitis
• Treatment is much more difficult in patients with AIDS.
Nystatin often is ineffective. Topical clotrimazole is associated
with an improved response

38. HIV-ASSOCIATED PERIODONTAL DISEASE
• Three patterns of periodontal disease are associated
strongly with HIV infection:
• Linear gingival erythema
• Necrotizing ulcerative gingivitis
• Necrotizing ulcerative periodontitis
• The treatment of NUG and NUP revolves around debridement
, antimicrobial therapy, immediate follow-up care, and long-term
maintenance.
• The initial removal of necrotic tissue is necessary. combined
with povidoneiodine irrigation.
• The use of systemic antibiotics usually is not necessary. but
metronidazole has been administered to patients with
extensive involvement that is associated with severe acute
pain.

43. Diagnosis
Confirmation of HIV infection can be made by viral culture or by detection of HIV
antibodies or antigens. The standard screening tool is the enzyme immunoassay
(EIA) for antibodies to HIV. This test can have false-positive results or cross-reactions:
therefore. It should be repeated
TreatmentandPrognosis
The introduction of highly active antiretroviral therapy (HAART) has altered the
course of the epidemic
ANTIRETROVIRAL MEDICATIONS
1. Nucleoside reverse-transcriptase inhibitors
2.Non nucleoside reverse transcriptase inhibitors
3. Proteaseinhibitors