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Oral viral infections Prof. Elsanousi M Taher BDS, MSc., FFDRCSI

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1 Oral viral infections Prof. Elsanousi M Taher BDS, MSc., FFDRCSI
LIMU Dental School

2 Virus structure

3 The nature of viruses small size (10-300 nm)
obligate intracellular parasites ( lacks ribosomes for protein synthesis ): on entry into a susceptible host the virus NA transcribed into - or itself acts as- virus specific messenger RNA nucleic acid: DNA or RNA as a single or double stranded shape variation

4 Structure of viruses Nucleic acid core ( genome): of either DNA or RNA
Capsid: consist of small subunits called capsomeres Envelop: (in some viruses) consist of lipoproteins most of envelop viruses like herpes viruses are more susceptible to physiochemical agents

5 Viral replications process
Attachment Penetration Viral synthesis Virion assembly and replication Release Invasion of another cells or tissue and replicate

6 Classification of viruses
No generally accepted classification RNA VIRUSES: Picorna virues: hepatitis A enteroviruses: coxackie, polio ...etc rhinoviruses Myxoviruses: orthomyxoviruses: influenza paramyxoviruses: measeles, mumps, parainfluenza Retroviruses: HIV

7 DNA VIRUSES: Herpes viruses ( 8 types) Hepadana virus: hepatitis B virus Papovirus: human papiloma virus (HPV) Pox viruses: smallpox, molluscum contagiosum

8 Modes of viral infection
acute infection: latent infection: chronic infection: CMV, HBV oncogenic virus: benign as HPV malignant as some viruses that cause certain lymphomas and leukemias

9 Disadvantages: Laboratory investigations for virus infection
Detection of the virus or its components (antigens or nucleic acids) "foot prints" Electron microscopy diagnosis can be made within minutes Disadvantages: insensitive only morphological diagnosis can be made not very useful for clinical purposes Direct antigen detection by immunofluorescence or immune assay: Enzyme linked immunosorbant assay (ELIZA) Radio-immune assay (RIA) Can be done on cells, serum or other body fluids

10 Detection of viral nucleic acid
by using nucleic acid hybridization and polymerase chain reactions (PCR) in clinical specimens Detection of virus inclusion bodies: too non specific to be useful in clinical diagnosis

11 Lab. animals: rabbits, mice, monkeys (less commonly used nowadays)
Culture of the virus: Lab. animals: rabbits, mice, monkeys (less commonly used nowadays) Chick emberyonated eggs Tissue cultures:

12 Tissue cultures: most cultures can be propagated in cultures of suitable cells depends on preparation of single layer (monolayer) of actively metabolizing cells adherent to glass surface in a test tube or Petri plates) for continuous cell line, human rhabdomyosarcoma is used almost all virus isolation is nowadays done by tissue culture the diagnosis is made by detection of cytopatheic effect (CPE) once the virus in cell culture is recognized, its identity has to be confirmed

13 The main disadvantages of tissue culture:
the time taken by most viruses to grow to detectable levels (4 days for HSV & 3-4 weeks for CMV) some viruses can't yet be cultured routinely in lab. like HPV, HBV, HAV

14 Serological investigation:
Detection of the antibodies is by far the most commonly used method for virological diagnosis in clinical practice Paired serum sample is taken: acute stage sample convalescent stage sample A fourfold rise in the titre of serum antibodies is indicative of infection Detection of IgM (the earliest antibodies to appear is only present if there is a recent infection with the virus) Limitation: retrospective

15 Detection of cytopathic changes in the infected tissue
Cytopathic effect or cytopathogenic effect (abbreviated CPE) refers to degenerative changes in cells, especially in tissue culture, and may be associated with the multiplication of certain viruses. Cytopathic effects have been shown in conjunction with non-viral infections as well, such as those changes seen in fibroblasts during the early lesion of periodontal diseases.

16 Herpes viruses

17 Herpes viruses include:
HSV: 1 & 2 HZ VARICELLA : chicken box & Shingles EBV: infectious mononucleosis & others Cytomegalovirus: salivary infection Human herpes viruses 6 and 7: skin rashes Human herpes viruses 8: Kaposi sarcoma

18 Herpes simplex virus (HSV) infection
HVs are double stranded DNA viruses: Transmitted in saliva Encountered early in life Characterized by latency Reactived by Immunosuppression Has two subtypes: HSV- 1: causes oral, skin above waist HSV-2 : causes genital, skin below waist and newborn babies

19 Primary herpetic gingivostomatitis Recurrent herpetic lesions:
HERPES SIMPLEX VIRUS CLINICAL CLASSIFICATION OF ORAL HERPETIC INFECTION Primary herpetic gingivostomatitis Recurrent herpetic lesions: Recurrent herpes labialis Recurrent intra oral herpes

20 Primary herpetic gingivostomatitis
Clinical features: Caused by HS1 USUALLY but in teenagers may be due to HSV2 transmitted sexually route of transmission: direct contact with saliva and body fluids incubation period 2-20 days (usually 4 days) most cases are subclinical (50%) or mild to be considered as teething process self limiting (10-14 days ) but may be fatal in immunocompromised host

21 prodromal signs & symptoms (pyrexia, headache and cervical lymphadenopathy)
Single episode of vesiculobullous oral lesion acute marginal gingivitis with edema and ulceration Ulcerations of oral mucosa excessive salivations Bilateral Cervical lymphadenopathy (jugolodigastric specially) Usually no hepatosplenomegally after primary infection, the virus reside in the dorsal root & trigeminal ganglion (neuroinvasive) and at local neural tissue to be reactivated later

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28 HSV 2 cause genital lesion in both males in females

29 D.D Acute necrotizing gingivitis HZV infection Erythema multiforme
Herpengina & HFMD Aphthous ulceration

30 Special investigations: diagnosis is mainly clinical
Cytology smear: rarely used nowdays HSV isolation Serology: fourfold rise in antibody titer in acute and convalescent stages Electron microscopy: not always available PCR for HSV-DNA: sensitive, rapid and expensive culture of the virus: takes days

31 The culture and serology take about 10 days to provide the result so they are of limited clinical value Chair side kits that can rapidly (within minutes) prove the presence of the HSV in a lesional smear using immunoflurosecence are available but their routine use is limited due to high cost

32 Management: Supportive measures
Reduce fever and pain: paracetamol and ibuprofen elixir Maintain hydration Soft diet Reduce secondary infection Rest Local antseptic (0.2% CHLORHEXIDINE mouth wash) Antiviral : in severe or immunocompromised cases (200 mg acyclovir five times a day for 5 days) Reassure the parents of the affected child about the nature and self limiting feature of the disease

33 Complications of HSV infection:
Herpetic whitlow Herpetic keratoconjuctivitis Herpetic encephalitis Eczematous herpeticum

34 Herpetic whitlow

35 Herpetic keratoconjuctivitis

36 HSV latency and reactivation (Recurrent herpes labialis)
Predisposing factors: Common cold & febrile infection Exposure to sun light Menstruation Local irritation e.g. Dental treatment Emotional upset Immunosuppression

37 Clinical features: Adults mainly affected
paraesthesia or burning & erythema Macular papular vesicles and ulcer appear 1-2 hours later at the mucocutaneuos junction of lip rupture of vesicles after 2 days & appearance of new vesicles Healing the whole cycle may take about 10 days secondary bacterial infection may induce impetiginous lesion

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42 D.D: Impetigo: Traumatic ulcers EM
contagious superficial skin infection among kids infection generally caused by Staphylococcus aureus or Streptococcus pyogenes, usually produces blisters or sores on the face, neck, hands, and diaper area. Traumatic ulcers EM

43 imptigo

44 Management: Prophylactic Symptomatic:
immunocmopetent: topical 5% acyclovir cream may be applied at early stage of the disease to reduce its duration and severity immunocompromised: systemic acyclovir

45 Recurrent intra-oral herpes
Rare Seen more commonly in immunocompromised patients as in HIV infection The hard palate is a common site In immunocompromised patients, systemic antiviral is given with supportive treatment

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47 Varicella zoster virus infection
Primary infection ( chickenpox) The virus is acquired by inspiration of contaminated droplets During the two weeks incubation period the virus proliferate within the macrophages with subsequent viraemia and dissemination into the skin and other organs including nerve ganglia in which it reside in latent form In children, it is preceded by little (malaise and fever) or no prodromal symptoms which are more severe in adults

48 Face and distal extremities are less commonly involved
The appearance of cough, dyspnea or chest pain within 2-5 days after the onset of the rash is indicative of severe pulmonary involvement Pruritus is the primary and most annoying feature of chickenpox and patient’s scratching contributes to secondary bacterial infections and scarring Abrupt discrete erythematous macules and papules over the chest, scalp and mucous membrane that appear in crops Face and distal extremities are less commonly involved Irritability and anorexia Mouth ulcers are indistinguishable from HSV BUT it doesn’t involve gingiva

49 Varicella zoster virus infection
The macules progress to clear, tense fragile vesicles which may rupture and become crusted Varicella lesions appear in 3 -5 distinct crops for up to 5 day period and lesions in all stages of development may be seen within one area ( an important difference from smallpox) The disease is highly contagious

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52 Chickenpox (oral lesions)

53 Secondary infection (zoster or shingles)
Predisposing factors: Old age Immunosuppression medication HIV Radiation Others

54 Secondary infection (zoster or shingles)
Zoster is latin for belt (belt like distribution) Is due to reactivation of latent virus in sensory ganglion The lesions are preceded by mild severe pre-eruptive itch, tenderness or severe pain; the last may be generalized over the entire nerve segment or localized to part of it, or referred The pain in the facial area mimic and be confused with toothache Neurological changes like hypo, hyperesthesia or dysthesia may be reported or detected

55 The interval between pain and the appearance of eruptions may be as long as 10 days but on average is 3-5 days Lesions are usually unilateral and involve face and/or oral cavity along the distribution of v cranial nerve and doesn’t cross the mid line The pain usually subsided in several weeks with scar formation Rarely the eruption may be bilateral Lesion on the tip of the nose may herald involvement of trigeminal nerve Trigeminal nerve is affected in about 15% of cases of shingles (most lesions are in thoracic area) May be complicated by post-herpetic neuralgia

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61 Secondary infection (zoster or shingles)
Investigations: cytological smear of the vesicle may show T zank cells viral culture antibody titre Electron microscopy examination investigate for underlying disease

62 Treatment of orofacial shingles
Healthy patient: maintain good OH painting of the lesions with tincture benzoin analgesics like opiates topical 5% acyclovir (early in the course) systemic acyclovir if severe (400 mg tds/ 10 days)

63 ocular involvement should be evaluated and managed by an ophthalmologist
it may treated with topical steroid and the lesion must be distinguished from herpes simplex keratitis where the steroid is contraindicated systemic antibiotic if secondarily infected arise

64 as above in addition to:
In immunocompromised patient: as above in addition to: systemic acyclovir (800 mg IV tds) zoster immunoglobulin acyclovir: reduce duration of pain, time of healing, post-herpatic neuralgia systemic steroid for a short period appear to reduce the post-herpatic neuralgia. It should be started early after skin eruption

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66 Complications of shingles:
Ophthalmic: corneal ulcers and scarring & blindness Motor palsy: may result from spread of the lesion from the posterior horn into the ant. horn of spinal cord Disseminated HZ: in immunocompromised patients and cause gangrenous and necrotic lesions, varicella pneumonia and encephalitis are potentially fatal post-herpatic neuralgia

67 Post-herpetic neuralgia
Occurs in 9-15 % of patients with shingles Tricyclic antidepressant (amitriptyline) Phenothiazines Combined treatment of carbamazepine ( mg/day) or phenytoin sodium ( mg) mg nortryptaline Intralesional or subcutaneous injection of triamcinolone 0.2 mg/ml into the affected dermatome Repeated cryosurgery of the area affected with by postherpatic neuralgia is reported to cause long-term relief of pain Transcutaneous electrical stimulation may be useful in patients with intractable pain Postherpetic neuralgia is thought to be nerve damage caused by herpes zoster. The damage causes nerves in the affected dermatomic area of the skin to send abnormal electrical signals to the brain. These signals may convey excruciating pain, and may persist or recur for months, years or for life. Signs and symptoms Symptoms: With resolution of the HZ eruption, pain that continues for 3 months or more is defined as PHN. Pain is variable from discomfort to very severe and may be described as burning, stabbing, or gnawing. Signs: Area of previous HZ may show evidence of cutaneous scarring. Sensation may be altered over involved areas, in the form of either hypersensitivity or decreased sensation. In rare cases, the patient might also experience muscle weakness, tremor or paralysis — if the nerves involved also control muscle movement.

68 Ramsay Hunt syndrome is the reactivation syndrome of herpes zoster in the geniculate ganglion. It has variable presentation which may include a lower motor neuron lesion of the facial nerve, deafness, vertigo and pain. See Facial Pain

69 Epstein -Barr virus This virus is being associated with many conditions: infectious mononucleosis Burkitt's lymphoma Nasopharyngeal carcinoma Hairy leukoplakia

70 Transmitted by saliva, blood transfusion and may become latent in B-lymphocytes and pharyngeal epithelial cells Infected lymphocytes appear in peripheral blood as atypical lymphocytes It has relatively long incubation period ( days)

71 Infection with EBV EBV is present in pharyngeal epithelium and appears in saliva of patient with infectious mononucleosis and for several months after recovery Close contact transmit the disease (kissing disease) sub clinical (asymptomatic) acute (infectious mononucleosis) chronic infection

72 Infectious mononucleosis
Common in adolescents & young adults Fever and Malaise Sore throat Tonsillar exudates that mimic diphtheria Cervical lymphadenopathy Hepatomegally and abnormal liver function tests Splenomegally Palatal petechiae in 30 % of cases Oral ulceration Skin rash on ampicillin administration (non allergic type)

73 Skin rash on ampicillin administration

74 Palatal petechiae in 30 % of cases

75 Blood film: large atypical nononuclear lymphocytes

76 Complications of infectious mononucleosis:
Hairy leukoplakia Burkitt’s lymphoma Nasopharyngeal carcinoma Chronic infection and persistent malaise

77 Infectious mononucleosis
D.D: CMV mononucleasis diphtheria HIV infection acute lymphonodular pharyngitis leukemia

78 Infectious mononucleosis
Investigations: CBC with lymphocytosis Blood film: large atypical nononuclear lymphocytes Serology: Paul-Bunnel or monospot test (positive heterophil antibody test) Antibody to EBV viral capsid antigen (VCA)

79 Infectious mononucleosis
Management: Supportive Acyclovir is of little benefit SYSTEMIS steroids if there is pharyngeal oedema severe enough to compromise the airway

80 Cytomegalovirus infection
About 80% of adults by the age of 40 are CMV seropositive The prevalence of CMV in homosexuals, IVDA, is almost 100% where it is present in all body fluids Contracted from infected saliva, urine and body fluids, blood transfusion, can cross the placenta 20-40 days incubation periods The virus is usually latent in salivary gland, kidney, liver and lung The CMV can cause: congenital CMV: abortion, mental retardation and physical defects and expels the virus in urine for months or years (reservoir for virus) CMV mononucleosis

81 CMV mononucleosis Infection usually subclinical
In healthy individuals it Cause CMV mononucleosis syndrome: Headache Sore throat Back and abdominal pain Atypical Lymphocytosis but Paul- Bunnell test is negative Lymphadenopathy are not conspicuous feature as in EBV

82 In immunocompromised (HIV and kidney transplant) patients infection or activation of latent virus may be very serious as it cause opportunistic infections in: Lung and Liver GIT CNS EYE Treatment is asymptomatic but Ganciclovir is active against CMV AND INDICATED FOR IMMUNOCOMPROMISED patients

83 Coxsackie viruses RNA viruses group A type is responsible for:
Herpangina Hand, foot and mouth disease Acute lymphonodular pharyngitis

84 Herpangina Epidemic & contiguous disease usually seen among school children Transmitted by contaminated saliva and fecal-oral routes Affect mainly children and young adults May present with low grade fever, anorexia, sore throat or dysphagia Orally 4-6 ulcers are predominantly affect post. Part of the oral cavity and soft palate Lymphadenopathy is less common Self limiting ( lasts for few days)

85 Oral lesions of herpangina

86 D.D: HSV HZV herpetiform aphthous ulceration
The main D.D is herpetic gingivostomatitis but in herpengina: occurs in epidemics milder & ulcers are less painful the gingiva is not affected affect post. part of oropharyngeal cavity the smear doesn't show cythopatic changes

87 Hand, Foot and Mouth disease (HFM)
clinical features are similar to herpangina but: Has painful maculo-papular and vesicular lesions on dorsum of palm of hands and soles of feet and between digits and mucosa of the pharynx, soft palate and tongue Diagnosis and management is as herpangina Self limiting disease Foot & mouth disease (of cattle) is quite different rhinovirus infection which rarely affect humans

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