A viral infections of mouth


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Clinical Microbiology
Fifth Year

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A viral infections of mouth

  2. 2. Common Oral Conditions • Acquired • Developmental • Congenital
  3. 3. Acquired Oral Conditions • Infections: Viral Bacterial Fungal -Candida • Ulcers • Autoimmune lesions • Glossitis • Discolored teethth
  4. 4. INFECTIOUS DISEASES • DIAGNOSTIC CRITERIA – Obtain medical history – Obtain dental history – Conduct complete clinical examination – Obtain necessary laboratory and radiographic studies.
  5. 5. Viruses causing oral lesions • • • • • • Human Herpes virus(HHV) Human papilloma virus (HPV) Coxasackie virus Mumps virus Measles virus Rubella virus
  6. 6. Human Herpes virus(HHV) • HHV infections are common in oral cavity • 8 types of HHV have been linked with oral disease • HHV 1 – primary herpetic gingivostomatitis, latent infections (common sore) • HHV 2 – oral lesions clinically similar to HHV1 • HHV 3 ; Varicella –Zoster virus (VZV)Chicken pox and Shingles
  7. 7. • HHV 4 ; Ebstein-Barr virus (EBV) - Oral hairy leukoplakia, Infectious mononucleosis, Nasopharyngeal ca, Burkitt’s lymphoma • HHV 5; Cytomegalovirus (CMV)- primary infection of salivary glands • HHV 6&7 - Infects CD4 cells(Roseola infantum) • HHV8 - Kaposi’s sarcoma
  8. 8. General features of Herpes viruses • • • • Herpen = To creep in crops Enveloped, Icosahedral ds DNA viruses Replicate in host cell nucleus. TRANSMISSION – Saliva, direct , skin to skin, skin to mucosal contact (oral genital) • SPREAD – penetrate mucosal epithelial cells, Cutaneous nerve fibers and sensory ganglia • Remain LATENT in infected cells. • Periodic reactivation
  9. 9. HERPETIC GINGIVOSTOMATITIS – HHV 1 • Primary lesions occur in children and adolescents • Many infections are asymptomatic • Lesions – small, multiple, clustered umbilicated vesicles anywhere in and around oral cavity, peri oral skin, pharynx, rupture to form large painful ulcers, • Recurrent herpes lesions – cold sores, keratinized mucosa (lips, gingiva, hard palate) • Other C/F – fever, malaise.
  10. 10. HERPETIC GINGIVOSTOMATITIS • Diagnosis: – Age: Young patients History – First exposure to HSV – Viral culture, serum antibody. EM, PCR, Vesicle develop on the lips, tongue, gingival, palate
  11. 11. • Triggers for recurrence – sunlight exposure, stress physical or emotional systemic illness, trauma(dental procedures) • Travel retrograde sensory neuron to local ganglion, remain latent (trigeminal ,sacral, lumbar ganglion) • Trigeminal neuralgia (HHV1). • HHV-2 causes similar lesions but less common
  12. 12. HHV3 (VARICELLA OR SHINGLES) • • • • • Intra oral and pharyngeal vesicles may occur Virus becomes latent in dorsal root ganglia Recurrent Varicella (Herpes zoster or Shingles) Usually affects single dermatome. In mouth vesicles or ulcerations stop sharply at midline • Prodrome of pain, burning or itching that mimics toothache may occur.
  13. 13. Human herpesvirus (HHV) type 3. Intraoral herpes zoster closely resembles recurrent HHV-1 infection, but the lesions generally follow a dermatome and stop sharply at the midline, as shown here. However, the rules for common sites of occurrence of HHV1 and HHV-3 often do not apply to patients who are immunocompromised.
  14. 14. Ramsay- Hunt syndrome • Seen when HHV3 emerges from latency in geniculate ganglion • Facial nerve (VII) is involved. • C/F – paralysis of facial muscles, levator palati, loss of secretory function, vertigo, tinnitus, pain, vesicles in pharynx eardrum. • Persistent facial nerve weakness or deafness may follow.
  15. 15. HHV 4 (EBV) • Primary infection - Infectious mononucleosis • Infected saliva (kissing disease) Subclinical, young adulthood. • Spreads to B and salivary glands and multiplies • T lymphocytes (If the patient is immunocompetent, cytotoxic T cells become activated and a characteristic lymphadenopathy posterior cervical nodes accompanies tonsillitis and hepatosplenomegaly.) • Latent infection in B cells
  16. 16. • • • • Infectious mononucleosis Nasopharyngeal ca African Burkitt's lymphoma Oral hairy leukoplakia
  17. 17. A 21-year-old woman with infectious mononucleosis presents with a petechial lesion on her palate. Infectious mononucleosis
  18. 18. Oral Hairy leukoplakia (HHV4) • White patches in the mouth • Benign lesion in Immunocompromised adults • Asymptomatic white lesions on the dorsal or ventral,sides of tongue and rarely on buccal mucosa. • Lesions- Greyish white, corrugated, linear appearance, granular or nodular or may have hair like projections. • May be the first manifestation of IC status (HIV) other conditions
  19. 19. • OHL can look like thrush (CANDIDA), • Thrush usually comes off when it is lightly scraped with a toothbrush, whereas OHL does not. • Patches do not usually cause discomfort and generally do not affect the taste of foods or liquids.
  20. 20. HHV 8 (Kaposi’s Sarcoma associated Herpes virus KSHV) • Seen commonly in IC or IS patients, rarely in children. • The lesion may appear as a red, purple or dusky patch that enlarges into a plaque and later progresses into a tumorous mass. • Palate is initial site of intra oral KS, others include gingiva, tongue and Tonsillar area.
  21. 21. HHV-Diagnosis and treatment • • • • • • Most of the times Clinical findings alone Smear of intact vesicle for HHV 1,2 & 3 Direct immunofluorescence(DIFAT) Culture - Cell cultures, Embryonated egg. Biopsy for confirmation of KSHV and others. Molecular methods- PCR,
  22. 22. HHV-MANAGEMENT • HHV1,2 - Analgesics, Acyclovir IN EARLY stages • HHV3 - Acyclovir WITHIN 48-72 hrs, Valcyclovir or Famciclovir better in reducing pain and lessening post herpetic neuralgia, Vaccine (live attenuated)12 months onwards. • EBV – conservative approach for oral hairy leukoplakia (topical PODOPHYLLIN, TRETINOIN less useful, systemic antivirals rarely)
  23. 23. HHV 8 (KSHV) MANAGEMENT • Referred to expert, improve systemic immune status, low dose radiation therapy when lesions are confined to mouth, intra lesional injections of Vinblastine and/or sodium tetra decyl sulfate, and/or interferonalfa(IFN-A) • Regular follow up for immune status
  24. 24. HUMAN PAPILLOMA VIRUS • • • • Papovaviridae family PA PO VA = PApillma, POlyoma, VAcuolisation. Small icosahedral, NE, circular dsDNA virus. Transmission - close skin to skin contact, sexual, oro-genital contact. • Penetrates the mucosal epithelium & invades the cells of basal layer. • Rate of HPV carriage in oral cavity of healthy adults is 5-80%.
  25. 25. • At least 106 types of HPV- High risk (16, 18, 33, 35) and Low risk types(1,2, 3,4, 27, 29, etc…) • HPV 16 associated with dysplasia and carcinoma in oral cavity, cervix. • HPV lesions are more common in IC (HIV) patients • Play role in oral pre malignancy and malignancies (Squamous cell carcinoma)
  26. 26. Common lesions • Verrucca vulgaris or Common warts (HPV types 2, 4) • Condyloma acuminata 0R Genital warts (HPV types 6,11) • Focal epithlial hyperplasia or Heck’s disease(HPV types 13, 32)
  27. 27. A mnemonic for remembering the microscopic and clinical shapes of verruciform oral lesions: • Verruca vulgaris is shaped like a series of inverted V's. • Condyloma acuminata are shaped like a series of C's placed on their sides. • Papillomas are pedunculated like the letter P.
  28. 28. VERRUCCA VULGARIS or COMMON WARTS (HPV2, 4) • The name "verruca" is Latin for wart • A local growth of the outer layer of the skin caused by a virus • White, sessile, verrucous, solitary or multiple elevated lesions with discrete borders. • Common on skin(lips, hard palate or gingiva) • In patients with oral infection, commonly seen on digits.
  29. 29. • Human papillomavirus (HPV). Verruca vulgaris on the lateral border of the tongue exhibits the multiple, sharp-tipped, white, verrucous appearance, which is classic for this lesion in the oral cavity. Not all verrucae are so clinically diagnostic. • This verruca on the retromolar pad shows much less keratinization and a broader base. • Verrucae and papillomas may be difficult to differentiate, but both are usually surgically excised.
  30. 30. This is a verruca vulgaris of the anterior maxillary gingiva in a healthy young male. He had recently resolved a wart on his finger. These small papillomas on the lateral tongue of a young woman showed histologic evidence of HPV in the form of extensive koilocytosis.
  31. 31. Condyloma acuminata or Genital warts (HPV types 6,11) • Can affect oral mucosa, cerebriform, pink, sessile, solitary or multiple. • Occur commonly on non keratinised mucosa(genital area) Condylomata on the lower lip
  32. 32. Focal epithlial hyperplasia or Heck’s disease(13, 32) – Epidemic in young adults. • Multiple smooth sessile nodules and mucosal surface of lower lip or buccal mucosa. •
  33. 33. Laboratory diagnosis • Immunohistochemical detection of HPV structural proteins • Enzyme immunoassays – very sensitive • PCR DNA amplification – excisional biopsy • Histologic findings –koilocytosis, dark shrunken nuclei and cytoplasmic vacuolisation.
  34. 34. Management • Oral lesions are treated with excisional biopsy • Topical agents are used – Cidofovir antiviral • Intralesional injections – Bleomycin (cytotoxic polypeptide that inhibits DNA synthesis in cells and viruses. • IFN-A - Naturally occurring cytokine with antiviral, antibacterial, anticancer and immunmodulatory • Systemic agents – Retinoids or systemic vitamin A anologs • Imiquimod 5% - toll like receptor 7 activator • Vaccine – oral HPV related disease is not yet known.
  35. 35. Coxsackie virus • PicoRNAviridae family, Enterovirus genus • Enteroviruses 4 subgroups – Polio viruses, Coxsackievirus group A,B and ECHO viruses. • Infect humans via fecal-oral route. • Attach to mucosal epithelium in pharynx to ileum. • Spreads to regional lymph nodes cervical and mesenteric – viraemia. • Most infections subclinical, IP 3-5 days
  36. 36. • Hand Foot and Mouth disease – vesicular, eryhematous lesions in mouth(tongue, buccal mucosa, soft palate) hands and fingers, feet and toes. • Herpangina – sudden onset of sore throat, fever and painful swallowing, vesicles on soft palate. • Acute lymphonodular pharyngitis – variant of herpangina, lesions remain papular without progressing to vesicles and ulcers.
  37. 37. HFMD - vesicular eruption in the mouth
  38. 38. HERPANGINA = Painful mouth and throat ulcers
  39. 39. Diagnosis and Management • Diagnosed mainly on clinical grounds. • Confirmed by Virus isolation(cell culture, most widely used), PCR, serological testing. • Treatment not required usually, prevent secondary infections, topical anesthetics and coating agents, analgesics paracetamol.
  40. 40. Rubella (German measles) • RNA virus, Family Togaviridae, genus Rubi virus • Unstable virus killed by lipid solvents trypsin, formalin, UV light and extreme Ph. • Acute exanthematous viral infection similar to Measles infection. • Spread – droplet (Inhalation), replicates in nasopharynx and lymph nodes
  41. 41. Clinical features • Lymphadenopathy (major manifestation)- post auricular, post cervical and sub occipital lymph nodes. • Intraorally (Forchheimer sign) – dark red papules on soft palate, arise at onset of rash, enanthem consisting petechial lesions, seen in 20% of cases.
  42. 42. Forchheimer sign- Petechial lesions in mouth
  43. 43. Diagnosis and management • • • • Clinical evaluation Virus isolation ELISA for IgM, IgG antibodies. Vaccine – live attenuated vaccine available (MMR)
  44. 44. Mumps • • • • • • Paramyxoviridae family, genus Rubula virus Endemic through out the world. Transmission- droplets, direct contact, fomites URT & Regional lymph nodes. Viraemia – glandular and neural tissues. Epidemic parotitis , acute generalized infection in children 5-15 years.
  45. 45. Clinical features – Parotitis • Low grade fever, malaise, headache, earache tenderness of parotid glands simoultaneously on both sides. • Recurrent acute and chronic sialadenitis are complications. • Earlobes on affected side lifted upwards and outwards • Trismus – difficulty in eating and speaking • Intraorally enlargement and redness of opening of Stensen’s duct.
  46. 46. Complications • CNS – Aseptic meningitis(asymptomatic 60%), headache, neck stiffness in 15% • Orchitis (testicular inflammation) 20-50% post pubertal males, atrophy in 50% , sterility is uncommon. • Pancreatitis - uncommon complication • Deafness - acquired sensory neural deafness
  47. 47. Diagnosis and management • Clinical diagnosis • Supportive – analgesics, liqid diet, isolation, bed rest • Prevention – Live attenuated vaccine( Jeryl – Lynn strain) given with Measles and Rubella, at least 2 doses before 4-6 years, life long immunity.
  48. 48. Measles (Rubeola) • • • • Family Paramyxoviridae, genus Morbillivirus Acute, highly contagious disease in children Spread – droplets from respiratory secretions Initial site of infection is upper respiratory tract epithelium, lymph nodes  primary viraemia  Reticulo Endothelial System. • Secondary viraemia after breakdown and necrosis of RES cells
  49. 49. Clinical features • IP 10-14 days, Exanthematous fever, and cough, coryza, • Rash – erythematous, maculopapular spreading from head to toe direction. • Koplik’s spots pathognomonic for measles. • Located on buccal mucosa in premolar and molar area, bluish grey pecks against Erythematous background (rains of sand) • Plaque like or nodular and oval or round
  50. 50. Koplik spots in measles. They are small, white spots (often on a reddened background) that occur on the inside of the cheeks early in the course of measles.
  51. 51. Diagnosis and Management • Virus isolation- blood, urine, nasopharyngeal • Serology – IgM detection. • Histology - Warthin- Finkeldy cells MNG cells, neutrophils in koplik spots • PCR • Antibiotics for secondary bacterial infections, Vit A, Ribavirin in Immunocompromised • Prevention – MMR vaccine(EdmonstonEnders strain)
  52. 52. Complications • No oral complications have been reported. • Diarrhea, otitis media, pneumonia are common. • Sub acute sclerosing pan encephalitis (SSPE) – CNS disease years after primary infection, progressive deterioration of higher functions, seizures, motor functions eventually death.