various viral infection t heir manifestations prevention treatment

1. C
VIRAL INFECTIONS
IN THE ORAL CAVITY

2. C
HERPES SIMPLEX
VIRUS(HSV)

3. • Herpes simplex virus infections are vesicular eruptions of the skin and mucosa that occur
in two forms:
• Primary as a result of initial infection of an uninfected person.
• Secondary as the result of viral reactivation in a previously infected
individual.

4. Etiology and Pathogenesis:
• The infection spreads through:
• Physical contact with an infected person
• Exposure to body fluids

5. • During the primary infection, only a small percentage of individuals show
clinical signs and symptoms of infectious systemic disease, however the
vast majority face subclinical diseases which can be identifies by
laboratory detection of antibodies to HSV.

6. • The incubation period after exposure ranges between several days to two
weeks.
• A vesiculoulcerative eruptions( primary gingivostomatitis) occur in the oral
and perioral tissues usually at the original site of contact.

7. • To be capable of remaining in a latent/sequestered state, the virus migrate along the
periaxonal sheath of the trigeminal nerve to the trigeminal ganglion.
• During latency, no infectious/free virus is produced.

8. The reactivation of HSV may follow:
• Exposure to sunlight(fever blisters)
• Prior to a cold (cold sores)
• Trauma
• Menstrual cycle
• Stress
• Immunosuppression

9. Clinical Features:
• Vesicular eruptions on skin, vermilion, and oral mucous membranes.
The recurrent form of the disease:
• Lesions are confined to the lips, hard palate, and gingiva.

10. Primary lesions are accompanied by:
 Fever
Malaise
Headache
Cervical lymphadenopathy.

11. Patients usually have prodromal symptoms of:
Tingling
Burning
Pain in the site of lesion

12. Diagnosis:
• Tzank smear ( this test is helpful only if it is positive)
• Serology
• Viral culture
• Immunohistochemistry
• Polymerase chain reaction testing

13. Treatment:
• Acyclovir and its analogs have shown the greatest efficacy in treating HSV infection.
NOTE: Any drug essential to be used as soon as possible after the detection of the prodromal
features.

14. C
HERPANGINA

15. Etiology and Pathogenesis:
• Herpangina, also called mouth blisters, is a painful viral mouth infection produced by several
coxsackie type A virus. It is similar to hand-foot mouth disease (HFM) and it is characterized by
small, blister like ulcers on the roof of the mouth and in the back of the throat. These viruses are
highly infectious and can easily be transmitted from person to another by infected saliva and
sometimes through contaminated feces. Herpangina is more common in children aged 3 to 10 than
in adults and usually occur in summer or early autumn.

16. Clinical Features:
• Herpangina is a vesicular eruption inside the mouth in certain places especially the soft palate and
tonsillar pillars. The lesions start as red macules then vesicles and lastly to ulcerations which can be
2-4 mm in size. The symptoms of herpangina can include:
1. Sudden onset of fever
2. Sore throat
3. Headache
4. Neck pain
5. Swollen lymph glands
6. Difficulty in swallowing
7. Loss of appetite
8. Drooling ( in children)
9. Vomiting (in children)

17. Diagnosis:
• Diagnosis can be made from clinical signs and symptoms. The vesicular eruption which have
mild symptoms occurring in summer or early autumn, and with diffuse pharyngitis distinguishes
the condition from streptococcal pharyngitis, and the systemic symptoms distinguish it from
apthous stomatitis. Laboratory verification can be completed by virus isolation or by detection
of serum antibodies

18. Treatment:
• Herpangina is a self-limiting, mild and of a short duration virus so treatment ahead of limited
measures is typically not required. Antibiotics aren’t an effective form of treatment instead some
measures may be taken into consideration such as:
• Usage of Ibuprofen or acetaminophen
• Usage of topical anesthetics such as lidocaine
• Increased fluid intake especially cold milk and water

19. C
VARICELLA-ZOSTER
INFECTION
Name: Alaa Mohammad Nasreddine
ID number: 201500465
Section A

20.  Varicella-Zoster infection is one of the herpesviruses that infects humans. It affects humans only.
 In seronegative individuals, primary varicella zoster infection is known as Varicella or Chickenpox
mostly affects childrens, teens, and young adults , whereas in secondary or reactivated disease is
known as Herpes Zoster or Shingles affecting older adults and very rare in childrens.

21.  This virus is very similar to Herpes Simplex virus with the DNA core, protein capsid, and lipid
envelope.
 Varicella-Zoster infection multiplies in lungs and causes many symptoms. After primary infection
(chickenpox) the virus goes dormant in the nerves, including the cranial nerve ganglia, dorsal root
ganglia, and autonomic ganglia. Many years after the patient has recovered from chickenpox, the
zoster virus can reactivate to cause neurologic conditions.

22. Pathogenesis:
 Varicella is transmitted predominantly through direct contact by contaminated droplets from skin lesions
or by inhalation of aerosolized virus. Virus can spread from one person to another. It eventually, in a
normal host, the immune response is able to limit the replication of this virus.
 The infection is self limiting and lasts for several weeks.
 Oral mucous membranes are involved in the primary disease and usually are described as shallow
ulcers that are preceded by evanescent vesicles.
 The sensory nerves of the trunk and head and neck are commonly infected. This involvement of
various branches of the trigeminal nerve may results in unilateral oral, facial, or ocular lesions.

23.  Varicella, or chickenpox, develops after an individual is exposed to VZV for the first time
especially during childhood. Symptoms range from fever, headache, stomach ache, or loss of
appetite before breaking out in the classic pox rash. This rash quickly develops into vesicular
eruptions that becomes ulcerations eventually. Chickenpox usually occurs in late winter and
early spring months.

24. o During the second week of incubation, virus proliferates within macrophage causing viremia and
dissemination of skin and organs. Host defense mechanism of non specific interferon production and
specific humeral and cell mediated immune response are triggered.
o Herpes Zoster: During the disease process, VZV may progress along sensory nerves to the sensory
ganglia where it hides as a latent. Reactivation of this latent Virus characterized by decline in cell
mediated immunity with the presence of immunosuppressed resulting from malignancy, drug
administration, HIV infection, radiation, surgery of spinal cord or local trauma leads to this lesion.

25.  Differential diagnosis: Varicella is clinically diagnosed by the history of exposure and by the type
and distribution of lesions. Both chickenpox (varicella) and shingles (zoster) can usually be diagnosed
by symptoms. If a diagnosis is still unclear after a physical examination, laboratory diagnostic tests
may be required. These tests use samples of fluid taken from the blister.
Chickenpox vaccine:
The live-virus varicella vaccine (Varivax) produces immunity against chickenpox. The vaccine can
prevent chickenpox or reduce the severity of the illness if it is used within 3 days, and possibly up to
5 days, after exposure to the infection.
Shingles Vaccine:
The herpes zoster (shingles) vaccine (Zostavax) is a stronger version than the chickenpox vaccine.
Because the vaccine contains live virus, it cannot be administered to people with weakened
immune systems. A single shot of the vaccine can reduce the risk of developing shingles by 55 -
70%

26. How do you prevent shingles from spreading?
1.Keep the rash covered.
2.Avoid touching or scratching the rash.
3.Wash your hands often to prevent the spread of varicella zoster virus.
How can you avoid getting shingles?
To prevent shingles, adults who are 60 years old and older should receive the shingles vaccine. To
relieve pain, you can apply a cool washcloth to the blisters. Keep the rash covered as much as possible to
avoiding spreading the varicella virus to others

27. The first symptoms of shingles are usually pain and burning. The pain is usually on one side of the body and
occurs in small patches. A red rash typically follows.
 Rash characteristics include:
•Red patches
•Fluid-filled blisters that break easily
•A rash that wraps around from the spine to the torso
•A rash on the face and ears
•Itching
 Some people experience symptoms beyond pain and rash with shingles. These symptoms may
include:
•A fever
•Chills
•A headache
•Fatigue
•Muscle weakness
 Rare and serious complications of shingles include:
•Pain or rash that involves the eye, which should be treated in order to avoid permanent eye damage
•Loss of hearing or intense pain in one ear, dizziness, or loss of taste on your tongue, which can be symptoms
of ramsay hunt syndrome
•Bacterial infections, which you may have if your skin becomes red, swollen, and warm to the touch

28. C
EBV
&
ORAL HAIRY LEUKOPLAKIA
(HL)

29. What is EBV ?
• EBV is the Epstein Barr Virus belonging to the herpes family, also known as human herpesvirus 4.
• Disease Names:
• Infectious mononucleosis (Heterophile-positive)
• Burkitt’s lymphoma
• AIDS-related lymphoma
• Posttransplant lymphoproliferative disease (PTLD)
• Nasopharyngeal carcinoma

30. • It is one of the most common human viruses. EBV is found all over the world. Most people get
infected with EBV at some point in their lives(90% of the population has been infected by EBV)
.
How common is EBV?

31. EBV Symptoms?
• Fatigue
• Fever
• Inflamed Throat
• Swollen Lymph Nodes In The Neck
• Swollen Liver
• Enlarged Spleen
• Rash

32. EBV symptoms observation
• Many people become infected with EBV in childhood.
• EBV infections in children usually do not cause symptoms, or the symptoms are not distinguishable
from other mild, brief childhood illnesses.
• People who get symptoms from EBV infection, usually teenagers or adults, get better in 2-4 weeks.
However, some people may feel fatigued for several weeks or even months.
• After you get an EBV infection, the virus becomes latent (inactive) in your body.
• In some cases, the virus may reactivate. This does not always cause symptoms, but people with
weakened immune systems are more likely to develop symptoms if EBV reactivates.

33. How is EBV transmitted?
EBV spreads most commonly through:
1. Bodily fluids; especially saliva ( oropharyngeal secretions).
However, EBV can also spread through:
1. Blood or blood transfusions (rarely)
2. Semen
3. During sexual contact
4. organ transplantations.

34. Can EBV spread from infected person’s used objects?
• EBV can be spread by using objects, such as a toothbrush or drinking glass, that an infected
person recently used or even by having contact with toys that children have drooled on.
• The virus probably survives on an object at least as long as the object remains moist.
At-Risk Populations:
• Typically greater risk of disease in immunocompromised hosts or following bone marrow or solid
organ transplantation.

35. Lifespan of EBV
• The first time you get infected with EBV (primary EBV infection) you can spread the virus for
weeks and even before you have symptoms.
• Likelihood of secondary transmission is moderate.
• Once the virus is in your body, it stays there in a latent (inactive) state. If the virus reactivates,
you can potentially spread EBV to others no matter how much time has passed since the initial
infection.

36. EBV diagnosis?
• Diagnosing EBV infection can be challenging since symptoms are similar to other illnesses.
• EBV infection can be confirmed with a blood test that detects antibodies. About 9out of 10 of
adults have antibodies showing a current or past EBV infection.

37. EBV vaccination?
• There is NO vaccine to protect against EBV infection.
How to protect yourself against EBV?
• You can help protect yourself by not kissing or sharing drinks, food, or personal items,
like toothbrushes, with people who have EBV infection.

38. EBV treatment?
• There is no specific treatment for EBV.
• However, some things can be done to help relieve symptoms, including:
1. Drinking fluids to stay hydrated.
2. Getting plenty of rest.
3. Taking over-the-counter medications for pain and fever.

39. What is hairy Leukoplakia?
• Hairy leukoplakia is a form of leukoplakia, which refers to white patches on the mucous
membranes of the mouth often arising in response to chronic irritation.
o It is characterised by: Irregular, Non-movable, corrugated or "hairy" white lesion on the lateral
margins of the tongue and occasionally elsewhere on the tongue or in the mouth. (No report
describes HL in mucosal sites other than the mouth.)
o HL is in group 4, category C2 of the original Centers for Disease Control (CDC) definition of AIDS and in B3
of the 1993 criteria.

40. Clinical Appearance and Manifestations?
• HL lesions vary in size and appearance and may be unilateral or bilateral.
• The surface is irregular and may have prominent folds or projections, sometimes markedly resembling
hairs. Occasionally, however, some areas may be smooth and flat.
• Lesions occur most commonly on the lateral margins of the tongue and may spread to cover the entire
dorsal surface . They may also spread downward onto the ventral surface of the tongue, where they
usually appear flat.
• HL lesions can also occur on the buccal mucosa, generally as flat lesions. Rarely, lesions occur on the
soft palate.
• HL usually does not cause symptoms.

42. Who has Hairy leukoplakia?
o Occurs in all risk groups for HIV infections, although less commonly in children than
in adults and is usually also associated with EBV infection.
o HL occurs in about 20% of persons with asymptomatic HIV infection and becomes
more common as the CD4+ T-cell count falls.
o HL has occurred in non-HIV-infected people including recipients of bone marrow,
cardiac, and renal transplants.

43. Diagnosis?
• HL should be diagnosed by biopsy for definitive diagnosis. Experienced clinicians can make a
presumptive diagnosis of HL in association with HIV disease from the clinical appearance,
although HL can be confused with oral candidiasis.
•

44. Is there a treatment?
• Hairy leukoplakia usually is asymptomatic and does not require treatment.
• HL is almost always a manifestation of HIV infection, and clinicians should arrange evaluation
of HIV disease and appropriate treatment for patients with HL.
• HL has disappeared in patients receiving high-dose acyclovir for herpes zoster, presumably
because of the anti-EBV activity of acyclovir. Doses of acyclovir (2.5 to 3 mg per day for 2 to 3
weeks) usually eliminate HL, but the lesion usually recurs with cessation of treatment.
• Occasionally, Candida albicans may be found in HL lesions. Treatment consists of antifungal
medications.

45. C
MEASLES

46. Etiology and Pathogenesis:
• Measles is a viral infection caused by the genus morbillivirus, a member of the paramyxovirus family. The
virus known simply as measles virus which is an RNA-enveloped virus that is related structurally and
biologically to viruses that also cause mumps and influenza.

47. • Typically, the measles rash consists of:
 Early pinpoint elevations over the soft palate with an ultimate involvement of the pharynx and tonsils.
• German measles Or Rubella, is caused by unrelated virus of the togavirus family. It shares some clinical features
with measles, such as fever and rash.
• Clinical features:
• Because of the widespread vaccination programs , those at risk of infection are individual who have not been
vaccinated.
• In 1 to 2 days, pathognomonic small erythematous macules with white necrotic centers appear in the buccal
mucosa known as Koplik’s spots.
• The rash initially affects the head and neck followed by the trunk, and then the extremities.
• Secondary infection may develop as otitis media or pneumonia.

48. Histopathology:
• Infected epithelial cells, which eventually become necrotic, overlie an inflamed connective tissue that
contains dilated vascular channels and a focal inflammatory response. Lymphocytes are found in
perivascular distribution.
• In lymphoid tissues and tonsils large characteristic multinucleated macrophages which are known as
Warthin-Finkeldey giant cells are observed.

49. Differential Diagnosis:
• Besides the prodromal symptoms and rash which are sufficient evidence of measles, laboratory
criteria for diagnosis include several tests including positives measles immunoglobins M (IgM),
immunoglobin G (IgG), isolation of the measles virus.

50. Treatment:
• No specific treatment for measles is known. Supportive therapy of bed rest, fluids, adequate
diet and analgesic are described.
•

51. C
CYTOMEGALOVIRU
S

52. •Cytomegalovirus (from the Greek cyto-, "cell", and -megalo-, "large") is a viral genus of
the viral family known as Herpesviridae or herpes viruses.
•The species that infects humans is commonly known as human CMV (HCMV) or human
herpesvirus-5 (HHV-5), and is the most studied of all cytomegaloviruses

53. Properties of the CMV
• Belong to the betaherpesvirus subfamily of herpesviruses
• Double stranded DNA enveloped virus
53

54. tegument
200 nm
envelope
glycoproteins
capsid
DNA core
Human Cytomegalovirus Virion
Structure

55. Why are herpes viruses (and especially CMV) so fascinating
from an evolutionary standpoint?
1. They are ancient
2. Latency = highly evolved
3. While many viruses deal with evolution “passively” (i.e. mutate), herpesviruses
“actively” target mechanisms

56. Human Cytomegalovirus
•A complex -herpes virus
•Slow replicating
Infects 60-90% of the population worldwide, typically asymptomatic
infection
Infection in immunocompromised individuals life threatening:
•Stem cell and solid organ transplant recipients
•HIV infected individuals
56

57. Spread of CMV
CMV spreads from person to person through body fluids, such as blood, saliva, urine,
semen and breast milk. CMV spread through breast milk usually doesn't make the baby
sick. However, if pregnant and develop an active infection, can pass the virus to baby.

58. Consequences of CMV Infections
• Cancer patients receiving intensive chemotherapy treatments can get infected
• Mild to severe hearing loss
• Cognitive deficits
• Physical abnormalities
58

59. Pathogenesis
•Once infected, the virus remains in the person for life and my be
reactivated from time to time, especially in immunocompromised
individuals.
•The virus may be transmitted in utero, perinatally,or postnatally.
Perinatal transmission occurs.
•.

60. Complications
•Intestinal complications.
•CMV infection of intestines can result in
diarrhoea, fever and abdominal pain;
inflammation of colon; and blood in
stool.

61. Laboratory Diagnosis
• Virus isolation
• Conventional cell culture is regarded as gold standard but requires
up to 4 weeks for result.
• More useful are rapid culture methods such as the deaff test which
can provide a result in 24-48 hours.
• Serology
• The presence of cmv igg antibody indicates past infection.
• The detection of igm is indicative of primary infection although it
may also be found in immunocompromised patients with
reactivation. 61

62. Treatment
•Perinatal and postnatal infection - it is usually not necessary to treat such patients.
•Immunocompromised patients - it is necessary to make a diagnosis of CMV infection
early and give prompt antiviral therapy. Anti-CMV agents in current use are ganciclovir,
forscarnet, and cidofovir.

63. Prevention
•CMV infection can be contagious if the infected person comes in close or
intimate contact with another person. One should avoid kissing and sexual
contact with an infected person.
•The virus may also spread among young children in day care
settings.
•When planning blood transfusions or organ transplants, the CMV status of the
donor can be checked to avoid passing CMV to a recipient who has not had
CMV.

64. Thank you!