Herpesviruses - Copy.pdf hsii jaio hdio ud

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1. Human Herpesviruses
Infectious Diseases, AIDS & Clinical Immunology Research Center
INFECTIOUS MONONUCLEOSIS

2. •Herpes simplex type I (HHV-1)
•Herpes simplex type II (HHV-2)
•Varicella-zoster virus (VZV/HHV-3)
•Epstein-Barr virus (EBV/HHV-4)
•Cytomegalovirus (CMV/HHV-5)
•Human herpesvirus type 6 (HBLV/HHV-6)
•Human herpesvirus type 7 (HHV-7)
•Kaposi's sarcoma herpesvirus (KSHV/HHV-8)
HUMAN HERPESVIRUS TYPES

3. •HSV-1 causes Oral-facial infections,
Gingivostomatitis and pharyngitis
•HSV-2 is a sexually transmitted infection that causes
genital herpes
•Varicella-zoster virus causes Shingles (herpes zoster) and
Chickenpox
•Epstein-Barr virus causes Infectious mononucleosis
•Cytomegalovirus causes CMV mononucleosis and
immunocompromised host infections
•Human herpesvirus type 6 causes childhood illness
known as roseola infantum or sixth disease.
•Human herpesvirus type 7 cause a skin condition in
infants known as exanthema subitum,
•Human herpesvirus type 8 cause Sarcoma Kaposi's

4. •People who become infected with HSV will
have the virus for the rest of their lives.
Even if it does not manifest symptoms, the
virus will continue to live in an infected
person’s nerve cells. Some people may
experience regular outbreaks. Others will
only experience one outbreak after they
have been infected and then the virus may
become dormant

5. •Even if a virus is dormant, certain stimul can
trigger an outbreak. These include:
•General illness (from mild illnesses to serious
conditions)
•Fatigue
•Physical or emotional stress
•Immunosuppression due to AIDS or
suchmedicationsaschemotherapyorsteroids
•Trauma to the affected area, including sexual
activity
•Menstruation

6. •HSV-1 is transmitted by
oral-to-oral contact to cause
oral herpes

7. •The virus spreads more quickly when
an infected person is experiencing an
outbreak. Anywhere from 30 to 95
percent of adults are seropositive for
HSV-1, though they may never
experience an outbreak.

8. Herpes simplex type I (HHV-1)

9. Herpes simplex type I (HHV-1)

10. •HSV-2 is a sexually transmitted
infection that causes genital
herpes

11. •Pregnantwomen with genital
herpes should talk to their
doctor, as genital herpes can be
passed on to the baby
duringchildbirth.

12. Treatment, Prevention, &Control
•Antiviral drugs acyclovir, valacyclovir, and vidarabine.
•Acyclovir is currently the standard therapy. All are inhibitors of viral DNA
synthesis.
•The drugs may suppress clinical manifestations, shorten time to healing, and
reduce recurrences of genital herpes.
•Drug-resistant virus strains may emerge.
•Experimental vaccines of various types are being developed.
Vidarabine

13. VARICELLA-ZOSTERVIRUS
Varicella (chickenpox) is a mild, highly contagious disease, chiefly
of children, characterized clinically by a generalized vesicular
eruption of the skin and mucous membranes. The disease may be
severe in adults and in immunocompromised children.
Zoster (shingles) is a sporadic, incapacitating disease of adults or
immunocompromised individuals that is characterized by a rash
limited in distribution to the skin supplied by a single sensory
ganglion. The lesions are similar to those of varicella.

14. ➢CHICKENPOX ALSO KNOWN AS
VARICELLA
➢DNA VIRUS
➢MOST COMMON IN WINTER and
SPRING

15. SYMPTOMS
➢LOSS OFAPETITE
➢COLD
➢FEVER
➢ABDOMINALPAIN
➢HEADACHE
➢GENERAL FEELING OFlLLNESS
➢RASH
➢FATIGUE
➢SORETHROAT
➢FEVER MAY BE HIGH FOR FIRST FEWDAYS

16. DIAGNOSIS
BY SIGNS
&
SYMPTOMS
LAB
DIAGNOSI
S

17. LABDIAGNOSIS
➢LAB DIAGNOS IS USUALLY NOT
REQUIRED BUT IF REQUIRED THERE
ARE SOME TESTS.
➢MOST FREQUENT SOURCE OF
ISOLATION IS VESICULAR FLUID.
➢STAINED SMEARS FROM VESICULAR
SCARPINGS.
➢SEROLOGY TESTS FOR VARICELLA
IgM ANTIBODY.
➢ELISA ARE ALSO USEFUL.

18. ETIOLOGY
➢CHICKENPOX – PRIMARY LESION
➢HERPES ZOSTER – REACTIVATED
LESION
➢INCUBATION PERIOD IS 3 WEEKS
➢MOST CONTAGIOUS

19. TRANSMISSION
➢THE VIRUS ENTERS THE BODY BY
INFECTING CELLS IN THE RESPIRATORY
TRACT.
➢IT SPREADS TO MANY OTHER PARTS OF
THE BODY, INCLUDING THE SKIN,WHERE
IT CAUSES THE CHARACTERISTIC RASH.

20. PATHOGENESIS
➢DAY 0-3 - INFECTION OF
CONJUCTIVAE AND MUCOSA OF THE
UPPER RESPIRATORY TRACT.
➢VIRAL REPLICATION INREGIONAL
LYMPHNODES

21. VESICULAR RASH
EXCORIATIO N

22. STAGES OFCHICKENPOX
INCUBATION PERIOD USUALLU(14 -21
DAYS)
PRODROME(1-3 DAYS) VESICLES
PUSTULES
SCABS
RECOVERY TYPICALLY 7 -9 DAYS AFTER
RASH APPEARS

23. ➢A PERSON WITCH CHICKENPOX IS
CONTAGIOUS 1-2 DAYS BEFORE THE
RASH APPERS AND UNTILL ALL
BLISTER HAVE FORMED SCABS.
➢IT MAKES FROM 10-21 DAYS AFTER AN
INFECTED PERSON FOR SOMEONE TO
DEVELOP CHICKENPOX.

24. COMPLICATION
➢BACTERIAL INFECTION OF LESIONS
➢PNEUMONIA
➢HOSPITALIZATION:3 PER 1000 CASES
➢DEATH:1 PER 60000 CASES
➢CNS INVOLVEMENT LEADS TO
ENCEPHALITIS,TRANSVERSE
MYELITIS,GUILLAIN BARRE SYNDROME
AND REYE’S SYNDROME
➢MYOCARDITIS,NEPHRITIS,ARTHRITIS AND
BLEEDING DIATHESES

25. INCREASED RISK OF
COMPLICATION

26. CHICKENPOX DURING PREGNENCY MAY
RESULT IN:
➢CONGENTIAL VARICELLA SYNDROME
➢SEVERE VARICELLA SYNDROME
➢RISK OF NEONATAL DEATH

27. TREATMENT
➢DRUGS USED IN THE TREATMENT OF
CHICKENPOX ARE ANTIVIRALDRUGS,
ANTIHISTAMINES & ANTIPYRETICS.
➢ANTIVIRAL MEDICINES CAN BE TAKEN
ORALLY INTRAVENOUSLY OR APPLIED
ON THE SKIN-OINTMENT.

28. PREVENTION
➢CHICKEN POX OR VARICELLA VACCINE
PROTECT 70% TO 90% OF THOSE PEOPLE
WHO ARE VACCINATED.
➢VARICEELA VACCINE CONTAINS LIVE VIRUS
AND SO IS NOT RECCOMENDED TO
CHILDREN HAVING COMPROMISED IMMUNE
SYSTEM OR SEVERE ILLNESS.
➢THE VACCINE SHOULD NOT BE GIVEN TO
CHILDREN WHO ARE ALLERGIC TO
NEOMYCIN OR GELATIN.
➢THIS VACCINE IS GIVEN TO ADULTS WHICH
ALSO PREVENTS SHINGLES.

29. INFECTIOUS
MONONUCLEOSIS

30. Infectious mononucleosis also known
as kissing disease

31. INFECTIOUS MONONUCLEOSIS
Definition
Infectious mononucleosis, also known as
heterophile-positive infectious mononucleosis
(IM), is viral infection, which is characterized
by fever, sore throat, lymphadenopathy, and
atypical lymphocytosis.

32. Infectious mononucleosis (IM) and Epstein-
Barr virus (EBV)
EBV is a gamma herpes virus.
In developing countries, subclinical infection
in childhood is virtually universal.
In developed countries, primary infection
may be delayed until early adult life.
The virus is acquired from asymptomatic
excreters via saliva, by droplet infection, or
by kissing.
EBV is not highly contagious ,isolation is
unnecessary.

33. EBV is also associated with several human
tumors, including nasopharyngeal carcinoma,
Burkitt’s lymphoma, Hodgkin’s disease, and
(in patients with immunodeficiencies) B cell
lymphoma.

34. History

35. The Epstein–Barr virus was first identified
in Burkitt's lymphoma cells by
Michael Anthony Epstein and
Yvonne Barr

36. •The virus was name
"mononucleosis" because it's
associated with an increase in
certain white blood cells called
lymphocytes in the bloodstream.

37. ETIOLOGY
The virus is approximately 122 nm to 180 nm in
diameter and is composed of a double helix (spiral)
of DNA and containing about 85 genes

38. EPIDEMIOLOGY
•EBV infections occur worldwide.
•These infections are most common in early
childhood
•By adulthood, more than 90% of individuals
have been infected and have antibodies to the
virus.
•IM is usually a disease of young adults

39. Transmission

40. •EBV is spread by contact with oral secretions
(is spread via saliva)
•The virus is frequently transmitted from
asymptomatic adults to infants and among
young adults by transfer of saliva during
kissing.

41. •EBV has been transmitted by blood
transfusion and by bone marrow
transplantation.
•More than 90% of asymptomatic
seropositive individuals shed the virus in
oropharyngeal secretions.

42. PATHOGENESIS

43. The virus then spreads through the bloodstream.
The proliferation and expansion of EBV-infected
B cells along with reactive T cells during IM
result in enlargement of lymphoid tissue.
Polyclonal activation of B cells leads to the
production of antibodies to host-cell and viral
proteins.
EBV infection of epithelial cells results in viral
replication and production of virions.

44. CLINICAL
MANIFESTATIONS

45. •The incubation period for IM
in young adults is ~4–6 weeks
•In young children this period may
be shorter

46. •Fatigue
•Sore throat, which doesn't get better with
antibiotic use
•Fever
•Swollen lymph nodes in the neck and
armpits
•Swollen tonsils
•Headache
•Skin rash
•Splenomegaly , hepatomegaly
SIGNS AND SYMPTOMS OF MONONUCLEOSIS
MAY INCLUDE:

47. The nature of disease defends on the
patients age and immune status
Most EBV infections in infants and young children either
are asymptomatic or present as mild pharyngitis with or
without tonsillitis.
Adolescents and adults develop typical Infectious
mononucleosis syndrome (up to 75% of infections).
Immunecompromised patients can develop
lymphoprolifetarive disease

48. IM in the elderly presents relatively often as nonspecific
symptoms, including:

•prolonged fever,
•fatigue,
•myalgia,
•and malaise.
In contrast, pharyngitis, lymphadenopathy, splenomegaly,
and atypical lymphocytes are relatively rare in elderly
patients.

49. A prodrome of fatigue, malaise, and
myalgia may last for 1–2 weeks
before the onset of fever, sore throat,
exudative pharyngitis and
lymphadenopathy.
A prodrome

50. •Fever is usually low-grade and is most common
in the first 2 weeks of the illness; however, it
may persist for >1 month.
•Lymphadenopathy and pharyngitis are most
prominent during the first 2 weeks of the illness.
• while splenomegaly is more prominent during
the second and third weeks

51. Lymphadenopathy most often affects the posterior cervical
nodes but may be generalized.
Enlarged lymph nodes are frequently tender and symmetric
but are not fixed in place (movable nodes).

52. •Pharyngitis, often the most prominent sign, can be
accompanied by enlargement of the tonsils with an
exudate resembling that of streptococcal pharyngitis.
The pharyngitis is frequently accompanied by enlarged tonsils

54. •A morbilliform or papular rash, usually on the arms or
trunk, develops in ~5% of cases
A morbilliform or papular rash,usually on the arms or trunk

55. InfectiousMononucleosis
IM with rash after treatment with amoxicillin orampicillin

56. •Most patients have symptoms for 2–4 weeks, but
malaise and difficulty concentrating can persist
for months.

57. Signs
•Lymphadenopathy 95 (83–100)
•Fever 93 (60–100)
•Pharyngitis or tonsillitis 82 (68–90)
•Splenomegaly 51 (43–64)
•Hepatomegaly 11 (6–15)
•Rash 10 (0–25)
•Periorbital edema 13 (2–34)
•Palatal enanthem 7 (3–13)
•Jaundice 5 (2–10)
Manifestation
Median percentage of Patients (range)

58. The white blood cell count is usually elevated and peaks
at 10,000 – 20,000/μL during the second or third week
of illness.
Lymphocytosis is usually demonstrable, with >10%
atypical lymphocytes.
The latter cells are enlarged lymphocytes that have
abundant cytoplasm, vacuoles, and indentations of the
cell membrane
Laboratory findings

59. DIAGNOSIS

60. Serologic testing
•Tests for heterophile antibodies are positive in
40% of patients with IM during the first week of
illness and in 80–90% during the third week.
•Tests usually remain positive for 3 months after
the onset of illness, but heterophile antibodies can
persist for up to 1 year.

61. EBV-specific antibody testing
IgM antibody to VCA (viral capsid antigen) is most
useful for the diagnosis of acute IM because it is present at
elevated titers only during the first 2–3 months of the
disease
IgG antibody to VCA is usually not useful for diagnosis of
IM but is often used to assess past exposure to EBV
because it persists for life

62. Complications of
infectious mononucleosis

63. Most cases of IM are self-limited.
Deaths are very rare and most often
are due to complications of infectious
mononucleosis.

64. •Spleenic rupture,
•Upper airway obstruction (because of Hypertrophy of
lymphoid tissue)
•Bacterial superinfection.
•CNS complications (meningitis, encephalitis)
•Autoimmune hemolytic anemia
•thrombocytopenia
•Fulminant hepatitis
•myocarditis or pericarditis
•pneumonia with pleural effusion
Complications

65. TREATMENT

66. •Therapy for IM consists of supportive
measures, with rest and analgesia.
•There is no treatment for mono, but
supportive care involves resting and
drinking plenty of fluids.
•The illness resolves without treatment, but
symptoms may last from several weeks to
months.

67. Prednisone (40–60 mg/d for 2–3 days, with
subsequent tapering of the dose over 1–2 weeks) has
been used for the prevention of airway obstruction
in patients with severe tonsillar hypertrophy, for
autoimmune hemolytic anemia, and for severe
thrombocytopenia.

68. Acyclovir has had no significant clinical impact on
IM in controlled trials. In one study, the
combination of acyclovir and prednisolone had no
significant effect on the duration of symptoms of
IM.

69. THANKS
FOR ATTENTION