virus

1. CMV
(CYTOMEGALOVI
RUS)
NUR FARRA NAJWA BINTI ABDUL AZIM
082015100035

2. OBJECTIVES
At the end of the seminar, all of the student should be able to :
Define what is herpes and CMV
Understand the pathophysiology of herpes and CMV
Describe the morphology of Human Herpes Viruses (HHV)
and its type
Describe the morphology of CMV and its type

3. HERPES

5. INTRODUCTION
Herpes viruses also known as chronic latent infection.
In latent infection, viruses persist in a noninfectious
form, with periodic reactivation and shedding of
infectious viruses.
Latency is defined as the inability to recover infectious
particle from cells that harbor the viruses.
There are 8 type of human herpes viruses, mainly
divided to 3 subgroup based on type of cell frequently
affected and site of latency.

7. CLASSIFICATION OF HERPES VIRUSES
HERPES
VIRUSES
α-group
virus
HSV-1 (HHV-1)
HSV-2 (HHV-2)
VZV (HHV-3)
EPITHELIAL CELLS NEURONS
Lymphotropic
β group
CMV (HHV-5)
HHV-6
HHV-7
VARIETY CELL TYPE
γ group
virus
EBV (HHV-4)
HHV-8
LYMPHOID CELLS LYMPHOID CELLS
HHV ( Human Herpes Virus)
HSV (Human Simplex Virus)
EBV (Epstein Barr Virus)
VZV (Varicella Zoster Virus)

8. HERPES SIMPLEX VIRUSES (HSV) -
PATHOPHYSIOLOGY
 HSV-1 and HSV-2.
 Replicate in skin and mucous membrane at the site of initial inoculation.
 Usually oropharynx or genital, causing vesicular lesion.
 After epithelial infection, virus spread to associated sensory neurons and then by
retrograde axonal transport to the sensory neuron ganglia to establish latent
infection .
 During reactivation, virus spread from regional ganglia back to skin or mucous
membrane.
Classic HSV lesions include large, pink-purple, virion containing
intranuclear inclusion (Cowdry-type A inclusion) as well as inclusion
bearing multinucleated syncytia.

10. MORPHOLOGY (gross)
FEVER BLISTER OR COLD
SORES
Facial skin
around orifice
(lips, nose)
Distributed
bilateral,
Dermatome
independent
Burst or crust,
superficial
ulceration
GINGIVOSTOMATITIS
Children, HSV-1,
Tongue to
retropharynx,
Cervical
lymphadenopthy
INFANTS-
HERPETIC
WHITLOW
GENITAL HERPES
HSV-2 >
HSV-1
Vesicle >>>
superficial
ulcer G
F

12. MORPHOLOGY (gross)
CORNEAL
LESION
KAPOSI
VARICELLIFORM
ERUPTION
ECZEMA
HERPETICUM
NEONATAL
HERPES
N
E
C
K

14. MORPHOLOGY (gross)
HERPES
ENCEPHALITIS
HERPES BRONCHO
PNEUMONIA
HERPES
ESOPHAGITIS
HERPES
HEPATITIS
H4

16. Last but not least… .. . (HSV)
HSV lesion range from self limited cold sores and
gingivostomatitis (HSV-1) to genital sores (HSV-2) to life
treatning disseminated visceral infection (hepatitis and
bronchopneumotitis) and encephalitis
Herpes corneal lesion lead to subsequent neovascularization,
scarring, and corneal opacification lead to blindness

17. HERPES VIRUS HISTOPATHOLOGY (LM)
Large, surrounded by
clear halo
Pink to purple
intracellular inclusion in
balloon cell
Consist of intact and
disrupted virions
Stained host cell
chromatin
Eosinophilic (Cowdry-type A inclusion)

19. CYTOMEGALOVIRUS
(CMV)

20. INTRODUCTION
β group herpes virus, variety disease manifestation
Depending on
Host age
Host immune response
Infect/latent at monocyte and bone marrow progenitors,
reactivated when immune response low.
Infection usually asymptometics in immunocompetant host
but can manifest as mononucleosis like syndrome

22. CMV – PATHOPHYSIOLOGY
It cause marked cellular enlargement characterized by
large intranuclear inclusion surrounded by a clear halo
and smaller basophilic cytoplasmic inclusion
CMV carried in breast milk, respiratory droplet, blood and
saliva and can have, transplacenta venereal, fecal-oral,
transfusion or organ transplantation modes of
transmission
CMV can affect dendritic cell and cause transient but
severe immunosuppressive

23. CMV Cont
Viruses remain latent in leukocyte
CMV mainly cause manifestation in immunosuppressive
patient and infants.
Its common oppurtunistics viral pathogen in AIDS
Survived infant usually deafness and mental retardation

24. 1. CONGENITAL INFECTION
 Acquired in utero/mother with primary
infection
 95% cases asymptometics
 Classic cytomegalic inclusion diseases
 Resembles erythroblastosis fetalis
 Affected infants
Intrauterine growth retard
 ill
Jaundice
Hepatosplenomegaly
Anemia
Bleeding
Microcephaly
Foci of calcification
 Survived infants had permanents deficits
Mental retard
Hearing loss
Pneumonitis, hepatitis, haematologic
disorder
(some recover but mental retard
developed)

25. 2. CYTOMEGALY MONONUCLEOSIS
Asymptomatics in young and healthy children/adult
Had previous exposure to CMV as 50% to 100% in adults
shows antibody to CMV in serum
Common clinical manifestation – in immunocompetent
patient beyond neonatal period is infectious
mononucleosis like illness

26. 3. CMV IN IMMUNOSUPPRESSIVE INDIVIDUAL
Immunocompromised individuals
Transplant patient
HIV-infected people
Recepients of solid organ transplant (CMV from donor)
Can be either primary infection or reactivation of latent
CMV
Can cause life threating colitis or pneumonitis, hepatitis,
chorinretinitis and meningoencphelitis
CMV is common opportunistic viral pathogen in AIDS

27. CMV HISTOPATHOLOGY (LM)
ENLARGEMENT OF
INFECTED CELL
Prominent
Intranuclear
basophilic
inclusion
AFFECTED CELLS
Strikingly enlarged (gigantism)
Surrounded clear halo
Cellular and nuclear pleomorphism

29. SUMMARY
Answer em’!!
What is herpes virus?
What is CMV ?
What is pathophysiology of herpes?
What is pathophysiology of CMV?
What is morphology of Human Herpes Virus (HHV) ?
What is morphology of CMV ?

30. REFERENCES
Robbins and Cotran, Pathology Basis of Diseases, Eight Edition
http://www.histopathology-india.net/HSV.htm
http://www.meddean.luc.edu/lumen/MedEd/orfpath/herpes.
htm
http://www.webpathology.com/image.asp?case=231&n=4
http://learningradiology.com/notes/chestnotes/varicellapage.
htm
http://www.pcds.org.uk/clinical-guidance/eczema-eczema-
herpeticum