Herpes Viruses Lecture
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HERPES VIRUSES
Properties
Enveloped, dsDNA Viruses
Replication in nucleus of host cell
Have a similar morphology (Icosahedral).
Causes primary and latent infection
Reactivation occurs during immunosuppressive condition.
Classification
Alpha herpesvirus Herpes
simplex virus type 1 Herpes simplex virus type 2 Varicella-zoster virus
Beta herpesvirus cytomegalovirus Human
HSV-1 HSV-2 VZV
herpesvirus type 6
CMV HHV-6
Gamma herpesvirus Epstein-Barr
virus Human herpesvirus type 8
EBV HHV- 8
HERPES SIMPLEX VIRUS
Herpes simplex virus
HSV-1 infect the upper part of the body.
HSV-2 infect the lower part of the body genital infections
There is little cross protection.
HSV-1 and HSV-2 can be differentiated by DNA sequencing and type specific antisera.
Herpes simplex virus
Transmission:
HSV-1 is transmitted primarily by saliva and HSV-2 by sexual contact.
Vice versa can occur due abnormal sexual practice.
Neonates can be infected during passing through the infected birth canal.
Pathogenesis Entry by skin or mucous membranes viral multiplication
sensory nerve
lysis of cells
root ganglia HSV-1 → Trigeminal ganglia & HSV-2 → Lumbosacralganglia
vesicles ulcers
latency Reactivation
Cold, Fever, Surgery Unknown
Pathogenesis
Reactivation:
Many factors can provoke a recurrence
These include: physical or psychological stress, infection, fever, irradiation, sunlight, and menstruation.
Clinical condition HSV is involved in a variety of clinical manifestations which includes: 1. Acute gingivostomatitis 2. Herpes Labialis (cold sore) 3. Ocular Herpes 4. Herpes Genitalis 5. Other forms of cutaneous herpes 7. Meningitis 8. Encephalitis 9. Neonatal herpes
Clinical condition
Gingivostomatitis:
Characterized by fever, irritability and vesicular lesion in mouth.
Usually a self limiting disease which lasts around 2-3 weeks.
Clinical condition Herpes labialis (cold sore) Characterized by cops of vesicles at mucocutaneous junction of the lips or nose.
Clinical condition Ophthalmic: Keratoconjunctivitis Corneal ulcers Repeated attacks can lead to blindness
Clinical condition Cutaneous lesions Among the health care workers Painful lesions no pus Eczema herpeticum occurs in patients with eczema. Herpetic whitlow typically affect the fingers.
Clinical condition
Genital lesion:
Painful vesicular lesions ingenital area.
Sites: penis, vulva, vagina, cervix, anus, urethra, prostate etc.
May be asymptomatic
Clinical condition Neonatal herpes: Both HSV-1 & HSV-2 can cause severe infection acquired Infection may be milder form like: lesions in the skin, mouth & eyes or severe disseminated infection (encephalitis). Severe infection occurs if mother suffers from primary infection. Can be prevented by cesarean section.
Clinical condition
Encephalitis:
Caused by HSV-1 & is characterized by fever, headache, vomitting & neurological symptoms.
Lab. diagnosis:
Specimens: aspirate from vesicle, scraping from base of ulcer & serum / CSF for antibody.
Virus can be isolated by cell culture & confirmed by detecting cytopathic effect.
Detection of multinucleated giant cell.
Viral DNA can be dtected by PCR.
Electron microscopy of vesicle fluid - rapid result but cannot distinguish between HSV and VZV
Immunofluorescence of skin scrappings - can distinguish between HSV and VZV
Thank You
Varicella zoster
Varicella zoster
Double stranded DNA, enveloped virus
One antigenic serotype only.
Humans are natural Host.
Transmission:
Highly contagious disease.
Transmitted through respiratory droplet & direct contact.
Pathogenesis of Varicella Entry & replicate in mucosa of upper respiratory tract Primary viremiaspread to skin skin rash: macule > papule > vesicle > crust Virus latent in sensory (Dorsal) ganglion Later life virus reactivate & causes Zoster
Varicella; skin rash ■Incubation period 1421 days. ■ Mild prodrome: fever, malaise. ■ Rash appears on trunk & spread to head & extremities ■Itching is prominent during rash.
Varicella; skin rash
Herpes Zoster (Shingles)
Reactivation of varicella zoster virus can occur years or even decades after illness with chickenpox.
Painful vesicles along the course of a sensory nerve.
Generally associated with anything that causes reduced immunocompetence.
Congenital Varicella Syndrome
Greater risk usually occur in the 1st trimester of pregnancy with primary infection of VZV
Varicella syndrome;
low birth weight,
atrophy of extremity with skin scarring,
brain and eye defects
deafness
Varicella zoster Complications Bacterial infection of skin lesions
Pneumonia (viral or bacterial)
Central nervous system manifestations
Reye syndrome
post-infetion encephalitis
congenital and neonatal varicella
Pain and hyperaesthesia
Pain and hyperaesthesia
Laboratory Diagnosis of VZV Detection of multinucleated giant cell. Direct detection electron microscopy; vesicle fluid immunofluorescence; skin scrapping Serology IgG -> past infection IgM -> recent primary infection Definitive diagnosis by isolation of virus by culture. Rapid varicella virus identification using PCR
Prevention
Varicella vaccine contains live, attenuated virus approved for persons 1-2 years of age.
Measles-mumps-rubella-varicella vaccine approved for children 12 months through 12 years.
Vaccine prevents vericella but not zoster.
EPSTEIN BARR VIRUS (EBV)
EPSTEIN BARR VIRUS
Morphologically identical but antigenically different to other herpes virus.
Humans are the natural host.
Primary infection & latency occurs in B lymphocytes.
EPSTEIN BARR VIRUS
Transmission: Occurs by kissing & exchange of saliva.
Affects adolescents and young adults
worldwide distribution.
EPSTEIN BARR VIRUS
EBV causes: Infectious mononucleosis, Burkits lymphoma, Other B cell lymphoma, Nasopharyngeal carcinoma & Hairy leukoplakia in AIDS patients.
Symptoms The classic triad of mononucleosis is: sore throat, Fever Lymphadenopathy (usually in the neck, groin or under the arms)
Symptoms Other symptoms include: Fatigue and malaise Rash Enlargement of the spleen and liver Hepatitis & encephalitis can develop.
Symptoms Hairy Leukoplakia
Oral Hairy Leukoplakia
Nonmalignant hyperplastic lesion of epithelial cells
Burkitts lymphoma
It usually occurs in children aged 3-14 years.
BL cells show translocation of c-myc oncogene between the long arm of chromosome 8 and chromosomes 14.
Lab. diagnosis Hematological: Atypical lypmhocytosis. Immunolobical: Monospot test, agglutination test to detect hetarophil antibody (Monospot test relies on the agglutination of horse RBCs by heterophile antibodies in patient's serum). EBV specific IgM & IgG detection. Paul-Bunnell test: Determination of the highest dilution of the patient's serum (heterophile antibodies) will agglutinate sheep erythrocytes.
Cytomegalovirus (CMV)
Cytomegalovirus Cytomegalovirus or Human Herpesvirus 5 Single serotype. Forms giant cell hence called “cytomegalo”.
Cytomegalovirus Transmission: Fetus: from mother via placenta Infant: during birth or breast feeding. From person to person through saliva, urine, or other bodily fluids. Can be transmitted by sexual intercourse Also transmitted by transplanted organs, and rarely from blood transfusions.
Clinical finding
CMV infection of newborn: When infection occurs in 1st trimester, neonate suffers from an asymptomatic infection to a disease with fever, hepatosplenomegaly, mental or motor retardation and sometimes death.
In immunocompetent adult: causes heterophilnegative infectious mononucleosis without sore throat.
Clinical finding
In immunocompromised persons: It may include CMV retinitis, diarrhea , respiratory infection, and encephalitis.
Lab. diagnosis Isolation of virus. Detectionof nucleic acid by PCR. Fluorescence microscopy. Antibody titre. Microscopic detection of giant cell.
HUMAN HERPES VIRUS 8
HHV8 Transmitted
sexually or by organ
transplant. Causes kaposis sarcoma in AIDS patients.
Properties
Enveloped, dsDNA Viruses
Replication in nucleus of host cell
Have a similar morphology (Icosahedral).
Causes primary and latent infection
Reactivation occurs during immunosuppressive condition.
Classification
Alpha herpesvirus Herpes
simplex virus type 1 Herpes simplex virus type 2 Varicella-zoster virus
Beta herpesvirus cytomegalovirus Human
HSV-1 HSV-2 VZV
herpesvirus type 6
CMV HHV-6
Gamma herpesvirus Epstein-Barr
virus Human herpesvirus type 8
EBV HHV- 8
HERPES SIMPLEX VIRUS
Herpes simplex virus
HSV-1 infect the upper part of the body.
HSV-2 infect the lower part of the body genital infections
There is little cross protection.
HSV-1 and HSV-2 can be differentiated by DNA sequencing and type specific antisera.
Herpes simplex virus
Transmission:
HSV-1 is transmitted primarily by saliva and HSV-2 by sexual contact.
Vice versa can occur due abnormal sexual practice.
Neonates can be infected during passing through the infected birth canal.
Pathogenesis Entry by skin or mucous membranes viral multiplication
sensory nerve
lysis of cells
root ganglia HSV-1 → Trigeminal ganglia & HSV-2 → Lumbosacralganglia
vesicles ulcers
latency Reactivation
Cold, Fever, Surgery Unknown
Pathogenesis
Reactivation:
Many factors can provoke a recurrence
These include: physical or psychological stress, infection, fever, irradiation, sunlight, and menstruation.
Clinical condition HSV is involved in a variety of clinical manifestations which includes: 1. Acute gingivostomatitis 2. Herpes Labialis (cold sore) 3. Ocular Herpes 4. Herpes Genitalis 5. Other forms of cutaneous herpes 7. Meningitis 8. Encephalitis 9. Neonatal herpes
Clinical condition
Gingivostomatitis:
Characterized by fever, irritability and vesicular lesion in mouth.
Usually a self limiting disease which lasts around 2-3 weeks.
Clinical condition Herpes labialis (cold sore) Characterized by cops of vesicles at mucocutaneous junction of the lips or nose.
Clinical condition Ophthalmic: Keratoconjunctivitis Corneal ulcers Repeated attacks can lead to blindness
Clinical condition Cutaneous lesions Among the health care workers Painful lesions no pus Eczema herpeticum occurs in patients with eczema. Herpetic whitlow typically affect the fingers.
Clinical condition
Genital lesion:
Painful vesicular lesions ingenital area.
Sites: penis, vulva, vagina, cervix, anus, urethra, prostate etc.
May be asymptomatic
Clinical condition Neonatal herpes: Both HSV-1 & HSV-2 can cause severe infection acquired Infection may be milder form like: lesions in the skin, mouth & eyes or severe disseminated infection (encephalitis). Severe infection occurs if mother suffers from primary infection. Can be prevented by cesarean section.
Clinical condition
Encephalitis:
Caused by HSV-1 & is characterized by fever, headache, vomitting & neurological symptoms.
Lab. diagnosis:
Specimens: aspirate from vesicle, scraping from base of ulcer & serum / CSF for antibody.
Virus can be isolated by cell culture & confirmed by detecting cytopathic effect.
Detection of multinucleated giant cell.
Viral DNA can be dtected by PCR.
Electron microscopy of vesicle fluid - rapid result but cannot distinguish between HSV and VZV
Immunofluorescence of skin scrappings - can distinguish between HSV and VZV
Thank You
Varicella zoster
Varicella zoster
Double stranded DNA, enveloped virus
One antigenic serotype only.
Humans are natural Host.
Transmission:
Highly contagious disease.
Transmitted through respiratory droplet & direct contact.
Pathogenesis of Varicella Entry & replicate in mucosa of upper respiratory tract Primary viremiaspread to skin skin rash: macule > papule > vesicle > crust Virus latent in sensory (Dorsal) ganglion Later life virus reactivate & causes Zoster
Varicella; skin rash ■Incubation period 1421 days. ■ Mild prodrome: fever, malaise. ■ Rash appears on trunk & spread to head & extremities ■Itching is prominent during rash.
Varicella; skin rash
Herpes Zoster (Shingles)
Reactivation of varicella zoster virus can occur years or even decades after illness with chickenpox.
Painful vesicles along the course of a sensory nerve.
Generally associated with anything that causes reduced immunocompetence.
Congenital Varicella Syndrome
Greater risk usually occur in the 1st trimester of pregnancy with primary infection of VZV
Varicella syndrome;
low birth weight,
atrophy of extremity with skin scarring,
brain and eye defects
deafness
Varicella zoster Complications Bacterial infection of skin lesions
Pneumonia (viral or bacterial)
Central nervous system manifestations
Reye syndrome
post-infetion encephalitis
congenital and neonatal varicella
Pain and hyperaesthesia
Pain and hyperaesthesia
Laboratory Diagnosis of VZV Detection of multinucleated giant cell. Direct detection electron microscopy; vesicle fluid immunofluorescence; skin scrapping Serology IgG -> past infection IgM -> recent primary infection Definitive diagnosis by isolation of virus by culture. Rapid varicella virus identification using PCR
Prevention
Varicella vaccine contains live, attenuated virus approved for persons 1-2 years of age.
Measles-mumps-rubella-varicella vaccine approved for children 12 months through 12 years.
Vaccine prevents vericella but not zoster.
EPSTEIN BARR VIRUS (EBV)
EPSTEIN BARR VIRUS
Morphologically identical but antigenically different to other herpes virus.
Humans are the natural host.
Primary infection & latency occurs in B lymphocytes.
EPSTEIN BARR VIRUS
Transmission: Occurs by kissing & exchange of saliva.
Affects adolescents and young adults
worldwide distribution.
EPSTEIN BARR VIRUS
EBV causes: Infectious mononucleosis, Burkits lymphoma, Other B cell lymphoma, Nasopharyngeal carcinoma & Hairy leukoplakia in AIDS patients.
Symptoms The classic triad of mononucleosis is: sore throat, Fever Lymphadenopathy (usually in the neck, groin or under the arms)
Symptoms Other symptoms include: Fatigue and malaise Rash Enlargement of the spleen and liver Hepatitis & encephalitis can develop.
Symptoms Hairy Leukoplakia
Oral Hairy Leukoplakia
Nonmalignant hyperplastic lesion of epithelial cells
Burkitts lymphoma
It usually occurs in children aged 3-14 years.
BL cells show translocation of c-myc oncogene between the long arm of chromosome 8 and chromosomes 14.
Lab. diagnosis Hematological: Atypical lypmhocytosis. Immunolobical: Monospot test, agglutination test to detect hetarophil antibody (Monospot test relies on the agglutination of horse RBCs by heterophile antibodies in patient's serum). EBV specific IgM & IgG detection. Paul-Bunnell test: Determination of the highest dilution of the patient's serum (heterophile antibodies) will agglutinate sheep erythrocytes.
Cytomegalovirus (CMV)
Cytomegalovirus Cytomegalovirus or Human Herpesvirus 5 Single serotype. Forms giant cell hence called “cytomegalo”.
Cytomegalovirus Transmission: Fetus: from mother via placenta Infant: during birth or breast feeding. From person to person through saliva, urine, or other bodily fluids. Can be transmitted by sexual intercourse Also transmitted by transplanted organs, and rarely from blood transfusions.
Clinical finding
CMV infection of newborn: When infection occurs in 1st trimester, neonate suffers from an asymptomatic infection to a disease with fever, hepatosplenomegaly, mental or motor retardation and sometimes death.
In immunocompetent adult: causes heterophilnegative infectious mononucleosis without sore throat.
Clinical finding
In immunocompromised persons: It may include CMV retinitis, diarrhea , respiratory infection, and encephalitis.
Lab. diagnosis Isolation of virus. Detectionof nucleic acid by PCR. Fluorescence microscopy. Antibody titre. Microscopic detection of giant cell.
HUMAN HERPES VIRUS 8
HHV8 Transmitted
sexually or by organ
transplant. Causes kaposis sarcoma in AIDS patients.
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