Professional Documents
Culture Documents
1. 2. 3. 4. 5. 6. 7. 8. HSV1: HSV2: VZV: CMV: EBV: HHV6: HHV7: HHV8: Gingivostomatitis, whitlow, Keratoconjunctivitis Genital herpes,Neonatal Infection, Meningitis Fever, Vesicular rash, Encephalitis, Zoster Congenital and postnatal infection IM, BL, NPC Exanthema subitum, Mononucleosis with cervical lymphadnopathy Exanthema Subitum Kaposis sarcoma, Burkitts Lymphoma
Herpes Viruses:
Family: Herpetoviridae Members:
1. 2. 3. 4. 5. 6. 7. 8.
Properties:
Herpes simplex virus type 1 (HSV-1) Herpes simplex virus type 2 (HSV-2) Varicella-zoster virus (VZV) Cytomegalovirus (CMV) Epstein-Barr virus (EBV) Human herpes virus 6 (HHV-6) Human herpes virus 7 (HHV-7) Human herpes virus 8 (HHV-8)
1. 2. 3. 4. 5.
Icosahedral symmetry, enveloped, ds DNA Diameter: 120-200 nm Nuclear replication Oncogenicity Latency and Reactivation
Fever Sun light Cold Ultraviolet Menstrual cycles Hormonal changes Emotional upset Immune deficiency Other infections
Reactivation
Clinical Illness Cold Sore (Fever Blister)
2. 3. 4. 5. 6.
Keratoconjunctivitis: Corneal ulcer Meningoencephalitis: Brain lesions Ulcerative pharyngitis: Young adults Herpetic whitlow: Dentists, Doctors, Nurses In 1979: Link between HSV-1 and Alzheimers disease by damaging the nervous system by the virus
B. C.
Latent Infection: Virus present in latent state in nerve cells Recurrent Infection: Herpes Labialis (cold sore or fever blister)
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Cold Sore = Fever Blister = Herpes Labialis (HSV) It is a recurrent infection of HSV1 Small painful blisters around lips, nose, inside mouth Virus stay dormant permanently in nerve cell ganglia On reactivation, virus travel via nerve to lips and cause cold sore Not every one who get HSV develop cold sore It is contagious, spread by direct contact with oral secretion or by contaminated hand Wash hand frequently if you have cold sore or you are around infected person Disappear within 7-10 days.
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Epidemiology (HSV-1)
Spread:
Direct contact with Saliva, Food, Water Close contact with infected persons Mainly in children Family spread Poor socioeconomic: Early life Upper socioeconomic: Adolescence Age Ab: 60%- 100% have Abs. From mother to child during delivery in birth canal
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Primary Infection:
Serology: CFT: 4 Fold Rise- Recent Infection IFT, EIA, RIA: IgM and IgG
Control: (HSVI)
Vaccine: under trial. Ideal vaccine should induce immune response to prevent or reduce primary infection, that will reduce the source of virus for recurrent or transmission.
1.
Antiviral:
Acyclovir: Inhibit viral DNA polymerization, may stop the progression of Alzheimer disease Reduce severity and duration of symptoms Does not prevent latency Resistant strain exist Inhibit viral DNA synthesis
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Disease
Latent Infection
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HSV-2
Clinically:
Incubation: 5-7 days Vesicular eruption on genital area ulceration Lesion Vesicle Pustules Ulcer Crust Healing Fever,Malaise,Myalgia, Dysuria, Meningitis, Lymphadenopathy. Severity, Lesions: More in women. Urethra, Cervix: high infection Neonatal herpes: Infants have jaundice, hepatosplenomegaly, Vescicle on skin (60% die or neurological sequelae).
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HSV-2
Epidemiology and transmission:
Sexual transmission Increased number of sexual partners Female more than male HIV infection: risk factor Duration of sexual relationship Genital secretion Infected birth canal fetus infection Lab. people Nurses World wide: Increase in incidence.
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HSV-2
Prevention:
Hygiene (Mother, Others) Special attention: Mother child Asymptomatic carrier shed from saliva, urethra, cervix. Observation for symptoms. Patients with lesions: Isolation Acyclovir: reduce severity and duration of symptoms, doesnt prevent latency Vaccine: inactivated, gives partial protection in women who are seronegative to HSV1 and HSV2
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Zoster Shingles
Reactivation Older Age No seasonal peaks Less infectious
5- Generalized infection
6- Spread: Via blood 7- Occur: Normal host 8- Symptoms: Rash, Fever, Mild RTI 9- Complication: Pneumonia in adult Secondary bacterial infection Encephalitis 1-2 per 1000 Congenital defects Disseminated varicella
Localized Infection
Via nerve fiber Old people, mainly immunocomp. Painful blisters on face trunk, neck
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Varicella: Child disease, very infectious by respiration, vesicule. Nosocomial infection: big problem High rate of transmission: in group setting Active case of HZ transmit VZV to susceptible people
Direct contact: with respiratory secretions, vesicles Airborne: inhalation of nasopharyngeal secretion Varicella patients: Strict isolation Zoster patients: no strict isolation Outbreaks: in healthcare setting Via ventilation system.
5.
Transmission:
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B.
Recommended when
Patient is immunosuppressed VZV in a neonate In a suspected immune person In complications or unusual clinical syndromes From vesicle, stain with Tzanek, Giemsa, HE Look for intranuclear inclusions Not specific for VZV as HSV give same result
C.
Smear:
Viral culture in HEL: difficult and slow to grow, low sensitivity EIA for
IgG: Immunity after natural infection or vaccine IgM: recent infection, may cross react with HSV-1 IgM, may occur in zoster
IFT:
For Ag Biopsy specimen Rapid and sensitive 20
Vaccine:
In 1995: live attenuated (Varivax), reduce incidence, hospitalization and death of varicella Effective for >10 yrs Second dose recommend before school entry In 2006: Live attenuated (Zostavax) for shingle prevention in old people, reduce postherpetic neuralgia.
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Cytomegalovirus (CMV)
Herpesvirus, ds DNA, Env, Icosahedral, 120-200 nm Primary infection Latency Reactivation Virus excretion: Saliva, Urine for several month. Opportunistic infection: Immunocompromised patients (Pneumonia, Hepatitis) Transplants patients: Major problem (Re-activation) Immunity: IgM, IgG: and CMI important Symptoms: fever, sore throat, fatigue, swollen salivary gland.
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Clinical Features: Fever, Swollen salivary glands, sore throat Congenital Infection: Placenta Fetus virus shed
Maternal infection Mostly symptomless Fetal damage can be in all trimesters Primary and reactivation can infect fetus Signs: Jaundice, Hep. Spl.megaly, Microcephaly, Mental Retardation, Deaf, Vision loss Postnatal Disease:Widespread, mostly symptomless In young children, adult (Hepatitis, CMV mononucleosis) In immunocomp. Patients (Pneumonia, Retinitis, Gastroenteritis)
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Similarities:
Disease: Self limited Incubation: 3-6 wks Symptoms: Fever, Malaise, Hepatosplenomegaly Transmission: Blood Transfusion, Saliva Atypical Lymphocytes: Similar in both Viruses
B.
Differences:
Properties
Pharyngitis Lymphadenopathy Hetrophil Abs Specific Abs
EBV-Mono
+ve +ve (P-B Test) +ve EBV-IgM +ve
CMV-Mono
-ve -ve -ve CMV-IgM +ve
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Worldwide: person to person Saliva, Sexual, Urine, Blood, Breast Milk. Close contact via body fluid 50-90% of adult get infected Widespread in developing countries and lower socioeconomic Common in immunocompromised patients.
Lab Diagnosis:
Isolation in T/C (HEL) EIA, IFT: IgM, IgG PCR: for early diagnosis and treatment.
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Prevention:
Donors of blood / Organs: must be Seronegative Blood treated to remove WBC Hygiene: wash hands, gloves
Treatment:
a) Ganciclovir: Inhibit CMV replication, reduce severity of infection, used in life-treat. In Immunocomp. (Pneumonia, Retinitis) and for infants with severe congenital CMV Foscarnet: CMV retinitis in AIDS patients Vaccine: Still in research CMV-IG: given I.V. as prophylaxis for transplant patients.
b) c) d)
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Similarities:
Disease: Self limited Incubation: 3-6 wks Symptoms: Fever, Malaise, Hepatosplenomegaly Transmission: Blood Transfusion, Saliva Atypical Lymphocytes: Similar in both Viruses
B.
Differences:
Properties
Pharyngitis Lymphadenopathy Hetrophil Abs Specific Abs
EBV-Mono
+ve +ve (P-B Test) +ve EBV-IgM +ve
CMV-Mono
-ve -ve -ve CMV-IgM +ve
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Association of EBV with Burkitts Lymphoma (BL) and Nasopharyngeal Carcinoma (NPC)
Majority of NPC and BL Patients have EBV-Abs
BL: Malignant tumor of jaw, ovaries, Lymphoid tissue, common in African children, sporadic worldwide
NPC: Malignant tumor of nasopharynx epithelium, common in China and Africa 29
Latent Infection: In T-lymphocytes, Salivary glands. CMI: control HHV6 replication. Immunosupp. Patient and drug induced hypersensitivity reactivate the virus. Infection: Most children by age 2 years, 90% of adults sero (+). Transmission: Saliva, close contact, respiratory route, persistent shedding from oropharynx. Serological test: 95% of worlds population are HHV6-Abs positive, indicating immunity. 30
PCR : HHV6 and EBV are cell associated, so little free virus found in sera, so if DNA found in serum indicate active infection Virus isolation: difficult, time consuming, cannot tell if active or latent virus.
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Control:
Medicine to control fever, pain Bed rest Vaccine: not yet Antiviral: (cidofovir, Foscarnet: under trial)
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50% of transplant recipients and HHV8 +ve will develop KS African people at high risk due to high prevalence of the virus 30-51% HIV seropositive gay men (high risk group) 15 - 20% seronegative gay men Gay men at high risk for infection with HHV8 (why ?) How the virus is transmitted? Sexual, saliva, others
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Lab.:
PCR for HHV8 in KS lesion or blood IFT, EIA for IgG Abs Virus isolation difficult Samples saliva or tumor cell lines
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