Viral Diseases Name Title - PowerPoint Presentation

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Viral Diseases

Name

Title

Company Name

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The Herpes Virus Family

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Cytomegalovirus

Chapter 21

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Etiology

Classified as a herpesvirus

Large enveloped DNA virus

Cell associated, spreads from cell to cell.

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Epidemiology

Transmission: oral, respiratory or venereal.

Urine, saliva, feces, breast-milk, cervical secretions, virus-infected grafts semen, vaginal fluid and respiratory droplets. Blood transfusions.

Latent

Infection: infection persists in latent state and are activated by various conditions.

Congenital

Infection: maternal CMV infection can be transmitted in utero. Maternal antibodies provide protection for developing newborn.

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Figure 21-01.

   Four-month-old child with symptomatic congenital cytomegalovirus (CMV) infection manifesting severe failure to thrive, hepatitis with hepatosplenomegaly, bilateral inguinal hernia, and micropenis.

(From Krugman S et al:

Infectious diseases of children,

ed 9, St Louis, 1992, Mosby.)

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Signs and Symptoms

Acquired Infection: usually asymptomatic

Incubation 2-3 weeks

Sore throat, fever, swollen glands, chills, profound malaise and myalgia

Congenital Infection

Cytomegalic inclusion disease (CID)- may be fatal.

Intracranial calcification, mental retardation, deafness, vision defects, microcephaly and motor dysfunction.

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Figure 21-02.

   Brain of infant with congenital CMV infection. Note extensive periventricular necrosis and calcification.

(From Krugman S et al:

Infectious diseases of children,

ed 9, St Louis, 1992, Mosby.)

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Immunologic Manifestations

Immune System Alterations:

Alters immune system.

Interferes with immune responses.

Linked to malignancies.

Serologic Markers:

Infected cells show several antigens.

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Laboratory Evaluation

Passive Latex Agglutination for Detection of Antibodies to CMV in Human Serum- not recommended for immunocompromised patients.

Other Assays: see Table 21-1.

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Table21-1

Laboratory Diagnosis of Cytomegalovirus (CMV) Infection

Target

Test Method

Recommended Use

CMV cell

Culture,

Immunofluorescence

Diagnose CMV infection

Gold Standard test for tissue

CMV

PCR

Rapid test for diagnosing CMV in immunocompromised patients or organ donors.

CMV DNA quantitation

PCR

Diagnose CMV infection.

Monitor disease state in organ transplant and HIV patients

CMV: whole blood or bone marrow

PCR

Diagnose CMV infection.

CMV antibodies: IgG and IgM

Latex agglutination

Screen pregnant women and infants possibly infected with CMV. Infants may test positive during first 6 months due to maternal antibodies. Discriminate between current (IgM) and prior infections (IgG)

CMV

antibodies: total

Solid-phase agglutination

Screen organ donors

CMV antibody, IgM

ELISA

Confirm equivocal CMV IgM results

CMV antibody, IgG

Chemiluminescent immunoassay

Confirm equivocal CMV IgG results

Modified from ARUP Laboratories,2008,www.arup.com.

*a negative result (<2.6 log copies.mL, or <390 copies/Ml) does not rule out the presence of polymerase chain reaction (PCR) inhibitors in the patient specimen or CMV nucleic acid in concentrations below the assy’s level of detection. Inhibition may also lead to underestimation of viral quantitation. HIV, Human immunodeficiency virus; ELISA, enzyme-linked immunosorbent assay.

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Herpes Simplex types 1 and 2

Etiology

Epidemiology

Signs and Symptoms

Immunologic manifestations

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Epstein-Barr Virus

Etiology

Epidemiology

Signs and Symptoms

Immunologic manifestations

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Varicella, Herpes Zoster

chickenpox

Etiology

Epidemiology

Signs and Symptoms

Immunologic manifestations

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Human Herpes 6:

Roseola

Human Herpes 7:

Roseola

Human Herpes 8: Kaposi Sarcoma

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Chapter 23

Viral Hepatitis

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General Characteristics of Hepatitis

Etiology:

Most common liver disease world wide.

Primary Hep viruses- A, B, C, D, E and G.

Secondary hep viruses- EBV, CMV, Herpesviruses and others.

Incidence:

Account for 95% of all hep infections

Signs and

Symptoms:

Acute- chronic

Mild asymptomatic- severe and fatal

.

Hepatitis – carcinoma

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Hepatitis A

Etiology:

HAV- small RNA,

picornavirus

.

Successfully grown in culture.

Epidemiology:

Formally known as infectious hepatitis.

Primarily found in young children.

Routine vaccinations began in 1999.

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Hepatitis A

Signs and Symptoms:

Symptoms appear

on average at 4 weeks.

Patients usually anicteric.

Does not progress to chronic liver disease.

Immunologic Manifestations:

IgM appears after fecal shedding.

IgG follows days later.

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Hepatitis A

Diagnostic Evaluation

:

Total Hep A antibodies

Hep A antibody, IgM antibody

EIA

Prevention and Treatment:

Vaccine

Safer food

Safer water

1945 - gamma globulin shots

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Figure 23-02.   Clinical sequelae of hepatitis A.

(Redrawn from Gollan JL: Viral hepatitis. In

International Review of Internal Medicine,

Boston, 1995, Brigham and Women’s Hospital, Harvard University Medical School, pp 781-792.)

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Figure 23-01.   Electron micrographs of hepatitis viruses. A, Hepatitis A virus (HAV). Electron micrographs of hepatitis viruses. B, Hepatitis B virus (HBV). Note Dane particles (see Figure 23-3).

(From Krugman S et al:

Infectious diseases of children,

ed 9, St Louis, 1992, Mosby.)

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Hepatitis A virus

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Hepatitis B

Etiology:

HBsAg (formally known as Australia antigen)- discovered in 1966.

Blood transfusion virus.

DNA virus- Dane Particle- double shelled particle.

Epidemiology:

Long incubation hepatitis.

Transfusion related disease decreased in the 1990’s.

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Figure 23-03.

   Dane particle of hepatitis B virus.

(From Bauer JD:

Clinical laboratory methods,

ed 9, St Louis, 1982, Mosby.)

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Hepatitis B

Signs and Symptoms:

Rash, glomerulonephritis, vasculitis, arthritis and angioneurotic edema.

Asymptomatic infections, jaundice

Laboratory Assays:

HBsAg

HBeAg

: associated with HBV core structure

anti-HBc

Anti-Be

Anti- HBs

Hep B viral DNA

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Hepatitis B

Hepatitis e Antigen

Associated with core of HBV (DNA and DNA polymerase)

Rarely found in absence of

HBsAg

Its detection indicative of active viral replication

Detectable in chronic carriers

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Hepatitis B

Diagnostic Evaluation

:

Testing should be ordered based on patient history, signs and symptoms.

Differentiating Acute and Chronic Hepatitis and the Chronic Carrier State:

Care must be taken to differentiate between acute, chronic and carrier states (asymptomatic) of Hep B.

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Hepatitis B

Prevention and Treatment

:

Vaccine introduce in 1991. 98% reduction in infection of <15 year olds.

Vaccine- 3 doses over 7 months, 80-95% effective.

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Figure 23-05.   Serologic and clinical patterns observed during acute hepatitis B viral infection.

(Redrawn from Hollinger FB, Dreesman GR. In Rose RN, Friedman H, editors:

Manual of clinical immunology,

ed 2, Washington, DC, 1980, American Society for Microbiology.)

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Hepatitis D

Etiology:

Delta Agent- Hepatitis delta agent-1977

Replication defective, incomplete RNA

Unable to cause infection alone, HBV needed. Contracted by superinfection with HBV

Epidemiology:

Common in S. Europe and Amazon.

Severe and rapidly progressive liver disease.

Spread by direct contact.

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Hepatitis D

Signs and Symptoms:

Benign and brief.

Chronic HDV- liver disease and cirrhosis.

Immunologic Manifestations

:

Partially represses HBV replication.

HDV Ag found in serum.

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Hepatitis D

Diagnostic Evaluation:

Total antibody by EIA

IgM assay by RIA

Antigen detection by immunodiffusion

HDV RNA hybridization

Reverse-transcription PCR

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Hepatitis C

Etiology:

“non-A, non-B” - HCV

Viral Characteristics:

Small enveloped single-stranded RNA virus

Mutates rapidly

6 genotypes

50 subtypes

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Hepatitis C

Epidemiology:

3.5 million in US have chronic HCV

Major cause of liver disease

Viral Transmission:

Spread by contact with infected blood or products

Drug abusers

Infants from infected mothers

Sex

Needle sticks

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Hepatitis C

Signs and Symptoms:

Variable, asymptomatic

Mild to fatal

Acute to chronic

Laboratory Assays:

EIA

Western Blot

PCR

Serum Titers

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Hepatitis C

Diagnostic Evaluation:

Acute HCV- jaundice, fatigue and nausea, increases ALT and anti-HCV.

Chronic HCV- mild (asymptomatic) to severe (cirrhosis and end stage liver disease).

Prevention and Treatment:

Interferon alpha – naturally occurring glycoprotein.

No vaccine or immunoglobin at present.

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Figure 23-06.   Hepatitis C infection after accidental needlestick injury.

(Modified from Hernandez ME et al: Risk of needlestick injuries in the transmission of hepatitis C in hospital personnel,

J Hepatol

16:56-58, 1992; Mitsui T et al: Hepatitis C infection in medical personnel after needlestick accident,

J Hepatol

16:1109-1114, 1992.)

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Figure 23-07.   Hepatitis C infection: natural history.

HCC,

Hepatocellular carcinoma.

(Modified from Gollan JL: Viral hepatitis. In

International Review of Internal Medicine,

Boston, 1995, Brigham and Women’s Hospital, Harvard University Medical School, pp 781-792.

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Hepatitis E

Etiology:

Virus recently identified.

Epidemiology:

Only a few cases reported.

Transmitted fecal- oral route

Signs and Symptoms:

Incubation period 2-9 weeks

Self-limited, mild infection

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Hepatitis E

Immunologic Manifestations:

Short-lived IgM.

Diagnostic Evaluation

:

Specific serological test for IgM and IgG anti-HEV.

Prevention and Treatment:

Gamma globulin shots do not work.

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Hepatitis G

Etiology:

RNA virus

Epidemiology:

Blood-borne agent

Co-infection of HCV

Signs and Symptoms:

Role remains unclear.

Diagnostic evaluation:

Chronic HGV- rare.

Does not cause liver disease.

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Transfusion-Transmitted Virus

Etiology:

TTV- non-enveloped single stranded DNA virus, with 3739 nucleotides.

Epidemiology:

Associated with non A-G viruses

Found everywhere.

Signs and Symptoms:

Human virus with no clear disease association.

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Chapter 24

Rubella Infection

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Etiology

Isolated 1962

Acquired rubella- German measles- 3-day measles.

Enveloped single-stranded RNA virus.

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Epidemiology

Vaccine – 1969

Epidemics every 6-9 year intervals

2 problems with vaccines:

Unvaccinated preschool children.

Vaccine failures.

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Signs and Symptoms

Acquired

Infection

:

Incubation period 10-21 days.

Contagious for 12-15 days.

Acute phase lasts 3-5 days, usually mild.

Congenital

Infection

:

1

st

trimester – fetal death or congenital defects

( Rubella Syndrome)

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Figure 24-01.

   Rubella.

(From Odom RB, James WD, Berger TG:

Andrews’ diseases of the skin: clinical dermatology,

ed 9, St Louis, 2000, Saunders.)

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Figure 24-02.

   Rubella rash.

(From Krugman S et al:

Infectious diseases of children,

ed 8, St Louis, 1985, Mosby.)

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Immunologic Manifestations

Acquired

Infection

:

IgM- recent infection (associated with clinical signs and symptoms)

IgG- protect indefinitely (immunity)

Congenital Rubella

Syndrome

:

Neonates- IgM shows congenital rubella syndrome.

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Figure 24-03.

   Congenital malformations of rubella.

(From Krugman S et al:

Infectious diseases of children,

ed 8, St Louis, 1985, Mosby.)

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Diagnostic Evaluation

Hemagglutination

Inhibition (HAI):

Standard test- detects IgM and IgG.

Titer cutoff 1:8.

Other

Methods

:

Latex procedures

EIA- enzyme immunoassay

FIA-fluorescent immunoassay

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Chapter 25

Acquired Immunodeficiency Syndrome

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Etiology

Viral Characteristics:

1983- isolated from homosexual men, HTLV type III

1984 – HTLV III caused AIDS

From retrovirus family, type D retrovirus

Oncovirus – HTLV-I, HTLV-II –tumors

2 types HIV- type 1 and 2

HIV-1: 9 subgroups: group M (A-H), group N, and group O.

HIV-2: 2 subgroups – A and B.

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Epidemiology

Incidence:

leads the world’s cause of death in Sub-Saharan Africa.

4

th

leading cause of death world-wide.

Classification Sy

stem: see handout

Infectious Patterns:

Three patterns prevalent.

N&S America, W. Europe,

Africa, Caribbean, parts of S. America

E. Europe, N. America, Middle East. Asia, Australia, New Zealand

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Epidemiology

Modes of Transmission

: 2 Ways

Actual virus

As a cell associated with HIV and carried in a body fluid

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Signs and Symptoms

Early infection

:

asymptomatic or mild or chronic lymphadenopathy (lasts months to years)

Opportunistic Infections

:

Kaposi’s Sarcoma – rare tumor

Cryptosporidiosis -

Disease Progression:

Several factors – see figure 25-4

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Pneumocystis jiroveci

(

carinii

)

from tracheobronchial aspirate; stained with

methenamine

silver.

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Kaposi’s sarcoma. A,

Early lesion consisting of

violaceous

macules and plaques.

Kaposi’s sarcoma. B,

Purple nodules are seen most often on the lower legs.

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Figure 25-04.   Evolution of AIDS.

(Redrawn from Habif TP:

Clinical dermatology,

ed 2, St Louis, 1990, Mosby.)

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Immunologic Manifestations

Cellular Abnormalities:

Prefers CD4+ subset of lymph’s

Has a receptor site

Alterations in Immune System:

Gp120 breaks off virus and infects CD4 molecules – body destroys both

Serologic Markers

:

Body mounts a massive response against virus.

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Diagnostic Evaluation

HIV testing includes:

Detection of HIV antibodies

Detection of HIV antigens (p24).

Detection or quantification of viral nucleic acids.

Viral culture

Viral RNA/DNA

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Testing Methods

Human Immunodeficiency Virus (HIV-1) Antibodies:

EIA (1985) - blood

HIV Antigen and Genome Testing:

P24- blood and CSF, can be diagnostic before seroconversion, PCR, EIA

Confirmatory Testing:

Western Blot – recognizes major HIV proteins.

Line immunoassay – HIV antigens, popular

IFA – locates HIV-1 antigen within cells.

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Testing Methods

Fourth Generation Testing

Architect Ag/Ab (Abbott Diagnostics)

GS HIV Combo Ag/Ab (Bio-Rad Labs)

Rapid Testing:

Used as a screening test, must be confirmed.

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Prevention and Treatment

Prevention:

HIV screening – routine part of medical care (13-64 year olds)

No vaccines yet.

Treatment:

Anti-retroviral agents – 3 types

New drugs – fusion inhibitors, integrase inhibitors and protease inhibitors.