lec slides on common viral infection

Common viral infections
• Measles
• Rubella
• Mumps
• Varicella or chicken pox
• Influenza
• Hepatitis
• Epstein barr virus or glandular fever
• Cytomegalic virus
• Parvo virus
measles
• Etiologic agent- paramyxovirus
-a common viral infection usually affecting children
-very contagious and is spread by infected people coughing out droplets infected with the virus
characterised by a skin rash or exanthem
-begins with a 4 day prodromal period
consisting of high fever
bright red conjunctivitis
a harsh cough and coryza
development of a maculopapular eruption
maculopapular lesions
starts behind the ears and spreads onto the face, arms, trunk and arms
It becomes confluent and fades by desquamation and staining.

• Koplik spot
• Pathognomonic
of measles
• It is usually an uneventful illness
--but may be complicated by
-viral pneumonia
- secondary bacterial infections
rubella
• caused by the rubella virus
• mild infection of little consequence unless contracted during pregnancy.
• characterised by
– Malaise
– headaches
– conjunctivitis
– and fever
• On the second day a rash of rose-pink or macular spots appears
then fades within 1 to 3 days.
There is accompanying lymphadenopathy
Mumps
• Etiologic agent- paramyxovirus
• usually contracted in childhood
• may be asymptomatic
• or associated with only fever and malaise
It is characteristically associated with
• parotitis
• pancreatitis
• oophoritis
• orchitis
• and lymphocytic meningitis.
Varicella or chicken pox
Etiologic agent --varicella-zoster virus
-infection usually contracted in childhood
initial or primary infection is characterised by
- fever and an eruption
• prodromal period of 1 to 2 days consisting of
– Malaise
– fever
– and vomiting which is followed by the appearance of an eruption
This begins as a macule which rapidly progresses through papule, vesicle, pustule and crust within 48
– Complications in childhood are rare and consist of secondary bacterial infections
– Varicella then becomes a latent viral infection and reactivation may occur 40 to 50 years later as
– -- varicella zoster or shingles
varicella zoster or shingles
• manifests itself usually by recurrence in
• skin
• motor nerves
characterised by the onset of
• severe pain
• hyperaesthesia
• malaise and slight fever
After 3 to 4 days the area affected develops an erythematous rash which is followed by the appearance of closely grouped vesicles. These vesicles rapidly progress to pustules and crusts.
• After 3 to 4 days the area affected develops an
• erythematous rash
• closely grouped vesicles
• pustules and crusts.
Influenza
• Caused by orthomyxoviruses
There are three types of influenza, A, B and C
Type C infuenza - relatively uncommon
type B - produces endemic and small epidemics of influenza
type A virus - produces endemic, epidemic and pandemics of influenza
Influenza
• characterised by
• sudden onset of fever, headaches, myalgia and a cough.
fever usually settles by the third day and the illness by about one week.
The illness may be complicated by a viral or secondary bacterial pneumonia.

VIRAL HEPATITIS
• caused by agents whose primary tissue tropism is the liver.
at least five hepatitis viruses have been recognised, and these have been named:-
Hepatitis A, B, C, D and E.
Clinical Features
• majority of infections are totally asymptomatic
common clinical features include: anorexia, nausea, vomiting, right upper quadrant pain and raised liver enzymes
• Jaundice is the hall mark of infection, but tends to develop late.
Anicteric cases are also very common.
• ENTERICALLY TRANSMITTED HEPATITIS: A and E
PARENTERALLY TRANSMITTED HEPATITIS B , C , D and G
• Hepatitis A - "Infectious Hepatitis"
Caused by a picornavirus, Enterovirus 72
Clinical Features
Incubation period 3-5 weeks (mean 28 days)
-Milder disease than Hepatitis B
-asymptomatic infections are very common, there is no chronic form of the disease.
• Complications:
• Fulminant hepatitis is rare: 0.1% of cases
Pathogenesis
Virus enters via the gut; replicates in the alimentary tract and spreads to infect the liver, where it multiplies in hepatocytes.
Viraemia is transient. Virus is excreted in the stools for two weeks preceding the onset of symptoms.
• Transmission - Enteric
Contamination of food or water with sewage
– Infected food handlers
– Shell fish grown in sewage-polluted water
• Diagnosis
diagnosis is made on the presence of HAV-specific IgM in the patient's blood.
• Prevention
1) Passive immunisation -
Travellers to third world countries
– Household contacts of acute cases
2) Active Immunization
Inactivated cell culture-derived vaccine has recently become available; not in general use
Hepatitis E
• Calicivirus
Recently identified cause of enterically transmitted non-A, non-B (NANB) hepatitis
Clinical Features
Incubation period 30-40 days
Acute, self limiting hepatitis, no chronic carrier state
Age: predominantly young adults, 15-40 years
• Complications
• Fulminant hepatitis in pregnant women. Mortality rate is high (up to 40%).
• Pathogenesis
Similar to hepatitis A
• Diagnosis
No routine laboratory tests are available as yet
Hepatitis B
• Clinical Features
• Incubation period 2 - 5 months
• Insidious onset of symptoms. Tends to cause a more severe disease than Hepatitis A.
• Asymptomatic infections occur frequently.
Pathogenesis
• Infection is parenterally transmitted
The virus replicates in the liver and virus particles, as well as excess viral surface protein, are shed in large amounts into the blood.
Viraemia is prolonged and the blood of infected individuals is highly infectious.
• Complications
• 1) Persistant infection:-
• 5% of infected individuals fail to eliminate the virus completely and become persistantly infected
• The virus persists in the hepatocytes and on-going liver damage occurs because of the host immune response against the infected liver cells
Chronic infection
• Chronic persistent Hepatitis - the virus persists, but there is minimal liver damage
Chronic Active Hepatitis - There is aggressive destruction of liver tissue and rapid progression to cirrhosis or liver failure
• 2) Patients who become persistently infected are at risk of developing hepatocellular carcinoma (HCC)
• 3) Fulminant Hepatitis
• Rare; accounts for 1% of infections.
• Hepatitis B is parenterally transmitted
1) Blood:
• Blood transfusions, serum products,
• sharing of needles, razors
• Tattooing, acupuncture
• Renal dialysis
• Organ donation
2) Sexual intercourse
3) Horizontal transmission in children, families, 'close personal contact'.
.4) Vertical transmission –
perinatal transmission from a carrier mother to her baby
Diagnosis: Serology
A. Acute infection with resolution
Viral antigens
• 1) Surface antigen (HBsAg) - presence in serum indicates that virus replication is occurring in the liver
• 2) 'e' antigen (HBeAg) - Its presence in serum indicates that a high level of viral replication is occurring in the liver
• 3) core antigen (HBcAg) core protein is not found in blood
Antibody response
1) Surface antibody (anti-HBs) –
- indicates immunity following infection-
- It remains detectable for life and is not found in chronic carriers (see below).
2) e antibody (anti-HBe)
-It indicates low infectivity in a carrier.
3) Core IgM rises early in infection and indicates recent infection

4) Core IgG rises soon after IgM, and remains present for life in both chronic carriers as well as those who clear the infection.
• Prevention
• 1) Active Immunization
• Two types of vaccine are available:
– Serum derived - prepared from HBsAg purified from the serum of HBV carriers
– Recombinant HBsAg - made by genetic engineering in yeasts

• Vaccine should be administered to people at high risk of infection with HBV:
– 1) Health care workers
– 2) Sexual partners of chronic carriers
– 3) Infants of HBV carrier mothers

• 2) Passive Antibody
• Hepatitis B immune globulin should be administered to non immune individuals following single episode exposure to HBV-infected blood.
For example: needlestick injuries
Hepatitis C
• The major cause of parenterally transmitted non A non B hepatitis
In 1989, the genome was cloned from the serum of an infected chimpanzee.

Togavirus
Clinical Features
• Incubation period 6-8 weeks
Causes a milder form of acute hepatitis than does hepatitis B
• But 50% individuals develop chronic infection, following exposure
• Complications
• 1) Chronic liver disease
2) Hepatocellular carcinoma
Transmission
• Blood transfusions, blood products
• organ donation
• Intravenous drug abusers
• community acquired: mechanism unclear. ?Vertical transmission
• ?sexual intercourse
Diagnosis
• 1) Serology
Reliable serological tests have only recently become available.
HCV-specific IgG indicates exposure, not infectivity

• 2) PCR detects viral genome in patient's serum
Delta Agent
• Defective virus which requires Hepatitis B as a helper virus in order to replicate.
Infection therefore only occurs in patients who are already infected with Hepatitis B.
Clinial Features
• Increased severity of liver disease in Hepatitis B carriers
Hepatitis G
• originally cloned from the serum of a surgeon with non-A, non-B, non-C hepatitis, has been called Hepatitis G virus.
It was implicated as a cause of parenterally transmitted hepatitis, but is no longer believed to be a major agent of liver disease.


On hiv
Treatment
• attempt to bolster the body's ability to fight HIV

• "therapeutic" vaccines+anti-viral therapy
• may improve the body's response to HIV.

• Other treatments boost CD4 count (T-cells), though this approach is not believed to be useful unless it is combined with an antiviral treatment
Tests That Monitor The Immune System
• HIV viral load.
• testing measures the amount of HIV in blood plasma.
• CD4 count
• measures the number of CD4 cells in a blood sample.
• The CD4 count is one indicator of how much damage HIV has caused to the immune system.
• CD8 count
• CD8s are a different subset of T-cells that include suppressor T-cells and "killer" T-cells.
• At this stage, several things can happen
• The new virus ("provirus") can remain inactive for a long time without triggering the reproduction of virus,
• divide into two proviruses- mitosis
•
• or it can start producing new virus
•
• budding off from the T-cell wall-- eventually destroying the T-cell.
• In the process of viral reproduction
•
• the virus destroys increasing numbers of T-cells
•
• leaving the body open to
• opportunistic infections
•
• How HIV Is Spread
• Requirements For Transmission to Occur
•
• 1. HIV must be present
• 2. In sufficient quantity
• 3. And it must get into the bloodstream.
• Where is HIV Found in the Body?
• HIV can be transmitted from an infected person to another through:
• Blood (including menstrual blood)
• Semen
• Vaginal secretions
• Breast milk
• Possibly infectious "bodily fluids"
• Pre-seminal fluid (pre-cum)
•
•
• Non-infectious "bodily fluids"
• Saliva
• Tears
• Sweat
• Feces
• Urine
•
• Activities That Allow HIV Transmission
• there are three primary ways in which this can happen:
• 1. Unprotected sexual contact
• 2. Direct blood contact
• including injection drug needles, blood transfusions, accidents in health care settings or certain blood products
• 3. Mother to baby
• before or during birth, or through breast milk
• Sexual Routes Of Transmission
• Sexual intercourse (vaginal and anal)
•
• Oral sex (mouth-penis, mouth-vagina)
•
• Heterosexual transmission studies
• Sexual intercourse (vaginal and anal)
•
• Oral sex (mouth-penis, mouth-vagina)
•
• Heterosexual transmission studies
• Non-Sexual Routes Of Transmission
• Sharing injection needles
• Needle sticks
• Blood transfusions
• Hemophilia treatments
• pooled blood of many donors
• Other blood products
• Mother to Child
•
• HIV Is NOT Transmitted By
• Insect bites
• Casual contact
• sharing of dishes/foods
• Donating blood
• Swimming pools/bath tubs
• Pets
• Contact with saliva, tears,sweat,urine,feces
• Rape/sexual assault?
• Transmission Through Tattooing, Piercing, Acupuncture, Electrolysis, and Shaving
•
• What is the risk?
•
• Universal precautions
•