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70 Cards in this Set

  • Front
  • Back
General Characteristics of Viruses
Require LIVING cells for growth and
replication (cell cultures, embryonated
eggs, living animals/plants)
• Have DNA or RNA…NEVER both!
• Multiply by separate synthesis of nucleic
acid and protein, combine to form virus
particles
• Size varies from 10 nm-300 nm
Basic Components of Viruses
Nucleic Acid
-infectious genetic
material
Protein Coat
Surface Antigens
-protein or
carbohydrate
-highly variable
Replication
Adsorption
. Penetration and uncoating
Nucleic acid and protein synthesis
Assembly
Release
How do we detect viral infections?
1. Detect the virus itself!
2. Detect the immune response…antibodies against the
virus!
Viral Diagnosis- A. Detection in clinical
specimens
1. Visualisation by
Electron microscopy
2. Cell culture (cytopathic
effects, hemagglutination,
immunofluorescence)
3. Detection of viral
antigens (ELISA)
Viral Diagnosis- Detection of patient’s immune responses
Antibody detection, presence or absence (ELISA)
– IMMUNITY TEST
• Rise in antibody titre or high antibody titre
– DIAGNOSTIC TEST
What types of viruses will we learn about?
1. Viruses of the breathing
2. Enteric viruses
3. Viruses of diarrhea
4. Viruses of the rashes
1. Viruses of the glands
2. Viruses of the liver
3. Viruses of the brain
4. Viruses of the immune system…aka…HIV
Respiratory disease
• Different families
1. Influenza viruses
2. Parainfluenza viruses
3. Respiratory syncytial viruses
4. Rhinoviruses
5. Adenoviruses
6. Echoviruses, coxsackie viruses, herpes viruses
(occasional respiratory tract infection)
types of Influenza Viruses
Influenza virus type A: major epidemics
• Influenza virus type B: milder disease
Produce haemagglutinin (diagnostic)
• Frequent recombination which means that there are new types which sprea throughout the world causing pandemics of influenza.
= High antigenic variability
= Pandemics
Influenza Viruses clinical, diagnosis, serum, prevention
Clinical:
– fever, variable respiratory symptoms
– Infants and elderly more susceptible
• Diagnosis:
– Throat washings, naso-pharyngeal aspirate
inoculated into cell culture
• Serum:
– Paired sera (acute and convalescent stage)
• Prevention:
– Annual vaccination
especially for high risk groups
The WHO Pandemic response and planning is a
direct reflection of disease SPREAD and not of
disease SEVERITY
What about disease severity?
Greater disease burden in <25 yrs than in
>65 yrs
– Unusual for seasonal flu
• Certain groups have risk of complications
– Pregnant women, asthma, diabetes, immune
suppression, heart disease, kidney disease
– Same as for seasonal flu
What does the H1N1 virus look like?
Has been termed “swine” flu
• Influenza genome has 8 segments
• 2009 H1N1 segments
– 3 from classical swine
– 2 from asian swine
– 2 from avian
– 1 from human
H1N1 2009 vaccine
Vaccination is major effort of PHAC to fight
pandemic flu
• Canada has a dedicated vaccine manufacturer
• Adjuvanted vs. unadjuvanted vaccine
– Why adjuvant?
• To reduce the amount of vaccine protein per dose
– Why new adjuvant?
• Existing adjuvants have never worked well for flu shots
– Why controversial?
• Little data on adjuvant in children, pregnant women
• New adjuvant had not been used in other vaccines
Parainfluenza viruses
Infants and young children
• Respiratory infection that could have serious
complications
• Croup (barking cough, high pitch sound on
inhalation)
• Bronchiolitis, bronchopneumonia
• No vaccine
Respiratory syncytial virus
Major respiratory pathogen for children < 2years
• Pneumonia and bronchiolitis; occasionally fatal
• Epidemics
• No vaccine
• Antiviral: Ribavizine
Rhinovirus
Common colds
• > 100 serotypes; no cross-immunity
• Repeated infections
Adenovirus
Pharyngitis and conjunctivitis; pneumonia in
young children
• Children most commonly infected
• Asymptomatic infection common
• Vaccines used in army
ENTERIC VIRUSES- general information
Enterovirus = Enteric virus
• Infect intestinal / lymphoid cells
• Poliovirus, coxsackievirus, echovirus
• Multiply in GI tract, but RARELY cause gastroenteritis
• Infection via respiratory or GI tract
• Spread to other target organs in body
• 95% inapparent infection, 4-5% minor illness,
1% serious illness
Poliovirus
Humans are the ONLY natural host
• Types 1, 2 and 3
• Causes poliomyelitis
– Highly infectious, invades the host nervous system
and can cause total paralysis in as little as a few
hours
Global Polio Eradication Initiative
– Launched in 1988 by WHO, goal was to eliminate
poliovirus in the same manner as smallpox was
eliminated
– Since 1988, number of cases has decreased by
~99% (from > 350,000 cases in 1988 to 1997 cases
in 2005)
– Currently polio is only found in parts of Africa and
South Asia (Nigeria, India, Pakistan, Afghanistan)
Poliovirus Diagnosis
Isolation from stool samples (up to 5-6
weeks after infection), CSF and pericardial
fluid
• Serology: acute and convalescent phases
* Carriers with inapparent infection are able
to spread the disease to susceptible
individuals*
Polio Prevention
VACCINATION
– Salk vaccine (Jonas Salk)
• Killed/inactivated vaccine; does not produce local
immunity in GI of host (IgA); Virus can still colonize
host GI tract and SPREAD to the community!!!
• used for immunocompromised
– Sabin vaccine (most common; Albert
Sabin)
• Live attenuated; host will produce IgA and IgG, so
is protected against intestinal colonization and
virus can NOT replicate and spread
• Oral administration
Coxsackieviruses
minor respiratory illness (mainly group B)
aseptic meningitis (both group A and B)
herpangina and hand-foot-and-mouth disease (group A)
pleuodynia, pericarditis, and myocarditis (group B)
Coxsackieviruses
Groups A and B
• Seasonal variation
• Diagnosis by stool
sample and paired
sera (same as polio)
• NO VACCINE
Echoviruses
Several types
• Enteric cytopathogenic human orphan viruses
• Minor respiratory illness
• Aseptic meningitis
• Same diagnosis as coxsackie and polioviruses
• NO VACCINE
Viruses of Diarrhea
ROTAVIRUS
– Epidemics in infants (6 months-2yrs); mainly
in winter
– Replication in small intestine
– Acute gastroenteritis vomiting, diarrhea,
fever
– Highly infectious!!!
Rotavirus diagnosis epidemiology and prevention
Diagnosis
– EM or immunological testing of virus from stool
samples (within 3 days)
• Epidemiology
– Short incubation (2-3days)
– Fecal-oral route, aerosols (explosive diarrhea), fomites
– Outbreaks in daycare centres, children’s hospitals
• Prevention
– Rapid diagnosis and isolation of patient
– Proper handwashing
– No vaccine…..
Norovirus diagnosis, epidemiology and prevention
Outbreaks of gastroenteritis in older children and
adults
• Diagnosis: first exclude bacterial cause, then
can be differentiated from bacterial
gastroenteritis
• Epidemiology: VERY CONTAGIOUS; survives
well on objects/environment
– Fecal-oral route; food-borne outbreaks
• Prevention: no vaccine; handwashing and
isolation of infected individuals
US CDC estimated in 1999 (Mead et
al.) that of all foodborne illness:
30% is bacterial
 3% is parasitic
 67% is viral
Of viral foodborne outbreaks:
More than 90% attributed to
Noroviruses
Adenoviruses (also a respiratory virus!)
Some types cause gastroenteritis in children
– Can NOT cultivate diarrhea type in cell culture
– Diagnosis by EM
Calici- and Astro- viruses
Sporadic gastroenteritis in children
– EM diagnosis
– Fecal-oral route of transmission
Viruses Causing Rashes
Common epidemiological features of
viruses causing rashes:
– Humans are the only reservoir
– Highly contagious!
5 virus names causing rashes
Measles
• Rubella (German measles)
• Varicella (chickenpox)
• Herpes simplex (HSV)
• Papilloma virus
Measles
One of the highest infectivity rates
• Clinical: rash first appears behind
ears, forehead and nostrils then
spreads to whole body;
BLOTCHY appearance
• Lifelong immunity after natural
infection
• Complications: secondary
bacterial infections ie
bronchopneumonia
– Encephalitis (rare)
– Exacerbation of TB and
leukemia
Measles diagnosis and prevention
• Diagnosis:
– Serological
– Confirmation of Suspected Case:
• IgM Ab in single blood specimen against measles OR a rising
IgG Ab titer against measles in paired blood
– Immune status
• Circulating measles specific Ab IgG
• Prevention
– Immunoglobulin: can suppress disease if given within
5 days of contact with virus
– Live attenuated vaccine: very effective, widely used.
Administer after 12 months of age
• MMR
Rubella (German Measles)
VERY dangerous for non-immune pregnant
women birth defects
• Largest danger is in first trimester
– 50% chance of damage to the fetus if non-immune
mother is infected between 0-4 weeks
• Birth defects:
– General: abortion, death of newborn
– Localized: cataracts (infection during 6
th week)
deafness (infection during 9
th week)
heart defects (infection during 5
th
-10
th
week)
Other: low birth weight, cleft palate, mental deficiency
Rubella epidemiology
Clinical: similar to measles but milder; lifelong immunity
• Epidemiology and Immunity: pre-vaccine
era, seen in school children during winter
in spring, outbreaks every 7-10 years, lead
to life-long immunity
– Now most cases (60%) are seen in those 15
years and olderRub
Rubella diagnosis
Lab Diagnosis:
– Suspected cases:
detection of rubella
specific IgM or rising
Ab titer in paired sera
– Immunity status:
detection of circulating
Rubella Ab (IgG)
Rubella prevention
Prevention of congenital rubella:
– Check immune status of women of childbearing age
– Diagnosis in hospitals
– Rubella serology screening of men and women
starting work in hospitals
– Vaccination of non-immune
– Isolation of rubella cases in hospitals
• Vaccination-live attenuated vaccine
– Do NOT give vaccine to women who are already
pregnant!
Varicella
Chickenpox: Varicella
Zoster Virus (VZV)
• Clinical: childhood
febrile illness with
characteristic rash
– Successive crops of fresh
vesicles appear within 3-
4 days of onset
– In non-immune adults,
occasional pneumonia,
may be fatal
Varicella (shingles portion)
Herpes Zoster (Shingles)
– LIMITED rash, along
trajectory of ONE nerve
– Late recurrence of latent VZV
(chicken pox) infection
• Diagnosis: ID of virus
particles in pustules by EM
or immuno methods,
followed by cell culture
• Prevention: no vaccine;
detection of susceptible
persons by serological
methods
Herpes Simplex Virus (HSV)
Widespread
• Become LATENT after initial infection; lesions
reappear periodically
• High percentage of inapparent infections
• Epidemiology:
– HSV1: “cold sores” oral and ocular lesions;
transmitted via oral and respiratory secretions
– HSV2: “herpes genitalis” associated with genital tract;
infected females can transmit to the newborn
• Diagnosis: ID of virus particles by EM or immuno
methods; cell cultures; Serology NOT usefu
Herpes clinical forms and prevention
Clinical forms (other than cold sores):
– Genital infections: recurrent in both sexes
– Herpetic encephalitis: RARE (see CNS viruses)
– Neonatal Herpes: acquired during birth from
asymptomatic mother; difficult to prevent; can result in
death or severe sequelae (see CNS viruses)
– Herpetic Whitlow: affects fingers, occupational hazard
of health care workers; nosocomial infections in
neonates
– Corneal and Conjuntival Infection: can cause
ulceration of cornea and blindness
• Treatment and Prevention: antivirals; C-section
for symptomatic mothers; NO VACCINE
Papilloma Viruses
Cause different types of warts
– Common warts on hands and feet
– Genital warts: sexual transmission, asymptomatic
carriers
– Some types associated with cancer: cervix, vulva,
penis
• Diagnosis: immuno techniques and DNA
hybridization techniques; no cell cultures
available
• Prevention: Vaccine now available (Gardasil)
Viruses Causing Glandular Enlargement
MUMPS
– Childhood disease; bilateral inflammation of parotid
glands; many inapparent infections
– Complications: meningitis, orchitis (can lead to
sterility), ovaritis
– Epidemiology: spread by salivary and respiratory
secretions; incubation 18-21 days
– Prevention: MMR vaccine (live, attenuated)
facts about MMR
As of January 2008, 777 confirmed cases…
 Mostly 23 and 24 year old people (university students)
 Many potentially exposed while celebrating St. Patrick's Day
packed bars
can you tell someone to “self-isolate” when they had no
symptoms? Is this an exercise in futility?
 In old days, many only had 1 MMR shot (nowadays you get 2)
 Handling of vaccine by physicians
Infectious Mononucleosis (Epstein-Barr Virus)
Belongs to Herpes virus family
• Mild disease; children and young adults; can be
prolonged and debilitating
• Transmission by saliva (kissing disease)
• Symptoms: lymphadenopathy, fever, sore throat, atypical
lymphocytes, enlargement of liver and spleen
• Latent virus
– Chronic disease (rare) or asymptomatic shedding (common) for
lifetime of host
• Diagnosis: blood picture ( in atypical lymphocytes)
Monospot Test (detects RBC agglutination)
Presence of EBV antigens
• NO VACCINE
Cytomegalovirus (CMV)
Herpes family, infection usually asymptomatic
and latent BUT dangerous for
– Pregnant women: neonatal infection with jaundice,
enlarged liver and spleen, mental retardation and
motor disorders
– Transplant patients: disseminated infection can cause
transplant rejection
– AIDS and other immunocompromised patients:
frequent infection, GI tract ulceration and retinitis
CMV diagnosis
Diagnosis:
– Isolation of virus from urine, blood, organ biopsies
(slow process, but accurate)
– CMV antigen detection, DNA hybridization and PCR
in leucocytes much faster
– Serology screening for donors and recipients before
transplant
• Treatment: antivirals
• Prevention (immunocompromised):
– Match CMV immune status between donor and
recipient in transplants
– Preventative administration of antivirals
– Universal precautions to prevent transmission
– NO VACCINE
Hepatitis Viruses
Hepatitis = Inflammation of the liver
– Malaise, fatigue, nausea, loss of appetite and
jaundice
• Hep A, B most common and well
characterized
– Hep C, E, G less common
• *Other viruses and bacteria can cause
hepatitis as a complication of infection*
• Diagnosis: serological
Hepatitis A
Mainly children and young
adults
• Sporadic cases and small
epidemics
• Epidemiology:
– Transmission by fecal-oral route
– Incubation 15-50 days
– Stools infectious 2-3 weeks
before onset
– Mild or inapparent infection in
children
– No chronic hepatitis
– Life-long immunity
Hepatitis A diagnosis
Diagnosis:
– Suspected clinical cases:
detection of IgM
– Immunity: detection of IgG
(before travel)
• Prevention:
– Vaccine for high risk
populations
– Commercial γ-globulin for
prevention after exposure
Hepatitis B
Sporadic cases; all ages
• Epidemiology:
– Contaminated blood/blood products;
saliva, urine, semen
– Avg. incubation 90 days
– Infective serum 30-60 days before onset of
symptoms
– Carriers
• Clinical
– More severe than HepA
– Chronic hepatitis and chronic carrier-state
Hepatitis B Diagnosis
• Diagnosis:
– Blood test for HepB surface antigen (HBsAg)
– Antibodies are produced several months after onset
of symptoms
• Used as markers of infection and immunity
Hepatitis B Prevention
Prevention
– Universal precautions for blood and
body fluids
– Proper handling of needles
– Screening
– Vaccination
– HepB immunglobulins after exposure
– HepB carriers
Hepatitis C
Epidemiology:
– Blood and sexual transmission
– Initially mild disease but can cause chronic
hepatitis
• Diagnosis:
– Serological
• Prevention:
– Same as HepB
– NO VACCINE
– Treat with recombinant interferon and
ribavirin
Hepatitis Delta Agent
• Epidemiology:
– Blood and sexual transmission
– “Viroid”-relies on HepB presence for
replication in cells
– Increases severity of HepB infection
• Diagnosis:
– Serological
• Prevention:
– Vaccination against HepB
Hepatitis E
Transmission via fecal-oral route
• Incubation 15-50 days
• Symptoms similar to HepA BUT 20%
mortality in pregnant women
• Endemic in India, Pakistan, Nepal, Burma,
North Africa and Mexico
Hepatitis G
Epidemiology:
– Blood and sexual transmission
– Incubation 14-180 days
– Initially mild and no jaundice, can cause chronic
hepatitis
• Diagnosis:
– Detection of viral DNA by PCR or other molecular
methods
• Prevention:
– NO VACCINE
Yellow Fever Virus
Haemorrhagic fever with hepatitis
• Endemic in Africa, South America
and Caribbean
• Mortality rates as high as 50%
• Transmitted by mosquito
• Travellers to endemic countries
receive live attenuated vaccine
Viruses affecting the CNS
Clinical Manifestations
– Aseptic meningitis
– Encephalitis
– Meningo-encephalitis
– Poliomyelitis
– Slow progressive, persistant infections
CNS Viruses general diagnosis
*Always first exclude possibility of
bacterial or fungal infection*
– Lumbar puncture X4
– Other specimens
• Blood, urine, aspirates,
• throat swabs
• stools, sera
CNS Viruses with a Human
Resevoir
Usually an extension of a primary infection in
another part of the body
– Mumps-aseptic meningitis in children
– Enteroviruses-aseptic meningitis in infants and
children
– HSV1-RARE cause of herpetic encephalitis in young
adults
– HSV 1 or 2-RARE cause of meningo-encephalitis in
neonate or young adult
– Vaccination for mumps, measles and polio (entero)
CNS Viruses with an Animal
Reservoir
RARE: Humans are accidental or dead-end
hosts
– Arbovirus:
• over 200 different types
• Tropical rainforest areas
• Encephalitis
• Eg. West Nile
– Rabies virus
• Fatal, acute encephalitis
• Infects mammals, transmitted via saliva
• Long incubation (30-60 days)
• Combined active and passive immunization
• Prevention by vaccination of wildlife and pets
HIV and AIDS
Severe immunosuppressive condition;
often fatal; predisposition to opportunistic
infections and cancers
• HIV causes depletion in helper T-cells
making the host very susceptible to other
infections
• Frequent antigenic changes
HIV inactivation, pathogenesis
Inactivation
– Virus often protected by living inside cells, protect it
from disinfecting action
• Transmission
– Sexual, blood/blood products, congenital, organ
transplants, sperm donation
– Lengthy asymptomatic period increases spread of
disease
• Pathogenesis
– Virus is cytocidal to helper T4 cells
– AIDS develops from decreasing immune status
HIV clinical diagnosis
• Clinical
– Incubation 6 months-several yrs
– AIDS-related Complex disease, progress to AIDS
– Terminal stage patients develop dementias, other
neurological problems, many opportunistic infections
• Lab Diagnosis
– Serology based; seropositivity can take months to
occur
– Isolation of virus from blood, plasma, semen, cervical,
vaginal secretions
HIV prevention
Prevention
– Universal precautions for healthcare personnel
– Screen blood, organ and semen donors
– Heat inactivation of plasma for haemophilia patients
– Sexual education
– Education of drug users
– Testing pregnant women at risk
– NO VACCINE yet, but is a key focus of current
research
HIV treatment
Treatment
– MANY forms of treatment
– Most effective is cocktail of treatments
• HAART
– Protease inhibitor (stops viral maturation)
– Reverse transcriptase (stops viral replication)
– Bad side-effects
– Expensive
– Treatment and Prevention in developing
countries very difficult