Transcript Rabies_Corona_Rubella_Rotaviruses

Chair of Medical Biology, Microbiology, Virology,
and Immunology
Lecturer As. Prof. O.Pokryshko
Rubellaviruses
The rubella virus is a member of the genus
Rubivirus in the family Togaviridae.
Rubella
(German measles) is a common mild disease
characterized by a rash. It affects children and
adolescents worldwide and can also affect young
adults.
When rubella virus infects susceptible women
early in pregnancy, it may be transmitted to the
fetus and may cause birth defects. Therefore,
accurate diagnosis is critical in pregnancy.
Abnormalities Associated with Congenital
Rubella Syndrome
Type of defects
Examples
Ocular defects
Cataracts
Microphthalmia
Glaucoma
Retinitis
Heart defects
Patent ductus arteriosus
Atrial septal defect
Ventricular septal defect
Peripheral pulmonic artery stenosis
Hearing impairment
Sensorineural deafness
Abnormalities Associated with Congenital
Rubella Syndrome
Type of defects
Examples
Central nervous
system
Mental retardation
Meningoencephalitis
Progressive rubella panencephalitis (rare)
Microcephaly
Other
Growth retardation
Radiolucent borne disease
Hepatosplenomegaly
Hemathologic abnormalities:
Thrombocytopenia, purpura
Pneumonitis
Endocrine dysfunction:
Insulin dependent diabetes mellitus, thyroididtis
Cataract
a child born with cataracts as a result of
CRS (Congenital Rubella Syndrome)
Glaucoma
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Shape: bullet
Genome: -ssRNA
enveloped virus
CPE: Negri body
Structure of Rabies Virus
Reservoir
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Urban forms: Dogs and cats
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Sylvatic forms: Bats, foxes,
raccoons, wolves, skunks, coyotes,
mongooses, and biting animals
Transmission
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By animal bite or scratch
Via saliva
Airborne ( bats)
Transmission of Rabies
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Usually thru infected saliva entering bite wounds.
Virus migrates up peripheral nerves to the spinal
cord and ends up in the brain.
Aerosol transmission has been documented from
caves with large populations of infected bats.
Organ donations—documented from early corneal
transplantation.
In 2004 four US citizens died from rabies acquired via organ transplantation
from the same donor.
Strictly neuronotropic virus
No viremia
Pathology of Rabies Infection
Incubation of Rabies
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Averages three to eight weeks
Can be as short as 1 week or up to 1 year
Bite location and amount of virus present are the
two most important factors in incubation of the virus.
Virus migrates from peripheral nerves to the spinal
cord and ends up in the brain. The Virus replicates
in neurons and migrates out of the brain into the
salivary glands
Clinical Signs of Rabies
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Normally has 3 defined stages
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1. Prodromal Phase—Behavioral changes
This stage lasts 1-3 days
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A. Friendly animals become shy and fractious
B. Wild animals loose their fear of humans
C. Nocturnal animals come out in the day
Clinical Signs of Rabies
2. Hyperactive Stage
It lasts 1-4 days.
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A. Easily Excited
B. Bite anything close by
C. Bite imaginary objects
In some cases the animal does not exhibit the Hyperactive
stage. These animals appear to be in a stupor. This is
called “dumb” rabies
Clinical Signs of Rabies
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3. Paralytic Stage
Viral damage to motor neurons results in paralysis.
This is usually seen first in the hind legs. In
coordination is one of the first signs of the paralytic
stage of Rabies.
Paralysis of the throat causes drooling and the
inability to swallow. Loss of Jaw tone, dropped Jaw.
This stage lasts 1-2 days and is followed by death due
to respiratory failure
Rabies Virus
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Virus multiplies in skeletal muscles and then
brain cells, causing encephalitis
Initial symptoms may include muscle spasms
of the mouth and pharynx and hydrophobia
Rabies disease time course
Prevention of Rabies
Preexposure prophylaxis:
Injection of human diploid cells vaccine
(HDCV)
 Postexposure treatment:
Vaccine plus rabies immune globulin
(RIG)
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No
effective treatment exists.
Postexposure Prophylaxis/PEP:
3 steps
1. Wound care: immediate thorough washing with
soap and water and a virucidal agent such as
povidine-iodine or 1-2% benzalkonium chloride.
Shown
to be protective if performed within 3 hours of
exposure
If puncture, swab deeply in wound and around edges
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2. Passive Immunization: Human rabies
immunoglobulin (HRIG) 20 IU/kg ASAP, but
not longer than 7 days after vaccine given.
Infiltrate entire dose around wound, any
remaining IG inject IM at a site distant from
the vaccine.
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3. Human diploid cell vaccine (HDCV): 1
ml (deltoid) on days 0,3,7,14,28.
HRIG and HDCV: give in
different anatomical sites
and never in the same
syringe
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Challenge Virus Standard
Fatal encephalo-myelitis
Acute rabies
Pasteur Virus strain
Abortive rabies (myelitis) with paralytic
sequelea
Abortive rabies
Rabies vaccine types
Human Diploid Cell Vaccine
(HDCV)
 Rabies Vaccine adsorbed (RVA)
 Purified chicken embryo cell
(PCEC)
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Red Book 2003
Laboratory diagnosis
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Diseased dog: viral antigen and Negri body in
brain tissue.
Patient: IF assay, PCR.
Diagnosing Rabies
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1.Negri Bodies
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Italian Physician discovered them in 1903.
Cytoplasmic inclusion bodies in neurons
Rapid and easy to do in the lab
Neuron with Negri body
Diagnosing Rabies
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2. Mouse Inoculation Test
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Very accurate
Disadvantage is it can take 2 to 3 weeks to make
the final conclusion.
Not in common use due to the accuracy of the
florescent antibody test
Diagnosing Rabies
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3. Fluorescent Antibody Test
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99%+ accurate
Postmortem on brain tissue
Different Serotypes are present, approximately 8
virus variants
PRIMARY METHOD
USED TODAY
Immunofluorescent viral inclusions in a peripheral nerve in a cryostat
section from a patient with rabies, obtained via an antemortem
nuchal skin biopsy.
Rupprecht CE, The Lancet Infectious Diseases Vol 2 June 2002
Rotavirus structure
Naked double
shell capsid
11 segment
double
stranded RNA
genome
Replication in
cytoplasm
Rotaviruses infections
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Account for 50-80% of all cases of viral gastroenteritis.
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Usually endemic, but responsible for occasional outbreaks.
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Causes disease in all age groups but most severe symptoms
in neonates and young children.
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Asymptomatic infections common in adults and older
children. Symptomatic infections again common in people
over 60.
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Up to 30% mortality rate in malnourished children,
responsible for up to half a million deaths per year.
More frequent during the winter.
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Rotavirus / Pathogenesis
Fecal oral transmission, fomites
Highly infectious, 90% of children are
seropositive by age 3
1012 particles/ml in stool; infection can result
from 10 particles
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Incubation period 1-3 days
 24-48 hr incubation period followed by an
abrupt onset of vomiting and diarrhoea, a low
grade fever may be present.
Rotavirus Clinical Features
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Fever, vomiting, watery diarrhea dehydration
 No blood or leukocytes in stool
 Virus replicates in epitheal cells of villi in
small intestine
 Damage to epithelium major cause of
diarrhea
 One virus gene product is an enterotoxin
 Causes loss of electrolytes and prevents
readsorption of water
Self limiting; can be fatal in malnourished or
dehydrated children
Gastrointestinal symptoms generally resolve in 3 to 7 days
Rotavirus Complications
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Severe diarrhea
Dehydration
Electrolyte imbalance
Metabolic acidosis
Immunodeficient children may have more
severe or persistent disease
Clinical appearance of dehydration
Photo Credit: Dr. D. Mahalanabis, World Health Organization
DIAGNOSIS
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Antigen detection in stool
ELISA, LA (Group A rotavirus),
immunochromatographic assay
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Culture- Group A rotaviruses can be cultured in
monkey kidney cells
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Serology for epidemiologic studies
Treatment and prevention
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Treatment
Supportive- oral, IV rehydration
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Prevention
Hand hygiene and disinfection of surfaces
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Vaccine
Live oral vaccine
Coronavirus
•Viral genome structure:
 The non-segmented RNA genome
 The virions is about 100 to 140
nm in diameter
• Viral protein structure:
 Pleomorophic and enveloped
particles
 Characteristic long projected
surface protein (spike) about 20
nm long
www.cell-research.com/ 20033/sars.jpg
Transmission
 SARS-CoV is predominantly spread in droplets shed
from respiratory secretions of patients direct or indirect
contacts
 Less likely by oral-fecal transmission fecal or
airborne transmission
• Viral load is peaked at around 10 days and 13 -14
days in stool
• Clinical course:
Symptoms
 short incubation period (6 days)
 time period from exposure to onset of symptoms
ranging from 2 to 16 days
 intensive care usually required about 10 days after
onset of symptoms
•There are generally 3 phases:
 week 1: cold like symptoms,fever, myalgia, chill and a
sore throat
 week 2, recurrence of fever. Onset of diarrhea, and
oxygen desaturation
 only 20% of patients reach this phase, requires
ventilatory support
 The fatality rate is about 10% upon infection
S
y
m
p
to
m
s
www.health24.com/ images/center/sars_flu.jpg
Breathing
difficulties 3-7
days from onset
of symptoms
Sudden onset of high fever (>38°C) & dry cough
Chills and shivering & muscle aches
Antiviral drugs/Vaccines
•Currently, no specific antiviral drugs available for SARS-CoV
•Vaccines are under development:
 In China, a second-phase human trials of a SARS
vaccine- using inactivated SARS-CoV
The first U.S. SARS vaccine trial at NIH by using
recombinant plasmid for S protein expression
 Development of transgenic tomato and tobacco
expressing SARS-CoV S protein
 An experimental attenuated Vesicular Stomatitis Virus
(VSV)-based vaccine
Control measures
• Close contacts of a probable or suspect case of
SARS are at high risk of becoming a case, and
should be isolated in the community during their
potential incubation period
• Travelers from areas with recent local
transmission of SARS should be given advice
about whom to contact, and what to do if they
develop a fever within their potential incubation
period
• Health departments should assign staff to
undertake contact tracing and daily review of
contacts in the community. Ideally, this should be
in conjunction with a 24-hour SARS hotline
• The recovered patients will be quarantined at
home for at least 14 days after discharged from
hospital
Wearing mask was one of the
main public preventive
measures against SARS