Polio Virus, Rota virus, Rabies virus

Dr. Md. Abdullah Yusuf

Assistant Professor, Dept. of Microbiology
National Institute of Neurosciences & Hospital
Dhaka, Bangladesh
Email: ayusuf75@yahoo.com

Learning Objectives

Structure
virological Characters
mode of transmission
Pathogenesis
Complications
Lab Diagnosis
treatment
Prevention

Classification
Family: Picornaviridae (pico means small)
Genera: 9
Enterovirus
Rhinovirus
Hepatovirus-HAV
Par-echovirus
Aphthovirus-Foot-and-mouth disease viruses
Cardiovirus

Enterovirus
Classification: 5 species
Polivirus: types1,2,3
Coxsachie viruses (town of Coxsackie, N.Y.-1st
isolated)
Group A: types 1-24 (There is no type 23)
Group B: types 1-6
Echovirus: types 1-33 (Missing types 10,22,23 or 28)
(echovirus is derived from enteric cytopathic human
orphan )
Enterovirus: types 68-78 (Missing type 72)

Polio virus: Structure

ssRNA virus
Icosahedral
Non-enveloped (Naked)

Electron micrograph of poliovirus

Virological Characters
Inactivated at 550 C heat for 30 minutes
Higher Conc. of Chlorine needed to disinfect sewage

Mode of transmission
Faeco-oral route

Disease
Poliomyelitis

Pathogenesis
replication in the oropharynx and small intestine (especially in
lymphoid tissue)
the virus spreads through the bloodstream or retrograde along
nerve axons to the CNS

In CNS, replicates in the motor neurons in the anterior horn

cells of the spinal cord

Death of these cells

paralysis of the muscles innervated by

those neurons

CNS invasion by poliovirus.

Remember
Paralysis is not due to virus infection of muscle cells.
The virus also affects the brain stem
leading to "bulbar" poliomyelitis with respiratory
paralysis
but rarely damages the cerebral cortex

Immunity
In infected individuals, the immune response consists
of both
intestinal IgA
humoral IgG to the specific serotype.
Infection provides lifelong type-specific immunity.

Clinical Features
Incubation Period: 7-14 days
Clinical Types: 4 types
1. in apparent, asymptomatic infection
2. abortive poliomyelitis or Minor illness
3. Non-paralytic poliomyelitis or aseptic meningitis
4. paralytic poliomyelitis, major illness

inapparent, asymptomatic illness

results if the viral infection is limited to the
oropharynx and the gut
occurs in 90 to 95% of cases
causes
no disease
no sequelae

Abortive poliomyelitis or Minor illness

a nonspecific febrile illness
occurring in approximately 5% of infected people
Occur within 3 to 4 days of exposure
Fever
Headache
Malaise
sore throat
vomiting
Most patients recover spontaneously.

Non-paralytic poliomyelitis or aseptic

meningitis
occurs in 1% to 2% of patients
Progresses into CNS and meninges, causing
fever
headache
stiff neck
back pain
muscle spasms
in addition to the symptoms of the minor illness
This also usually resolves spontaneously

Paralytic Poliomyelitis, Major Illness

flaccid paralysis- predominant finding

Painful muscle spasms also occur
permanent motor nerve damage
In paralytic polio, meningo-encephalitis involved
meningo-myelo-encephalitis= meninges+Spinal
cord+Brain
Maximal recovery
within 6 months

Complications
Bulbar poliomyelitis
more severe
involve the muscles of the
Pharynx
vocal cords
respiration
death in 75% of patients

Post-polio Syndrome
sequel of poliomyelitis
occur much later in life (30 to 40 years later)
20% to 80% of the original Affected people suffer a
deterioration of the originally affected muscles
Poliovirus is not present
Syndrome is believed to result from a loss of neurons
in the initially affected nerves.
result of physiologic and aging changes in paralytic
patients already burdened by loss of neuromuscular
functions

Post-poliomyelitis syndrome or Progressive

Post-poliomyelitis Muscle Atrophy
Approximately 20-30% patients who partially or fully
recover from paralytic poliomyelitis a new onset of
muscle weakness
Pain
Atrophy
fatigue 25 to 35 years after the acute illness
specific syndrome
Not due to consequence of persistent infection

Conti
A recrudescence of paralysis and muscle wasting has
been observed in individuals decades after their
experience with paralytic poliomyelitis.

Lab Diagnosis
Specimen
throat swabs taken soon after onset of illness
rectal swabs
stool samples
cerebrospinal fluid
Specimens should be kept frozen during transit to
the laboratory.

Cultures
Cultures of human or monkey cells
Cytopathogenic effects appear in 36 days
identified and typed by neutralization with specific
antiserum
by polymerase chain reaction (PCR) assays.

Serology
Paired serum specimens are required to show a
rise in antibody titer during the course of the
disease.

Treatment
Specific antiviral agents
not available

Management
supportive and symptomatic

Prevention
Types of Vaccine
killed vaccine (Salk vaccine, inactivated vaccine,
IPV)
live, attenuated vaccine (Sabin vaccine, oral
vaccine, OPV)

Conti

Both vaccines induce humoral antibodies

neutralize virus entering the blood
prevent CNS infection and disease
Both killed and live vaccines contain all three
serotypes

Difference between Salk & Sabin Vaccines

Attribute

Killed
(Salk)
Prevents disease
Yes
Interrupts transmission
No
Induces humoral IgG
Yes
Induces intestinal IgA
No
Affords secondary protection by No
spread to others
Interferes with replication of
No
virulent virus in gut
Reverts to virulence
No

Live
(Sabin)
Yes
Yes
Yes
Yes
Yes
Yes

Yes
(rarely)

Difference between Salk & Sabin Vaccines

Co-infection with other
enteroviruses may impair
immunization
Can cause disease in the
immunocompromised
Route of administration
Requires refrigeration
Duration of immunity

No

Yes

No

Yes

Injection Oral
No
Yes
Shorter Longer

Live Vaccine
Advantages
(1) Interrupts fecaloral transmission
by inducing secretory IgA in gastrointestinal tract
(2) more readily accepted due to give orally

live vaccine has four disadvantages

(1) reversion of the attenuated virus to virulence
especially for the type 3 virus
(2) Can cause disease in immunosupressed persons
should not be given to them
(3) infection of GIT by other enteroviruses
can limit replication of the vaccine virus
reduce protection
(4) Must be kept refrigerated
to prevent heat inactivation of the live virus

Rotavirus

Learning Objectives

Structure
virological Characters
mode of transmission
Pathogenesis
Complications
Lab Diagnosis
treatment
Prevention

Family
Reovirus

Structure
segmented, double-stranded RNA genome
double-layered icosahedral capsid
Non-envelope

Disease
Most common cause of viral gastroenteritis in young
children
most common in children between ages 6 months
and 2 years

Transmission
by the fecaloral route.
Infection occurs worldwide
by age 6 years most children have antibodies to at
least one serotype

Pathogenesis
Rotavirus replicates in the mucosal cells of the small
intestine =the excess secretion of fluids and
electrolytes into the bowel lumen=consequent loss
of salt, glucose, and water leads to diarrhea
No inflammation occurs
Diarrhea is non-bloody
Watery diarrhea is caused primarily by stimulation of
the enteric nervous system.

Clinical Findings

Nausea
Vomiting
watery, non-bloody diarrhea
Gastroenteritis is most serious in young children
dehydration
electrolyte imbalance
Adults usually have minor symptoms.

Complications

Dehydration
Acidosis
Shock
Death

Lab Diagnosis
detection of rotavirus in the stool by using
radioimmunoassay
ELISA

a 4-fold or greater rise in antibody titer

Treatment
No specific treatment
replacement of fluids and restoration of
electrolyte balance either intravenously or
orally

Prevention
a live rotavirus vaccine (RotaTeq)
contains five human rotavirus strains
The immunogen is the outer surface protein
given orally
replicates in the small intestine.

The five rotaviruses in the vaccine are

reassortants in which the gene for the human
outer surface protein is inserted into a bovine
strain of rotavirus.

Rabies

Learning Objectives

Structure
virological Characters
mode of transmission
Pathogenesis
Complications
Lab Diagnosis
treatment
Prevention

Rabies
Structure
Negative sense ssRNA
helical nucleocapsid
envelope

Pathogenesis
Transmitted by bite of rabid animal
Replication in cytoplasm; budding
Spread by axonal transport to brain
long incubation period
Fever, nausea, hydrophobia, coma
Almost always fatal

Diagnosis
Viral antigen or nucleic acid, Negri bodies

Treatment/prevention
Inactivated viral vaccine for humans after
exposure, live virus vaccine for animals