Detail description of Rabies and Poliomylitis

1. Rabies
Aman Ullah

2. Rabies
 Rabies is an acute fatal viral illness of
the central nervous system (CNS)
 The word rabies is derived from the Latin
verb to rage, which suggests the
appearance of the rabid patient
 It can affect all mammals and is
transmitted between them by infected
secretions, most often by bite
 It was first recognized more than 3000
years ago and has been the most feared
of infectious diseases

3. Rabies virus
 The rabies virus is a bullet-shaped,
enveloped, single-stranded RNA virus of
the rhabdovirus group
 Knob-like glycoprotein excrescences,
which cover the surface of the virion
 Strains from different sources are
antigenically heterogeneous

4. Epidemiology
 Rabies exists in two epizootic forms, urban
and sylvatic.
 The urban form is associated with
unimmunized dogs or cats, and the sylvatic
form occurs in wild skunks, foxes, wolves,
raccoons, and bats but not rodents or rabbits
 Worldwide, the occurrence of human rabies is
estimated to be about 15,000 cases per year,
with the highest attack rates in Southeast
Asia, the Philippines, and the Indian
subcontinent
 Risks to humans are from bites by infected
carnivores, omnivores, and bats
 Aerosol spread from exposure in bat caves

5. Pathogenesis
 The essential first event in human or
animal rabies infection is the
inoculation of virus through the
epidermis, usually as a result of an
animal bite
 Inhalation of heavily contaminated
material, such as bat droppings, can
also cause infection
 Rabies virus first replicates in striated
muscle tissue at the site of inoculation

6. Pathogenesis
 Immunization at this time is presumed to
prevent migration of the virus into neural
tissues
 In the absence of immunity, the virus then
enters the peripheral nervous system at the
neuromuscular junctions and spreads to the
CNS, where it replicates exclusively within
the gray matter
 It then passes centrifugally along autonomic
nerves to reach other tissues, including the
salivary glands, adrenal medulla, kidneys,
and lungs
 Passage into the salivary glands in animals
facilitates further transmission of the disease
by infected saliva

7. Pathogenesis
 The pathognomonic lesion is the Negri body, an
eosinophilic cytoplasmic inclusion distributed
throughout the brain, particularly in the
hippocampus, cerebral cortex, cerebellum, and
dorsal spinal ganglia
 The incubation period ranges from 10 days to a
year, depending on the amount of virus
introduced, the amount of tissue involved, the
host immune mechanisms, the innervation of
the site, and the distance the virus must travel
from the site of inoculation to the CNS
 Thus, the incubation period is generally shorter
with face wounds than with leg wounds.
Immunization early in the incubation period
frequently aborts the infection

8. Clinical manifestation
 After an average incubation period of 20 to
90 days the disease begins as a nonspecific
illness marked by fever, headache, malaise,
nausea, and vomiting
 Abnormal sensations at or around the site of
viral inoculation occur frequently and
probably reflect local nerve involvement
 The brainstem infection causes cranial nerve
dysfunction and painful contractions of
pharyngeal muscles with swallowing liquids
("hydrophobia")
 This results in an inability to swallow saliva
and "foaming of the mouth."

9. Clinical manifestation
 Death ultimately occurs secondary to
respiratory center dysfunction

10. Lab diagnosis
 The test of choice in a live patient is
detection of rabies antigen by
immunofluorescent stain of a nape of the
neck biopsy
 PCR of CSF or saliva may supplant the
neck biopsy
 Laboratory diagnosis of rabies in animals
or deceased patients is accomplished by
demonstration of virus in brain tissue
 Histologic examination of their brain tissue
shows Negri bodies in 80% of cases

11. Polio virus (Poliomyelitis)

12. Important properties
 Belong to Picornaviridae
 Positive-strand, single-stranded,
nonsegmented RNA genome
 Non-enveloped, icosahedral

13. Transmission and Pathogenesis
 Fecal-oral route
 Poliovirus infections
may follow one of
several courses:
1. Asymptomatic
infection, which
occurs in 90 to 95
percent of cases and
causes no disease
and no sequelae
2. Abortive infection;
3. Nonparalytic
infection;
4. Paralytic
poliomyelitis

14. Pathogenesis
 The classic presentation of paralytic poliomyelitis is
flaccid paralysis, most often affecting the lower limbs
 This is a result of viral replication in, and destruction of,
the lower motor neurons in the anterior horn of the
spinal cord
 Respiratory paralysis may also occur, following infection
of the brainstem
 Permanent weakness is observed in approximately two
thirds of patients with paralytic poliomyelitis
 Complete recovery is less likely when acute paralysis is
severe, and patients requiring mechanical ventilation
because of respiratory paralysis rarely recover without
some permanent disability
 Approximately 20 to 30 percent of patients who partially
or fully recover from paralytic poliomyelitis experience a
new onset of muscle weakness, pain, and fatigue 25 to
35 years after the acute illness.

15. Center nervous system invasion
by Polio virus