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Dr: MONA BADR
Assistant professor
Consultant virologist
Viral zoonotic diseases
 Divided into two groups:
 1- Arboviruses
zoonotic diseases.
They are transmitted from animal to human through the
bite of arthropode sucking blood vector such as
mosquitoes, ticks and sand flies .
 Arboviruses cause hemorrhagic fever , encephalitis or
febrile illness .
Viral zoonotic diseases
 2- Non
arboviruses zoonotic diseases. This
group include
rabies, Marburg, Ebola ,
Lassa and Hanta viruses .They are
transmitted from infected animal to human through the
bite of rabid animal (rabies) , direct exposure to
blood and tissues from infected monkeys , ( Marburg
& Ebola ) or direct exposure to infected rodents
excreta ( Lassa and hanta).
RABIES
 Rabies is also known as hydrophobia.
 Rabies virus causes an encephalomyelitis leading to
degeneration of neurons in CNS
usually FATAL.
Rabies cycle :
 Wolves, foxes, skunks , raccoons and bats serve as
the natural reservoir for the virus .
 Dogs and cats serve as the most important sources of
human infection , because of their close CNTACT with
humans.
TRANSMITION
 Animal Natural Reservoir all over the world
are
non-domesticated mammals ( wild animals)
as(FOX,WOLVS,BAT) which accidentally bite
domestic animals usually
dogs ,cats
 The virus rarely affects rodents, rabbits or horses
 Humans usually become infected through DOG bites
 Human to human transmission is extremely rare.
Natural reservoir for rabies (WILD ANIMALS).
Natural reservoir for the virus .
Source of human
infection(DOMESTIC ANIMALS)
INCUPATION PEROID
 The incubation period varies depending on the
nature ,severity of the bite(virus concentration in the
saliva of the animal) and on location of the bite
(head ,neck ,trunk, extremities,foot,leg)
 Bites involving the head or neck has short
 The IP can be from 10 days
 (2 WEEKS
2 MONTHS)
IP.
ONE YEAR
Pathogenesis of Rabies
Structure and classification .
 Family : Rhabdoviridae .
 genus : lyssa virus
 The virus is bullet shaped, with helical nucleocapsid.
 The viral genome is ss
–RNA.
 Virion contain the enzyme transcriptase.
 One major antigenic type exist in nature .
Rabies virus .
Pathogenesis .
 After entry the virus replicate s in muscles and
connective tissue at the site of the bite .
 The virus then travels through peripheral nerves to
the spinal cord and the brain .
 After replication in the CNS, the virus spreads through
the peripheral nerves to the salivary
sheds in
saliva .
glands
and
Clinical features
 The incubation period in human depends on the site of
the bite( usually between 1 – 4 months ).
 A bite on the face or neck tend to produce a shorter
incubation period than a similar wound on the foot or leg .
Clinical features
 1--The
prodromal phase:
malaise, headache, nausea , vomiting and fever .
Usually there is discomfort or paresthesia at the site of the
bite .
 2--The
excitement phase:
anxiety, agitation, increased nervousness, hyper
reactivity, pupillary dilation, increased salivation.
painful laryngeal and pharyngeal spasms triggered by
swallowing saliva ( hydrophobia ).
Clinical features
 3-- Paralytic phase : soon a wide variety of the CNS
signs appear including hallucination, lack of coordination,
mental confusion and paralysis .
 4--
finally coma develop and death .
 Recovery from rabies is extremely rare.
 Only six documented cases of human survival from clinical
rabies have been reported.
.
Laboratory diagnosis of rabies .
 In human or animals
by detection of rabies
virus –RNA in saliva, spinal cord ,brain tissue,cornea or
skin by immuno flourecent or PCR .
 Detection of rabies antigen in skin biopsy from the neck,
using direct immuno flourescent technique
( IF ).
Laboratory diagnosis of rabies in animals
.
 In dead animals: by detection
of rabies
antigens in brain tissue, using direct immuno-flourescent
technique
(IF ) .
 Or demonstration of
Negri bodies
,
intra- cytoplasmic inclusion bodies, in the brain tissue.
Negri bodies .
Negri bodies
Negri bodies
Pre-exposure immunization
 Generally confined to those occupationally at risk such
as veterinarians, animal holders, and long term visitors to
endemic areas.
3-doses of the human
diploid vaccine one month apart, with a booster
 They should be given
dose two years later .Tow booster doses should be given
if they are exposed to infection.
Post –exposure or suspicion of
exposure
 Active immunization :
 The main vaccine is the human
diploid cell
vaccine.
 Contains: inactivated virus disrupted into subunits.
 Prepared : in human embryo lung cell.
 Administered : intramuscularly in 5-doses spaced at
0, 3, 7, 14 & 30 days .
Post- exposure, or suspicion of exposure
 The wound should washed thoroughly with
soap and water
and alcohol or iodine solution.
 Patients should be given combined passive and active
immunization.
 Passive immunization: by injecting of
human anti-rabies immunoglobulin( RIG ). The dose is 20
Iu/kg, half given around the bite wound and the other half
intramuscularly
Prevention
 Stray animals should be destroyed.
 Vaccination of pet dogs and animals should be
mandatory
A live attenuates vaccine is available for
immunizing
dogs and cats .
Marburg and Ebola virus infection
 Marburg virus was discovered in 1967, when outbreaks
of hemorrhagic fever occurred simultaneously in Marburg
in Germany .
 Ebola virus was discovered in 1976 and named as a
river in Congo (ZAIRE).
 They have been classified in the family
filoviridae.
 They have ss-RNA genomes with negative polarity .
Marburg and Ebola virus infections
 They cause
hemorrhagic fever with multiple organs
dysfunction and high mortality rate .
 They infect human and non-human primates
(chimpanzees, gorillas and monkeys).
 ANIMAL to HUMAN transmission occur by a direct
contact with blood , tissues & secretion from infected
chimpanzees, gorillas and monkeys .
 HUMAN TO HUMAN transmission seems to be
important in human outbreak via direct contact with
infected blood, organs or secretion of infected person.
Ebola virus .
Pathogenesis
 Ebola & Marburg viruses
micro- vascular
cause damage
to the
resulting in increased
vascular permeability, which may contributing to the
hemorrhagic manifestation .
Clinical features OF
HAEMORRAGIC FEVER due to Marburg
and Ebola virus.
 Short incubation period ranging from 5
– 10 days .
 The two viruses cause diseases with similar clinical
picture .
 The disease is started with fever, myalgia, and headache
 Mucosal bleeding from nose, gum, conjunctiva, GIT
and vagina
 Nausea, vomiting and diarrhea.
 CNS symptom: mental confusion and coma.
Prognosis of
HAEMORRAGIC FEVER due to Marburg and
Ebola virus. .
 During the second week of infection the patient either begin
recovery or develop fatal multiple organ failure.
 Mortality rate ranges from 25
Ebola.
– 90 % , higher with
Laboratory diagnosis
 Hemorrhagic fever viruses are classified as
SAFTY
level class
BIO-
4 pathogens ( BSL-4 ) .
 Lab diagnosis must be accomplished under maximum
biological containment conditions .
 The two most commonly used lab methods are, detection
of the
viral genome in the patient blood using PCR or
isolation of the virus in tissue culture followed by
identification of the virus by PCR .
Treatment and prevention

Treatment is supportive and some trial using
INTERFERON and RIBAVIRIN seems promissing .
 There is no vaccine available yet for Ebola and
Marburg infections.
Rodent- transmitted viruses .
 1– Lassa virus ( family: Arenaviridae).
 2– Hantavirus ( family : Bunyaviridae ).
Lassa fever
 Caused by Lassa virus was discovered in 1969, in Nigeria .
 ss-. RNA with negative polarity .
 Infected rodents shed the virus in their excreta (urine,
saliva and feces ). Humans are infected by direct contact
with rodents excreta, or eating foods contaminated with
these excreta OR through inhalation of tiny particles
contaminated with rodents excreta.
Person to person transmission occurs by direct contact
with infected blood and body fluids OR contaminated
medical instruments .
Clinical features of hemorrhagic fever
(lassa virus)
 Incubation period: 6 – 21 days.
 Lassa fever is an acute viral
hemorrhagic fever with
multi-organ dysfunction (see before).
 About 80% of infected individuals show no symptoms or
had mild illness .
 The remaining 20% develop severe multi-systemic disease
and hemorrhage with high mortality rate.
Lab diagnosis
 Must be accomplished under maximum biological
containment conditions.
 Isolation of the virus in tissue culture, followed by
identification of the isolated virus.
 Detection of the viral
PCR .
RNA in the patient blood using
Treatment & prevention
 There is no specific anti-viral drug therapy.
 Treatment is supportive.
 Prevention:
By controlling rodents.
There is no vaccine available yet .
Hantavirus
The virus was named Hanta as the river Hantaan in
Korea .

Enveloped ,ss-RNA virus with negative polarity .

 The virus is excreted in the urine, saliva and
feces of infected mice
 Humans are infected when they come in direct
contact with rodents excreta .
 No Human to Human transmission has been
recorded
Hanta virus .
Deer mouse
Transmission of hanta virus .
Types of diseases.
 Hantavirus infection ranges from mild to severe .
 Severe cases may take the form of:
1- Renal hemorrhagic syndrome ( RHS ).
2- Hanta pulmonary syndrome ( HPS ) .
The initial symptoms of both syndromes are similar:
Fever, headache, myalgia, nausea, vomiting, and abdominal
pain .
1- Renal hemorrhagic syndrome ( RHS ) .
 Incubation period : 1-5 weeks.
 The disease ranges from mild cases to severe .
 The virus infects the endothelial cells of the blood vessels
in the kidneys, leading to increase vascular permeability,
decreased blood pressure and hemorrhage .
 In severe cases, there will be hemorrhage, renal
dysfunction. Proteinuria and oliguria .
2- Hanta pulmonary syndrome ( HPS ).
 The disease ranges from mild cases to severe .
 The virus affects endothelial cells of the small blood
vessels in the lungs, leading to increase vascular
permeability, decreased blood pressure and hemorrhage .
 In severe cases, tachycardia, shortness of breath,
dyspnea, pleural effusion and hemorrhage are developed .
 Mortality rate is about 50- 70 % .
Lab diagnosis
 1 -- By isolation of the virus in tissue culture, followed by
identification of the isolated virus .
 2– by detection of the
PCR .
viral – RNA , using
Treatment & prevention.
 There is no specific anti-viral drug therapy.
 Treatment is supportive .
 There is no vaccine available yet .