Cow Pox Dan Ebola 18

POXVIRIDAE (COWPOX)
FEDIK ABDUL RANTAM, DVM, Dr., Prof.

POXVIRIDAE (VACCINIA)
Objective :
Students should be able
to describe in the
outline the major pox
virus infections of
domestic animals
THE ROLE OF COWPOX DISEASE
History (1770 to 1790).
Therapy causing disease agent
Prevention Pathogenesis
Diagnostic Transmission
methods CACAR SAPI/VARIOLA
/COW POX
One Health:
Solution ?
Animal
Emerging disease ?
Reemerging disease ? Human
(EID) Environment
Definition
Cowpox is an infectious disease by cattle caused by
cow pox virus it the part of poxviridae. This virus
closely related with vaccinia virus.
DISCOVERY
 In the years from 1770 to 1790, who had contact with a cow
had independently tested cowpox vaccine as an immunization
for smallpox in humans.
 the English farmer Benjamin Jesty, in Dorset in 1774 and the
German teacher Peter Plett in 1791.
 Jesty inoculated his wife and two young sons with cowpox, in
a successful effort to immunize them to smallpox, an
epidemic of which had arisen in their town
Orthopoxvirus
• Orthopoxvirus is a genus of poxviruses that
includes many species isolated from mammals
, such as Buffalopox virus, Camelpox virus,
Cowpox virus, Monkeypox virus,
Rabbitpox virus, Volepox virus and Ectromelia
virus, which causes mousepox. The most
famous member of the genus is Variola virus,
which causes smallpox. It was wiped out using
another orthopoxvirus, the Vaccinia virus, as a
vaccine.
Virus and Replication
 Huge, up to 450 nm long with a complex capsid
symmetry. The poxviruses are subdivided into
genera which differ in external structure by electron
microscop
 Poxviruses survive for years in dust.
 Up to 30 different structural proteins.
 Nonstructural proteins include viral epidermal
growth factor and viral DNA and RNA polymerases to
allow intracytoplasmic replication within obvious
inclusion bodies.
CULTURE
 Most poxviruses grow in host cell lines and on
the external surface of chick chorioallantoic
membrane in-ovo,
in-ovo (ectoderm for pox
compared to endoderm for myxoviruses),
where they produce nodular lesions, "pocks".
Infected cells enlarge with vesicles and very
large eosinophilic intracytoplasmic inclusion
bodies (ballooning).
TERGET INFECTION
• Cows,
Cows skin of teats and udder. Control is by
improving herd management, i.e. milking hygiene.
• Cats,
Cats perphaps the original host. Contact infection
through abraded skin. A variety of lesions from
‘shallow , crater-like ulcers filled with white pus’ to
‘flat red, glistening areas’. They are usually on
paws, head or lips and may generalise or cause
pruritis. The respiratory form is rare but fatal.
• Man Cats or cows can infect man to produce
pocks on the forearm or face. These can
generalize if the person is immunosuppressed,
immunosuppressed so
take care.
• Pseudocowpox is a different pox virus which is

less serious and more common in cows. It is also
zoonotic and causes milker's nodules.
PATHOGENESIS
• Primary replication in
abraded squamous
epithelium.
• Viraemia then multiple
infections of skin epidermis.
• Ballooning then necrosis of
the epidermal cells of the
skin with a proliferation of
the adjacent epidermal cells
in response to epidermal
growth factor encoded by
the virus. This proliferation
provides the virus with new
host cells.
Pathogenesis
 The proliferation, ballooning, and final
necrosis (hydropic degeneration) of infected
cells gives rise to the classical sequence of
lesions seen as papule, vesicle, pustule, and
scab The centre of the pock can
finally, scab.
become secondly infected. Resolution in 3-4
weeks.
 Other poxviruses spread to the upper
respiratory tract e.g fowlpox and cat pox.pox
More rarely virus will replicate in the viscera
giving rise to multiple focal lesions which are
often fatal, e.g. sheep pox.
pox
Transmission
Direct transmission (through skin)
Arthropods (vectors)
Milk
Types of lesions
Bumps
Blisters
Pustules
Crusts
Emerging disease
 In Brazil
 It is classified as a zoonotic disease
 to be eradicated by vaccination efforts worldwide
 emain prevalent in certain communities and continue to infect
humans, such as the cowpox virus (CPXV) in Europe, vaccinia in
Brazil, and monkeypox virus in Central and West Africa.
 To occur in human beings who work directly with cattle, the milkers
The hemagglutinin gene of the isolate

clustered with a Russian cowpox virus
strain, and more distantly, with other
cowpox and vaccinia virus strains.
• Vaccinia Virus in Household Environment
during Bovine Vaccinia Outbreak, Brazi
Emerging Infectious Diseases •

www.cdc.gov/eid • Vol. 19, No. 12, December
2013
 Figure. Phylogenetic trees based on orthopoxvirus nucleotide sequences, including
vaccinia virus (VACV) from Brazil (VACV-BR). Phylogenetic analysis was performed
for A56R (A) and A26L (B) gene sequences and grouped VACV-BR strains into 2
branches: group 1 and 2. The Carangola virus (CARV) isolate is indicated by the
black dots. Both trees show grouping of CARV into VACV-BR cluster composed of
Guarani P2 virus (GP2V), Cantagalo virus (CTGV), and other viruses. Trees were
constructed by using the neighbor-joining method, the Tamura-Nei model of
nucleotide substitutions, and bootstrap values of 1,000 replicates in MEGA version
4.0 (Arizona State University, Phoenix, AZ, USA). GenBank accession numbers are
indicated in parentheses. Values along the branches indicate bootstrap values.
Scale bars indicate nucleotide substitutions per site. MURV, Muriaé virus; MARV,
Mariana virus; HSPV, horsepox virus; MPXV, monkeypox virus; ARAV, Araçatuba
virus; PSTV, Passatempo virus; VARV, variola virus.
Diagnosis
Fig. 2.Anti-comet test. After BS-C-1 cells were infected with the IHD strain of
vaccinia virus, pooled serum diluted 1:50 from mice immunized twice with MVA
(106 to 108 pfu) or once with Dryvax was added to the liquid overlay medium. After
48 h, the monolayers were stained with crystal violet.
PREVENTION
 Immunity to cowpox is gained when the smallpox vaccine is
administered.
 Though the vaccine now uses vaccinia virus, the poxviruses
are similar enough that the body becomes immune to both
cow- and smallpox.
 FINAL CONSIDERATIONS Vaccinia virus infections are
extremely relevant for public health and dairy economy in
Brazil, although little is known about the virus fl ow in the wild
and its natural hosts
References
• Abbas, K. (2003). Cellular and Molecular Immunology (Fifth
ed.). Philadelphia: Saunders. ISBN 0-7216-0008-5.
• Rat-to-Elephant-to-Human Transmission of Cowpox
Virus". EID Journal. 14 (4): 670–671. 2008
• Plett PC (2006). "[Peter Plett and other discoverers of cowpox
vaccination before Edward Jenner]". Sudhoffs Arch (in
German). 90 (2): 219–32. PMID 17338405
EBOLA VIRUS
Fedik Abdul Rantam, DVM., Dr. Prof.

Virology and Immunology, Faculty of Veterinary
Medicine, Universitas Airlangga
2016
THE ROLE OF EBOLA DISEASE
History (1976).
Therapy causing disease agent
Prevention Pathogenesis
Diagnostic Transmission
methods EBOLA DISEASE
h ?
lt
Hea
e
On Emerging disease ?
MEAT AND WILD MARKET
VIRUS EBOLA
Familiy Filoviridae, yang mempunyai single, linear,
negativesense ssRNA genomes.
Filoviruses dibagi dua genus: Ebola-like viruses
spesiesnya; Zaire, Sudan, Reston, Cote d’Ivoire,
dan Bundibugyo; and Marburg-like virus dengan
single species Marburg.
Semua spesies diatas sebagai penyebab
hemorrhagic fevers pada primata. Ditandai
banyak perdarahan berakibat fatal dan koagulasi
abnormal.
HISTORI
Penyakit virus Ebola dikenal sebagai penyakit Hemorrhagic
disease yang berat , fatal, menyerang pada manusia dan non-
human primates . Tahun 2014 terjadi outbreak
Virus ini menyebar di beberapa negara di African, termasuk
Sierra Leone, Guinea, dan Liberia.
Virus Ebola pertama kali muncul di Democratic Republic of the
Congo (formerly Zaire) pada musim panas 1976.
Kebanyakan outbreaknya kecil tetapi menjadi perhatian dunia
karena tingkat kematiannya tinggi 90% karena menyerang organ
viscera yang diakhiri dengan kematian.
Virus ini mempunyai kemampuan keluar tubuh, yang bisa
ditangkap oleh mata
MOLECULAR OF VIRUS EBOLA
Phylogenetic of Ebola virus
LIVE CYCLE OF VIRUS EBOLA
TRANSMISSION
TRANSMISSION OF EBOLA VIRUS
Secreted liquid from animal or human infected Ebola virus

High risk with through aerosol with patients sick.
Very possible to use for biological weapon,
Japanese terrorist cult Aum Shinrikyo once unsuccessfully
attempted.
PATHOGENESIS
 Ebola virus entry to the body through mucosal membrane
then infected (monocytes, macrophages, dendritic cells,
endothelial cells, fibroblasts, hepatocytes, adrenal cortical
cells and epithelial cells).
 Incubation time 6 days, but through the direct contact 10 days
 Ebola virus spreading from area lymph nodes the spreading to
liver, spleen and adrenal gland.
 Hepatocellular necrosis asosiation with disregulation factor
coagulation then became coagulopathy.
 Ebola virus induced pro-inflammatory cytokines then caused
multi-organ failure and shock.
 Primata fatal disease
VIRUS EBOLA INFECTED CELLS
IMMUNE SYSTEM TO VIRUS EBOLA
 High fetality rate caused immune respons

 antibody-dependent enhancement is predominant factor
related with heat labil serum and Fc antibodies.
 Through decrease of heat can influence infectivity enhancing
ability antiserum to glycoprotein.
ENHANCEMENT MECHANISM
 Multiple IgG antibodies bind GP epitopes

then binded to C1 in area Fc antibody
 Binded C1q ligands on cell surface then
interaction between Fc dan virus.
 These cases are inculding monocytes
/macrophages and endothelial cells finally
coming hemorrhagic.
 So antibody to make Ebola virus can attach on
cell surface.
DIAGNOSIS
 Symptomatic
 Enzyme linkage Immunosorbance Assay (ELISA) to
glycoprotein
 Immunofluorescence Assay (IFA)
 Reverse transcriptase polymerase chain reaction (RT-PCR)
Montage Fundus Photographs 10 Weeks after Slit-Lamp Photograph of the Left

the Onset of Ebola Virus Disease Eye 14 Weeks after the Onset of
Ebola Virus Disease
• undus Photograph of the Left Eye 14 Weeks
after the Onset of Ebola Virus Disease.
PREVENTION AND TREATMENT
No vaccine and drugs.

No progress of vaccine human, hand non human primata.
Still on going to search replication model to find drug of
antiviral.
Left Eye 14 Weeks after the Onset of

Ebola Virus Disease
CONCLUSION
 Ebola virus is zoonosis virus, single, linear, negativesense ssRNA
genomes. Family Filoviridae.
 Reservoir by fruits bath
 Infected human with haemorragic fever, fatal pada human dan
non human primates
 Respons immune is still not clear, ttetapi menyebabkan antibody
dependent enhancement (ADE)
 Ebola virus can serious cell distroyer diakhiri dengan kematian
sekitar 90%
 There are tree clade in phylogenetic analysis, that are Gabon,
Sudan and Reston, Margburg
 Macrophage have important role in viral infection, juga
menyerang beberapa tipe sel
QUISTIONS
 What kinds of strategy to diagnostic of ebola

virus and cowpox disease ?
 What kinds of prevention to protect infection
of cowpox virus and ebola virus ?
 Please make a concept to eradicate of cowpox
disease and Ebola disease ?
 How do you mind which one strategy for the
prevention of wild infection, explain please ?

Cow Pox Dan Ebola 18

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POXVIRIDAE (COWPOX)

FEDIK ABDUL RANTAM, DVM, Dr., Prof.

Therapy causing disease agent

• Pseudocowpox is a different pox virus which is

The hemagglutinin gene of the isolate

Emerging Infectious Diseases •

Fedik Abdul Rantam, DVM., Dr. Prof.

Therapy causing disease agent

Secreted liquid from animal or human infected Ebola virus

 High fetality rate caused immune respons

 Multiple IgG antibodies bind GP epitopes

Montage Fundus Photographs 10 Weeks after Slit-Lamp Photograph of the Left

No vaccine and drugs.

Left Eye 14 Weeks after the Onset of

 What kinds of strategy to diagnostic of ebola

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