LIVESTOCK LINE, APRIL 2020 1

LIVESTOCK LINE, APRIL 2020 2

 LIVESTOCK LINE
VOL.13 ISSUE 12 APRIL 2020

˝…’yékÕºø˘ ˝…’Hé
Editor : B. SHIV SHANKAR
Associate Editor : B. KALYAN KUMAR

TECHNICAL EDITORIAL BOARD

Dr. P.K. Shukla, Jt.Commissioner Poultry, G.O.I., New Delhi.
Dr. V. RAMA SUBBA REDDY, Retd. Professor, Agrl. Uni. Hyd.
CONTENTS
Dr. D. NAGALAKSHMI, Asst. Professor, S.V.V.U. Hyderabad.
1. Avian Pox Viruses: ....Organized Poultry Sector
Dr. S.T. VIROJI RAO, Sr. Scientist, AGB, S.V.V.U. Hyderabad.
- Sabarinath T ......................................................... 4-9
Dr. M. KISHAN KUMAR, Sr. Scientist, S.V.V.U. Hyderabad.
Dr. M. KOTESWARA RAO, Vet. Asst. Surgeon, RAHTC, KMNR. 2. Fascioliasis in Ruminants
Dr. P.K. SINGH, Asst. Prof. (A.N.), Bihar Vet. College Patna. - Deepak Sumbria ................................................ 10-11
Dr. S. NANDI, Sr. Scientist, CADRAD, IVRI, Izatnagar, U.P.
Dr. INDRANIL SAMANTA, Lecturer (Micro), WBUAFS, Kolkata. 3. Lumpy skin disease
Dr. M. KAWATRA, Sr. Manager-Bayer Animal Health, Thane (W), Mumbai. - Jeny K John ...................................................... 12-13
Dr. DEVENDRA S VERMA, Tech. Mgr, Biomin Singapore B'lore.
4. Parasitic aortitis in ....to Onchocerca armillata
Dr. R.K.S. BAIS, Sr. Scientist, CARI, Izatnagar, Bareilly.
- K.H. Bulbul ........................................................ 14-17
Dr. VIJAY KUMAR M, Asst. Prof., Vet. College Bidar.
Dr. MD MOIN ANSARI, Asst. Prof., SKUAST, Srinagar, J&K. 5. Post vaccination complication
Dr. AZMAT ALAM KHAN, Asst. Prof., SKUAST, Srinagar, J&K. - Ashok Kumar .................................................... 18-22
Dr. S K MUKHOPADHAYAY, Asst. Prof., (Vety Pathology) WBUAFS, Kolkata.
Dr. SUBHA GANGULY, Scientist, AICRP-PHT, Kolkata Centre. 6. Present Status of Livestock in India
Dr. AIJAZ AHMED DAR, Ph.D. Scholar, IVRI, Izatnagar, Bareilly. - SurajAmrutkar ................................................... 23-29
Dr. SARADA PRASANNA SAHOO, Ph.D. Scholar, IVRI, Izatnagar.
7. Calciumhomeostasis and its associated disorders
Dr. SHRIKANT KATOLE MVSc, Ph.D.(A.N.) Asst. Prof., Anand Agri. University
- Kennady Vijayalakshmy ......................................... 29
Dr. RAKESH ROY, Ph.D, Uttar Banga Krishi Viswavidyalaya,Kalimpong,W.B.
Dr. PRASANNA PAL, PhD Scholar, Animal Physiology, ICAR- NDRI, Karnal. 8. Waste Management at Dairy Farms
- Srijana Sharma .................................................. 30-32
INDEX OF ADVERTISEMENTS
9. Zoonotic Diseases of Cattle
1. Alltech Biotechnology Pvt. Ltd. Title Cover II
- Dr.M.Jeyakumar ................................................. 33-38
2. Alembic Pharmaceuticals Ltd. III

3. Jaysons Agritech Pvt. Ltd. Title Cover IV Livestock Line may not necessarilty
subscribe to the views expressed in the Articles
4. Provimi Animal Nutrition India Pvt.Ltd. Title Cover I
published herein.
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 Avian Pox Viruses: A Bane to Organized Poultry Sector
Sabarinath T1, G.Venkatesan2, S.K.Gupta3, Mageswary R4, S. Chandra Sekar4 and Amit Kumar2
Clinical Bacteriological Laboratory, Division of Virology, IVRI, Mukteshwar- Uttarakhand
1

2
Pox Virus Laboratory, Division of Virology, IVRI, Mukteshwar- Uttarakhand
3
PPR Laboratory, Division of Virology, IVRI, Mukteshwar- Uttarakhand
4
Biochemistry Laboratory, Division of Virology, IVRI, Mukteshwar- Uttarakhand
Email: drsabari143ivri@gmail.com, gnanamvirol@gmail.com, schand_vet@yahoo.co.in
Synonyms: Bird pox, Avian Diptheria, Contagious Epithelioma, Molluscum Contagiosum, Gefluegelpocken
(German), Viruela Aviar (Spanish), Variole Aviaire (French), Bouba (Portuguese).
U
Introduction: Avian pox is a relatively slow- Historical Perspective:
developing disease characterized in birds by Avian pox infections were among the earliest
proliferative lesions on the skin of the head, toes, described avian diseases because of the ease in
legs or mucous membranes of the mouth and identiûcation of the obvious external lesions.
upper respiratory tract. Systemic infections may Bollinger in 1873 and Borrel in 1904 were the ûrst
also occur. Avipoxvirus subgroup as genus of the to demonstrate a relationship between histologic
family poxviridae contains a number of species and lesions and structure of inclusion bodies, setting
strains that vary in their pathogenicity and host the stage for histopathologic techniques being
speciûcity. This widespread avian disease has employed to conûrm visual diagnoses. Evidence
been found in bird families such as Phasianidae that avian poxvirus was associated with the
(Pheasants, Partridges, Jungle fowl, Chickens, inclusion bodies and was the etiological agent was
Turkeys, Quail, and Peafowl) and Emberizidae conclusively demonstrated by Woodruff and
(Buntings, Finches, Grosbeaks, Juncos and Goodpasture in 1930. Cunningham in 1966 cultured
Sparrows). In most birds, avian pox infections are avian pox virus on the ectodermal chorioallantoic
mild and rarely result in death. However, when membrane (CAM) of embryonated chicken eggs.
lesions are on mucous membranes of the oral and Today, identiûcation of avian pox strains has moved
respiratory cavities or on the eyelids, mortality can into the molecular arena, with the use of Gel-
be high. Those avian populations that have been electrophoresis and PCR (Polymerase chain
isolated on islands (for example, Canary Islands, reaction) analyses of mitochondrial DNA
Hawaiian island chain, Galapagos Islands) are sequences.
more greatly impacted than are birds in continental Virus Characteristics:
situations where the hosts, vectors, and viruses
Avian pox virus particles are large, about 150 to
have had a longer co-evolutionary history. As with
250 nm by 265 to 350 nm in size and are either
many other diseases that are density dependent,
oval or brick-shaped and covered with irregularly
avian pox transmission is enhanced with increasing
spaced surface knobs. Fowl pox virus multiplies in
vector and host densities. Therefore, this disease
the cytoplasm of epithelial cells with the formation
is found to have a greater signiûcance in captive
of large intracytoplasmic inclusion bodies (Bollinger
situations such as zoos, bird rehabilitation centers
bodies) that contain smaller elementary bodies
and game farms where birds occur in much higher
(Borrel bodies). The inclusions can be
densities than in the wild. In the wild, the warmer demonstrated in sections of cutaneous and
and mesic regions of the world support more diphtheritic lesions by the use of Haematoxylin and
potential vectors, thus in these areas the prevalence Eosin (H&E), Acridine Orange or Giemsa stains.
of avian pox is higher, particularly in ûocking wild Genomes of avian poxviruses are composed of a
birds. single double-stranded, 300 Kb DNA. This DNA

LIVESTOCK LINE, APRIL 2020 4

 containing, enveloped virus develops in the
cytoplasm of infected avian epithelial cells. Avian
poxviruses can withstand extreme environmental
conditions, particularly desiccation, sometimes
surviving on perches and in dried scabs for months
and years. Much of this can be attributed to the
very large size of the virus. The virus is resistant to
ether, with the pigeon pox virus being resistant to
both chloroform and ether. Avian pox virus particles
can withstand 1% phenol and 1:1,000 formalin for
nine days, but that 1% potassium hydroxide or
heating to 50°C for 30 minutes (or 60°C for eight
minutes) inactivates the virus.
Based on host speciûcity, poxvirus strains have
been identiûed and classiûed as mono-, bi-, or tri-
pathogenic. A Northern Flicker (Colaptes auratus)
virus strain is a good example of a monopathogenic
strain because among 19 species of inoculated wild
and domestic birds, only the Northern Flicker was
found susceptible to infection. Scientists have
argued that strains adapted to various avian hosts
were not different enough to consider them valid
poxvirus species because their basic virus
characteristics appeared to be identical. However,
utilizing recent increases in the sophistication of
molecular research, Avian poxviruses have been
listed as Fowlpox, Turkeypox, Canarypox,
Pigeonpox, Quailpox, Sparrowpox, Starlingpox,
Juncopox and Psittine poxviruses as valid species.
To this species list, further additions include
Peacockpox, Penguinpox, Mynahpox, and
Albatrosspox viruses.
Epidemiology:
The geographic distribution of avian poxviruses is
worldwide with a higher prevalence rate in
temperate and warmer areas of the globe. The
distribution of avian pox in Wild Turkeys (Meleagris
gallopavo) over North America revealed that even
within continents, avian pox distributions tend to be
conûned to localized regions since the disease was
found concentrated in the moister and warmer
southeastern United States, even though Wild
Turkeys occur in every state except Alaska. In
remote islands of the globe such as Hawaii (USA),
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Galapagos (Ecuador) and Canary Islands (Spain),
it was observed that the disease spread rapidly with
much higher prevalence rate in the native avifauna
compared to introduced avian species. Reports
indicate avian pox infections in 278 bird species
from 70 families and 20 orders. It is interesting that
avian pox has never been reported from Tinamous
(Tinamiformes), Loons (Gaviiformes), Nightjars
(Caprimulgiformes), and Kingûshers
(Coraciiformes). Avian pox has been regularly
observed in waterfowl such as ducks and geese.
Avian pox has been also reported in Falconiformes,
Columbiformes, and Psittaciformes.
There are a number of biotic and abiotic factors
that affect the distribution and prevalence of avian
pox. Weather conditions, host densities and
numbers of poxviruses that are present all interact
in a synergistic fashion to mold the epizootiological
framework of avian pox distribution among bird
species and their populations. These factors also
determine in a large part the character and primary
causes of an avian pox outbreak. The other
important factors inûuencing avian pox
epizootiology are host susceptibility and numbers
of vectors that occur within a certain space and
time of the environment. Avian pox can occur at
any time of the year in wild birds. In temperate
regions, where vectors are not active during the
winter period, infections occur primarily in the
summer. In warmer regions of the world, avian pox
is reported throughout the entire year, but most often
during fall and winter months. It is at this time that
host densities are highest because young-of-the
year are present, complemented by the post
breeding ûocking behavior of many bird species.
In addition, those vectors that are speciûc to
poxvirus transmission are usually most abundant
during the fall and early winter period. In California,
avian pox infection occurred throughout the year in
a population of House Finches, but highest
prevalence was during the fall and winter months.
In Florida, peaks of avian pox infection in Wild
Turkeys were observed in fall that occurred
subsequently to peak mosquito activities. In Hawaii,
peak infections were found in fall and early winter.
5
 In temperate regions of North America, during the
fall and early winter the cutaneous form of avian
pox is most common, whereas late in the winter
the diphtheritic form predominates.
Transmission:
Avian poxviruses can be transmitted in a number
of different ways. Even though they are unable to
penetrate unbroken skin, small abrasions are
sufficient to permit infection. The most common
method of transmission is by means of biting
insects such as mosquitoes, mites, midges, and
ûies. At the time of year when vectors are at the
highest numbers, avian pox transmission is
greatest. Many biting insects have been shown to
be mechanical vectors only, transferring virus from
infected to susceptible birds by contamination of
their skin-piercing mouthparts. Transmission can
also occur directly by contact between infected and
susceptible birds or by contact with contaminated
objects such as bird-feeder perches. Aerosol
transmission, although rare, can occur from viruses
being carried along with dust, particularly in conûned
situations.
Clinical manifestations:
Avian pox occurs primarily in two different forms:
(1) the skin form (most common), in which
discrete, wart-like, proliferative lesions develop on
the skin (Fig. A) and the less common diphtheritic
cannot ûnd food. Moreover, when birds are blinded
in the wild, emaciation follows and birds quickly
succumb because of the inability to procure food
or due to predation. In wild birds such as Albatross
(Diomedea immutabilis) that have webbed feet, pox
lesions appear along the ramiûcations of blood
vessels in the foot webs. Focal epithelial
proliferation and later necrosis and sloughing occur
mainly on the plantar surfaces of the webs and toes.
When fully developed, these lesions appear as
circular pocks, 3 to 5 mm in diameter, with central
areas of necrosis, bordered by zones of erythema.
In perching wild birds, lesions start as a swelling
on the toe, leg, or facial region. The swelling
appears smooth, reddish, and dome shaped.
Eventually the swelling cracks or bursts and lesions
begin to form.
In some advanced cases, lesions are present on
both mucous membranes and skin. Lesions of the
mucous membranes, particularly of the mouth and
upper air passages, most often result in high
mortality. In chickens that had the diphtheritic form
of pox, mortality rates were higher than in birds with
cutaneous pox. In canaries, acute systemic
infections are commonly associated with many
deaths. In the wild, birds are rarely found alive with
advanced avian pox infections because they usually
die or are preyed upon prior to reaching this level
of intensity.

form (Fig. B), in which moist, necrotic

lesions develop on the mucous
membranes of the mouth and upper
respiratory tract. A third form, systemic
infection, is rarely found in wild birds.
Lesions are most common on the
unfeathered parts of the body—the
legs, feet, eyelids, base of the beak,
and the comb and wattles of Fig A: Pock lesions in the comb of poultry due to Fowl
gallinaceous birds. A preponderance pox Virus
of lesions on the eyelids may cause Fig B: Diphtheritic lesion in upper respiratory tract of
mortality, as seen in granivorous birds, poultry due to Fowl pox Virus
such as pheasants, quail, and turkeys
Fig C: Pock lesions in Chorio-allantoic membrane of
that have become unable to see and
embryonated egg

LIVESTOCK LINE, APRIL 2020 6

 Pathogenesis:
Upon successful entry of the poxvirus into avian
host epithelium, within one hour the virus penetrates
cell membranes and then uncoats prior to synthesis
of a new virus from precursor material. In the host
dermal epithelium, biosynthesis involves two
distinct phases, the ûrst being host response during
the ûrst 72 hours, followed by synthesis of infectious
virus from 72 to 96 hours. Beginning at 36 to 48
hours, synthesis of host DNA is accompanied by
epithelial hyperplasia, with host DNA declining
abruptly at 60 hours. Hyperplasia ends at 72 hours
with a 2.5-fold increase in cell numbers. The
replication of viral DNA in the avian host begins
between 12 to 24 hours, followed by an exponential
rate of synthesis between 60 to 72 hours. The ratio
of viral to host DNA increases up to 2:1 at 100 hours,
with the maximum titer of virus attained following
cell proliferation. The next phase consists of a
relatively long latent period, with areas of viroplasm
within the cytoplasm surrounded by incomplete
membranes. The viroplasmic particles condense
and acquire an additional outer membrane to
become incomplete virions. These virions migrate
to vacuoles of the inclusion bodies and thus acquire
a membrane coat. The virus then emerges from
the cells by a budding process, resulting in an
additional outer membrane that is obtained from
the cell membrane. This process produces the
classical inclusion body (Bollinger body) that is
observable via light microscopy. Bollinger body is
not always a structure indispensable for the
development and maturation of avian pox in birds
and that infectious virus may be produced by cells
in which matrix inclusion bodies only are present.
In chickens, cutaneous lesions become inûamed
and hemorrhagic just prior to regression.
Desiccation and scab formation then follows, with
eventual sloughing and replacement by normal skin.
This same pattern also occurs in wild birds, but
cutaneous lesions are few and the whole process
of development, regression, and healing of lesions
may be much prolonged. Perhaps the fewer
number of lesions in wild birds occurs because of
LIVESTOCK LINE, APRIL 2020
a high natural resistance to infection, combined with
minimal host response.
Diagnosis:
The visual observation of lesions on birds does not
represent a deûnitive diagnosis of avian pox
infection. Candidiasis, Capillariasis, and
Trichomoniasis all cause lesions in the oral cavity
that look similar to the diphtheritic form of avian pox.
Virus isolation in embryonated eggs & cell
culture:
Isolation via the propagation of virus on
chorioallantoic membranes of chicken embryos
should be used as the deûnitive diagnosis showing
characteristic pock lesions (Fig. C).
Histopathological examination of the CAM lesions
will reveal eosinophilic intracytoplasmic inclusion
bodies following staining with H&E. However, some
strains of avian poxvirus in wild birds such as
Peregrine Falcon (Falco peregrinus) cannot be
cultured on chicken egg CAM, so they were cultured
in Peregrine Falcon eggs itself. Reports suggest
the use of House Finch eggs to culture the avian
poxviruses from Hawaiian bird species such as
Hawaii Amakihi (Hemignathus virens), Apapane
(Himatione sanguinea), Laysan Finch (Telespiza
cantans), and Scarlet Honeycreeper (Vestiaria
coccinea).
Different cell cultures have been used for the
propagation of FPV like Chicken Embryo Fibroblasts
(CEF) (Fig. D), Chicken Embryo Liver (CEL)
Culture, Chicken Embyo Kidney (CEK) Culture,
Duck Embryo Fibroblasts (DEF) and Chicken
Embryo Dermis (CED) Culture. Cell cultures
derived from embryonated chicken eggs offer an
economic and convenient means for pursuit of
many virus investigations as well as for production
of effective viral vaccines. FPV as well as eleven
Avipox virus isolates including Junco Pox and
Pigeon Pox grew well in Quail Testis-35 (QT-35)
cell lines but was unable to grow in mammalian
cell lines. Further, Avian pox viruses can easily be
propagated in continuous Duck Embryo cell lines
such as DEC-99. Characteristic cytopathic effects
7
 (CPE) produced by Avipox virus isolates include
an initial phase of rounding of cells followed by a
second phase of degeneration, plaque formation,
necrosis and sloughing of monolayer (Fig. E).
Fig D: Uninfected monolayer of Chicken
Embryo Fibroblast (CEF)
Fig E: Infected CEF cells showing rounding,
necrosis, degeneration & plaque formation
Electron Microscopy:
Demonstration of typical avian poxvirus particles by
electron microscopy would provide a positive
conûrmation of an avian pox infection. Electron
microscopy of avian pox inclusions reveals viral
particles embedded in a rather homogeneous matrix,
typical of poxviruses.
Serological Tests:
Serological tests such as Virus Neutralization (VN),
Agar gel immunodiffusion (AGID), Passive
Haemagglutination, Immunoperoxidase Test (IPT),
Fluorescent Antibody Test , Immunoblotting (FAT)
as well as Enzyme Linked Immunosorbent Assay
(ELISA) are used routinely to measure specific
humeral antibody responses against avian
poxviruses. AGID is helpful but the test suffers from
limitations such as cross-reactions since one cannot
differentiate different species or strains of avian
poxvirus. AGID is designed to detect avian
poxviruses that cross-react with FPV and pigeon pox
virus strains that commonly affect domestic birds.
ELISA has replaced AGID as it is used in commercial
flock monitoring kits. VN tests are more specific but
are technically more demanding. Passive
haemagglutination is more sensitive than AGID. The
test will give cross-reactions among avian pox
viruses. FAT along with IPT has been used by
researchers to detect the presence of fowl pox viral
LIVESTOCK LINE, APRIL 2020
antigens in whole chicken embryos as well as cell
cultures (Fig. F) and it was noticed that the areas
undetected in IPT for presence of virus revealed
fluorescence in FAT indicating it to be more sensitive
than IPT. However, IPT has the advantage that the
sections can be examined with the light microscope
and can be stored for an extended period without
loss of colour. Antigenic variations between strains
of fowlpox virus can be evaluated by means of
immunoblotting or Western Blotting. However,
Western Blotting is not convenient for routine
diagnosis.
Molecular Methods:
Restriction fragment length polymorphism (RFLP)
analysis can be used for comparison of field isolates
and vaccine strains of fowl pox virus. However, this
procedure is not used in routine diagnosis. Cloned
genomic fragments of FPV can be used effectively
as nucleic acid probes for diagnosis of fowl pox. Viral
DNA isolated from lesions can be detected by
hybridization either with radioactively or non-
radioactively labeled genomic probes. This method
is especially useful for differentiation of fowl pox from
infectious laryngotracheitis when tracheal lesions are
present. Genomic DNA sequences of various sizes
can be amplified by the polymerase chain reaction
(PCR) using specific primers. This technique is
useful when there is only an extremely small amount
of viral DNA in the sample. A nested PCR has been
developed targeting the 4b core protein gene of FPV
in which external primers amplified 578 bp (Fig. G)
DNA fragment while internal primer pair amplified a
419 bp fragment.
Fig F: IFAT of CEF showing presence of Fowl
pox Virus (FPV)
Fig G: PCR amplicon (4b core protein gene of
FPV) in scab, diphtheritic lesion & CEF
8
 Prevention and Control:
Avian pox virus outbreaks that are being transmitted
by vectors, control should be targeted at reduction
of vector populations. Control can also be achieved
by preventing vector access to birds. Where birds
are being artiûcially concentrated, such as in
aviaries, feeders and perches should be sterilized
at least every two weeks using antiseptic cleaning
agent such as bleach. In aviaries, diseased birds
should be kept in separate, isolated, screened
cages. Scientists have found that applying ûowers
of sulfur directly to the lesion or giving it orally
proved beneficial to birds infected with avian
poxviruses. Removal of the lesions and washing
in bicarbonate soda may prove useful, but caution
needs to be taken not to further spread the virus.
Applying silver nitrate, iodine, or 1–2% saline
solution directly to the lesion has also shown some
success in reducing the level of infection. Broad-
spectrum antibiotics are routinely given to birds with
avian pox in an attempt to reduce the chance of
secondary bacterial infection.
Vaccination:
Vaccination of healthy chickens aged 8 weeks or
older is recommended but at least 4 weeks prior to
start of lay. When used properly, vaccine will prevent
clinical signs caused by the virulent field strains of
fowl pox virus. Evidence of successful
immunization with vaccine can be determined by
examining a flock 7-10 days after vaccination for
‘takes’. A take consists of a swelling of the skin or a
scab at the site where the vaccine was applied and
its presence is evidence of successful
immunization. Swelling and scabs will disappear
at about 2 weeks following vaccination. The
absence of take may indicate that the birds were
immune before vaccination or that improper
vaccination methods were used. Fowl pox vaccine
is applied by a wing web stab method. Passively
acquired immunity is a crucial factor to be taken
into consideration during vaccination of progeny
from flocks that has been recently vaccinated. As
passive immunity (for 2–3 weeks) may interfere
with vaccine virus multiplication, such progeny
U
LIVESTOCK LINE, APRIL 2020
should be vaccinated only after the decline of
passively acquired antibody.
References:
1. Singh, P., T.J. Kim, and D.N. Tripathy, 2000:
Re-emerging fowlpox: evaluation of isolates
from vaccinated flocks. Avian Pathol. 29, 449–
455.
2. Singh, P., T.J. Kim, and D.N. Tripathy, 2003:
Identification and characterisation of fowlpox
virus strains using monoclonal antibodies. J.
Vet. Diagn. Invest. 15, 50–54.
3. Singh, P., W.M. Schnitzlein, and D.N. Tripathy,
2003: Reticuloendotheliosis virus sequences
within the genomes of field strains of fowlpox
virus display variability. J. Virol. 77, 5855–5862.
4. Singh, P., and D.N. Tripathy, 2000:
Characterization of monoclonal antibodies
against fowl poxvirus. Avian Dis. 44, 365–371.
5. Srinivasan, V., and D.N. Tripathy, 2005: The
DNA repair enzyme, CPD-photolyase restores
the infectivity of UV damaged fowlpox virus
isolated from infected scabs of chickens. Vet.
Microbiol. 108, 215–223.
6. Tripathy, D.N., 1993: Avipoxviruses. In: Virus
Infections of Vertebrates – Virus Infections of
Birds, Vol. 4, McFerran J.B. & McNulty M.S.,
eds. Elsevier Science Publishers, Amsterdam,
the Netherlands, 5–15.
7. Tripathy, D.N. and L.E. Hanson, 1976: A smear
technique for staining elementary bodies of
fowlpox. Avian Dis. 20, 609–610.
8. Tripathy D.N., L.E. Hanson and A.H. Killinger,
1973: Immunoperoxidase technique for
detection of fowlpox antigen. Avian Dis. 17,
274–278.
9. Tripathy, D.N., L.E. Hanson and W.L. Myers,
1970: Passive hemagglutination test with
fowlpox virus. Avian Dis. 14, 29–38.
10. Tripathy, D.N. and W.M. Reed, 2013: Pox. In:
Diseases of Poultry, 13th edition, Swayne D.E.,
Glisson J.R., McDougald L.R., Nolan L.K.,
Suarez D.L. & Nair V. eds. Wiley-Blackwell,
USA, 333–349.
9
 Fascioliasis in Ruminants
Deepak Sumbriaa, L.D Singlab
a
Post-Doctoral Research Associate, Address: University of Tennessee, Knoxville, USA
b
Department of Veterinary Parasitology, College of Veterinary Sciences, Guru Angad Dev Veterinary and
Animal Sciences University, Ludhiana-141004, Punjab, India
U
Fasciolosis is a main parasitic disease of both
cattle and ovine, caused mainly by Fasciola
hepatica andFasciola gigantica. In some country
like United Kingdom the annual predictable loss
to cattle industry is £23 million.Fasciola
hepatica and Fasciola gigantica are dispersed
across the world and has a broad host range,
including humans. It also leads to a condition
known as “black disease” and is more common
in sheep and usually fatal.
Life cycle:
Eggs are passed in the feces, and miracidia
develop within as little as 9–10 days (at 22°–
26°C). Hatching only occurs in water, and
miracidia are short-lived (3 hr approximate).
Miracidia penetrate inside the lymnaeid snails,
in which asexual growth and multiplication occur
through the stages of sporocysts, rediae,
daughter rediae, and cercariae. After 6 to 7 week,
cercariae emerge from snails, encyst on aquatic
vegetation (like grass blade etc.), and become
metacercariae. After ingestion by the host, usually
with herbage, young flukes excystment take
place in the duodenum, and the immature fluke
penetrate the intestinal wall, and enter the
peritoneal cavity, where they migrate to the liver.
The young/immature flukes penetrate the liver
capsule and tunnel through the parenchyma for
6 to 8 week, growing and destroying tissue. They
then enter small bile ducts and migrate to the
larger ducts and, sometimes, the gallbladder,
where they mature and begin to produce eggs.
The prepatent period is generally 2 to 3 months,
depending on the fluke burden. Adult flukes may
live in the bile ducts of sheep for years
LIVESTOCK LINE, APRIL 2020
Pathogenesis and clinical sign:
Fasciolosis ranges in severity from a devastating
disease in sheep and mainly an asymptomatic
infection in cattle. The course usually is
determined by the number of metacercariae
ingested.
Disease has two form i.e. acute, sub-acute and
chronic. In acute disease,which occurs 2 to 6
week after the ingestion of large numbers of
metacercariae (usually >2,000) over a short
period lead to distended, painful abdomen;
anemia; and sudden death occurring within 2 to
6 week after infection. The acute syndrome can
be problematical by synchronized infections
with Clostridium novyi, consequential in “black
disease” (clostridial necrotic hepatitis), although
this is now less common due to immunization
against clostridial diseases. In subacute disease,
large numbers (500-1,500) of metacercariae are
ingested over longer periods of time; survival is
longer (7-10 week), even in cases with significant
hepatic damage, but deaths occur due to
hemorrhage and anemia. Main form is chronic
and chronic fasciolosis can be seen in all
seasons but shows primarily in late fall and
winter. It occurs as a result of ingesting moderate
numbers (200 to 500) of metacercariae over
longer periods of time. Chronic infection lead to
hepatic fibrosis and hyperplastic cholangitis. In
hepatic fibrosis due to migration of fluke the blood
flow decrease and it lead to coagulative necrosis.
After infection collagen is laid down and fibrotic
band formation occur. At the same time stretching
of scar tissue occur and it disrupt the normal
hepatic architecture. So in order to restore the
normal architecture band are laid to connect the
fibrotic tissue to normal tissue and as a result lobes
are formed. Hyperplastic cholangitis occurs due to
10
 presence of adult fluke in the duct. The tissue near
the fluke became hyperplastic. After some time,
inflammation occur and lymphocyte enter the
lamina propria and it lead to cholangitis. Due to all
these effect protein losses occur form blood. In the
end calcification of lesion start and it lead to the
formation of clay pipe stem liver. The main signs
of chronic infection are anemia, unthriftiness,
submandibular edema, and reduced milk
production, but even heavily infected cattle may
show no clinical signs although their immunity
to other pathogens.
Lesions:
Rigorousness depends on the number of
metacercariae ingested, the phase of
development in the liver, and the species of host
involved. During the first phase, immature,
wandering flukes destroy liver tissue and cause
hemorrhage. The second phase occurs when the
flukes enter the bile ducts, where they ingest
blood and damage the mucosa with their
cuticular spines. In acute fasciolosis, damage is
extensive; the liver is enlarged and friable with
fibrinous deposits on the capsule. Migratory tracts
can be seen, and the surface has an uneven
appearance. In chronic cases, cirrhosis
develops. The damaged bile ducts become
enlarged, or even cystic, and have thickened,
fibrosed walls. In cattle but not sheep, the duct
walls become greatly thickened and often
calcified. Aberrant migrations occur more
commonly in cattle, and encapsulated flukes may
be found in the lungs. Mixed infections
with Fascioloides magna can be seen in cattle.
Tissue destruction by wandering flukes may
create a microenvironment favorable for
activation of clostridial spores.
Diagnosis:
The oval, operculated, golden brown eggs must
be distinguished from those of paramphistomes
(rumen flukes), which are larger, clear and has
clear embryonic mass. Eggs of Fasciola cannot
be demonstrated in feces during acute
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LIVESTOCK LINE, APRIL 2020
fasciolosis. In subacute or chronic disease in
cattle, the number varies from day to day, and
repeated fecal sedimentation may be required.
Diagnosis can be aided by an ELISA
(commercially available in Europe) that enables
detection ~2–3 wk after infection and well before
the patent period. Plasma concentrations of ã-
glutamyltransferase, which are increased with
bile duct damage, are also helpful during the late
maturation period when flukes are in the bile
ducts. At necropsy, the nature of the liver damage
is diagnostic. Adult flukes are readily seen in the
bile ducts, and immature stages may be
squeezed or teased from the cut surface.
Control:
Control measures for Fasciola ideally should
involve elimination of flukes in affected animals,
lessening of the intermediate host snail
population, and inhibition of livestock access to
snail-infested pasture. In practice, only the first
of these is used in most cases. Although
molluscicides can be used to decrease lymnaeid
snail inhabitants, those that are available all have
disadvantages that restrict their use. Copper
sulfate, if applied before the snail population
multiplies each year, is effective but toxic to ovine,
which must be kept off treated pasture for 6 wk
after application. Other such chemicals are
generally too expensive and have ecologically
undesirable effects. Prevention of livestock
access to snail-infested pasture is frequently
impractical because of the size of the areas
involved and the consequent expense of erecting
adequate fencing.
Several drugs are available to treat infected
ruminants, including triclabendazole, clorsulon
(cattle and sheep only), albendazole, netobimin,
closantel, rafoxanide, and oxyclozanide.
Anthelmintic resistance by F. hepatica to various
compounds, including albendazole, clorsulon,
and triclabendazole, has been demonstrated,
further complicating control programs based only
on anthelmintic usage.
11
 Lumpy skin disease
Jeny K John1, Jobin Jose Kattoor2, Naresh Chandra1, Tarun K. Sarkar1, M.V.Jithin1,
Ajit K.Singh1, Atul. K. Verma1, Vinod K Varun1
1
Department of Veterinary Clinical Complex, College of Veterinary and Animal Sciences, SardarVallabhbhai Patel
University of Agriculture and Technology, Meerut, 250110
2
Department of Animal Husbandry, Kerala
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Introduction acidic/alkaline pH (OIE, 2012; Abutarbush et al.,
Lumpy skin disease (LSD) is an economically 2015)
significant disease of domestic ruminants. It is Host
caused by lumpy skin disease virus (LSDV), Cattle and water buffaloes are the natural host
prototype Neetling virus of genus capripoxvirus, for LSDV. Only experimental infections are
and family poxviridae. Earlier, the virus was reported in goat and sheep. Crossbred or
restricted to sub-Saharan Africa but now spread Holstein Friesian breed cattle’s are more
to Asia and Europe (Woods, 1988). It was first susceptible to LSDV. Mortality and morbidity
reported from India in 2019. The primary mode rates are higher in these breeds than local zebu
of transmission of the virus is by arthropod cattle’s. All age group of animals and both sexes
vectors. Cattles and buffalos are the natural hosts are vulnerable to LSDV.
for LSDV. It causes severe economic loss due
Transmission
to reduction in the milk quantity, hide quality,
infertility problems and death. It is a notifiable The primary mode of transmission is arthropod
disease. It is characterized by the presence of vectors. More transmission is reported in humid
nodules in skin and other parts of the body. summer when the arthropod number is more.
Mosquitoes, biting flies and ticks are the possible
Etiology
arthropods involved in transmission. The
LSD is caused by a poxvirus in the genus disease is more prevalent in the low ground
capripox. LSDV is an enveloped, double- and near water bodies. Scabs and crusts from
stranded DNA virus with a genome size of 151 the nodules are an important source of
kilobase pairs (kbp). Capripoxvirus genus infection, whereas placental transmission is
consists of goat pox virus, sheep pox virus and also reported for the virus. The virus was also
lumpy skin disease virus. The viruses are usually isolated from blood, saliva, semen, nasal and
host-specific. LSDV is very stable for long ocular discharges.
periods at ambient temperature in necrotic and
Clinical sign
dried skin lesions. The virus is also stable in dark
areas for long periods. The virus is susceptible The incubation period in natural infection varies
to sunlight, organic solvents, chloroform, ether, from 2 to 5 weeks and in experimental infections
formalin, sodium hypochlorite (2-3%), 0.5% 1-2 weeks. LSD can be grouped into two forms,
quaternary ammonium compounds and highly mild and severe forms. In the mild form, the

LIVESTOCK LINE, APRIL 2020 12

 animal will show fever, few nodules, depression,
anorexia, discharge from eyes and nose, and
agalactia. Nodular lesions are painful and
hyperemic and may be observed in the skin of
muzzle, nares, back, legs, scrotum, perineum,
eyelids, lower ear, tail, nasal and oral mucosa.
Mild form lasts for few days only. In severe cases,
the animal will show high fever, anorexia,
depression and a large number of nodules all
over the body. Later nodules will disappear,
leaves ulcerated lesions on the skin.
Lymphadenopathy is also a feature of LSD.
There is a reduction in milk yield, mastitis,
abortion, orchitis and infertility problems
associated with this disease. The skin lesions
will lead to permanent damage to hide
(Abutarbush et al., 2015)
Differential diagnosis
LSD should be differentiated from a wide variety
of diseases like Ringworm, mite infestation,
allergy, photosensitization, Streptotrichosis,
bovine papular stomatitis, bovine viral diarrhoea,
and malignant catarrhal fever.
Diagnosis
1. Based on clinical signs and gross lesions
2. Electron microscopy
3. Polymerase chain reaction: Quick method
Samples required: Skin nodules and scabs,
saliva, nasal secretions, and blood
4. Virus isolation and identification
5. Serological tests: But can’t distinguish the
three viruses in Capripoxvirus genus
1. Virus neutralisation: Gold standard test
2. Western blot
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LIVESTOCK LINE, APRIL 2020
3. Enzyme-linked immunosorbent assay
(OIE, 2012)
Treatment
Treatment strategy for LSD includes supportive
and symptomatic therapy, including wound
dressing, administration of anti-inflammatory
drug, and prevention of secondary bacterial
infection.
Prevention and control
1. Vaccination : Homologous and heterologous
vaccines are available
2. Restriction of animal movement
3. Proper disposal of dead animals
4. Vector control(OIE, 2012)
References
1. Woods JA. (1988). Lumpy skin disease-A
review. Trop Anim Health Prod. 20(1):11–7.
2. Abutarbush SM, Ababneh MM, Al Zoubi IG,
Al Sheyab OM, Al Zoubi MG, Alekish MO, et
al. 2015. Lumpy skin disease in Jordan:
disease emergence, clinical signs,
complications and preliminary-associated
economic losses. TransboundEmerg Dis.
62(5):549–54
3. OIE Terrestrial Manual. Aetiology
Epidemiology Diagnosis Prevention and
Control References Oie. 2012:1–5.World
Organisation for Animal Health (OIE). Lumpy
Skin Disease: Aetiology Epidemiology,
Diagnosis, Prevention and Control
References. Paris: Organization
International des Epizootics; 2012.
13
 Parasitic aortitis in cattle due to Onchocerca armillata
K.H. Bulbul, R. A. Shahardar, Z. A. Wani, I. M. Allaie, Nazir Ahmed*
Division of Veterinary Parasitology, Faculty of Veterinary Sciences & Animal Husbandry, SKUAST-Kashmir,
Shuhama, Srinagar, 190006 *KVK Budgam, SKUAST-K
U
Onchocerca armillata, an elongate, 1910) (cervical ligaments and
filariform worm found in bloodstream connective tissues of buffaloes) and
and in around arcus aorta (Ozyildiz O. gibsoni (Cleland and Johnston,
et al., 2013), especially found in the 1910) (nodules and worm nests in the
wall of the aorta of cattle, buffalo, subcutaneous connective tissues of
sheep, goat and camels and rarely in cattle).
donkeys causes parasitic aortitis. O.
Transmission of disease:
armillata occurs in brachiocephalic
truncus, cervical and brachial arteries Although black flies and mosquitoes
and the abdominal aorta up to the iliac K.H. Bulbul are thought to be vectors of O.
bifurcation regions. The adult parsites armillata but life cycle are unknown.
are found in tortuous tunnel and nodules in the aorta. fillies play aThe worldwide
great rule todistributions
establish aof direct
these
Onchocercosis in animal has not received much relationship with climate and the incidence of the
attention due to its cryptic nature (Nelson, 1970) of disease.
the parasites but the infection may be common and
Pathogenesis:
has been seen up to 90% of cattle (Soulsby,
1982).The disease is highly prevalent in older cattle In early infection raised tunnels and a few nodules
than the younger cattle. In the majority of the are seen while in older infections the aortic wall is
animals there is no obvious clinical evidence to thickened, the intima shows numerous tortuous
indicate the microfilariae. The age of the infected tunnels and there are numerous nodules containing
animals varied from 1½ to 5 years. The infection yellow caseous or slimy fluid and coiled worms.
was more in male as compare to female with Affected aortic intima layers have undulant
slightly more infection in crossbred than in local appearance. Moreover, numerous tunnels and
cattle Begam (Begam et al., 2015). nodules are found in the media. These nodules
show protrusions towards the intima and media
Distribution of the disease:
layers. Besides survived mature microfilaria may
The occurrence of parasitic aortitis due to bovine be exceeded through the circulation, the parasitic
onchocerchosis is worldwide distributed mostly in tunnels are filled with a thin connective tissue
many temperate and tropical countries (Cheema without inflammatory cells. Granulomatous
and Ivoghli, 1978), has not received much attention, nodules present around the dead, degenerate or
partly because of its cryptic nature. O. armillata is calcified parasite larvae, contain dominantly
generally observed in the south of the Asian regions eosinophils and leukocytes. Granulomatous foci in
and African continent closer to the equator. In India the vessel wall can be localized over time.
the disease is reported from Orissa, Uttar Pradesh
The parasitic cysts, live, dead and calcified tissues
and Assam. The onchocercosis was also reported
and the compatible degenerated or calcified cysts
in the Bangladesh, Iraq, Iran, Tanzania, Turkey,
are located close to each other. Similarly,
Cameroon, Nigeria Venezuela and in the Greece.
degenerated or calcified cysts are also surrounded
In India 3 species of Onchocerca are in prevalence
by the parasitic granulomas that contain giant cells,
in animals i.e. Onchocera armillata (Railliet and
eosinophils, macrophages, lymphocytes and
Henry, 1909) (in the tunica intima of aorta in cattle,
fibroblasts. The absence of any inflammatory
buffaloes and goats); O. gutturosa (Neumann,
reaction around tunnels and some parasitic cysts

LIVESTOCK LINE, APRIL 2020 14

 is remarkable. However, in some cases, these
parasite tunnels are found to be calcified. It is
pertinent to mention that no inflammatory reaction
occur against to live and vibrant forms of parasite.
A substance released from live cuticula of parasite
body prevents reaction against to the parasite.
Neutral fat is in parasites and surrounding cells.
Both changes often occurred in the same
specimen and many samples have parasites but
no tissue reaction. Hypersensitivity, foreign-body
reactions and parasitic toxins apparently may be
involved in the genesis of these lesions.
There are three stages of inflammatory reactions
occurs in aorta when infected with O. armilata viz.
acute, subacute, and chronic granulomatous
aortitis.
Acute aortitis:
It is mostly started at adventitial vessels of infected
animals. The sporadic eosinophils, neutrophils and
macrophage infiltrations are increased in a linear
style from intimal vessels to muscle bundles
(Soulsby, 1982). The dilated blood vessels, rounded
endothelial cells, inflammatory oedema and
hyalinization of muscle bundles are noticed around
the parasitic cysts in some part of the affected
areas. The intima is thicker because of oedema,
haemorrhage and heavy infiltrations, predominantly
by eosinophils with some lymphocytes and plasma
cells in acute aortitis. Congested blood vessels are
swollen and have round endothelial cells in the
media. Accumulated cellular infiltration in irregular
masses around blood vessels form linear streaks
between elastic and smooth muscle fibres.
Oedema and cellular infiltration are in the adventitia
and surrounding loose connective tissue.
Subacute aortitis:
A great number of eosinophils, a few numbers of
macrophages, lymphocytes and plasma cell are
infiltrated surroundings of medial and adventitial
layers. These cells are moving towards to the dead
and caseous parasitic cysts. This cellular infiltration
is generally localized around the old or calcified
tunnels in the affected areas. The formation of new
blood vessels due to presence of few fibroblasts in
some areas may also be detected.
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Chronic granulomatous aortitis:
The chronic granulomatous aortitis, the most
common type are frequently occurred in very old
cattle. In this case, the nodules become calcified,
the aortic wall is thin, with linear, broken, calcified
ridges, and aneurysms may be seen (Cheema and
Ivoghli, 1978). Granulomatous reaction may be
occurred around tunnels containing degenerate,
dead and calcified worms. In early stages there is
much necrotic debris at the centre surrounded by
a radially-arranged row of elongated cells that have
fused to form giant cells. The tunnels are fewer in
these cases, white, flat or depressed and nodules
may be rare or absent. There are aneurismal
dilations up to 3.5 centimeters in diameter in some
cattle. There are chronic granulomatous reactions
characterized by accumulation of macrophages,
lymphocytes, plasma cells, giant cells, calcification
and fibrosis around degenerate and dead parasites.
Hyperchromatic and multinucleated giant cells are
observed around the dead, degenerated or calcified
parasitic cyst walls. Moreover, a large number of
eosinophilic infiltrations are present between giant
cells. This infiltration is supported by dense
macrophages, lymphocytes, and plasma cells. The
outermost composed from granulation tissue that
including fibroblasts, fibrocytes and newly formed
blood vessels. In some areas, inflammatory cell
infiltration is decreased while sclerosis is
increased. In some other cases, arteriosclerotic foci
with presence of clefts at their centers composed
of lymphocytes, macrophages, fibroblasts, and
fibrocytes are also noticed.
Clinical symptoms:
Clinical signs are not usually attributable to the adult
although Patnaik (1962) suggested that epileptic
fits, blindness and periodic opthalmia may be seen
in some cattle with high counts of microfilariae.
Onchocercosis often do not show any significant
clinical symptoms but sometimes the bulls show
neural symptoms. Sometimes microfilaria localized
at ocular regions causes recurrent ophthalmitis.
Onchocerca armillata mostly settles in the arcus
aorta region causing calcified nodules which are
responsible for aneurysms in very old animals.
15
 Gross lesions:
The parasitic tunnels, nodules, roughening and
calcification in the aortic walls are concentrated in
the upper thoracic aorta but also are in the
brachiocephalic trunk and bicarotid artery in some
cattle. Generally one circumscribed area of raised
tunnels forming intricate patterns and one or two
nodules at the edge of affected areas in mild early
infection may be encountered in young cattle. The
aortic walls are thicker and intimal surfaces uneven
because of numerous tortuous tunnels while
nodules are observed in heavily infected older
cattle. The affected vessel walls, in general,
thickened, crusty in consistency and lost flexibility
are observed in aortic onchocercosis. In some
cases the vessel walls are also in appearance of
rubber tube and their lumens are severely
narrowed. The openings of intercostal arteries are
constricted and wrinkled.
The intima, media and adventitial layers of the aorta
show the following accordingly;
Tunica intima: The yellowish gray coloured
nodules measuring 0.5-4.0 cm in size, especially
in areas close to the bifurcation, projecting to the
vessel lumen, hard in consistency, bright and white
surface, cross-sectional areas of calcification felt
creaking. Finally the affected areas are become
tough and an irregular surface. In cut surfaces, dry
and caseous structures are noticed which is
cleaved easily and surrounded by a tough
connective tissue to the size varies from lentils to
nuts. In some areas, upturned edges formed crater-
like foci which cause shrinkage of the surface with
the star-like connective tissue indurations. However,
the caseous foci, easily cleaved and yellowish gray
in color may also be observed in cross section of
the tunica intima.
Tunica media: The tough and an irregular surface
are found in cross section of the affected areas.
Thickening of the medial layer are occurred due to
granulomas formed by the parasites. The dark red-
brown old hemorrhage areas hard in consistency
are observed along with the long axis in some
areas.
Tunica adventitia: The parasitic bud-like nodule
located sometimes single, sometimes combined
LIVESTOCK LINE, APRIL 2020
with each other in groups of two to three in the
adventitial layer. These types of nodule formations
are observed rarely. The diameter of the
granulomas is quite large (up to 4 cm) in this layer
compared to the intimal layer. When granulomas
those over-flow out of the vessels, they become
hard in consistency, and often surrounded by a
broad connective tissue. The presence of large
caseation and small amount of calcified areas are
observed in cross-section of tunica adventitia. In
the adventitia they resembled lymph nodes, are firm
and sometimes sessile. The nodules originated in
the media and, depending upon their location,
projected either towards the lumen or the periphery.
They usually had thick capsules and contained
yellow caseous material, small amounts of clear
slimy liquid, coiled worms and sometimes blood.
The older ones had dry calcified contents.
Microscopic lesions:
In histopathological examination generally, varying
degrees of tissue reactions are perceived in the
aorta. Microscopically there are acute changes with
oedema, haemorrhages and cellular infiltrations
predominantly by eosinophils. The majority of
parasitic tunnels contain dense haemorrhagia
without inflammatory cell infiltrations are located in
the intima and media. It is pertinent to mention that
the calcium deposits are found in some regions of
these parasitic tunnels. There are round or
ellipsoidal cavities containing one or more intact
parasitic sections, some with microfilariae. The
tunnels have a thin lining of fibrous tissue but no
cellular infiltrations. There are spaces between the
lining and the worm sections, but their contours
indicated the parasites had fitted tightly into the
tunnels during life. Worms and its structure
surrounding thin cuticula may be appeared to reside
within around or ellipsoidal cavity, with a space
between the worm section and the host-derived
lining. However, some parts of the parasitic cysts
may be restricted by a thin connective tissue
without any inflammatory cell infiltration. Moreover,
a thin halo may be found between larvae and the
connective tissue capsule. The hyalinised muscle
fibers around the parasitic cysts and tunnels are
the microscopic evidence of the parasitic aoritis in
16
 cattle. In stereo and light microscopic examination,
parasitic loops appeared to be hanging free in the
lumen. They always may found to be covered with
thin layers of medial and intimal tissues.
Masson’s trichrome stain may be used for the
presence of collagen, connective tissue around the
parasitic tunnels and granulomatous lesions. When
Haematoxyllin and Eosin stain is used the calcium
deposits around and in the parasitic cysts and
tunnels appear as basophilic. Verhoeff‘s stain
shows sharp breaks, deflection and compression
of elastic fibres of the aortic media around the
parasitic tunnels. Fine fibrils of regenerated elastic
tissue may be seen in the areas of healing. Bright
red with PAS and rose-red with Masson’s trichrome
are found in homogeneous material of the parasitic
tunnels. Giant cells are also noticed in PAS-positive
material. Neutral fat are also seen in the intact
parasitic sections and in the cells around the
degenerate and dead parasites.
Treatment:
Use of anti-helmenthic drugs and pesticides
decreased the presence of Onchocerca spp. in the
both vectors and hosts.
Significance importance:
Many, but not all, filarial nematodes carry within their
tissues endosymbiotic, Rickettsia-like bacteria of
the genus Wolbachia. The majority of filarial
nematodes have been found to contain the
endosymbiont Wolbachia. It has been suggested
that Wolbachia may be important in evading the
host immune response in those species
of Onchocerca associated with the bacteria. O.
armillata contain Wolbachia in the hypodermis of
adult female worms and in intrauterine structure of
female reproductive tract. Recent finding of
endosymbiont Wolbachia in O. armilleta (Neary et
al., 2010) is expected to initiate new direction in
research and clinical medicine towards this
unattended filarialparasite in cattle.
Conclusion:
Formation of tortuous tunnels and nodules in the
arcus aorta of both in adult and young cattle,
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LIVESTOCK LINE, APRIL 2020
epileptic fits, blindness and periodic ophthalmia may
be exhibited in cattle. This is assumed to be due to
higher vector availability and activity. Recent
findings of endosymbiont Wolbachia in O. armilleta
are anticipated to instigate new advancement
towards the goal of research in the field of
unattended filarial parasite in cattle.
References:
Alibasoglu, M., Golesuk, K., Erturk, E. and Guler,
S. (1969). Turkiyede sigilarde gorulen
onchocerciasis olayari (Onchocerca armillata
Raillet ve Henry 1909). Vet. Fak. Derg. Ankara. Univ.
16: 50-60.
Al-Zubaidy, A. J. (1973). Observations on parasitic
aortitis in cattle in Iraq. Trans. R. Soc. Trop. Med.
Hyg. 67: 636.
Begam, R., Islam, S., Saikia, M., Kalita, A., Bulbul,
K. H., Bam, J. and Pathak, P. (2015). Prevalence
of aortic onchocerciasis in cattle of Assam.
Veterinary Practitioner, 16(2):225-227.
Cheema, A. H. and Ivoghli, B. (1978). Bovine
onchocerciasis caused by O. armillata and O.
gutturosa. Vet. Pathol. 15: 495-505.
Neary, J.M., Trees, A. J., Ekale, D.D., Tanya, V.N.,
Hetzel, U. and Makepeace, B. L. (2010).
Onchocerca armillata contains the endosymbiotic
bacterium Wolbachia and elicits a limited
inflammatory response. Vet. Parasitol. 174(3-4):
267-276.
Nelson,G.S. (1970). Onchocerciasis. Adv.
Parasitol. 8: 173-224.
Ozyildiz, Z., Yilmaz, R., Ozsoy S. Y. and Ozkul, I.
A. (2013). Parasitic aortitis due to Onchocerca
armillata in slaughtered cattle in the southeastern
region of Turkey. Kafkas Univ. Vet. Fak. Derg. 19:
589-594.
Patnaik, B. (1962). Onchocerciasis due to O.
armillata in cattle in Orissa. J. Helminthol. 36: 313-
326.
Soulsby, E. J. L. (1982). Healminths, Arthropods
and Protozoaof domesticated Animals. 7thEdn.
Bailliere and Tindall, London. pp-325-326.
17
 Post vaccination complication
Ashok Kumar*, Vishal Rai, Ajay Kumar Yadav, Laxmi Upadhyay, Mukesh Bhatt
ICAR-Indian Veterinary Research Institute, Izatnagar, Bareilly, U.P.-243122
*Corresponding author: vetashok5@gmail.com
U
Introduction
Vaccination can be defined as administration of an
antigen (vaccine) to stimulate a protective immune
response against an infection. It continues to be
the only safe, reliable, and effective way of protecting
animals against the major infectious diseases.
Vaccine related complication is usually rare, mild
and transient and hypothetical side effects most
not dominate our perceptions. Nevertheless the use
of vaccine is not free of risk.The issue of risk
associated with vaccination remains in large part
a philosophical one, since the advantages of
vaccination are well documented and extensive
whereas the risks for adverse effects are poorly
documented. Traditionally adverse events are
reported voluntarily by veterinarians to
manufactures or government agencies.In
determining whether a vaccine causes adverse
effects or complication, following three principles
should apply.
1. Consistency: It means the clinical responses
should be same if the vaccine is given to a different
group of animals, by different investigators and
irrespective of the method of investigations.
2. Specificity: It means the association should
distinctive and the adverse event linked specifically
to the vaccine concerned. An adverse may be
caused by vaccine adjutants and additives other
than the active component.
3. Temporal relation: it means administration of
vaccine should precede the earliest manifestations
of the event or a clear exacerbation of a continuing
condition.
Classification
Post vaccination complication or adverse effects
of vaccine can be classified in following ways.
1. Complication due to normal toxicity.
LIVESTOCK LINE, APRIL 2020
2. Complication due to errors.
3. Complication due to inappropriate responses.
1. Complication due to normal toxicity
Vaccines commonly elicit transient inflammatory
reaction and some degree of inflammation is
required for the efficient induction of protective
immune responses. This may cause pain. More
commonly local swellings may present at the
reaction site. These may be firm or edematous and
be warm to touch. They may appear about one
day after vaccination and can last for about one
week. Unless an injection site abscess develops
these swellings leave little trace. Vaccines
containing gram negative organisms may be
intrinsically toxic owing to the presence of
endotoxins that can cause cytokine release, leading
to shock,fever and leucopoenia. Vaccinating
pregnant animals may lead to abortion.
2.Complications due to errors:
These types of complications may arise either due
to errors in manufacture or errors in
administration.If during administration of vaccine,
sterilized procedure are not followed then there will
be contamination leading to clinical disease. Also
during vaccination there will be stress leading to
reactivation of latent infection. For example,
activation of equine herpes virus infection has been
demonstrated following vaccination against African
horse sickness. In case of complication due to
errors in manufacture, if proper aseptic measures
are not taken, then there will be contamination
leading to clinical disease and fatal death. Again if
there will be improper activation of the vaccine
agents’ then abnormal toxicity may appear.
Vaccines such as blue tongue vaccine have been
reported to cause congenital anomalies in offspring
of ewes vaccinated while pregnant. Further, due to
residual virulence, there may be some
18
 complications as in case of modified live herpes
virus vaccine or calcivirus vaccine which are given
intranasal spread to oropharynx & cause persistent
infection. Such a virus vaccine may infect other
animals in contact. Even if these vaccines do not
cause overt disease, they may reduce the rate of
growth of farm animals with significant economic
losses. In case of modified live parvovirus vaccine
there is transient decrease in lymphocyte
blastogenesis or even a lymphopenia in some
puppies. Some poly canine viral vaccines cause a
transient drop in absolute lymphocyte numbers and
their responses to mitogens. This occurs even
though the individual components of these vaccines
may not have this effect. Several vaccine
combinations may cause changes between 5 &11
days after vaccination. For example CAV1&2 with
CD is especially suppressive of canine lymphocyte
responses to mitogens.
3. Complication due to inappropriate response:
These complications are produced because of not
inducing proper immune responses. These are
classified into broadly into three types.
A. Hypersensitivity reactions
(a) Type I hypersensitivity
(b) Type III hypersensitivity
(Fig.1: Mechanism of Type I hypersensitivity reaction)
LIVESTOCK LINE, APRIL 2020
(c) Type IV hypersensitivity
B. Neurological reactions:
(a) Neuritis(b) Encephalitis
C. Foreign body reactions:
(a) Fibrosarcoma
(b) Type IV reactions
A. Hypersensitivity reactions
(a) Type I hypersensitivity reaction--In this
complication the vaccine induces a normal
humoral antibody response by the same
mechanisms as for other soluble antigens, resulting
in the generation of antibody-secreting plasma cells
and memory cells. The main distinction from a
normal humoral response is that the plasma cells
secrete IgE antibody. Figure 1 shows the
mechanism of Type I hypersensitivity induced by
vaccine. After administration of vaccine B cells are
activated to form IgE secreting plasma cells. These
secreted IgE molecules bind to IgE specific Fc
receptors on mast cells and blood basophils.
Second exposure to the allergen leads to cross
linking of the bound IgE, triggering the release of
pharmacologically active mediators, vasoactive
amines, from mast cells and basophils. The
mediators cause smooth-muscle contraction,
increased vascular permeability, and
vasodilatations.
19

(Fig.2: vaccine induced Type I hypersensitivity)
(b) Type III hypersensitivity – This type of
hypersensitivity is immune complex mediated and
it is seen after 6-8 hours of administration of
vaccine. It is again classified as either local or
generalised type III hypersensitivity reaction.
(i) Local TypeIII hypersensitivity reaction-
Injection of an vaccine into an animal that has
high levels of circulating antibody specific for that
vaccine leads to formation of localized immune
reactions. This type of reaction can occur in the
eyes of dogs vaccinated against infectious canine
hepatitis. Some rabies vaccines may induce a local
complement mediated vasculitis leading to
ischemic dermatitis and local alopecia. This type
of reaction is most often seen in small dogs such
as Dachshunds, Miniature poodles, Bichon Fries
and Terriers.
(Fig.3: Blue eye condition in a dog vaccinated
with infectious canine hepatitis vaccine)
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(ii) Generalised Type III hypersensitivity
reaction-This type of hypersensitivity reaction has
been noticed in passive immunization in case of
dogs who had received a very large dose of equine
antitetanus serum. This reaction is called as serum
sickness and consists of a generalized vasculitis
with erythema, edema, and urticaria of the skin,
neutropenia, lymph node enlargement, joint swelling
and proteinuria.
(c) Type IV hypersensitivity reaction-The most
common reaction of Type IV hypersensitivity
reaction is granuloma formation at the site of
inoculation within 24-72 hr of vaccination. This may
be a response to depot adjuvants containing alum
or oil. Vaccine containing water-in-oil adjuvant
produce larger and more persistent lesions at
injection sites than vaccines containing alum and
aluminium hydroxide. These lesions can be
granulomas or sterile abscesses. If the skin is dirty
at the site of injection, these abscesses may
become infected. Fig. 6 shows the detailed
mechanism of Type IV hypersensitivity reaction
induced by vaccine. In this case when first injection
of vaccine is administered sensitized T cells are
produced. During second injection, the vaccine
antigen is captured by Langerhans cells and
presented to T cells. As a result the sensitized
memory T cells activated and produce Th1 effectors
cells. Now these Th1 cells migrate to site of
injection and secrete chemokines which attract
basophils, macrophages and more T cells. As a
result there will be inflammation followed by
granuloma formation.
B. Neurological reactions: Sometimes
neurological reactions are produced as a
complication to vaccination
(a) Neuritis- A polyneuritis has been associated
with the use of certain virus vaccines ( most notably
swine influenza in humans ) and the disease is
called as Gullain-Barre syndrome. One case has
been reported in dogs following vaccination with a
20
 (Fig.5: Mechanism of granuloma formation)
polyvalent distemper – hepatitis-parvovirus vaccine.
The pathogenesis of syndrome is unclear.
(b)Encephalitis- Rabies vaccine that contains
central nervous tissue may provoke autoimmune
encephalitis. Post vaccinational canine distemper
virus encephalitis is a rare complication that may
develop after administration of a modified live canine
distemper vaccine. The affected animal may show
aggression, incoordination and seizures or other
neurological signs. The pathogenesis of this
condition is unknown, but it may be due to residual
virulence, increased susceptibility or triggering of
a latent paramyxovirus by the vaccine.
C. Foreign body reaction – Vaccines when
administered can be treated as a foreign body to
produce either Type IV hypersensitivity reaction or
fibrosarcoma. Type IV hypersensitivity reaction has
already been described. Fibrosarcoma has been
seen in cats vaccinated against rabies & feline
leukemia with adjuvanted vaccine. It is seen mostly
in cervical, intercervical and femoral region.
LIVESTOCK LINE, APRIL 2020
Prolonged irritation by adjuvanted vaccine increase
the activation state of the cells involved in
inflammation and tissue repair. So local stem cells
number increased at the site of irritation and there
is possibility that some cells will mutate. During
chronic inflammation macrophages secrete growth
factors and angiogenic factors that enhance cell
growth. These factors will upregulate NF-kB activity
in affected tissues. Oxidants released from
activated macrophages may act as carcinogens,
especially in cells that are dividing rapidly. Although
the mechanism is not clear NF-kB promotes both
malignant transformation and metastases may
promote cancer cell formation by inhibiting
apoptosis of premalignant cells. Fibroblasts are
also stimulated to proliferate at sites of chronic
inflammation. In some of these fibroblasts the sis
oncogene is activated whereas in others there
appear to be mutations in the gene coding for tumor
suppressor factor. The cis oncogene codes for the
platelet derived growth factor (PDGF) receptor and
vaccine associated sarcomas have been shown
21
 to express both PDGF and its receptor. Besides
this vaccine associated sarcomas also express
mutated p53.
Precautions for post vaccination complication
Following precautions can be taken to prevent post
vaccination complications
a. Proper sterilization of syringe & needles before
vaccination.
b. Reconstituted vaccine should be discarded at
the end of each vaccination.
c. Training of immunization worker
d. Adrenaline (1: 1000 solutions) should be used
in the event of anaphylaxis
e. An injection of antihistaminic drug &
corticosteroid should be kept ready during
vaccination
Conclusion
Vaccination is the preventive measure to protect
individuals against the infectious diseases. But the
use of vaccine is not free of risk. Residual virulence
and toxicity, allergic reactions, disease in
immunodeficient hosts, neurological complications
and harmful effects on the fetus etc are the most
significant risks associated with the use of
vaccines. Veterinarians should use only licensed
vaccines and the manufacturer ’s
recommendations should carefully be followed.
Before using a vaccine, the veterinarian should
consider the likelihood that an adverse event will
happen, as well as the possible consequences or
severity of this event. These factors must be
weighed against the benefits to the animal. Thus a
common but mild complication may require a
different consideration than a rare, severe
complication.
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LIVESTOCK LINE, APRIL 2020
References
1. Edwards Ds, Henley WE, Ely ER, Wood JLN.
(2004). Vaccination and ill health in dogs: a lack
of temporal association and evidence of
equivalence. Vaccine 22: 3270-3273
2. Frank LA. (1998). Rabies vaccine- induced
ischemic dermatitis in a dog. Veterinary Allergy
Clinical Immunology 6: 9-12.
3. Gray A and Knivett S. (2000). Suspected
adverse reactions. Veterinary Record 147: 283-
284.
4. Hendrick MJ, Kass PH McGill LD and Tizard
IR. (1994). Post vaccinal sarcomas in cats,
Journal of National Cancer Institute 86: 341-
343
5. Kuby Immunology by Thomas J. Kindt , Richard
A. Goldsby , Barbara A. Osborne . Sixth Edition
6. Mayer EK. (2001). Vaccine associated adverse
events. Veterinary Clinical North America 31:
493-515
7. Moore GE, Guptill LF and Ward MP. (2005).
Adverse events diagnosed within three days
of vaccine administration in dogs. Journal of
Veterinary Medical Association 227: 1102-1108
8. Schrauwen E and Van Ham L. (1995). Post
vaccinal polyradiculoneuritis in a young dog.
Programme Veterinary Neurology 6: 68-70
9. Smith H. (1994). Reactions to strangles
vaccination. Australian Veterinary Journal
71:257-258.
10. Veterinary Immunology: An Introduction by Ian
Tizard. Eighth Edition.
11. Wilbur LA, Evermann JF and Levings RL.
(1994). Abortion and death in pregnant bitches
associated with a canine vaccine
contaminated with bluetongue virus. Journal of
American Veterinary Medical Association.
22
 Present Status of Livestock in India
Suraj Amrutkar1, SuhasAmrutkar2, Bharti Deshmukh3, Vinod Gupta4 and S. K. Gupta5
1. Scientist, Poultry Science, SKUAST-J, Jammu.
2. SMS, Animal Nutrition, Parbhani Veterinary College, Parbhani, MAFSU
3. Assistant Professor, GADVASU, Punjab
4. Senior Scientist & Head, KVK Samba, SKUAST-J
5. Professor & Librarian, Medicine Division, SKUAST-J
U
Table 1: Rank of India at World level:
Introduction:

The total Livestock

population is 535.78 million
in the country showing an
increase of 4.6 % over
Suraj Amrutkar Livestock census-2012.
Total Bovine population
(Cattle, Buffalo, Mithun and Yak) is 302.79 million
in 2019 which shows an increase of above 1% over
the previous census. The total number of cattle in
the country in 2019 is 192.49 million showing an
increase of 0.8% over the previous census. The
female cattle (Cow population) is 145.12 million,
increased by 18 % over the previous census
(2012). The exotic/cross bred population in India is
50.42 million. Indigenous /non destript female
population has increased by 10% in 2019 as
compared to previous census. The population of
the total exotic/crossbred cattle has increased by
26.9% as compared to previous census. However, Table 2: Cattle population top ten country of
the pace of decline of indigenous / non-descript World:
cattle population during 2012-2019 is much lesser
than as compared to the 2007-12 which was about
9%. The buffalo in the country is 109.85 million
showing an increase of 6.0% over the previous
census. The sheep population in the country is
74.26 million in 2019, increased by 14.1% over the
previous census. The goat population in the country
in 2019 is 148.88 million showing an increase of
10.1 % over the previous census. The total pigs in
the country is 9.06 million in the country census,
decline by 12.03% over the previous census. The
other livestock including Mithun, Yak, Horses,
Ponies, Mule, Donkeys, Camel together contribute
around 0.23% of the total livestock and their total
count is 1.24 million.
LIVESTOCK LINE, APRIL 2020 23
 Table 3: Distribution of livestock population in India:
Table 4: Livestock Population: Major species
during 2012 and 2019 census:
Cattle:
Total cattle population in the country is 192.49 million
during 2019. Total cattle is increased by 0.8 % over
previous livestock census (2012). Female cattle
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Table 5: Livestock population 2012 & 2019 of
major states
population increased by 18.0% whereas male cattle
decreased by 30.2% over previous census. About
36% of the total livestock is contributed by cattle.
Milch cattle of exotic crossbred has increased by
32.2% over previous census. Milch cattle of
indigenous / non-descript has increased marginally
by 0.8%.
24
 Table 6: In Milk, Dry and Milch cattle for Exotic Total 8: Buffaloes: Male, Female and Milch
/cross bred & Indigenous /Non-descript animals

Table 7: Cattle population 2012 & 2019 in Major

states
Table 9: Buffalo population 2012 & 2019 in
Major states

Buffalo:
Total buffalo population in the country is 109.85
million during 2019. Total buffalo has increased by
1.1 % over previous livestock census (2012).
Female buffalo population increased by 8.61 %
Sheep:
whereas male buffalo is declined by 42.35% over
previous census. About 20.5% of the total livestock Total sheep population in the country is 74.26 million
is contributed by buffaloes. Milch buffalo population during 2019. Total sheep has increased by 14.13
has increased marginally by 0.2% over previous
% over previous livestock census (2012). About
census in which in milk has increases by 4.3%
13.8% of the total livestock contributed by sheep.
whereas dry category has declined by 10.2 %.

LIVESTOCK LINE, APRIL 2020 25

 Table 10: Sheep population: Exotic/cross bred Goat:
and indigenous / non-descript
Total goat population in the country is 148.88 million
during 2019. Total goat has increased by 10.14%
over previous livestock census (2012). About 27.8%
of the total livestock is contributed by goats.

Table 13: Goat population 2012 and 2019 of

major states

Table 11: Sheep population 2012 & 2019 in

Major states

Poultry:

The total poultry in the country is 851.81 million in

2019, registered an increase of 16.8 % of the total
poultry. The total birds in the backyard poultry in
the country is 317.07 million. The backyard poultry
has increased by around 46% as compared to
previous census. The total commercial poultry in
the country is 534.74 million in 2019, increased by
Table 12: Goat Population: Male, female and
4.5% over the previous census.
Milch

Table 14: Poultry Population:

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 Table 15 : Poultry population 2012 & 2019 of
major cities

Camel:
Total Camel population in the country is 0.25 million
during 2019. Total camel population has decreased
by 37.1% over previous livestock census (2012).

Table 18: Camel Population 2012 and 2019

Pig:
Total pig population in the country is 9.06 million
during 2019. Total pig population has decreased
by 12.0 % over previous livestock census (2012).
About 1.7% of the total livestock is contributed by
pigs.

Table 16: Pig population 2012 and 2019 Table 19: Camel population 2012 and 2019 of
major states

Table 17: Pig population 2012 and 2019 of Major

states:

Horses, Ponies, Mules & Donkeys:

Total population of horses, ponies, mules and
donkeys in the country in the country is 0.35
million during 2019. Total population of horses,
ponies, mules and donkeys has decreased by
51.9 % over previous livestock census (2012).

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 Table 20: Horses, Ponies, Mules and Donkeys Table 23: Donkey population 2012 and 2019 of
population 2012 and 2019 Major states:

Table 21: Horses & Ponies population 2012 and

2019 of Major states:

Mithun:
Total population of Mithun in the country is 3.9 lakh
during 2019. Total population of Mithun is increased
by 30.0 % over previous livestock census (2012).

Table 24: Mithun population 2012 and 2019 of

Major states:

Table 22: Mules Population 2012 & 2019 of major

states

Yak:
Total population of Yak in the country is 58 thousands
during 2019. Total population of yak has decreased
by 24.67% over previous livestock census (2012).

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 Table 25: Yak population 2012 and 2019
U
Calciumhomeostasis and its associated disorders
Kennady Vijayalakshmy1,*Meenakshi Virmani2and Jyotsnarani Biswal3
1,*
Research Officer, International Livestock Research Institute (ILRI), New Delhi, India - 110012
2
Assistant Endocrinologist, Department of Veterinary Physiology, Lala Lajpat Rai University of Veterinary and Animal Sciences
3
Research Officer, International Livestock Research Institute (ILRI), New Delhi, India - 110012. *Corresponding Author e-Mail: drviji.vet6115@yahoo.com
U
Introduction: Extracellular calcium is essential for formation
of skeletal tissues, transmission of nervous tissue
impulses, excitation of skeletal and cardiac muscle
contraction, blood clotting, and as a component of
milk.Intracellular calcium, is involved in the activity of a wide
array of enzymes and serves as an important second
messenger conveying information from the surface of the
cell to the interior of the cell.
Ca homeostasis: Parathyroid hormone is secreted in
response to a decrease in serum calcium, which might be
caused by the loss of calcium from the serum pool to
lactation, growth, or foetal development.Calcium can also
be lost in pancreatic secretions and bile, which is called
endogenous faecal calcium loss. Parathyroid hormone
increases renal tubular reabsorption of calcium to reduce
urine calcium loss, increases osteocytic and osteoclastic
bone calcium release, and stimulates the kidney to produce
1,25 dihydroxyvitamin D (1,25(OH)2D).The 1,25(OH)2D
enhances the active transport of calcium across the
intestinal tract.Calcium can also be absorbed paracellularly
if diet calcium is high enough.
Diseases
Dietary calcium deficiency in young animals leads to failure
to mineralize new bone and contributes to retarded growth.
The following disorders include:
1. Osteoporosis 2. Osteomalacia
3. Rickets 4. Secondary nutritional hyperparathyroidism
5. Fibrous osteodystrophy
1. Osteoporosis: This is a thinning of the bone matrix as
more calcium is resorbed into the blood than is deposited
into the bone. Osteoporosis may be related to protein
deficiency (both dietary and due to prolonged anorexia),or
through disuse of bones. This may be as a result of being
confined in too-small spaces, or enforced inactivity such as
that experienced when fractures have been immobilized, or
as a result of long-term paralysis.Bones become brittle,
light, and easily broken.Pathophysiology behind this is the
balance between bone resorption and bone deposition is
determined by the activities of two principle cell types,
osteoclasts and osteoblasts, which are from two different
origins.Osteoclasts are endowed with highly active ion
channels in the cell membrane that pump protons into the
extracellular space, thus lowering the pH in their own
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LIVESTOCK LINE, APRIL 2020
Table 26: Yak population 2012 and 2019 of Major states:
microenvironment.This drop in pH dissolves the bone
mineral.The balance between the activities of these two cell
types governs whether bone is made, maintained, or lost.
2. Osteomalacia: This is softening of the bone and
decreased bone density due to decreased mineralization.
The body tries to compensate by depositing bone material
at the sites of greatest tension.Folding fractures and bowed
bones are common.Normal mineralisation depends on
interdependent factors that supply adequate calcium and
phosphate to the bones.Vitamin D maintains calcium and
phosphate homeostasis through its actions on the GI tract,
the kidneys, bone, and the parathyroid glands. Vitamin D is
obtained from the diet, or it can be produced from a sterol
precursor (7-dehydrocholesterol) in the skin following
exposure to UV-B light.Sequential hydroxylation of vitamin D
is required to produce the metabolically active form of vitamin
D. Hydroxylation occurs first in the liver and then in the
kidneys and produces 1,25-dihydroxyvitamin D.Dysfunction
in any of these metabolic steps results in osteomalacia
and secondary hyperparathyroidism in adults.
3. Rickets: Rickets is similar to osteomalacia, and occurs
in the young.The differences are most noticeable in x-rays
as it affects the bones in different ways.Bowing of the long
bones, sometimes severely deformed long bones, is the
most common outward signs of rickets.
4. Secondary nutritional hyperparathyroidism
Low levels of serum calcium stimulate the production of
PTH (parathyroid hormone), which causes the bones to
release calcium and phosphate, as well as stimulating 1,25-
dihydroxycolecalciferol, which increases calcium absorption
in the gut. The result is bones stripped of calcium, with
insufficient calcium available to replace the calcium lost
from the bone, and so the bone weakens. This results in
osteomalacia in adults and rickets in the young.
5. Fibrous osteodystrophy
This is most often seen in the jaw bones; they begin to
soften and bow outward as they continue to be pulled upon
by the muscles.The heads of some afflicted animals, such
as iguanas, tend to look small and rounded, juvenile in
appearance.Self-feeding becomes difficult, then
impossible, as the jaw bones become too soft.
Pathophysiology behind this is a defective bone
mineralisation.
29
 Waste Management at Dairy Farms
Srijana Sharma¹, S Praveen², Sadhana Tiwari³ and Prasanna Pal4
¹,²,³M.V.Sc Scholar, Livestock Production Management section
4
Ph.D Scholar, Animal Physiology Section
ICAR-National Dairy Research Institute, Karnal, Haryana-132001, INDIA. Email: srizanasky@gmail.com
U
ABSTRACT leather, and wool, etc.). During last decade, the
livestock keeping systems were changing to
Changing trend of livestock keeping adapted to
specialized dairy farming with zero grazing. It is
improve profitability have resulted environmental
termed as confined animal feeding operations
concern and a public health issue. However, the
(CAFO) which is intensive livestock farming.
disposal of these wastes continues to be challenge
Livestock waste is of two types: Liquid waste (It
from standpoints of cost, environmental safety, and
includes urine, washing water runoff water etc.)
bio security. The different livestock waste includes
Solid waste (It includes feaces and bedding
1. Solid waste (faeces, leftover feed, bedding
material, and daily left over fodder also) ).Lack of
material), 2. Liquid waste (Urine, washings, runoff
efficient waste management techniques may lead
water) 3. Gaseous waste (methane, carbon dioxide,
to higher incidence of diseases, pollution, loss of
ammonia ) . Lack of efficient waste management
organic fertilizer and decline in field crop production.
techniques may lead to higher incidence of
With production of two million tons of dung per day,
diseases, pollution, loss of organic fertilizer and
majority are used as manure in fields, some portion
decline in field crop production. With production of
as a cooking fuel in rural areas, and less portion
two million tons of dung per day, majority are used
for biogas production. The increasing use of
as manure in fields, some portion as a cooking fuel
petroleum products forced us to utilize the ability
in rural areas, and less portion for biogas
of livestock waste for various possible energy
production. Biogas production via anaerobic
products, among them biogas is most popular.
digestion, composting, vermi composting,
There is a need for new management system that
livestock-fish integration are some of the methods
make animal operations economically feasible and
in practice that need to be encouraged and
eco friendly. New management strategies and
propagated further. The results of initial trials of
technologies should be productive, cost effective
biogas bottling plants in India demonstrated that the
but furthermore must be ecologically sustainable.
biogas can be pure up to 98 % methane content.
Recent advancement in bio-oil production from algal
cultivation, improved diet composition for
ruminants, has contributed to sustainable
management of livestock waste. Livestock waste
can be recycled to combat rising energy prices.
New management strategies and technologies
should be productive, cost effective but furthermore
must be ecologically sustainable.
Introduction:
Livestock refers to domesticated animals
intentionally reared in an agricultural setting such
as family farms and organized commercial farms
to produce food or other products (Milk, meat,

LIVESTOCK LINE, APRIL 2020 30

 Various techiques used:
• Composting
• Vermi composting
• Dairy fish integration
• Integration of compost and vermi compost
• Biogas production
• Composting: Composting is a naturally
occurring process that farmers have used for
centuries. Under the right conditions,
microorganisms grow and multiply, converting
the original organic material into a more stable,
usable product. Livestock producers constantly
face the challenge of managing manure and
meeting environmental regulations.
Composting is a possible alternative for
handling manure. The benefits include reduced
volume, enhanced soil fertility and texture, and
reduced environmental risk.
• Vermicomposting: The earthworms eat the
organic matter and excrete little pelleted
material called “vermicompost”. During
Vermicomposting, the important plant nutrients,
such as N, P,K and Ca present in the organic
waste are released and converted into forms
that are more soluble and available to plants.
Secretions in the intestinal tracts of earthworms
make nutrients more concentrated, available
for plant uptake, including micronutrients. The
wastes left by a bovine of about 400 kg body
weight can produce 800-1000 kg
vermicompost a year which can fetch up to
Rs 16,000 to 20,000.
LIVESTOCK LINE, APRIL 2020
• Dairy fish integration: Integration of fish with
livestock farming is a good method for
recycling organic wastes. Cattle manure is
used extensively in India as a source of manure
in carp polyculture. A dairy farm of 5-6 cattle is
sufficient for a pond of 1 ha area which can
accommodate 8,000-10,000 fish fingerlings of
different species like catla, rohu, mrigal, silver
carp, grass carp and common carp. The
annual yield from fish culture may be around
5000-7000 kg. The annual profit may be around
Rs 3-4 lakh per ha. A unit of 5 cows provides
adequate manure to produce 3000kg of fish
ha/yr at a stocking density of 10,000 fingerling
per ha Biological oxygen demand of cow
manure is lower than other livestock manures
. Grass crap showed highest growth in
integrated farming .
• Integration of compost and Vermicompost:
The major problems associated with
composting are loss of nutrients, long duration
of process, the frequency of turning material
and heterogeneous nature of product. The
problem in Vermicomposting process is that it
must be maintained at temperature below 35 0
C. Thus integrated system that approach both
provides a product free of pathogens , and with
desirable characteristics. The lower C:N ratio
indicates good quality fertilizer, suggesting it
got intensely decomposed Concentration of N
was significantly higher, indicating
mineralization.
31

• Biogas: Biogas can be used as domestic
cooking, industrial heating, combined heat and
power (CHP) generation as well as a vehicle
fuel. In India, the estimate for the production of
biogas is about 20,757 lakh cubic meters in
2014-15 Equivalent to 6.6 crore domestic LPG
cylinders. This is equivalent to 5% of the total
LPG consumption in the country today.
Maharashtra tops the production with 3578 lakh
cubic meters while Andhra Pradesh comes
next with 2165 lakh cubic meters Biogas
contain significant amount of Methane, carbon
dioxide and hydrogen sulfide (H2S) gas which
needs to be stripped off due to its highly
corrosive nature. The removal of H2S takes
place in a biological desulphurization unit in
which a limited quantity of air is added to biogas
in the presence of specialized aerobic bacteria
which oxidizes H 2S into elemental sulfur.
Biogas development through anaerobic
digester (AD) would influence the activities of
agricultural, water, soil, and electrical sectors
more in the future as the need for animal waste
utilization, management, and using sustainable
energies increase.
Conclusion: Animal waste management and
engineering aspects of alternative sources of
energy production, with an emphasis on biogas as
a highly promising technology for converting animal
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LIVESTOCK LINE, APRIL 2020
waste into vast quantities of methane, which may
be used directly as an energy source through
utilization of animal manure for ensuring
environmental safety. Livestock waste can be
recycled by many modern ways in order to combat
rising energy crises, sustainable agriculture and
reduce environmental threats . Biogas is highly
promising technology for converting animal waste
into vast quantities of methane and directly used
as energy source. New management strategies
and technologies should be productive, cost
effective but furthermore must be ecologically
sustainable.
Reference:
Daljeet kaur, M Singla and A.L.Saini(2016). Profit
enhancing livestock waste management. Livestock
production under diverse constraints.
Handbook of Animal Husbandry (2012). ICAR
Publication
Sastry N.S.R.(2016). Waste to riches:Value addition
products from livestock and poultry farming wastes
for improving sustainability of local breed rearing. A
special publication of the ISAPM, pp524-532.
Sorathiya et al., 2014). Eofriendly and modern
methods of livestock recycling for enhancing farm
profitability.
https://www.nrcs.usda.gov
www.icar.org.in
32
 Zoonotic Diseases of Cattle
Dr.M.Jeyakumar, Assistant Professor
Department of Animal Genetics and Breeding, Veterinary college and research institute, Namakkal-637002.
U
Introduction
Zoonotic diseases are diseases that can be
transmitted from animals to humans and from
humans to animals. Zoonotic diseases may be
acquired or spread in a variety of ways: through
the air (aerosol), by direct contact, by contact with
an inanimate object that harbors the disease
(fomite transmission), by oral ingestion, and by
insect transmission. There are fifteen cattle
diseases with zoonotic potential, some of which
are more common than others. They include
anthrax, brucellosis, cryptosporidiosis,
dermatophilosis, Escherichia coli, giardiasis,
leptospirosis, listeriosis, pseudocowpox, Q fever,
rabies, ringworm, salmonellosis, tuberculosis, and
vesicular stomatitis.
Anthrax
Anthrax is a bacterial disease caused by Bacillus
anthracis, which forms spores that survive for
years in the environment. Cattle, sheep, and goats
are at the highest risk of developing anthrax, but
other farm animals, as well as wildlife and humans,
can contract the disease. Most animals are infected
by oral ingestion of soil contaminated with anthrax
spores. People develop anthrax when the organism
enters a wound in the skin, is inhaled in
contaminated dust, or is eaten in undercooked meat
from infected animals. Biting flies can transmit the
bacterium, which results in redness and swelling
at the bite site. The most common clinical sign in
animals is sudden death. Blood may be seen
oozing from the mouth, nose, and anus of animals
that died of anthrax. A vaccine for livestock is
available in areas where anthrax is a common
livestock disease. Animals suspected of dying from
anthrax should be examined by a veterinarian
immediately. Animals that have died of anthrax
should be burned or buried deeply and covered with
lime. The area should be thoroughly
decontaminated with lime, as anthrax spores can
survive in the soil for decades. Anthrax is prevented
by avoiding contact with animals that are
suspected to have anthrax and areas that may
contain bodies of animals that died from anthrax.
Brucellosis
Brucellosis is caused by the bacterium Brucella
melitensis, which can affect a wide variety of
animals including cattle, pigs, sheep, goats,
horses, and dogs. Brucella organisms can be
present in birthing tissues or fluids (aborted
fetuses, fetal fluids, placentas, and vaginal
discharges), and also in milk, urine, blood, and
semen. Transmission among cattle is through
ingestion of birthing fluids and milk and in utero.
The most common clinical sign in cattle is late-
term abortion, but many infected cattle do not show
any clinical signs. Most infections in humans are
associated with drinking or eating unpasteurized
milk products. Handling infected aborted fetuses
or afterbirth is another common means of human

Potential Human Exposure to Zoonotic Organisms

Note: Not all exposure results in clinical disease. Additionally, symptoms may be mild and may go unnoticed

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 infection, as the organism can enter through cuts
in the skin and the mucous membranes of the eye
and mouth. Common symptoms in humans are
undulating fever, weakness, headache, joint pain,
and night sweats. There is a Cooperative State
Federal Brucellosis program in the United States
to eradicate the disease from this country. States
are designated “Brucellosis Class Free” when there
are no cattle or bison infected with brucellosis for
12 consecutive months. Virginia is Brucellosis
Class Free, as are all states except Texas and
Idaho. There is a pocket of brucellosis in the bison
and elk herds of Yellowstone National Park, and
sporadic outbreaks of animal brucellosis have
occurred in western states. Human brucellosis is
prevented by not drinking unpasteurized dairy
products, and wearing gloves when handling
reproductive tissues. Hands should be washed
after touching or handling animals.
Cryptosporidiosis
Cyrptosporidium is a protozoal parasite that causes
diarrhea. Most animals can be infected with
Cryptosporidium, but clinical signs are most
commonly observed in calves less than 1 month
old. Infected animals shed the organism in their
feces, contaminating the environment.
Cryptosporidium can then be ingested from
infected food or water. Humans are infected by
consuming food or water contaminated with the
organism or by failing to wash their hands after
exposure to infective feces or animals. Most people
who are infected do not become sick. For those
individuals that show clinical signs, explosive
diarrhea and abdominal pain are common.
Vomiting, fever, and muscle cramps may also
occur. Young children, pregnant women, and
immune compromised adults are most severely
affected. Calves with diarrhea should be separated
from healthy ones, and the infected area disinfected
with bleach. Prevention efforts in humans focus on
hand washing, especially after handling or being
around animals and before eating or handling food.
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Dermatophilosis
Dermatophilosis is a bacterial skin disease caused
by Dermatophilus congolensis, and is also known
as rain rot, lumpy wool, and strawberry foot rot. It
most commonly affects cattle, sheep, goats, and
horses. The disease is spread by direct contact
with infected skin or through biting insects. Wet
conditions allow the bacteria to spread. It causes
thick scabs, and when the hair is pulled, the tuft of
skin looks like a paintbrush. Infections in humans
are rare, but people can develop sores that form
ulcers, often resulting in scarring. Infected animals
should be isolated and treated with antibiotics.
Human infections can be prevented by wearing
gloves and washing hands thoroughly after working
with infected animals.
Escherichia coli
Escherichia coli (E. coli) are bacteria normally
found in the intestines of people and animals.
However, some strains cause a severe, often
bloody, diarrhea in humans. Animals are the carriers
of the bacteria, and humans become infected by
ingesting contaminated food or water, especially
undercooked ground beef, unpasteurized juice and
milk, and vegetables. Humans may also become
infected after handling or being exposed to feces
of a carrier animal. Person-to-person transmission
can occur by lack of good hand washing following
diaper changes. E.coli can also be transmitted
through swimming pools. E. coli O157:H7 is a
particularly virulent strain of E. coli that in humans
can cause abdominal cramping, bloody diarrhea,
and occasionally, especially in young children and
the elderly, life threatening kidney disease and a
hemolytic uremic syndrome. E. coli O157:H7 may
cause diarrhea in young calves, but most infected
cattle show no clinical signs. Prevention focuses
on hand washing and proper food hygiene. Hands
and all cooking equipment should be washed with
soap and hot water after touching or handling raw
meat. Meats should be thawed in the refrigerator,
and ground beef should be cooked until it reaches
an internal temperature of 165°F and the juices run
clear. At restaurants, undercooked meats should
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 be returned to the kitchen. Do not drink
unpasteurized milk or milk products, juice, or cider.
Make sure drinking water, especially well water, is
adequately disinfected. Wash hands after handling
animals or being in animal facilities and do not eat
or drink around animals. Day-care facilities should
wash toys frequently, and individuals with diarrhea
should avoid swimming in public areas.
Giardiasis
Giardia lamblia is an intestinal protozoal parasite
that may or may not cause disease in cattle. Giardia
is present in soil, food, and water that have been
contaminated by infected feces. Humans become
infected by ingestion of contaminated food or water.
Infants and small children may place their hands
that have been contaminated with fecal material
directly into their mouth. Because a large number
of wild animals harbor Giardia, water from lakes,
streams, or ponds may be unsafe to drink. Giardia
causes diarrhea and abdominal cramping in
humans. It can be prevented by avoiding untreated
drinking water and thoroughly washing all fruits and
vegetables. Frequent hand washing is also
recommended.
Leptospirosis
Leptospirosis is a bacterial disease caused by
Leptospira interrogans that can occur in a large
number of animals, including cattle, sheep, goats,
pigs, horses, and dogs. Leptospirosis is spread
through the urine of infected animals and can
survive in water and soil for months. The most
common clinical signs in cattle are abortion and
weak newborn calves. Cattle, and especially
rodents, may show no signs of illness but carry
and pass the organism in their urine. Humans
acquire leptospirosis through direct contact,
ingestion, or inhalation of the bacteria. Infection
usually results in mild flu-like symptoms but may
progress to severe liver and kidney disease.
Prevention involves rodent control and elimination
of standing water. Avoid water, such as ponds,
where animals congregate and urinate, and wear
gloves when handling reproductive fluids or when
being exposed to urine.
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Listeriosis
Listeriosis is caused by the bacterium Listeria
monocytogenes. Cattle, sheep, and goats are
commonly affected. Common signs of infection in
livestock are circling, incoordination, and the inability
to chew and swallow. Pregnant animals may abort.
The organism lives in decaying vegetation and low-
lying wet areas. Consumption of spoiled or
improperly ensiled feed is often associated with
outbreaks in animals. Feeding good-quality corn
silage will decrease the risk of listeriosis in animals.
Moldy silage that has been exposed to air and
leftover silage from feed bunks should be discarded.
Most humans are resistant to infection, but
individuals who are immunosuppressed, pregnant,
or taking antacids are at increased risk of acquiring
infection. Infection in humans usually occurs after
eating contaminated processed meats or
unpasteurized milk products. Infections in humans
can result in abortions and septicemia (blood
poisoning). Prevention consists of washing
produce, cooking meats properly, and avoiding
unpasteurized milk and milk products. Pregnant
women should avoid deli meats and soft cheeses.
Gloves should be worn while assisting calvings and
hands washed afterward.
Pseudocowpox
Pseudocowpox is a virus that causes small raised
sores and scabs on the teats and udders of cattle.
The virus is spread from cow to cow by milkers
and milking equipment, and causes small raised
sores that later scab. Humans acquire
pseudocowpox by direct contact with infected
cows, and can develop painful scabby sores on
the hands and arms. Good milking hygiene and teat
dipping will decrease the spread of this virus.
People should wear gloves when handling infected
cows, and thoroughly wash hands and arms after
milking.
Q Fever
Q fever is caused by the bacterium Coxiella burneti
and causes abortions in cattle, sheep, and goats.
Animals acquire Q fever through contact with
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 reproductive fluids and milk from infected animals.
Humans are usually infected when they are
assisting the birthing process and are exposed to
reproductive fluids. They may also be infected by
drinking infected unpasteurized milk. Humans
develop a fever, night sweats, and pneumonia and
hepatitis in severe cases. Miscarriages, premature
delivery, and infections of the placenta are possible
in pregnant women. To prevent the spread of Q
fever, aborted fetuses and reproductive tissues
should be buried or burned. Wearing gloves and
protective eyewear when assisting in birthing and
washing hands thoroughly afterward are
recommended. Pregnant women should not assist
in birthing. Unpasteurized milk products should be
avoided.
Rabies : Rabies is a deadly viral infection affecting
all mammals, including humans. Rabies is spread
in the saliva of a rabid animal, typically through bite
wounds. Cattle may show changes in behavior,
excessive vocalization, have difficulty swallowing,
drool, and/or become paralyzed. People contract
rabies through exposure to infected saliva in open
wounds or mucous membranes (eyes, nose, and
mouth). This could occur during examination or
treatment of infected cattle. Rabies is almost
always fatal once clinical signs are evident. People
should not handle or feed wildlife. Contact your
veterinarian immediately if cattle behave
abnormally or have symptoms of rabies. Always
wear gloves and take safety precautions when
treating sick animals. A veterinarian should be
consulted if an animal dies of unknown causes. If
there is human exposure to an animal with rabies,
a physician should be contacted immediately so
post-exposure prophylactic injections can be
initiated.
Ringworm : Ringworm is a skin infection caused
by fungi of the Trichophyton or Microspora species.
Animals get ringworm by direct contact with an
infected animal or by being in an infected
environment, such as a barn. Ringworm is
characterized by hairless, crusty circular areas on
the skin. People are infected with ringworm through
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direct contact with infected animals. In humans,
ringworm forms itchy areas on the skin that are
round and irritated. Good hygiene and thorough
hand and forearm washing after handling infected
cattle will help decrease the risk of ringworm.
Salmonellosis : Salmonella are bacteria that are
shed in the feces of infected animals. Many animals
are susceptible to Salmonella, including cattle.
Infection occurs as a result of the ingestion of
contaminated feed, water, or grass. The bacterium
can live for months to years in the environment,
especially in wet and warm conditions. Young,
stressed or pregnant animals are the most
susceptible to Salmonella infection. Infection may
result in fever, foul smelling diarrhea, and severe
dehydration. People acquire Salmonella from
undercooked contaminated meat, infected eggs,
or unpasteurized milk products. If hands are not
washed after direct contact with infected feces,
then accidental ingestion of bacteria can occur.
Humans may develop diarrhea, abdominal
cramping, and fever, which can be very severe.
Animals with diarrhea should be isolated and the
area disinfected. Meat and eggs should be
adequately cooked and proper food handling
hygiene should be used. Always wash hands after
touching or working with animals.
Tuberculosis : Bovine tuberculosis is caused by
the bacterium Mycobacterium bovis which is shed
in respiratory secretions, feces, and milk of infected
animals. Cattle are infected by inhaling or ingesting
the bacterium. Weight loss, weakness, low-grade
fever, and coughing are common clinical signs of
infection in cattle. Humans may acquire
tuberculosis from unpasteurized dairy products
and can develop symptoms involving the lungs,
kidneys, spine, or brain. Infected individuals have a
persistent cough and often cough up blood.
Currently there is little tuberculosis in cattle as a
result of a federal eradication program. All states,
including Virginia, are currently accredited
Tuberculosis Free except Michigan, Minnesota, and
New Mexico. Prevention is by avoiding
unpasteurized dairy products.
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 List of zoonotic diseses of cattle

Vesicular Stomatitis Preventive Measures

1. Washing hands with soap after handling
Vesicular stomatitis is a viral disease, producing
animals is the most important precaution. Soap
blister-like sores on the mouth and feet of infected
should be readily available in the barn/lavatory
animals. The disease is transmitted by flies or direct areas.
contact. People acquire the virus by direct contact
2. Unpasteurized milk and milk products should
with infected animals. People develop flu-like
be avoided. This is especially true for children,
symptoms and occasionally develop blisters in their the elderly and pregnant women.
mouth and on their hands. Prevention is by wearing
3. All meat should be cooked to appropriate
gloves while handling animals suspected of having
internal temperatures. Ground beef should be
vesicular stomatitis. Hands should be thoroughly cooked until reaching an internal temperature
washed after handling any animals. of 165°F and the juices run clear.

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 4. Raw meat and eggs should be handled as if
they contain infectious organisms.
5. All surfaces and utensils used to prepare raw
foods should be thoroughly washed with hot
water and soap. Utensils used on raw foods
should not be used later in the cooking or
serving process.
6. If you suspect any of these diseases on your
farm, or you have questions about them,
contact your veterinarian.
7. If you suspect that you, one of your farm
employees, or anyone in your family has any
of these diseases, contact your physician
immediately.
Summary : There are numerous zoonotic diseases
that can be transferred from cattle to humans.
These diseases cause mild to severe symptoms
and are a definite concern for farmers and their
families. While some of the diseases are rare, their
potential for devastating outcomes makes it
necessary to take precautions for these diseases
seriously. Luckily, many of the precautions taken
to prevent these diseases are the same.
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