Download - Equine diseases
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Dr. Pavulraj.S5246
M.V.Sc., ScholarDivision of Pathology
Indian Veterinary Research Institute, Izatnagar, India
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Introduction
• Horse – a symbol of bravery and power
• Total population of equids in India is 1.18 million(2007)
– Horses – 52%
– Donkey – 37%
– Mule – 11%
• In India, diseases like glanders and equine influenza re-emerged
among equines in 2006-09
• There are many bacterial and viral diseases are endemic in India
• Many new emerging diseases threatening our equine health
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List of diseases
Viral diseases• Hendra• Equine influenza• Equine herpes virus• Equine infectious
anemia• African horse
sickness • Equine viral arteritis• West Nile fever• Equine encephalitis• Rabies
Bacterial diseasesGlandersStranglesTetanus Rhodococcus equiLeptospirosisBotryomycosis
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Hendra
• Acute febrile respiratory infection of horses
• Characterized by increased respiratory rate, profuse nasal
discharge, jaundice and neurological signs with fatal outcome
• Paramyxoviridae – genus Henipavirus (equine morbilivirus), don’t
agglutinate RBC
• Horses – only species naturally infected
• Fruit bat – Pteropus Sp., reservoir host
• Zoonotic
• First recognized in 1994, caused acute respiratory disease
Vanarsa Guillaume et.al.,
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50% seroprevalence of HeVantibodies in flying foxes in Australia
Satellite telemetry hasshown that old world fruitbats can travel more than2000 km in 1 year
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Epidemiology • Low transmission rate – not persist in environment for long time
• I.P – 5 to 10 days, disease last for 2 days
• Low morbidity, high mortality
• BSL-4 pathogen
• Human infection form infected horse
• Horse – nasopharynx inoculation. Shed virus in urinary tract
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Pathogenesis
• Pneumotropic and neurotropic virus
• Animal and human died after showing resp. signs
• Virus isolated from all the organs of the body including
blood
• Affect vascular endothelium – cause pulmonary edema
• Lesions in lung and brain – similar to CD, measles
Vanarsa Guillaume et.al.,
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Clinical signs
• Pyrexia, dyspnea, frothy/haemorrhagic nasal discharge, neurological signs,
ataxia, muscle trembling
Lesions
• Diffuse pulmonary edema and congestion
• Hydrothorax and hydropericardium
• Congestion of LN, S/C hemorrhages
Mic
• Interstitial pneumonia, alveolar edema, necrosis of alveolar walls and
thrombosis of blood vessels, Non suppurative encephalomyelitis
• Vascular lesions in visceral organs
• Syncytial cells in blood vessels – unique featureVanarsa Guillaume et.al.,
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Interlobular edema Petechial hemorrhages over lung
Brain vasculitis ovary vasculitis Lymphadenitis with syncytial cell formation. IHC staining of HeV N protein
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Equine influenza
• “Flu” or “two-year-old cough”
• Highly contagious respiratory viral disease of equines
• RNA virus – Influenzavirus A – family Orthomyxoviridae
• Two subtypes viz. H7N7 and H3N8
• H3N8 spreads very rapidly, cause severe clinical disease
• Characterized by pyrexia, dyspnea, dry hacking cough,
serous nasal discharge, edema of LN
• Re-emerged in India in last week of June, 2008 in Jammu
and Kashmir, 20 years after the first outbreak in 1987
• Entered to india by importing army horses for France
Vandanajay Bhatia et. al.,
Nithin virmani et. al.,
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Current status(2008-09)
Nithin virmani et. al.,
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Transmission
• Short I.P - <48hrs
• Morbidity – 60-90%
• Mortality - <1%
• Outbreak – close contact
• Direct contact – nasal secretion - Droplet
infection
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Pathogenesis
Attachment of virus to airway epithelial
cells(HA to Sialic acid residue)
Receptor mediated
endocytosis
Acidification of endosomal
compartment
Conformational change of HAFusion of viral
and cellular membrane and release of RNP
Entry of RNP into nucleus
Synthesis of viral proteins
Assembly and release
Inhalation
Ljubo Barbic et.al.,
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Pathogenesis
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Lesions
• Inflammation of resp tract
• Erosion of upper respiratory mucosa
• Pulmonary consolidation, pneumonia
• Myocarditis
Mic
• Hyaline membrane formation on
bronchiolar and alveolar epithelium
• Peribronchitis, bronchitis,
bronchopneumoniaLjubo Barbic et.al.,
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Exudate in the bronchial lumen and infiltration of inflammatory cells in bronchial epithelium and lamina propria
The alveolar architecture is obliterated by the presence of MNC, neutrophils, erythrocytes, and edema fluid in the alveolar lumina.
IHC for equine influenza A virus respiratory tissue
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EI in India
• The vaccination against EI is not practiced in India.
• The rise in HI antibodies against EIV, in the naive population in the country
which had not experienced any outbreak since 1987, indicated that the
animals were infected recently with EIV.
• NRCE regularly conducts routine sero-surveillance against infectious
diseases of equines from various parts of the country.
• The occurrence of the EI infection was confirmed in all the places by either
virus isolation or by demonstration of fourfold or more rise in serum HI
antibody titres.
Nithin virmani et. al.,
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Equine herpes virus
• Important cause of abortion, neonatal death, respiratory disease and
neurological diseases
• Caused by Equine herpesvirus (EHV1 &EHV4)
• Narrow host range – single target species
• Infect multiple types of cells
• Lytic and latent cycle
• Latency – trigeminal ganglia and CD8+ cells
• EHV-1 - major cause of neonatal foal mortality in a number of breeding
studs located in the Haryana, Punjab and Uttar Pradesh States of India. Tiwari S.C, et al.,
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Epidemiology and Transmission
• Horse - to – horse
• Ingestion and inhalation
• Aborted material, semen, aerosol droplet
• Reservoir – latently infected horses
• Stress, transport can reactivate latency
• Less persistent in environment
• Infection acquired in first weak of birth
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Pathogenesis
Inhalation
Replicate in upper resp. tract mucosa
In uterus – vasculitis– abortion
Disseminated in all organs including trigeminal ganglion,
CNS, uterus during viremia
Enter to lamina propria, endothelial
cells, CD8+ cells
Brain – vasculitis, thrombo-ischemia,
encephalopathy
Virus
Tiwari S.C, et al.,
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Clinical signs
• EHV1 – resp signs, abortion, neurological
signs
• Nasal discharge, conjunctivitis,
lymphadenopathy, no cough
• Abortion – last trimester
• Neonatal infection – fatal
• Stallion – poor semen quality
• CNS – ataxia, paralysis, bladder
dysfunction, incontinence
• EHV4 – resp signs
Neurological form of EHV1
Nasal discharge
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Multifocal hemorrhages, rubbery lung
Multiple necrotic foci in liver
Hemorrhage and necrosis of brain stem
Aborted fetus, enclosed in amnion
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Lesions
Necrotic foci in liverEosinophilic inclusions in hepatocyte
Vasculitis in CNS
Nuclear debris in splenicfollicle lymphocytolysis
EHV-1 particles nucleus. Organelles of the cytoplasm degeneration hydropic dilation of sER,mitochondria, detached ribosomes of rER
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Equine infectious anemia• Swamp fever, Coggins disease
• Equine infectious anemia virus, genus Lentivirus Family Retroviridae
• Contains reverse transcriptase (RNA dependent DNA polymerase)
• Characterized by icterus, anemia, edema of subcutis of ventral abdomen,
thrombocytopenia
• World wide distribution
• Transmitted mechanically by mosquito or biting fly or by infected blood
Maria Teresa Scicluna et al.,
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Current status
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Transmission
• Blood from infected animal – source of infection
• Mechanical transmission by Tabanus and Stomoxys
calcitrans (with in short time <4hrs, in short distance)
• Vertical transmission – in utero/colustrum feeding
• Venereal transmission – semen
• Iatrogenic – blood contaminated productsMaria Teresa Scicluna et al.,
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Pathogenesis
Kidney glomeruli have thickened basement membrane and mesangium with neutrophilicinfiltration and contained deposits of immune complex
Anemia – immune mediated destruction, intra & extra vascular hemolysis
Thrombocytopenia – suppression of platelets production and immune mediated destruction
Increase in proinflammatory cytokines causes fever, lethargy, inappetence
Infection of macrophages induces upregulation of TNFα, IL-1 and IL-6
Active infection of liver, LN, BM, lung, adrenal gland, kidney, brain
Viremia
Virus infect macrophages in spleen, tissue
Maria Teresa Scicluna et al.,
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Clinical signs
Pyrexia, edema of lower abdomen, sublingual and nasal haemorrhage
Anaemia, thrombocytopenia
Chronic form develop after the pass of acute form
Lesions
Acute disease
Icterus, haemorrhages on serous membrane
Edema of subcutis of abdomen, base of heart, perirenal and sublumbar fat
Hepatomegaly, splenomegaly, lympadenopathy
Chronic disease
Hypertrophy of spleen and bone marrow
Heart – haemorrhage in epicardium and pericardiumSpyrou et al.,
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Enlarged grey red liver showing lobular pattern
Replacement of BM fat with dark red hemopoietic tissue - erythroid hyperplasia
Pale cardiac muscle, focal white areas of myocardial degeneration
Kidney – infracts
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Microscopically
Edema, hyaline degeneration and lymphocyte infiltration around blood vessels.
Glomerular nephritis
Liver - lymphocytic infiltration, dilation of
sinusoids, haemosiderin pigment in kupffer
cells, centrilobular necrosis.
Periportal - lymphocytes and plasma cells.
Interface hypereosinophilic hepatocytes
with loss of cellular detail - piecemeal necrosis
Hyperplasia of BMSpyrou et al.,
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African horse sickness
• Non contagious, infectious, insect borne disease of equine
• Caused by African horse sickness virus, belong to genus – Orbivirus,
family – Reoviridae, Nonenveloped
• Transmitted by Culicoides spp.
• 9 antigenic serotypes
• Characterized by pyrexia, edema of lungs, pleura, S/C tissue and
hemorrhage of serosa of internal organs
• In 2006 - WOAH declared India free of African horse sickness
Kazeem.M.M et al.,
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Epidemiology
• Mortality rate - 70-95%
Transmission
• Not contagious
• Culicoides spp., - biological vector
• Occasional - mosquitoes - Culex, Anopheles and Aedes spp.; ticks - Hyalomma, Rhipicephalus
• Moist and warm temperatures favour the presence of insect vectors
• Virus movement over long distances via windborne infected vectors
Sources of virus
• Viscera and blood of infected horses
• Semen, urine and all shed and secreted products
• Viraemia up to 18 days Kazeem.M.M et al.,
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Pathogenesis
Cardiac form (serotype9)- degeneration and necrosis of myocardium, hydropericardium
Foals and naïve horses develop – peracute pulmonary form
Secondary viremia
Primary viremia – disseminate to endothelial cells of target organs – endothelial cell damages
Effusion in body cavities, serosal, hemorrhages
Initial multiplication in regional LN
Inoculation of virus
Gomez J.C. et al.,
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Pulmonary & cardiac form
AHS - Foam from nares due to pulmonary edema
Bilateral supra orbital edema –cardiac form Congestion and edema of conjunctiva
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Lesions
• Respiratory form: edema of the lungs, froth in trachea, hydro
pericardium, oedema of thoracic LN, petechiae in pericardium
• Cardiac form: S/C and I/M gelatinous edema, epicardial and
endocardial ecchymoses, myocarditis, haemorrhagic gastritis,
petechiae in ventral surface of tongue Gomez J.C. et al.,
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AHS - Pulmonary edema (distended interlobular septa)
edema in intermuscular fascia of neck
S/C edema
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Petechial hemorrhages on serosa Petechial hemorrhages on the diaphragm
AHS - Hydropericardium Subendocardial hemorrhagesSubcutaneous edema
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Microscopically
• Widening of interlobular septa
• Alveolar edema
• Perivasculitis
• Focal myocardial hemorrhage
• Degeneration of myocardial
fibers
Pulmonary edema
Myocardial necrosis
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Equine viral arteritis
• Infectious disease
• Caused by Equine arteritis virus belong to genus Arterivirus, family Togaviridae
• Characterized by depression, edema of limbs, intense pink or red conjunctiva, palpebral edema,
enteritis, pneumonic complications and abortions
• Principal lesions is degenerative and inflammatory changes in the endothelium and tunica media
of small arteries
• Serological survey indicate wide spread infection but clinical disease is not that common
• About 80% abortion during clinical disease
• The virus which causes EVA was first isolated from horses in Ohio in 1953
• India – one case in 1989
Holyoak G.R., et al.,
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Transmission
• Via respiratory route or by ingestion
• Venereal transmission by stallions
• Tissues and fluids of aborted fetus contained large mass of virus
• Virus shed in the urine Holyoak G.R., et al.,
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Pathogenesis
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Ocular edema and conjunctivitis (pink
eye)
Excess lachrymation
Urticarial type skin reaction - due to
lesions in blood vessels
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Lesions
• Congestion, petchiae in conjunctiva, resp tract and guttural
pouches, S/C tissue
• Hydrothorex, petichae in pleura, heart, pericardium and lungs,
• Ascites
• Enlargement of LN
• Petichae on endocardium, epicardium, mesentery
• Small intestine, caecum and colon oedematous and congested Holyoak G.R., et al.,
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Pulmonary hemorrhagesInterstitial pneumonia and emphysema
Enteritis with sub-serosal and sub-mucosal hemorrhages
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Microscopically
• Small arteries and necrosis and
deposition of eosinophilic mass in
tunica media with cellular
infiltration in adventitia
• Platelet thrombi in lumen
• Abortion -necrotizing myometritis
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West Nile virus: the Indian scenario• West Nile virus - arthropod borne flavivirus
• Causes a mild infection in human and horses
• Mosquitoes are the principal vectors
• Various Culex species - Transovarial transmission
• Very few clinical cases of human encephalitis due to WNV are observed - Neuroinvasive disease
• WNF in horses has not been documented in India.Paramasivam, et al.,
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Glanders
• Fatal, contagious and zoonotic disease
• Caused by Burkholderia mallei , Gram -Ve, non-motile, non-
sporulating obligate aerobic
• Acute or chronic form
• Characterized by nodular lesions in the lungs and nodular or
ulcerative lesions in the respiratory tract mucosa and skin
• Occupational disease of veterinarians, farriers and animal
workers
• Last report on glanders outbreak in India - June, 1985,
recently from july, 2006
Purulent nasal discharge
2010
Bazargani T.T, et al.,
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Transmission
• Excretions and discharges of affected animals skin and nasal mucosa
• Oral - chronic respiratory disease
• Intranasal - acute disease
• Virulence and immuno-evading factors
– Intracellular status
– Capsule and capsular LPS
– High level of genomic alterations in the host – such rapid genomic variation upregulate
virulence gene expression in B. mallei
– Genomic instability has had impact on vaccine development
• Pathogenesis not fully understood Bazargani T.T, et al.,
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Pathogenesis
Oropharynx or intestine
Bacteria penetrate the
mucosa and reach regional LN
Spread hematogenously
to the internal organs and lungs
From nasal cutaneous lesions
Other visceral organs also the sites of typical
nodules
Terminal signs -bronchopneumonia
Death is caused by anoxic anoxia
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Clinical signs and lesions
• Acute - cough and nasal discharge, ulcers on nasal mucosa
and nodules on the skin of lower limbs or abdomen.
• Chronic - chronic cough, epistaxis . Nasal and skin form
occur together
• Cutaneous lesions - medial hock
• Lymphadenopathy and cording of lymphatics
• Milliary nodules in lung
Microscopically - pyogranulomatous lesionsBazargani T.T, et al.,
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Mucopurulent nasal discharge
cutaneous nodules on legsUlcers and farcy buds along facial lymphatics.
Leg - non-ulcerated farcy buds.
Epistaxis
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Enlarged submaxillary LN and nodules rupture, release pus and ulcerate
Nodules of lymphatic vessel tracts in cervical region
Nodules in nasal mucosaLungs numerous gray, hard, small (2-10 mm) milliary nodules (resembling millet seeds)
Erosion in nasal mucosa
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Necrosis and inflammation of nasal mucosa and thrombosis of nasal vessels
Vessel wall infiltrated by degenerate neutrophils and fibrin
Nodules with necrotic debris, hemorrhage, epithelioid macrophages, neutrophils
Pyogranulomatous central necrosis
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Strangles
• Acute infectious disease of horses - Equine
distemper
• Caused by the bacterium Streptococcus equi
sub-species equi (S. equi)
• Characterized by abscess in pharyngeal and
maxillary LN, pericarditis, pleuritis,
suppurative pneumonia, presence of
abscesses on liver, kidney and spleen
Andrew S.Waller et al.,
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Pathogenesis
Attach to cells of crypts of lingual and palatile tonsils
Mandibular and suprapharyngeal LN
Failure of N to kill ( due to hyaluronic acid capsule, antiphagocytic SeMproteins, Mac proteins
Bacterial enzymes –Streptolysin, Streptokinase –cause abscess formation ( By damaging cell membrane and activating plasminogen
Spread to other organs
Abscess in LN, thorasic and abdominal organs – Bastard strangles
Andrew S.Waller et al.,
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Guttural pouch empyema
• LN swell, abscess and rupture either externally through the horse’s skin
• In retropharyngeal LN, usually internally into the guttural pouch.
• This air-filled sack is an enlargement of the eustachian tube that drains
into the nasal cavity.
• Drainage of abscess material into the nasal cavity from the guttural pouch
contributes to the mucopurulent nasal discharges commonly observed
during strangles.
• Residual pus becomes inspissated to form chondroids
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Edematous swelling of pharyngeal region
Rupture of submandibular abscess
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Guttural pouch empyema
Acute suppurative lymphadenitis
Bastard strangles – mesentric LN
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Metastatic abscess (brain)
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Tetanus
• Tetanus - lockjaw caused by exotoxins produced
by Clostridium tetani, motile, anaerobic, G+ve
bacilli
• Soil/intestinal inhabitant
• Horse – most sensitive animal to toxin
• Associated with deep puncture wound, naval
stump infection in foals
• Reduced oxygen tension promote the growth
Shoeing
Peter Reichmann, et al.,
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Pathogenesis
• Two toxins – tetanolysin, tetanospasmin
Peter Reichmann, et al.,
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Clinical signs
• I.P – 7-10days
• Rigidity of muscles around head and neck
• Trismus
• Prolapse of nictitating membrane
• Rigidity extend to limbs, elevated tail
• Saw horse
• Death due to asphyxia
Lesions
• Intramuscular hemorrhages, tendon avulsion, fracture of
long bones, aspiration pneumonia
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Rhodococcus equi
• Causes disease in young foals
• Pyogranulomatous pneumonia
• Pleomorphic, aerobic, non-motile, G+ve,
intracellular pathogen
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Pathogenesis
Organism multiply in macrophages R.equi activate
alternate pathway of complement and bind
to macrophage complement receptor
– CD3Large number of cells attracted –
granuloma formation - pneumonia Enter in to
macrophage through complement
receptor mediated phagocytosis
Phagosome –Lysosome fused, due
to lack of acidification –
organism multiply and kill host cell
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Lesions
Mesentric lymphadenitis Multifocal ulcerative colitis
Subcapsular splenic abscessesMultiple firm nodules in lung
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About NRCE
• NRCE has contributed a great deal towards diagnosis/management/ elimination of
diseases like
• Equine influenza outbreaks in India during 1987-1989 and 2008-2009
• Equine infectious anaemia 1991-1998
• Glanders outbreaks during 2006-2007, 2010, and in 2011-12.
• NRCE involved in nation-wide monitoring and sero-surveillance of important
equine infectious diseases with a view to manage, control and eradicate diseases
• Performing molecular characterization of equine pathogens
• Preparation of diagnostic kits for equine diseases
• preparation of vaccines against equine diseases
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Seroprevalence of various equine diseases in India 2010-11 (NRCE)
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Conclusion
• Many diseases are emerging and re-emerging in these days
• Understanding the pathogenesis, molecular characterization of the organism and
epidemiology of these diseases are very important for the implementation of
preventive and control measure.
• Spreading of diseases in the farm can be effectively prevented by good biosecurity
measures.
• Surveillance and monitoring of important equine diseases including emerging and
existing diseases is needed to avoid production losses
• Development of effective, affordable diagnostics and immunoprophylactics against
important diseases threatening equines in India
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