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Equine diseases


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important diseases of equines

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Equine diseases

  1. 1. Dr. Pavulraj.S 5246 M.V.Sc., Scholar Division of Pathology Indian Veterinary Research Institute, Izatnagar, India
  2. 2. 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
  3. 3. 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 diseases Glanders Strangles Tetanus Rhodococcus equi Leptospirosis Botryomycosis
  4. 4. 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,
  5. 5. 50% seroprevalence of HeV antibodies in flying foxes in Australia Satellite telemetry has shown that old world fruit bats can travel more than 2000 km in 1 year
  6. 6. 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
  7. 7. 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,
  8. 8. 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 feature Vanarsa Guillaume,
  9. 9. Interlobular edema Petechial hemorrhages over lung Brain vasculitis ovary vasculitis Lymphadenitis with syncytial cell formation. IHC staining of HeV N protein
  10. 10. 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.,
  11. 11. Current status(2008-09) Nithin virmani et. al.,
  12. 12. Transmission • Short I.P - <48hrs • Morbidity – 60-90% • Mortality - <1% • Outbreak – close contact • Direct contact – nasal secretion - Droplet infection
  13. 13. 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,
  14. 14. Pathogenesis
  15. 15. 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, bronchopneumonia Ljubo Barbic,
  16. 16. 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
  17. 17. 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.,
  18. 18. 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.,
  19. 19. 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
  20. 20. 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.,
  21. 21. 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
  22. 22. Multifocal hemorrhages, rubbery lung Multiple necrotic foci in liver Hemorrhage and necrosis of brain stem Aborted fetus, enclosed in amnion
  23. 23. Lesions Necrotic foci in liverEosinophilic inclusions in hepatocyte Vasculitis in CNS Nuclear debris in splenic follicle lymphocytolysis EHV-1 particles nucleus. Organelles of the cytoplasm degeneration hydropic dilation of sER,mitochondria, detached ribosomes of rER
  24. 24. 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.,
  25. 25. Current status
  26. 26. 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 products Maria Teresa Scicluna et al.,
  27. 27. Pathogenesis Kidney glomeruli have thickened basement membrane and mesangium with neutrophilic infiltration 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.,
  28. 28. 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 pericardium Spyrou et al.,
  29. 29. 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
  30. 30. 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 BM Spyrou et al.,
  31. 31. 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.,
  32. 32. 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.,
  33. 33. 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.,
  34. 34. Pulmonary & cardiac form AHS - Foam from nares due to pulmonary edema Bilateral supra orbital edema – cardiac form Congestion and edema of conjunctiva
  35. 35. 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.,
  36. 36. AHS - Pulmonary edema (distended interlobular septa) edema in intermuscular fascia of neck S/C edema
  37. 37. Petechial hemorrhages on serosa Petechial hemorrhages on the diaphragm AHS - Hydropericardium Subendocardial hemorrhagesSubcutaneous edema
  38. 38. Microscopically • Widening of interlobular septa • Alveolar edema • Perivasculitis • Focal myocardial hemorrhage • Degeneration of myocardial fibers Pulmonary edema Myocardial necrosis
  39. 39. 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.,
  40. 40. 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.,
  41. 41. Pathogenesis
  42. 42. Ocular edema and conjunctivitis (pink eye) Excess lachrymation Urticarial type skin reaction - due to lesions in blood vessels
  43. 43. 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.,
  44. 44. Pulmonary hemorrhages Interstitial pneumonia and emphysema Enteritis with sub-serosal and sub-mucosal hemorrhages
  45. 45. 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
  46. 46. 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.,
  47. 47. 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.,
  48. 48. 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.,
  49. 49. 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
  50. 50. 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 lesions Bazargani T.T, et al.,
  51. 51. Mucopurulent nasal discharge cutaneous nodules on legs Ulcers and farcy buds along facial lymphatics. Leg - non-ulcerated farcy buds. Epistaxis
  52. 52. Enlarged submaxillary LN and nodules rupture, release pus and ulcerate Nodules of lymphatic vessel tracts in cervical region Nodules in nasal mucosa Lungs numerous gray, hard, small (2-10 mm) milliary nodules (resembling millet seeds) Erosion in nasal mucosa
  53. 53. 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
  54. 54. 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.,
  55. 55. 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 SeM proteins, 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.,
  56. 56. 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
  57. 57. Edematous swelling of pharyngeal region Rupture of submandibular abscess
  58. 58. Guttural pouch empyema Acute suppurative lymphadenitis Bastard strangles – mesentric LN
  59. 59. Metastatic abscess (brain)
  60. 60. 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.,
  61. 61. Pathogenesis • Two toxins – tetanolysin, tetanospasmin Peter Reichmann, et al.,
  62. 62. 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
  63. 63. Rhodococcus equi • Causes disease in young foals • Pyogranulomatous pneumonia • Pleomorphic, aerobic, non-motile, G+ve, intracellular pathogen
  64. 64. 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
  65. 65. Lesions Mesentric lymphadenitis Multifocal ulcerative colitis Subcapsular splenic abscessesMultiple firm nodules in lung
  66. 66. 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
  67. 67. Seroprevalence of various equine diseases in India 2010-11 (NRCE)
  68. 68. 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