The One Health One Caribbean One Love project is implemented by University of the West Indies, School of Veterinary Medicine

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Dr Chris Oura Professor of Veterinary Virology

Veterinary Medicine, Trinidad and Tobago

Health One Caribbean One Love project is

1 Dr Chris Oura Professor of Veterinary Virology University of the West Indies, School of Veterinary Medicine, Trinidad and Tobago Priority Viruses affecting Poultry in Guyana Animal Disease Recognition and Response Workshop, Guyana April 2016 The One Health One Caribbean One Love project is implemented by University of the West Indies, School of Veterinary Medicine

2 Unhealthy Bird vs Healthy Bird Sneezing/Snickering Open mouth breathing Nasal/Ocular discharge Diarrhea Watery Green Bloody egg production Swelling/Oedema Discoloration Deformities Nervous signs

3 Many respiratory diseases look the same As a first responder in Guyana: What are you looking for? Clinical signs Respiratory noises snick (reverse sneezing) cough sneezing May be best to listen to birds during night / quiet time Gross lesions Mortality trends Production parameters: appetite, water intake, egg production Normal bird activities Listen to bird owners opinions

4 What are you looking for questions to guide you? Temporal association with possible sources of disease: Vaccines New birds in flock, different supplier? Transportation Exposure to other birds with unknown status Access to wild birds

5 Things to Keep in Mind Frequent secondary coliform (E. coli) involvement with many viral diseases Antibiotics may be rationally used to offset this impending mortality Morbidity and mortality associated with 2 disease often more severe than initial insult (e.g. IBV, LPAI) Workup and diagnosis of cause of respiratory diseases needed Cannot reliably differentiate between most causes of respiratory disease in poultry based upon clinical signs, gross descriptions, etc. Most diseases will need additional diagnostic testing: Bacterial culture and sensitivities PCR / sequencing Virus isolation Histopathology

6 Clinical signs of RESPIRATORY DISEASE Open mouth breathing Gasping/Labored Sneezing/Coughing Ocular/Nasal discharge Discolored combs and wattles

7 Clinical signs of RESPIRATORY DISEASE Swelling around head, neck, and eyes Not standing Ruffled feathers Squinting/closed eyes

8 Factors Complicating Respiratory Disease Concurrent (multiple) infections Immunosuppressive diseases Age / immune status of host Maternal antibodies Environmental factors Vaccine types / dosages / routes / combinations

9 Respiratory Disease of Poultry Avian Influenza Newcastle Disease Infectious Bronchitis Infectious Laryngotracheitis Fowl Pox Avian Pneumovirus Colibacillosis Fowl Cholera ORT Infectious Coryza Turkey Coryza Ornithosis Mycoplasma spp. Aspergillosis Dactylariosis

10 Paramyxovirinae: Rubulalavirus: Newcastle Disease Virus Probably the most important disease of poultry worldwide

11 Newcastle Disease Virus Caused by avian paramyxovirus type 1 OIE list A disease - Notifiable Produces a transitory conjunctivitis in humans Zoonotic Highly contagious, severity of clinical signs related to viral strain, immune status of host, environmental conditions. Affects many bird species (domestic & wild), e.g. chickens, turkeys, ducks, geese, cockatoos, cockatiels, parakeets, finches etc.

12 Newcastle Diseases outbreaks: Jan June 2015

13 Newcastle Disease Virus Transmission - Direct contact with secretions, particularly faeces, from infected birds. Contaminated food, water, fomites, droplets & virus-infected eggs Incubation period: 4-6 days Clinical forms: Velogenic (viscerotropic) % mortality Velogenic (neurotropic) % mortality Mesogenic 0-15% mortality Lentogenic low mortality

14 Newcastle Disease Virus Clinical signs Viscerotropic velogenic: acute lethal infections, haemorrhagic lesions in the intestines. Neurotropic velogenic: high mortality following respiratory and neurological disease, gut lesions absent. Mesogenic: respiratory and neurological signs, with low mortality. Lentogenic: mild infections of the respiratory tract. Asymptomatic enteric: avirulent infections, replication primarily in the gut.

15 Clinical Signs Lentogenic Mesogenic Velogenic Adult Chickens none to mild respiratory signs reduction in egg production sudden onset of mild depression and anorexia mild respiratory signs possible CNS signs in few birds egg production ceases within days no to low mortality marked dyspnea violent diarrhea conjunctivitis, ocular/nasal discharge, periorbital swelling tremors, twisting neck, paralysis sudden death (up to 100%) Young Chicks sudden onset of respiratory signs nasal and ocular discharge sudden onset of marked depression and prostration gasping, coughing, hoarse chirping, nasal discharge star gazing, CNS signs in up to 25% mortality up to 50% similar to MESOGENIC more acute progression mortality up to 100%

17 Cyanosis Torticollis Respiratory Distress Ocular Discharge

18 Egg shell deformities Hemorrhage (GI) Airsacculitis Hemorrhage (Trachea)

19 Videos showing clinical signs of Newcastle disease in broilers and layers vmf-vmn7qi Y2y54AN6ZQ

20 Newcastle Disease Virus - Diagnosis Specimens required: Lung, liver, trachea, spleen, brain, clotted blood samples or serum, cloacal swabs, tracheal swabs. Laboratory diagnosis: Virus isolation in 9-11 day old embryonated eggs, followed by assessment of haemagglutinating ability PCR Serological testing: ELISA, HI tests

21 Newcastle Disease Virus - Prevention No treatment - all in-all out systems Quarantine & testing of new additions Isolation during outbreaks, destruction of all infected & exposed birds Allow 21 days to pass prior to restocking Sanitation - Cleaning & disinfection Avoid contact with birds of questionable disease status Live and killed vaccines for endemic countries

22 Infectious Bronchitis Coronavirus: antigenic variation Four common serotypes: Connecticut Massachusetts Arkansas 99 O72

23 Occurrence: Worldwide in chickens Infectious Bronchitis Transmission: Aerosols & respiratory discharges. Spread via direct & indirect contact Persist on contaminated premises for more than 4 weeks Remain carriers and shedders for months after infection Clinical & pathological features: Most severe in young birds; mild in older birds. Coughing, gasping, exudative bronchitis, tracheal serous & catarrhal exudates. Loss of egg production - misshapened, rough or soft-shelled eggs. Some strains cause nephritis with sudden death

24 Gasping Airsacculitis Egg shell deformities

Infectious Bronchitis Diagnosis: Samples required: Trachea (swab), lungs & kidneys Virus cultivation in chicken epithelial cell cultures & susceptible chicken embryos.

25 Infectious Bronchitis Diagnosis: Samples required: Trachea (swab), lungs & kidneys Virus cultivation in chicken epithelial cell cultures & susceptible chicken embryos. Serotype ID via virus neutralisation tests Polymerase Chain Reaction (PCR) Fluorescent antibody testing on tracheal scrapings Prevention: Live attenuated vaccine 1-2 weeks of age in drinking water, followed by a sub-cutaneous killed vaccine 3-4 weeks later Control: Difficult due to presence of persistently infected birds and continuing emergence of antigenically variant viruses.

26 Infectious Laryngotracheitis (ILT) Etiological agent: Herpesvirus Occurrence: Worldwide in chickens Transmission: Direct & indirect contact, droplet infection Pathogenesis: Replication in epithelium of URT (primarily larynx & trachea). Virus travels along sensory nerves to become latent in the trigeminal ganglia

blood-stained mucus High morbidity, fairly low mortality Less virulent strains may

27 Clinical Signs: Clinical & pathological features Infectious Laryngotracheitis Mild to severe respiratory disease seen in young & older birds Coughing, dyspnoea, gasping & blood-stained mucus High morbidity, fairly low mortality Less virulent strains may only result in a mild sinusitis & conjunctivitis Congested & hyperaemic larynx & trachea

28 Infectious Laryngotracheitis (ILT) Marked respiratory distress Unthrifty birds Conjunctivitis Almond eye Expectoration of blood

29 Diagnosis and Prevention Infectious Laryngotracheitis Diagnosis: Samples required trachea / conjunctival swab & lung Gross lesions & intra-nuclear inclusion bodies suggestive FAT and PCR Prevention: Keep closed flocks MLV vaccines in drinking water or aerosols Vaccination cannot prevent infection or reactivation of latent virus Recovered birds may remain latently infected Avoid adding vaccinated, recovered, or exposed bird to a susceptible flock

30 Fowlpox Host range: Chickens, turkeys, grouse, quail, pheasants, canaries, pigeons, sparrows, starlings etc. Occurrence: Worldwide Transmission: Direct contact with infected birds, Fomites especially contaminated litter. Virus enters via skin abrasions or mosquito bites Oral/nasal mucosa via aerosol droplets Cannibalism

characterized by small papules on combs, wattles, around eyelids & featherless areas.

31 Fowlpox Extremely resistant virus - can survive for long periods in exfoliated scabs Clinical & pathological features: 2 forms: a) Cutaneous form b) Diphtheric form Cutaneous form: Most common, characterized by small papules on combs, wattles, around eyelids & featherless areas. Usually recovers within 1 month. Yellow nodules which become thick scabs

Diphtheric form: Fowlpox Associated with droplet infection & more severe as

Lesions seen in mouth, pharynx, trachea, orbit & sinuses.

32 Diphtheric form: Fowlpox Associated with droplet infection & more severe as often complicated by 2 bacterial infections. Lesions seen in mouth, pharynx, trachea, orbit & sinuses. Slightly elevated white opaque nodules which increase in size to become a yellow diphtheritic membrane. Mortality may be as high as 50% Must be differentiated from ILT Raised yellow plaques on mucous membranes with sinuses, nasal cavity, conjunctiva, pharynx, trachea, and/or oesophagus

Fowlpox diagnosis and control Diagnosis: Based on typical clinical & pathological findings Demonstration of Bollinger (aggregates) or Borrel bodies

33 Fowlpox diagnosis and control Diagnosis: Based on typical clinical & pathological findings Demonstration of Bollinger (aggregates) or Borrel bodies in tissue scrapings Growth on CA membrane (pock lesions) PCR (scabs / tissue scraping) Control 1. Vaccination 2. Mosquito control 3. Control cannibalism

34 Viruses that affects the immune system Prevention of immunosuppression is fundamental in maintaining a healthy poultry operation. Poor nutrition/ parasitism Coccidiosis, Runting-stunting syndrome Infection Diseases that attack immune organs Toxins -aflatoxins in mouldy feed Stress Overcrowding, aggression, change in climate, heat stress, housing

35 There are many viruses that affect the immune system of birds causing immunosuppression Reoviruses: Leads to change in size and structure of immune organs Adenoviruses (IBH / HPS, Hydropericardium syndrome) and EDS (Egg drop Syndrome) in chickens. Retroviruses: lead to atrophy of thymus and Bursa of Fabricious. Herpesviruses (Mareks): These viruses cause lymphoid neoplasms and cause bursal as well as thymic lymphocyte destruction. Birnaviruses (IBDV): Mainly infect Bursa of Fabricious (BF). Circoviruses (Chicken Anaemia Agent): Vertically transmitted viruses that cause anatomical, pathological and immunological lesions.

36 Infectious Bursal Disease (Gumboro): Jan June 2015

37 Infectious Bursal Disease Gumboro disease

Occurrence: Worldwide in chickens (usually 3-6 weeks old) Transmission:

38 Infectious Bursal Disease Also known as Gumboro disease Etiological agent: Avibirnavirus serotype 1 Serotype 2 isolates do not cause clinical signs. Occurrence: Worldwide in chickens (usually 3-6 weeks old) Transmission: Faecal-oral route, direct contact & indirect contact by fomites. Shed in faeces for 2 weeks post-infection

Infectious Bursal Disease Virus has an affinity for the B lymphocytes & the bursa of

& erosions at proventriculus and gizzard junction.

39 Infectious Bursal Disease Virus has an affinity for the B lymphocytes & the bursa of Fabricius becomes infected within 12 hours immune response impaired (immunosuppression) and ineffective response to vaccines. Swelling & oedema of the bursa of fabricius, diarrhoea, anorexia, depression, haemorrhages & erosions at proventriculus and gizzard junction. Severity of clinical signs & lesions dependent on virulence level of virus, age of bird & immune status. Proventriculus haemorrhage Haemorrhage of muscles Swelling & Oedema of the Bursa of Fabricius

immunodiffusion, virus isolation, virus neutralisation, immunofluorescence & RT-PCR Thorough cleaning & disinfection

40 Infectious Bursal Disease: Diagnosis & Prevention Samples required: Bursa of Fabricius, liver, spleen, kidney, lungs & blood Swollen & haemorrhagic Bursa of Fabricius is suggestive of disease Detection via ELISA, agar gel immunodiffusion, virus isolation, virus neutralisation, immunofluorescence & RT-PCR Thorough cleaning & disinfection of poultry houses Biosecurity measures Killed virus vaccines for breeders Attenuated live vaccines - drinking water or aerosol

41 Marek s Disease affects the immune and nervous systems of birds Etiological agent: Gallid herpesvirus 2 3 serotypes: 1 & 2 - affects chickens 3- affects turkeys Type 1 is oncogenic Occurrence: Worldwide in domestic fowl, turkeys & quail Most frequent in chickens between 8-20 weeks of age Transmission: Via respiratory tract through contact with infectious airborne dust particles (dust & dander)

Marek s Disease Pathogenesis: Entry into respiratory tract via infectious dust Infection of B lymphocytes of bursa of Fabricius, spleen & thymus (3-5 days after infection) Infection of T lymphocytes

42 Marek s Disease Pathogenesis: Entry into respiratory tract via infectious dust Infection of B lymphocytes of bursa of Fabricius, spleen & thymus (3-5 days after infection) Infection of T lymphocytes (mainly CD4+, less frequently CD8+) Latent Viraemia 2 cytolytic infection of feather follicle epithelium Shedding of cell-free virus in dust & dander Classical Form: Acute Form : Motor paralysis due to viral replication in peripheral nerves with or without visceral tumours Visceral tumours of the gonads, kidney, liver, lung, spleen, muscle & skin. Death can occur without paralysis Blindness if eye affected (ocular lymphomatosis)

43 Marek s disease: 8-20 weeks of age be.com/watch?v =BydP994Tp7E 20 sec

44 Diagnosis Marek s Disease Samples required: Whole birds in extremis Usually based on clinical signs & necropsy lesions - Paralysis/paresis with enlarged peripheral & autonomic nerves with a yellow, translucent appearance Visceral tumours, perivascular cuffing in the white matter of the cerebellum & infiltration of mononuclear cells in peripheral nerves Virus can be propagated in chick embryo kidney cells & duck embryo fibroblasts PCR

linked to the emergence of more virulent strains Vaccination prevents the development of tumours.

45 Marek s Disease: Prevention Vaccination of day old chicks against serotype 3 virus (turkey herpesvirus) Vaccination with attenuated and low path field virus strains In-ovo vaccination - 18 days of incubation (preferred) Vaccine failures have been linked to the emergence of more virulent strains Vaccination prevents the development of tumours. Vaccines do not prevent transmission of the virus - non-sterilizing. Vaccines reduce the amount of virus shed in the dander and hence reduce horizontal spread of the disease.

46 Thanks for Listening Any Questions? The One Health One Caribbean One Love project is implemented by University of the West Indies, School of Veterinary Medicine

Etiology. Paramyxovirus type 1 = Newcastle disease.

Etiology. Paramyxovirus type 1 = Newcastle disease. Newcastle Disease Many strains of similar virus cause signs ranging from mild respiratory signs (pneumotropic) with low mortality to severe neurological (neurotropic) and/or visceral lesions (viscerotropic)