Poultry 2

Question 1

salmonella nomenclature
- family
- species
- subspecies and serovard important for poultry

Answer 1

• Gram negative, Enterobacteriaceae family.
• Two species – S.enterica and S.bongori.
• In this lecture, we will focus on:
• Salmonella enterica sbsp. enterica, serovars Pullorum;
• Salmonella enterica sbsp. enterica, serovars Gallinarum.
• Salmonella Pullorum and Gallinarum affects several avian species > most important for chickens and turkeys

Question 2

two main types of salmonella infection? where do S. pollorum and S. gallinarum fall? what diseases do they cause?

Answer 2

Two main types of salmonella infection:
1) Typhoid (S. Pullorum and Gallinarum)
2) Paratyphoid infection.
- S. Pullorum = Pullorum disease
- S. Gallinarum = Fowl typhoid.

Question 3

typhoid salmonella infectins are adapted to what species? how does this compare to paratyphoid infections? zoonotic potential?

Answer 3

Typhoid infections are host adapted to avian species
- Pullorum (Pullorum disease)
and
Gallinarum (Fowl Typhoid)
- cause significant losses in poultry
- NO zoonotic potential and are not a concern for food-borne illnesses > minimal shedding of typhoid salmonellae by adult birds in production.
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paratyphoid infections are non-host adapted (can affect mammals and people)
- (Enteriditis, Heildeberg, Typhimurium, Hadar)
- usually do not cause significant disease in poultry (most commonly birds that are young or immunosuppressed).
- Serious zoonotic concern: food-borne pathogens. Infected birds are commonly asymptomatic but shed large numbers of salmonella through feces > heavy contamination of eggs and meat.

Question 4

salmonella pollorum causes what disease? who does it affect? mortality? carriers?

Answer 4

Salmonella Pullorum (Pullorum Disease – PD):
* Affects young chickens and turkeys.
* Characterized by high mortality in young birds and
asymptomatic adult carriers.

Question 5

Salmonella Gallinarum causes what disease? who is affected?

Answer 5

Salmonella Gallinarum (Fowl Typhoid – FT):
* Usually affects semimature and mature chickens and turkeys – can cause disease also in young birds.

Question 6

what type of transmission is key for S. pullorum and S. gallinarum

Answer 6

Vertical transmission is key for both diseases
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Vertical transmission is very important to understand pathogenesis and eradication programs.

Question 7

pathogenesis and horizontal transmission of S. pullorum and S. gallinarum
- transmission methods
- what cells colonized
- where they replicate
- tissues affected
- shedding
- contamination concern?

Answer 7

Oro-fecal or aerosol transmission.
> Colonization of mucosal epithelium and Peyer’s patches.
> Replication in macrophages.
> Dissemination to spleen, liver, bone marrow, ovary via macrophages
> Re-colonization of gut-associated lymphoid tissues (GALT) > shedding
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Shedding from feces is intermittent and in low amounts: little concern for contamination of eggs and meat.
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Bacteria persist within the macrophages and are disseminated in multiple tissues. Macrophages then recolonize the GALT (remember: macrophages/monocytes do circulate in the body), and the bacteria are shed with the feces.

Question 8

pathogenesis and vertical transmission of S. pullorum and S. gallinarum
- how it occurs
- signs
- carriers
- connection to horizontal transmission

Answer 8

Salmonella Pullorum or
Salmonella Gallinarum present in macrophages in the spleen.
> With egg production there is a decrease in the cellular immunity
> Salmonella P/G replicate, increase in numbers and reach the ovary (trans- ovarian transmission), and colonize the yolk.
> HATCH
> Salmonella P / G replicates and spread systemically in chicks.

=> Asymptomatic birds – > carriers.
=> Symptomatic > Enteritis and septicemia. Can become carriers if they survive.
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Vertically infected hatchlings will disseminate the bacteria horizontally through the barn.

Question 9

Salmonella Pullorum and
Salmonella Gallinarum lesions in chicks and semi-mature birds

Answer 9

• Bacterial shower (septicemia / bacteremia) causing multiple tissue granulomas
• Involvement of hock joint as consequence of septicemia

Question 10

Salmonella Pullorum and
Salmonella Gallinarum lesions in adult birds

Answer 10

Lesions are characterized by chronic inflammation of the oviduct, ovary and celomic cavity (remember the bacteria persist in the ovary)
- celomitis
- salpingitis

Question 11

pullorum disease and fowl typhoid control programs, when it was last seen in canada

Answer 11

• National Poultry Improvement Plan (NPIP) was created in US in 1940 to control Pullorum disease and Fowl typhoid.
• Ontario Hatchery Supply and Flock Policy (OHSFP) dovetails with the NPIP.
• Disease eradicated in commercial poultry also from US and many Western EU countries.
• In Canada, last PD case was reported in Vancouver in late 80s, in small backyard chicken flock (in Ontario last case was in 1971).
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  From OMAFRA website:
  The main objective of the Ontario Hatchery and Supply Flock policy is to assist in ensuring that Ontario hatchery supply flocks continue to serve as a reliable source of poultry hatching eggs and Ontario hatcheries maintain high standards of sanitation and disease prevention.
  This policy was developed jointly by industry, provincial and federal governments to establish standards for the valuation of poultry breeding flocks and hatchery products.
  The Ontario Hatchery and Supply Flock Policy is supervised by the Ontario Ministry of Agriculture, Food and Rural Affairs.
  The policy provides monitoring and testing of Ontario poultry breeding flocks to establish flock status for Salmonella Pullorum/typhoid under the regulations of the Federal Health of Animals Act.

Question 12

ontario hatchery and supply flock policy purpose, and surveillance methods?
do we need a PD and FT vaccine?

Answer 12

• To detect infected supply flocks (= breeder flocks) through screening procedures before they begin egg production.
• Active surveillance: Breeder flocks are monitored by a set schedule of blood testing (serology) and culturing of hatchery fluff.
• Passive surveillance: Excessive mortality (> 3% in chicks and 5% in poults by 14 days of age).
• Since eradication is in place, there is no vaccination for PD and FT.

Question 13

Why does the OHSFP put so much stress on the breeder flocks and hatching eggs?

Answer 13

• Because the poultry industry is highly hierarchical, and a few breeding flocks and hatcheries supply most of commercial flocks.
• Therefore, having breeder flocks that are free of vertically transmitted disease, ensures that all the other components of the poultry industry are free of the disease as well.
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  The policies of the OHSFP were initially implemented against S. Pullorum and Gallinarum, but have been also adopted for other diseases that are vertically transmissible, such as paratyphoid salmonellae and Mycoplasma gallisepticum, synoviae and meleagridis.
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  This is also important for small flock owners: Purchasing birds from hatcheries or co- ops ensures that birds are free form vertically transmitted diseases, and also guarantees that chicks are vaccinated against Marek’s disease and some respiratory diseases (such as infectious bronchitis virus).

Question 14

if a PD or FT outbreak is reported, what happens

Answer 14

*Federal control: Zoning and eradication of birds and destruction of contact materials (such as left over feed, crates etc.).
*Cleanup and disinfection costs borne by owner/producer.
*Compensation amounts are based on a preset fee schedule but with exotic or pet birds there is price negotiation.

Question 15

infectious laryngotracheitis (ILT)
- agent
- type of disease
- economic importance
- contagiousness, morbidity
- ontario presence?

Answer 15

Caused by Infectious Laryngotracheitis Virus (ILTV):
* Gallid Herpesvirus-1 (GaHV-1, alphaherpesviridae).
- Respiratory disease of chickens.
- Cause of multimillion dollar loss in U.S. and Canada.
- Highly contagious with high morbidity.
- Every year a few cases are reported in Ontario in both commercial and backyard poultry flocks.

Question 16

ILT vs Marek’s disease virus agent

Answer 16

ILT: Gallid Herpesvirus-1
Marek’s: Gallid herpesvirus-2

Question 17

ILTV pathogenesis
- who affected
- transmission
- replication, in what cells
- shedding, clinical signs timing
- latency, location

Answer 17

• Primarily a disease of chickens.
• Transmission > aerosol / inhalation.
• Replication in the respiratory epithelium > lesions.
• Peak of clinical signs and virus shedding between 6 to 14 days post infection.
• As any herpesvirus, it can become latent (in trigeminal ganglia and epithelial cells) and recrudesce when immune protection decreases.
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  Latency is very important to understand the epidemiology of the disease.

Question 18

ILT clinical signs
- acute and chronic
> who affected
> signs

Answer 18

Acute:
* Usually in non-vaccinated (immunologically naïve) flocks;
* Acute onset of respiratory disease:
> Nasal discharge, conjunctivitis, moist rales, coughing, gasping and expectoration of blood-stained mucous;
* Mortality rates may be high (never above 40%);
* Walls of the barn can be stained with blood.
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Chronic:
* Mostly affects breeders and layers that have poor immunity, either because poor vaccine application, or because not enough boosts are provided;
* Birds are unthrifty, conjunctivitis, sinus swelling, egg production drops;
* Catarrhal conjunctivitis and tracheitis.

Question 19

ILT
- sporadic cases occur in what birds?
- why do we see sporadic cases in heavy breeders or leghorns?

Answer 19

• Sporadic cases occur in all classes of birds, including hobby/show/game chickens, broilers, heavy breeders, and commercial leghorns.
• In the case of heavy breeders and leghorns, which are typically vaccinated against ILT, sporadic cases are often related to errors in vaccine application and to biosecurity failures: commercial table egg producers may desire to avoid the expense associated with eye drop administration of ILTV vaccine, and change to mass application. This change may result in inadequate protection.
• Since multiple–age layer complexes are common, and inadequately- vaccinated flock may be exposed to ILTV later, when a younger, vaccinated flock is moved into the complex and sheds the backpassaged vaccine virus, resulting in disease signs in the older flock.
• Cases in molted flocks that were not re-vaccinated, and the use of recently vaccinated “spiking males” in a poorly vaccinated, older breeder flock are other classic examples.

Question 20

ILT acute form - what signs will we see that are most obvious when we walk into a barn

Answer 20

• Open mouth breathing > respiratory difficulties.
• Bloody discharged is associated with the acute form of the disease.
• In the most severe cases, blood can be found spattered on the walls of the barn.

Question 21

ILT gross lesions, pathogenesis of these

Answer 21

• Morphologic diagnosis: tracheitis, fibrinous and hemorrhagic.
• The lesions are caused by damage to the mucosa (where the virus replicates) > ulceration > fibrin, hemorrhage and influx of inflammatory cells.

Question 22

ILT trachea histology / morphologic diagnostic features

Answer 22

Trachea: Presence of large syncitial cells with eosinophilic intranuclear inclusion bodies.
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Most important morphologic diagnostic features: SYNCYTIAL CELLS AND INTRANUCLEAR INCLUSION BODIES.

Question 23

ILTV diagnosis

Answer 23

*Cytology of the exudate > IN inclusions.
*Histology > IN inclusions and syncitia.
*Can have 24 hour turnaround time with histology.
*There is a qPCR as confirmatory test in addition to histology.
*Gene Sequencing to identify origin of virus (i.e., field or vaccine strain) maybe available.

Question 24

why do we do qPCR and sequencing for ILTV in addition to histology?

Answer 24

qPCR and sequencing is done to differentiate between wild or vaccine strains.

Question 25

what do we do if we get a positive ILTV diagnosis?

Answer 25

If test for ILTV is positive:
Laboratory is responsible for immediately notifying OMAF.

Question 26

ILT control, vaccination
- options, efficacy
- outbreaks
- who is vaccinated in ontario
- should we mix vaccinated and non-vaccinated birds? why?

Answer 26

Vaccination with live-attenuated vaccine:
* Tissue culture origin (TCO) > Eyedrop > Expensive;
* Chicken embryo origin (CEO) > Spray and Water > Cheaper;
* Other vaccines are vectored poxvirusor HVT (herpesvirus of turkey), but NOT as efficacious as TCO and CEO.
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- Live vaccination leads to latent infection, which in turn can lead to outbreaks of “vaccinal laryngotracheitis”.
- In Ontario, commercial layers, layer breeders and broiler breeders (long grow-out period) are vaccinated.
- Very important to keep separated vaccinated or convalescent birds from fully susceptible chickens.
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Remember: vaccine strains can cause outbreaks in immunosuppressed or older birds, for which immunity has declined over time.
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Control focuses on management practices, emphasizing strict biosecurity. Due to vaccination potential to cause disease, veterinary supervision is strongly recommended when the decision is made to go this route. Since both natural infection and vaccination have been shown to produce “carrier” birds, it is extremely important that susceptible chicken flocks are not exposed to vaccinated or previously infected chickens. Mixing of birds should only be done when a complete history of the birds is available, and it is absolutely certain that a potential ILT “carrier” is not present. Sanitation procedures, which include disinfection of equipment, boots and clothing and proper disposal of litter and carcasses, are essential components of ILT control.

Question 27

histomoniasis
- agent
- who it affects
- disease it causes
- signs
- other name
- economic significance
- geographic range

Answer 27

*Caused by protozoal parasite: Histomonas meleagridis.
*Most important parasitic disease of turkeys and important cause
of mortality for numerous game birds.
*Referred as:
* Blackhead:
* Due to initial observation that dead turkeys would
develop a darker head after dead (cyanosis).
* Not pathognomonic, only historical term.
* Other name: Infectious Enterohepatitis.
*Annual losses in the US from histomoniasis in turkeys are estimated > $2 million
*Important disease of commercial turkeys worldwide
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Historically a disease of turkeys. Now also observed in chicken layers, especially in aviary systems.

Question 28

histomoniasis etiology
- forms
- carriers birds, how they mmaintain the parasite

Answer 28

Histomonas meleagridis:
* Intestinal form: Flagellated protozoa, 10 um in diameter, in the cecal lumen of infected birds.
* Tissue form: Pleomorphic non-flagellated, 8-17um in diameter with pseudopodia.
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Carrier birds (chickens and pheasants) maintain the parasite in two ways:
1. Free vegetative form in the lumen.
2. Within the cecal nematode Heterakis gallinarum (symbiosis).

Question 29

histomoniasis hosts
- who is most susceptible
- who are resistant shedders

Answer 29

• Turkeys are most susceptible.
• Chickens and pheasants are considered to be resistant:
  > Shed the protozoa in the environment.
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  Other gamebirds can be susceptible, too:
• Partridges; * Peacock;
• Grouse;
• Quail.

Question 29

histomoniasis most important method of transmission

Answer 29

through the eggs and larvae of Heterakis gallinarum, which is an intestinal nematode that is present in the ceca of chickens and pheasants, and does not cause disease.

Question 30

histomonas meleagridis life cycle

Answer 30

Carrier birds: chickens and pheasants infected with H. gallinarum and H. meleagridis.
> H. meleagridis trophozoites infect the ovary of cecal worms (Heterakis gallinarum).
> H. gallinarum
produces eggs that are infected with H. meleagridis, and eggs are shed in the environment.
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> Heterakis eggs that carry histomonads are free in the soil.
> eaten by birds
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OR
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> Heterakis eggs are ingested by earth worms that function as paratenic host.
> worms eaten by birds
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- Histomonads infect the ovary of Heterakis gallinarum, and are shed with the eggs of this parasite.
- The eggs carrying the histomonads can be infectious for 2-3 years in the soil > very resistant.
- Earthworms contribute to concentration of histomonads by ingestion of nematode eggs > higher infectious dose!

Question 31

histomoniasis pathogenesis

Answer 31

1. Susceptible species ingest: * Infected heterakis eggs from soil;
   *Infected heterakis eggs or larvae in earth worms.
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2. Heterakis larvae develop, histomonads leave the larvae and colonize the cecal surfaces.
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3. Histomonads penetrate the cecal wall, cause
   inflammation (ulceration) and thickening of cecal wall.
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4. Histomonads enter bloodstream and reach the liver through portal circulation (hepatitis).
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5. Clinical signs within 7-12 days, mortality follows quickly.

Question 32

what can increase the severity of disease due to histomonas?

Answer 32

Interaction with coccidia and bacteria- including Clostridium perfringens and E. coli- increases the severity of disease with more tissue damage.

Question 33

two lesions of histomoniasis
do we need to see that parasite to diagnose?

Answer 33

1) Hepatitis and
2) Typhlitis (inflammation of the ceca).
The liver is reached through dissemination of histomonads by portal circulation.
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1) Hepatitis. Bull-eye appearance of necrotic areas in liver.
2) Typhlitis. Cecal cores.
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You do not always need to see Heterakis gallinarum to make a diagnosis, grossly. Lesions are highly suggestive anyways.

Question 34

occasinal route of transmission of histomonas in poults

Answer 34

on occasion the parasite can be transmitted though cloacal drinking (in poults)

Question 35

histomoniasis clinical signs
- when we see them
- what they are

Answer 35

Clinical signs usually observed between 7 to 12 days after infection.
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Non-specific:
* “Closed eye” (general depression / malaise);
* Drowsiness;
* Wing dropping;
* Diarrhea;
* Yellow feces (sulfur feces): when hepatic function is severely impaired, then bile pigments are extracted through the kidneys.

Question 36

histomoniasis control
- management
- products
> their uses, concerns

Answer 36

• Turkeys, quail, grouse, chukars cannot be raised in the same areas as chickens or pheasant.
• Do not raise these species in premises previously used to raise chickens or pheasant, since H. meleagridis can persist in the environment (eggs of heterakis in soil and earthworm) for years.
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• Histostat-50 (Nitarsone [Zoetis], 5 days withdrawal) is the only product approved in Canada as an aid in the prevention of Histomoniasis in turkeys.
• Recently withdrawn by the FDA – not used any longer in USA;
• It will not protect birds that are symptomatic > Prophylactic.
• Arsenic-based compound. It has 5 days withdrawal. Only preventive drug – not for treatment of clinical signs.
  > Withdrawn from use by FDA and Health Canada.
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• A new drug Paronomycin (aminoglycoside antibiotic [Huvepharma])
  > Imported in limited amounts for testing by Health Canada, to gather data regarding efficacy.
• Paronomycin has been used by veterinarians in Canada upon approval of an Emergency Drug Release from Health Canada.
• Currently, the drug has shown limited success for treatment of symptomatic flocks.
• No data about preventative (prophylactic) efficacy
  > Concerns for development of antimicrobial resistance against this important class of antibiotics.

Question 37

only drug for prevention of histomoniasis in turkeys, controvery

Answer 37

Histostat-50
* Recently withdrawn by the FDA – not used any longer in USA;
* It will not protect birds that are symptomatic > Prophylactic.
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Arsenic-based compound. It has 5 days withdrawal. Only preventive drug – not for treatment of clinical signs.
Withdrawn from use by FDA and Health Canada.

Question 38

possible drug for treatment of clinical signs due to histomoniasis, concerns

Answer 38

Paronomycin
- still in data collection phase
* Currently, the drug has shown limited success for treatment of symptomatic flocks.
* No data about preventative (prophylactic) efficacy
> Concerns for development of antimicrobial resistance against this important class of antibiotics.