salmonella nomenclature
- family
- species
- subspecies and serovard important for poultry
- 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
two main types of salmonella infection? where do S. pollorum and S. gallinarum fall? what diseases do they cause?
Two main types of salmonella infection:
1) Typhoid (S. Pullorum and Gallinarum)
2) Paratyphoid infection.
- S. Pullorum = Pullorum disease
- S. Gallinarum = Fowl typhoid.
typhoid salmonella infectins are adapted to what species? how does this compare to paratyphoid infections? zoonotic potential?
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.
salmonella pollorum causes what disease? who does it affect? mortality? carriers?
Salmonella Pullorum (Pullorum Disease – PD):
* Affects young chickens and turkeys.
* Characterized by high mortality in young birds and
asymptomatic adult carriers.
Salmonella Gallinarum causes what disease? who is affected?
Salmonella Gallinarum (Fowl Typhoid – FT):
* Usually affects semimature and mature chickens and turkeys – can cause disease also in young birds.
what type of transmission is key for S. pullorum and S. gallinarum
Vertical transmission is key for both diseases
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Vertical transmission is very important to understand pathogenesis and eradication programs.
pathogenesis and horizontal transmission of S. pullorum and S. gallinarum
- transmission methods
- what cells colonized
- where they replicate
- tissues affected
- shedding
- contamination concern?
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.
pathogenesis and vertical transmission of S. pullorum and S. gallinarum
- how it occurs
- signs
- carriers
- connection to horizontal transmission
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.
Salmonella Pullorum and
Salmonella Gallinarum lesions in chicks and semi-mature birds
- Bacterial shower (septicemia / bacteremia) causing multiple tissue granulomas
- Involvement of hock joint as consequence of septicemia
Salmonella Pullorum and
Salmonella Gallinarum lesions in adult birds
Lesions are characterized by chronic inflammation of the oviduct, ovary and celomic cavity (remember the bacteria persist in the ovary)
- celomitis
- salpingitis
pullorum disease and fowl typhoid control programs, when it was last seen in canada
- 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.
ontario hatchery and supply flock policy purpose, and surveillance methods?
do we need a PD and FT vaccine?
- 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.
Why does the OHSFP put so much stress on the breeder flocks and hatching eggs?
- 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).
if a PD or FT outbreak is reported, what happens
*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.
infectious laryngotracheitis (ILT)
- agent
- type of disease
- economic importance
- contagiousness, morbidity
- ontario presence?
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.
ILT vs Marek’s disease virus agent
ILT: Gallid Herpesvirus-1
Marek’s: Gallid herpesvirus-2
ILTV pathogenesis
- who affected
- transmission
- replication, in what cells
- shedding, clinical signs timing
- latency, location
- 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.
ILT clinical signs
- acute and chronic
> who affected
> signs
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.
ILT
- sporadic cases occur in what birds?
- why do we see sporadic cases in heavy breeders or leghorns?
- 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.
ILT acute form - what signs will we see that are most obvious when we walk into a barn
- 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.
ILT gross lesions, pathogenesis of these
- 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.
ILT trachea histology / morphologic diagnostic features
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.
ILTV diagnosis
*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.
why do we do qPCR and sequencing for ILTV in addition to histology?
qPCR and sequencing is done to differentiate between wild or vaccine strains.
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Birds 148
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Bird 262
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Bird 350
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Bird 455
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Bird 4 pt 218
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Bird 521
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Bird 641
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Bird 6 pt 238
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Bird 740
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Birds 7 pt 219
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Bird 831
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Bird 942
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Bird 9 pt 236
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Bird 1053
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Reptiles 142
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Reptiles 1 pt 227
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Reptiles 2: Clinical Techniques and Therapeutics48
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Reptiles 3 Infectious Diseases57
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Reptiles 4 Non-Infectious Diseases55
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Amphibians53
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Zoo21
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Poultry 133
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Poultry 239
