ornitho, salmonella

Ornithobacterium rhinotracheale

• gram nega, non motile

• Cytophaga-Flavobacterium- Bacteroides descending line (Superfamily V FRNA, Family Flavobacteriaceae).

• 18 serotypes A-R

• Highly pleomorphic rods.

serotype A OO

most prevalent globally

94% in chickens

57% in turkeys

target OO

higher in turkeys than broiler chickens

age OO

turkeys 2-6 and 12-20 weeks

broilers 4 weeks

reservoir OO

wild birds act as primary carriers

vertical and horizontal OO

OO MOT

vertical transmission OO

Infected breeder hens can transmit the disease agent directly t o their progeny, complicating eradication efforts.

adherence 1 OO

Pathogen attaches to host tracheal/lung epithelial cells within 3 hours using specific hemagglutinins and glycoproteins.

biofilm formation 2 OO

ORT produces biofilms that protect it from environmental stressors and host immune

responses.

Enzymatic Degradation 3 OO

Neuraminidase activity causes desialylation of host serum and tracheal mucus, paving the way for tissue colonization.

inflammation 4 OO

Severe exudative and purulent respiratory damage.

environmental stress triggers OO

High ammonia levels, inadequate ventilation, and temperature extremes act as catalysts,

dramaticaly increasing the severity of ORT pathogenesis

how ORT/OO increase mortality

ORT + other agents

viral synergies OO

Avian Metapneumovirus (aMPV),

Newcastle Disease (NDV),

Infectious Bronchitis Virus (IBV),

H9N2 AIV.

Bacterial synergies OO

Mycoplasma gallisepticum,

E.coli,

Pasteurella multocida,

Bordetella avium

head ss OO

Sneezing, nasal discharge, facial swelling, swelling of the infraorbital sinus, wet eyes

Respi SS OO

Coughing, gasping, labored breathing.

legs ss OO

Joint swelling, lameness, paralysis (due to arthritis/osteomyelitis).

systemic ss OO

Severe growth retardation, drop in egg production, smaller or misshapen eggs with poor shell quality, lethargy.

Lungs macroscopic lesions OO

Exudative, severe purulent pneumonia (often notably UNILATERAL). Hemorrhagic spots may be present in turkeys.

airsacs macroscopic lesions OO

yogurt-like" purulent airsacculitis.

head/trachea macroscopic lesions OO

Pericarditis and flattened tracheal mucosa with reddish mucus accumulation

sample collection OO

dry sterile swab maintained at 4 degrees upto 2 days

sample sites OO

Trachea and lungs are optimal. Infraorbital sinus also viable.

media OO

Blood agar, Columbia agar, or soybean casein agar.

Must be supplemented with 5-10% sheep blood.

selective agents OO

Essential t o add 10ug/mL gentamicin or polymyxin to prevent E. coli masking.

incubation OO

Fastidious requirements. Needs microaerophilic conditions with 7% CO2 at 37°C for 24-48 hours.

biochemical profiling OO

API-20NE kit at 30°C yields a highly specific biocode (0-2-2-0-0-0-4 or 0-0-2-0-0-0-4).

Positive for Oxidase, beta-galactosidase and urease

PCR OO

Targets 16S rRNA (784-bp amplicon) and rpoB genes. Highly specific and fast.

ELISA OO

Detects antibodies 1-4 weeks post-infection.

Highly reliable but requires longer execution time and higher costs.

Rapid Agglutination Test (RAT/SPAT) OO

Field-practical, low-cost, and rapid. Drawback: Prone to cross-reactions between certain serotypes (e.g., A and AB, or and L).

AMR OO

pOR1, encoding replication and heavy metal resistance

• Ampi and peni

• enro (link to gyrA mutations)

• genta and fosfomycin

• cotrimoxazole

Antibiogram (Antibiotic Sensitivity Test) OO

mandatory before initiating flock-level pharmacological interventions.

susceptible OO

• Amoxicillin / Clavulanic acid

• Florfenicol (High sensitivity noted in recent broiler/turkey studies)

• Tiamulin & Doxycycline

• Gamithromycin

chemical disinfection OO

using aldehyde-based chemicals or organic acid disinfectants (highly effective even a t low concentrations).

inactive bacterins OO

Highly effective when administered to broiler breeders oil adjuvant vaccines show best response). Protects progeny up to 4 weeks of age via maternal antibodies

autogenous vaccines OO

custom vaccines tailored to the specific serotype circulating on a farm (crucial since cross-protection between serotypes is not guaranteed).

recombinant subunit vaccines OO

(cloned in E. coli) are currently in development t o provide broad, heterologous protection across multiple ORT serotypes without causing clinical signs.

pullorum disease

AKA bacilliary white diarrhea

young chicks and poults <4wks

fowl typhoid

spreads more aggressive among growing and mature flocks

Salmonella enterica serotype gallinarum BIOVARS

biovar Pullorum ( S. pullorum) and Gallinarum (S. gallinarum)

morbidity SLS

40% or more

mortality SLS

100% days 1-21

host species SLS

primary: chickens and turkeys

pheasants, quails and backyards also affected

SLS status

successfully eradicated from US via the National Poultry Improvement Plan

MOT SLS

Vertical: egg

Horizontal direct: bird to bird, CANNIBALISM or feather pecking

Horizontal indirect: feces, water, feeds, litters, incubators, equipment

• viable in soil for up to a year

incubation period SLS

1-10 days

acute phase SLS

Rapid systemic septicemia

chronic phase SLS

survivors become ASYMPTOMATIC CARRIERS

bacteria PERMANENTLY localize in OVARIES and CECA

shedding SLS

activated by stress, leading to active horizontal (fecal) and vertical (egg) shedding

physical s/s SLS

stunting from 14 days onwards, poor feathering, labored breathing, swollen joints- lameness

behavioral s/s SLS

drowsy, weak, anorexic, swaying and huddling near neat sources

pathognomonic sign SLS

copious white sticky diarrhea causing pasty butt (dried fecal pasting blocking the vent)

fowl typhoid s/s in adult hens GENERAL SLS

asymptomatic carriers but present with pale, shrunken combs, severe dehydration and ruffled feathers

Pullorum disease in young chicks findings

yolksac: unabsorbed - omphalitis

GIT: firm cheesy material in ceca (cecal cores), raised plaques in lower intestinal mucosa

systemic: classic gray/white nodules in liver, spleen lungs, heart and gizzard; enlarged and congested liver and spleen

liver gross lesions FT

swollen, friable often bile stained marked WHITE coalescing necrotic foci

ovaries gross lesions FT

granulomatous oophoritis, flaccid hemorrhagic or atrophic follicles with caseous contents

heart and spleen gross lesions FT

granulomatous pericarditis and multifocal granulomatous splenitis

• 1-5mm white nodules

field screening SLS

rapid whole blood plate agglutination test and macroscopic tube agglutination for identifying ASYMPTOMATIC CARRIERS

definitive lab diagnosis SLS

bacte culture, isolation, serotyping from liver, intestine or yolksac

• culure required to DIFFERENTIATE S pullorum from S gallinarum

treatment not recommended SLS WHY

antibiotics may reduce immediate clinical signs and mortality but they DO NOT ELIMINATE carrier state

nutritional management SLS

fermenting feed and supplementing diets with pro/prebiotics can reduce suscep to salmonella colonization