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141 Cards in this Set
- Front
- Back
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What are fundamental factors in disease prevention in poultry?
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change litter & disinfect house after each group of birds
select dz free chicks all in all out: isolate young birds from older birds isolate poultry classes from each other & from livestock adequate feed & good water quality do not crowd poultry sound vaccination program regulate temperature, humidity, ventilation strict biosecurity composting or incineration of dead birds prompt dx & appropriate tx during dz outbreaks |
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What is the single most important diagnostic procedure performed in poultry?
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necropsy
perform on typically affected birds, fresh dead birds, & apparently normal birds |
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What are some pre-placement influences on disease development in poultry 0 to 2-3 weeks old?
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breeder farm
-healthy breeders: good nutrition, vaccinations -sanitation on farm, in incubator, in hatcher: want clean eggs w/ no pathogen exposure hatchery -consider heat, humidity, air exchange, turning of eggs in incubators, control by computers/machines |
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What are some causes of early mortality (0 to 2-3 wks) d/t mismanagement?
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chilling or overheating
ventilation: dust, ammonia (ammonia burn --> conjunctivitis) starve out (no feed in proventriculus or gizzard) & dehydration improper servicing persecution toxicosis |
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omphalitis
a. signalment b. etiology c. pathogenesis |
a. newly hatched chicks & poults
b. FECAL CONTAMINATION of eggs w/ bacteria (E. coli, Pseudomonas, Salmonella, Proteus, etc.) at BREEDER FARM OR HATCHERY c. BACTERIA PENETRATE SHELL MEMBRANE --> yolk sac infection --> navel inflammation --> incomplete closure --> death (late embryo stage – 3 wks. post hatch) |
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omphalitis
a. clinical signs b. gross lesions |
a. INFLAMED MOIST NAVEL, general weakness, lack of body tone, piling up of birds, enlarged abdomen
b. LARGE UNABSORBED YOLK SAC, peritonitis w/ fetid odor, edema of pectoral & abdominal mm. |
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omphalitis
a. dx b. tx c. control |
a. hx, signs, LESIONS, CULTURE OF YOLK SAC for bacteria
b. cull (not contagious) c. ID source, clean & disinfect to PREVENT CONTAMINATION |
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aspergillosis
a. signalment b. 2 forms |
a. many types of birds susceptible: turkeys, chickens, pets, wild birds
b. acute: young poultry -high morbidity & mortality: “brooder pneumonia” chronic: adult poultry -involves occasional bird, but majority are unaffected |
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aspergillosis
a. clinical signs b. gross lesions c. histo lesions |
a. DYSPNEA, gasping, tachypnea
b. LUNGS: white or yellow nodules or plaques (masses of fungal mycelium) AIR SACS & TRACHEA c. FOCAL PNEUMONIA: necrosis & nodular formations resembling tubercles fungal hyphae seen w/in nodules or plaques (requires special stains) |
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aspergillosis
a. pathogenesis b. dx |
a. Aspergillus fumigatus spores penetrate EGG SHELL --> infection of embryo
BREEDER FLOCKS: moldy feed or litter --> eggs HATCHERY: contaminated incubators or hatchers --> eggs & chicks or poults birds infected in HATCHERS OR ON FARM by RESPIRATORY ROUTE b. hx, signs, LESIONS mpression smear of lesions HISTOPATH showing fungal hyphae CULTURE |
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aspergillosis
a. tx b. control |
a. difficult: individual birds generally NOT treated
cull affected birds remove contaminated feed & water tx litter & feed w/ mold inhibitors b. ID source of contamination/infection: breeder farm, HATCHERY, BROODING properly store food to prevent mold growth maintain feeding, watering equipment & utensils free of mold properly adjust waterers |
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encephalomalacia
a. signalment b. pathogenesis |
a. chickens or turkeys b’twn 15-30 d. of age
b. deficiency of USABLE (ACTIVE) vitamin E in diet -long storage &/or too much heat --> inactivation of antioxidants -rations high in polyunsaturated fats or rancid fats inactivate vitamin E |
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encephalomalacia
a. clinical signs b. gross lesions c. histopath lesions |
a. ATAXIA, backward or downward retractions of head, +/- lateral twisting, forced movements, ↑ incoordination, rapid contraction & relaxation of legs, progresses to prostration & death
b. swollen, HEMORRHAGIC, softened CEREBELLUM edema of meninges c. cerebellum: hyperemia & edema, demyelination & neuronal degeneration |
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encephalomalacia
a. dx b. tx c. control |
a. signs, GROSS LESIONS, histopath
b. change feed to provide adequate vitamin E, supplement w/ vit. E & antioxidants (preservatives) c. adequate vitamin E in ration avoid rancid fats, long storage, & high temps add antioxidants: BHT, santoquin |
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encephalomyelitis
a. signalment b. etiology c. transmission |
a. primarily affects young chickens (also turkeys)
b. hepatovirus c. vertical transmission: egg from infected hen to chick/poult (most common) horizontal transmission -direct contact -indirect spread by contaminated feed, water, or equipment: virus can survive for up to 4 wks in fecal material |
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encephalomyelitis
a. clinical signs b. gross lesions c. histopath lesions |
a. progressive ataxia, TREMORS OF HEAD & NECK (accentuated by moving bird)
few birds showing signs will recover adult birds often asymptomatic except for ↓ EGG PRODUCTION, slight ↓ in egg size, & slight depression b. OFTEN NO GROSS LESIONS c. DISSEMINATED, NON-PURULENT ENCEPHALOMYELITIS w/ widespread & marked PERIVASCULAR CUFFING ganglioitis in midbrain lymphoid aggregates in muscles of proventriculus & gizzard |
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encephalomyelitis
a. dx b. tx c. control |
a. hx, signs, LACK OF GROSS LESIONS, HISTOPATH, serology
b. CULL c. obtain chicks/poults from IMMUNIZED BREEDER FLOCKS REPORTABLE DZ |
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splay leg
a. what is it b. signalment c. cause |
a. lateral deviation of leg originating at KNEE or hip
b. seen from 0-2 wks of age c. brooding birds on slippery surfaces (ex. brown paper) |
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rickets
a. signalment b. pathogenesis c. clinical signs |
a. poultry 2-4 wks old: turkeys > chickens
b. deficiency or imbalance of calcium, phosphorous, or VITAMIN D3 --> abnormal skeletal development d/t INSUFFICIENT CALCIFICATION of bones c. LAMENESS, leg weakness, ataxia, ↓ growth rate, poor feathering, ENLARGEMENT AT ENDS OF LONG BONES |
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rickets
a. gross lesions b. dx c. tx |
a. LONG BONES & beak: SOFT & springy
BEADING of ribs at junction w/ spinal column curvature of ribs & spine b. hx, signs, LESIONS determine source of deficiency: analyze feed c. change or supplement ration to provide proper amts of Ca, P, & VITAMIN D3 |
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What are the 2 classes of Salmonella organisms that cause GI dz?
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host specific, Ag similar: non-motile
-pullorum dz: Salmonella pullorum -fowl typhoid: S. gallinarum not host specific, Ag diverse: motile (public health concern) -paratyphoid infections: Salmonella spp. |
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What are the components of the National Poultry Improvement Plan (NPIP)?
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pullorum & fowl typhoid: reportable diseases
outbreaks quarantined: marketing of infected flocks is supervised control importation test exhibited birds: serology test breeder flocks & hatcheries: serology & culture |
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pullorum dz/fowl typhoid
a. signalment b. etiologies c. transmission |
a. young chickens & turkeys
b. pullorum dz: Salmonella pullorum fowl typhoid: Salmonella gallinarum c. vertical: egg, transovarian horizontal: fecal-oral, egg shell contamination, contamination of feed, water, equipment |
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pullorum dz/fowl typhoid
a. stability in environment b. clincal signs |
a. relatively resistant: can survive in organic material for months
destroyed by thorough cleaning to remove organic material killed by formaldehyde gas: fumigate eggs & incubation equipment b. acute death w/in days of hatch o depression, weakness, ruffled feathers, WHITE DIARRHEA, PASTING OF VENT (white feces stained a green color d/t bile), marked anorexia, ↑ water consumption |
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pullorum dz/fowl typhoid
a. gross lesions: acute & subacute b. histopath lesions |
a.
acute: GRAY NODULES (FOCAL NECROSIS) in lungs, LIVER, gizzard wall, heart, intestinal or cecal wall, spleen, or pericardium petechial hemorrhages or necrotic foci in LIVER subacute: white plaques in intestinal mucosa, caseous material in intestinal lumen & ceca (CECAL CORES) splenomegaly, urates in ureters b. intestines: mucosal hyperemia, hemorrhagic exudation, leukocytic infiltration, marked thickening of walls diffuse pulmonary congestion & hemorrhage |
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pullorum dz/fowl typhoid
a. dx b. tx c. control |
a. serology
definitive: BACTERIAL CULTURE -culture used for screening flocks: doesn't differentiate b'twn pullorum & fowl typhoid b. DO NOT give ABs: perpetuate carrier state! notify hatchery/breeder flock & regulatory officials of definitive dx: compensation possible c. obtain eggs from pullorum free breeder flocks & monitored hatcheries: NPIP prevent introduction of infection to breeder flocks, hatchery, & brooder farms REPORTABLE DISEASES |
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paratyphoid
a. signalment b. etiology c. pathogenesis |
a. young poultry
b. large # of Salmonella spp. NOT HOST SPECIFIC ANTIGENICALLY DIVERSE FREQUENT CAUSE OF HUMAN DZ: foodborne illness c. endotoxins contained in bacterial cell wall |
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paratyphoid
a. transmission b. dx c. tx d. control |
a. #1: contaminated feces
contaminated feed, water, litter, etc.: egg shell penetration or infection of newly hatched birds transovarian: not as common b. bacterial culture (used for screening flocks) c. ABs: DECREASING USE d. GOOD MANAGEMENT |
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crop mycosis
a. signalment b. etiology c. pathogenesis |
a. young turkeys & caged layers
b. Candida albicans -normal intestinal flora of healthy birds -opportunist or facultative pathogen c. debilitation, stress, alteration of normal flora, parasites, poor nutrition, infectious dz, poor sanitation, excess use of broad spectrum ABs --> yeast overgrowth --> invasion of tissues |
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crop mycosis
a. transmission b. clinical signs c. gross lesions |
a. environmental-oral, fecal-oral, "crop milk" (regurgitated feeding --> sick babies)
b. depression, ruffled feathers, diarrhea, failure to thrive in babies fed by crop milk c. whitish or thickened pseudomembranous or diphtheritic patches in CROP (most common), proventriculus, gizzard, etc. GRANULAR CHEESY EXUDATE |
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crop mycosis
a. dx b. tx c. prevention |
a. mucosal scrapings: BUDDING YEAST
histopath, fungal culture b. ANTI-MYCOTICS: mycostatin or gentian violet added to feed or Cu sulfate added to water ID PREDISPOSING DZ or MANAGMENT PROBLEM c. sanitation, avoid over-medication |
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coccidiosis
a. signalment b. etiology c. transmission |
a. young, growing birds (1-6 wks)
older birds develop immunity that is rather species specific b. Eimeria HOST SPECIES SPECIFIC: interspecies transmission does NOT occur c. fecal-oral, oocysts spread by FOMITES occurrence increases w/ confinement or intense product d/t inc. oocyst concentration |
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coccidiosis
a. clinical signs b. gross lesions c. dx |
a. depression, ruffled feathers, droopy wings, anorexia, brownish MUCOID DIARRHEA, WT. LOSS, POOR FEED CONVERSION
b. hemorrhage, severe compromise of gut mucosa: different Eimeria spp. cause lesions in different areas of gut c. GUT SCRAPINGS, FECAL FLOAT |
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coccidiosis
a. tx b. control |
a. not very successful
b. litter management, sanitation, biosecurity ANTI-COCCIDIALS in feed -not equally effective vs. all species -resistance develops: use in sequence or combinations vaccines oral: MULTIVALENT, LIVE -induces resistance to many Eimeria spp. -rxns possible since vaccine is live in-ovo |
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coronavirus enteritis
a. signalment b. mortality c. transmission |
a. TURKEYS: most severe in young
b. 50-100% in poults c. fecal-oral (direct & indirect) |
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coronavirus enteritis
a. clinical signs b. gross lesions c. histopath lesions |
a. FROTHY DIARRHEA, dehydration, cyanosis, anorexia, ↓ body wt., death, turkeys huddle around heat source
breeder hens: ↓ egg production, chalky egg shells b. intestinal contents: FLUID & FROTHY w/ mucus & casts petechial hemorrhages in intestinal mucosa; flaccid intestinal wall c. CAN'T ID SPECIFIC VIRUS BASED ON HISTOPATH ENTERITIS: CUBOIDAL EPI CELLS, VILLOUS ATROPHY, LOSS OF MICROVILLI, disappearance of goblet cells, mononuclear cell infiltration |
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coronavirus enteritis
a. dx b. tx c. control |
a. EM: FECES
fluorescent Ab (tissue), virus isolation (feces or tissue), serology b. SUPPORTIVE: heat, electrolytes, nutrients ABs: prevent secondary infection c. protect susceptible poults from potential carriers: avoid multiple age flocks on same farm sanitation & biosecurity |
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poult enteritis & mortality syndrome (PEMS)
a. signalment b. etiology |
a. SPIKING MORTALITY OF TURKEYS
b. CORONOAVIRUS, E. COLI, others |
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histomoniasis (blackhead)
a. signalment b. etiology c. clinical signs |
a. most severely affects TURKEYS
b. Histomonas meleagridis (protozoa) c. YELLOW-GREEN (SULFUR COLORED) DIARRHEA, cyanosis |
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What are the 3 methods of transmission of histomoniasis?
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1. direct
protozoans passed in droppings of infected birds --> ingested from fresh feces (“cloacal drinking”: turkeys) indirect: incl. flock to flock transmission 2. 1 transport host cecal worm (INTERMEDIATE HOST: Heterakis gallinarum) --> EGGS CONTAINING HISTOMONAS --> cecal worm eggs “contaminate” ingesta --> BIRDS INGEST INFECTED CECAL WORM EGGS --> infected w/ Heterakis & Histomonas 3. 2 transport hosts cecal worm (intermediate host) --> eggs containing Histomonas --> earthworms (ACCESSORY HOST) ingest infected cecal worm eggs --> BIRDS EAT EARTHWORMS --> infected w/ Heterakis & Histomonas labile in environment |
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histomoniasis
a. gross lesions b. dx |
a. CECA: enlarged, inflamed, filled w/ caseous plug or core
LIVER: irregularly round depressed ulcer like necrotic TARGET LESIONS (PATHOGNOMONIC) |
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histomoniasis
a. dx b. tx c. control |
a. GROSS LESIONS: liver & ceca
histopath b. metronidazole: individual birds (“off label” use) ABs: control 2º infections roxarsone (3-Nitro): some efficacy c. separate chickens from turkeys worm control (benzamidizoles) control exposure to earthworms |
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hemorrhagic enteritis
a. signalment b. pathogenesis c. transmission |
a. young turkeys (6-12 wks)
b. ADENOVIRUS --> replicates in spleen --> immunosuppression --> secondary infection (ex. E. coli) c. fecal-oral (direct & indirect) |
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hemorrhagic enteritis
a. clinical signs b. gross lesions c. histopath lesions |
a. ↑ mortality: sudden death
depression, ruffled feathers, BLOODY OR TARRY DIARRHEA b. INTESTINE: distended & filled w/ dark colored clotted blood from massive intestinal hemorrhage mucosa of duodenum & jejunum: red & congested SPLEEN: enlarged, friable, & mottled c. SI: severe congestion of mucosa, degeneration of epi cells & tips of villi, hemorrhage into gut lumen SPLEEN: hyperplasia of white pulp & necrosis of lymphoid cells, INTRANUCLEAR INCLUSION BODIES |
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hemorrhagic enteritis
a. dx b. tx c. control |
a. HISTOPATH OF SPLEEN & INTESTINE: intranuclear inclusion bodies in spleen
AGAR-GEL IMMUNODIFFUSION (AGID): ID Abs or virus b. non-specific ABs: ↓ 2º bacterial infections d/t immunosuppression c. VACCINES: given in water at 3-4 wks |
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infectious bursal dz
a. signalment b. etiology c. transmission |
a. young chickens (0-6 wks)
b. birnavirus c. horizontal: direct & indirect highly contagious & easily transmitted by contaminated feed, water, litter, fomites |
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infectious bursal dz
a. 2 forms b. gross lesions c. histopath lesions |
a. acute clinical form: 3-6 wks (age related susceptibility)
~100% morbidity, 0-30% mortality subclinical immunosuppressive form: 0-3 wks -occurs in chicks w/o maternal Abs b. urate deposits in kidneys & ureters, hemorrhages in thigh & pectoral mm., mucosa of proventriculus, ENLARGEMENT OF BURSA OF FABRICIUS early, atrophy later c. degeneration & necrosis of BURSAL lymphocytes (LYMPHOID NECROSIS) lymphoid necrosis also in spleen, thymus, & cecal tonsils |
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infectious bursal dz
a. dx b. tx c. control |
a. presumptive: hx, signs, LESIONS
definitive: histopath, fluorescent Ab test, virus isolation, serology, PCR b. none specific: keep warm c. biosecurity, sanitation VACCINATON: BREEDER HENS, embryos in ovo, chicks |
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Diseases of what body system is the most important cause of mortality during the middle growing period?
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respiratory
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What environmental factors contribute to development of respiratory dz?
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excessive dust --> pulmonary fibrosis
high ammonia --> impaired mucociliary apparatus |
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colibacillosis
a. signalment b. etiology c. dz syndromes |
a. young birds most susceptible
b. E. coli MOST avian E. coli not pathogenic to other animals (except 0157:H7) 150 serotypes: most NOT 1º PATHOGENS normal intestinal flora of domestic birds & mammals c. omphalitis, air saccullitis, acute septicemia, chronic localized lesions, etc. |
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colibacillosis
a. airsacculitis: causes b. acute sepicemia: signs c. acute septicemia: lesions d. types of chronic localized lesions |
a. dusty litter, poor ventilation
occurs secondary to 1º respiratory pathogens or immunosuppression (ex. HE, IBD) b. dehydration, sudden death c. green, bile stained liver w/ small white necrotic foci adhesive PERICARDITIS, fibrinous PERIHEPATITIS, ENLARGED CONGESTED SPLEEN d. polyarthritis, osteomyelitis, panophthalmitis, etc. |
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colibacillosis
a. dx b. tx c. control |
a. BACTERIAL CULTURE: avoid contamination
look for primary pathogens b. ABs: early in dz c. good management: sanitation, air quality, biosecurity, healthy flocks |
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mycoplasmosis
a. bacteria characteristics b. species of bacteria |
a. nutritionally fastidious WALL-LESS BACTERIA
require media supplemented w/ serum cannot survive for long outside host b. Mycoplasma gallisepticum (MG), M. synoviae (MS): turkeys & chickens M. meleagridis (MM): turkeys |
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M. gallisepticum
a. dz syndromes b. transmission |
a. chickens: “chronic respiratory dz”
turkeys: “infectious sinusitis” chickens & turkeys: “air sac dz”: respiratory virus + MG + E. coli b. TRANSOVARIAN, FOMITES, INFECTED CARRIERS endemic infections: commercial table egg flocks, backyard flocks, gamefowl (fighting chickens), house finches & some other songbirds most infections introduced to susceptible flocks: movement of birds, people, & equipment |
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M. gallisepticum
a. clinical signs b. gross lesions |
a. nasal d/c, SWELLING OF INFRAORBITAL SINUSES (TURKEYS: ALMOST PATHOGNOMONIC), conjunctivitis (chickens & songbirds)
slow chronic course, variable mortality --> condemnations at processing b. air sac dz: airsacculitis, fibrinous perihepatitis, adhesive pericarditis |
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Mycoplasma gallisepticum
a. dx b. tx c. control d. signs in house finches |
a. MYCOPLASMA CULTURE
PCR, serology b. quarantine ABs (tylosin, tetracyclines, etc.): expensive & often not effective depopulation c. obtain eggs or chicks/poults from MG FREE BREEDER FLOCKS: monitored by serology (NPIP) prevent introduction: biosecurity, sanitation d. conjunctival swelling, serous to mucopurulent ocular & nasal d/c |
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Mycoplasma synoviae
a. signalment b. lesions c. control |
a. chickens, turkeys
b. INFLAMMATION of synovial membranes of JOINTS & TENDON SHEATHS can sometimes cause respiratory dz c. NPIP REPORTABLE |
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Mycoplasma meleagridis
a. signalment b. transmission c. clinical signs |
a. TURKEYS
b. SEXUALLY TRANSMITTED (AI), transovarian, horizontal via respiratory tract c. adults: inapparent mild FOAMY AIR SACCULITIS in day old poults, dec. hatchability, inc. mortality |
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Mycoplasma meleagridis
a. dx b. tx c. control |
a. MYCOPLASMA CULTURE
serology, PCR b. ABs c. NPIP: MM free breeder flocks |
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Bordetella rhinotracheitis
a. signalment b. etiology c. transmission |
a. young TURKEYS (1-6 wks)
b. Bordetella avium c. CONTAMINATED WATER & LITTER (major source) shed in resp. & ocular secretions |
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bordtella rhinotracheitis
a. cliical signs b. gross lesions c. histopath lesions |
a. voice change (snicking: sneeze/cough), accumulation of mucus at external nares, mild foamy conjunctivitis
b. mucus in nasal sinuses & upper 1/3 of trachea, trachea partially collapses c. inflammation of NASAL SINUSES & TRACHEA LOSS OF CILIA from tracheal epithelium debris & mucus in airway |
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bordetella rhinotracheitis
a. dx b. tx c. prevention |
a. bacterial culture: tracheal or turbinate swabs, nasal or ocular d/c
serology b. ABs added to feed or water NOT effective against B. avium (can’t get efficacious levels to source of infection), but may ↓ 2º bacterial infections improve air quality, clean & disinfect waterers c. good management, esp. waterers vaccines -breeders: bacterins --> maternal Abs -poults: MLV (spray + water): expensive, not very effective |
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avian influenza
a. signalment b. types c. etiology |
a. chickens, turkeys, ducks
b. HIGH PATH form: acute, generalized dz w/ short course & high mortality = FOWL PLAGUE in chickens low path: respiratory signs (ddx: endemic Newcastle dz) NOT AN EXOTIC DZ: endemic in turkeys in some areas c. type A influenza virus (orthomyxovirus) antigenicity: serotypes (16 H, 9 N) |
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avian influenza
a. transmission b. clinical signs |
a. transovarian --> death of embryo
HORIZONTAL: oral/resp. transmission (direct & indirect) NATURAL RESERVOIRS: WATERFOWL & SHOREBIRDS -live bird markets, swine b. low path: none or mild resp. signs high path: sudden death severe ↓ in egg production, hatchability, & feed conversion respiratory signs, diarrhea, edema, cyanosis, convulsions, tremors |
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avian influenza
a. gross lesions b. dx |
a. VASCULAR DAMAGE: inflammation, congestion, swelling, & edema
pneumonia & airsacculitis necrotic foci in lungs, liver, kidney, & spleen b. serology: AGP, HI (in absence of vaccination): surveillance VIRUS ISOLATION: tracheal & cloacal swabs --> eggs --> HA (hemagglutinating virus) --> ID --> serotype & pathotype *PCR* |
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avian influenza
a. tx b. control |
a. low path: none specific
-supportive care, ABs to ↓ 2º bacterial infections -NOTIFY REGULATORY OFFICIALS: low path H5 & H7 can change to high path high path: depopulate; vaccination?: then can’t use serology for surveillance; development of new strains? b. good management & BIOSECURITY: prevent contact w/ wild birds, live bird markets, swine serologic monitoring: AGP test vaccinate (turkeys by permit): in some regions to control low path strains -antigenic diversity makes effective preventive vaccination difficult -control outbreaks? |
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Newcastle dz
a. signalment b. transmission c. clinical signs d. gross lesions |
a. chickens, turkeys (wide range of avian species)
b. same as AI c. same as AI d. same as AI |
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newcastle dz
a. etiology b. forms c. dx |
a. paramyxovirus: > 100 strains
b. endemic LENTOGENIC: mild path --> few or no signs MESOGENIC: moderate path --> resp. signs, encephalitis exotic (END): REPORTABLE VELOGENIC: high path --> rapid onset, acute course, high mortality c. serology (HI, ELISA: not that useful: rising titers may indicate vaccination or endemic strain VIRUS ISOLATION: swab brain, cloaca, trachea, & lung --> embryonating eggs --> HA (hemagglutinating virus) --> ID --> PATHOTYPE |
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What is viscerotropic exotic newcastle dz & what are the signs & lesions?
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1971: CA, 2002-03: CA, NV, AZ
signs rapid death: no gross lesions severe depression, high mortality CNS signs: tremors, torticollis, circling, paresis, paralysis, death lesions: cyanosis, facial & neck edema, hemorrhages in lining of proventriculus HEMORRHAGIC LYMPHOID TISSUES of GI tract, esp. cecal tonsils: viscerotropic |
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newcastle dz
a. tx b. control |
a. non specific
endemic: ABs to tx 2º bacterial infection END: quarantine --> depopulate; vaccination? b. chickens & turkeys: attenuated live & killed VACCINES -protect against ENDEMIC ND: NOT exotic ND REGULATIONS regarding importation of exotic birds, poultry, & poultry products were designed to prevent intro of END to US -now also used for AI & Chlamydia |
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What hx, signs, & lesions should make you highly suspicious of END or HPAI?
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respiratory, GI, CNS, marked ↓ in egg production, vascular damage, rapid death
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How do you definitively diagnose END or HPAI?
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serology: AI only
VIRUS ISOLATION: hemagglutinating virus AI (serotype) or ND --> pathotype --> HPAI or END |
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infectious bronchitis
a. signalment b. etiology c. transmission |
a. chickens
b. coronavirus: several antigenic serotypes immunity is serotype specific c. respiratory (direct & indirect): inhalation of virus containing aerosols rapid onset & spread thru flock |
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infectious bronchitis
a. clinical signs b. gross lesions c. histopath lesions |
a. gasping (open mouth breathing), rales, coughing, ocular & nasal d/c
eggs: 20-50% ↓ in production, misshapen, rough, soft shelled, water albumin, poorly formed yolks b. serous mucoid or caseous exudate in nasal passages, sinuses, & trachea conjunctivitis, airsacculitis lesions in ovaries or oviduct eggs or yolks in body cavity: internal layers acute nephritis: seen w/ nephrogenic strains c. TRACHEA & bronchi: deciliated, thickened mucosa & submucosa (cellular infiltration, edema) KIDNEYS: acute interstitial nephritis & tubular necrosis |
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infectious bronchitis
a. dx b. tx c. control |
a. VIRUS ISOLATION: lung & trachea --> embryonating eggs
serology (VN, modified HI, ELISA): can’t differentiate b’twn vaccination & field challenge RT-PCR: ID serotypes b. none specific ABs: ↓ problems w/ 2º bacterial infection c. vaccination: serotype specific -MLV: broilers & pullets -inactivated vaccines: layers & broiler breeders |
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chlamydiosis
a. signalment b. etiology c. transmission |
a. poultry (esp. TURKEYS), pet birds, etc.
ZOONOTIC b. Chlamydophila psittaci c. respiratory: inhalation of dust contaminated w/ feces, aerosols during processing of infected turkeys pigeons: often asymptomatic carriers |
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chlamydiosis
a. clinical signs b. gross lesions |
a. depends on pathogenicity
may be subclinical or show mild respiratory signs depression, anorexia, wt. loss, YELLOW-GREEN DIARRHEA, nasal & ocular d/c, respiratory distress b. gross lesions: pericarditis, hepatitis, air sacculitis, splenomegaly |
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chlamydiosis
a. dx b. tx c. control |
a. GOLD STANDARD: impression smears of air sacs, lung, liver, spleen, pericardium: use special stains & look for INTRACYTOPLASMIC INCLUSIONS
CULTURE & immunofluorescence other: histopath, EM; serology, dot immunobinding assay, PCR (evolving) b. turkeys: tetracyclines -↓ development of lesions: will not eliminate infection -may reduce exposure to processing plant workers c. confinement, exclusion of wild birds from poultry houses sanitation & BIOSECURITY: prevent introduction from personnel & equipment -employees can’t own pet or backyard birds REPORTABLE |
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bumblefoot
a. pathogenesis b. etiology c. tx |
a. poor management --> litter condition deteriorates --> irritation & abrasion of foot pads (pododermatitis)
b. Staph spp. c. commercial poultry: cull individual birds: ABs, sx |
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viral arthritis
a. signalment b. etiology c. clinical signs |
a. CHICKENS, esp. broilers
b. reovirus c. lameness, swollen joints, RUPTURE OF GASTROCNEMIUS TENDON (almost pathognomonic), ARTHRITIS, tenosynovitis |
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viral arthritis
a. dx b. tx c. control |
a. presumptive: hx, signs, lesions: RUPTURED TENDON, serosanguinous joint fluid
definitive VIRUS ISOLATION: synovial swab --> chick embryos or cell culture FA: virus in synovial cells serology: can’t differentiate vaccination from infection b. none c. MLV & killed VACCINES: broiler breeders, chicks |
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infectious synovitis
a. signalment b. etiology c. gross lesions |
a. chickens, turkeys
b. Mycoplasma synoviae c. swollen joints: moderately thick cream to gray colored exudate (may thicken w/ chronic lesions) |
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infectious synovitis
a. dx b. tx c. control |
a. serology, Mycoplasma culture, PCR
b. ABs: not effective in established cases c. NPIP obtain chicks/ poults from MS free breeder flocks biosecurity REPORTABLE |
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avian pox
a. forms b. etiology |
a. WET POX (diphtheritic form): diphtheritic lesions of mouth & esophagus, (upper respiratory tract)
DRY POX (cutaneous form): cutaneous lesions on featherless skin b. 4 classic strains of avian poxvirus: fowlpox (affects chickens), pigeon pox, turkey pox, & canary pox -can be affected by 1 or more pox virus |
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avian pox
a. signs: wet pox b. signs: dry pox c. transmission |
a. raised whitish-yellow PLAQUES in mouth; nasal & ocular d/c --> severe conjunctivitis --> ↓ vision, respiratory distress, ↓ egg production
b. wt. gain, ↓ egg production, low mortality; papules, vesicles, & pustules --> SCABS c. resistant in environment present in high amts. in dried exudate from pox lesions horizontal: oral/cutaneous abrasions, mosquitos |
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avian pox
a. histopath lesions b. dx c. tx d. control |
a. skin: EPITHELIAL HYPERPLASIA, EOSINOPHILIC INTRACYTOPLASMIC INCLUSION BODIES, inflammatory changes
b. HISTOPATH, virus isolation (embryonated turkey eggs) c. none specific VACCINATION during outbreak to dec. losses: virus progresses slowly CULL severely affected birds d. VACCINATION |
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fowl cholera
a. signalment b. etiology c. transmission |
a. chickens, turkeys
b. Pasteurella multocida -virulence, encapsulation, antigenicity all highly variable (hard to develop effective vaccines) c. organism in palatine (choanal) cleft of apparently healthy birds: asymptomatic or recovered carriers -contaminated excretions from external nares, mouth, or eyes: contaminate air, feed, or water -infected carcasses: dead bird disposal is important |
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fowl cholera
a. forms of dz |
a. ACUTE SEPTICEMIA: dead birds, cyanosis
SUB-ACUTE DZ: depression, anorexia, cyanosis, nasal or oral d/c, diarrhea, torticollis CHRONIC DZ: localized infections of comb or wattles, joints or tendon sheaths, conjunctival sac or infraorbital sinus, middle ear, & cranial bones |
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fowl cholera
a. dx b. tx c. control |
a. BACTERIAL CULTURE, blood smear or impression smears of liver, spleen, or lungs: G (-) bipolar rods
b. poultry -ABs: helps birds not severely or chronically affected -cull severely affected birds -vaccinate? waterfowl: dead bird disposal c. cull sick birds, dead bird disposal VACCINATION -meat turkeys: bacterin, live attenuated -breeder/laying flocks: boosted q. 4-6 wks for life |
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erysipelas
a. signalment b. etiology c. transmission |
a. TURKEYS (can also affect chickens, other birds)
swine: diamond skin dz, man: ERYSIPELOID (localized skin infection) b. Erysipelothrix rhusiopathiae resistant to environment & disinfectants, remains viable in soil for months to yrs c. shed in feces of infected turkeys ingestion of contaminated feed, water, or litter, persecution (toms) --> open wounds --> portal of entry |
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erysipelas
a. clinical signs b. gross lesions |
a. acute: dead birds
sub-acute to chronic: depression, resp. signs (nasal d/c), diarrhea, SWOLLEN REDDISH-PURPLE SNOODS & IRREGULAR DARK RED SKIN LESIONS ON FACE & HEAD b. septicemic dz generalized congestion & intramuscular ECCHYMOTIC HEMORRHAGES petechial hemorrhages in fat, epicardium, liver, spleen, & skin SPLENOMEGALY |
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erysipelas
a. dx b. tx c. prevention |
a. presumptive: hx, signs, lesions (SWOLLEN SNOODS, ECCHYMOTIC HEMORRHAGES in skin & muscles)
definitive BACTERIAL CULTURE & ID: liver, spleen, & BM impression smears: G (+) slightly bent thin rods b. injectable penicillin AND vaccination: erysipelas bacterin c. good management: trim snoods (less common recently) vaccination w/ erysipelas bacterin -meat turkeys: 8-12 wks -breeder turkeys: 16-20 & 20-24 wks |
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infectious laryngotracheitis
a. signalment b. etiology c. transmission |
a. maturing CHICKENS
b. herpesvirus variable pathogenicity destroyed by disinfectants, not resistant outside host remains viable in exudates & carcasses c. direct & indirect: relatively slow spread (compared to ND & infectious bronchitis) |
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infectious laryngotracheitis
a. clinical signs b. gross lesions c. histopath lesions |
a. severe respiratory signs: dyspnea, gasping, coughing, sneezing
BLOODY MUCOID TRACHEAL EXUDATE: “blood slinging chickens” conjunctivitis, nasal d/c, facial edema b. trachea w/ bloody mucous & PSEUDODIPHTHERITIC MEMBRANE(fibrinohemorrhagic), caseous plugs -separates from tracheal mucosa (unlike fowlpox diphtheritic membrane) c. edema & congestion of tracheal mucosa & submucosa -FIBRINOHEMORRHAGIC MEMBRANE -INTRANUCLEAR INCLUSION BODIES in multinucleate (syncytial) cells |
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infectious laryngotracheitis
a. dx b. tx c. control |
a. FLUORSECENT AB demonstration of virus in tracheal epi (fastest dx)
histopath: intranuclear inclusions in tracheal cells virus isolation in embryonating chicken eggs b. none specific c. eradication & biosecurity quarantine, area vaccinate by permission --> eradication REPORTABLE |
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fowl cholera
a. gross lesions: acute or subacute b. gross lesions: chronic |
a. vascular damage & generalized hyperemia, hepatomegaly, PNEUMONIA (characteristic changes should ↑ suspicion, esp. in turkeys: consolidated enlarged lobe: usually 1 side more involved than other)
b. localized suppurative or caseous lesions of joint, tendon sheaths, comb & wattle, conjunctival sac, infraorbital sinus, middle ear, or cranial bones at base of skull |
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avian tuberculosis
a. signalment b. etiology c. clinical signs |
a. ADULT chickens (< 1 yo) & other birds
infects swine, cattle, sheep, ZOONOTIC POTENTIAL for immunosuppressed people b. Mycobacterium avium c. gradual wt. loss, death |
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avian tuberculosis
a. gross lesions b. dx c. tx |
a. irregulary shaped & sized GRANULOMAS in VISCERAL ORGANS (SPLEEN, LIVER, INTESTINES: NOT LUNG!)
b. acid fast stain, culture, serology c. not recommended: potential zoonosis, tx not effective |
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Marek's dz
a. etiology & unique features b. relevance c. epidemiology |
a. ** α-herpesvirus w/ unique features **
-strictly cell associated -lymphoid tropism -carries an oncogene & induces lymphomas b. economic -poultry industry would not be economically viable w/o MD vaccines -economic losses of ~$1B annually research: Marek’s dz vaccine was 1st vaccine against a neoplastic dz c. ubiquitous affects primarily CHICKENS, but also turkeys, etc. |
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Marek's dz
a. classification of serotypes |
a. serotype 1: ONCOGENIC viruses isolated from chickens
-can be ATTENUATED in cell culture --> vaccines -subclassified into several pathotypes: MDV is ↑ in virulence serotype 2: naturally NON-oncogenic viruses isolated from chickens -used as vaccines serotype 3: naturally NON-oncogenic viruses isolated from turkeys (herpesvirus of turkey: HVT) -used as vaccines |
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Marek's dz
a. clinical signs b. tumor characteristics c. gross lesions |
a. chickens can show either non-specific clinical signs or NEURO signs: paralysis, torticollis, etc. (d/t enlargement of nn. d/t tumor)
b. MDV transforms CD4+ T cells --> lymphomas -can occur in ANY TISSUE -can be grossly observed as early as 3 WKS. OF AGE c. liver, heart, kidney, spleen, testes, ovary, lungs, proventriculus, muscle, eye (“white or gray eye”), SKIN (--> CONDEMNATION), nerves (enlarged, edematous, yellowish) |
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Marek's dz
a. dx b. control |
a. infection ≠ dz
VACCINATION does NOT protect against infection -only protects against dz (tumors) -EVERY CHICKEN in field is infected w/ MDV, but FEW develop MD b. biosecurity genetic resistance: trait used for breeding VACCINATION EFFICACY: serotype 1 > serotype 2 + 3 > serotype 3 -serotype 2 confers poor protection by itself, but is synergistic w/ serotype 3 administration -vaccinating w/ INFECTED CELLS since virus is strictly cell associated -route: SQ, IM, in ovo (embryos of 18 d.) -virus-host cell interaction: cell associated (frozen in liquid nitrogen), cell free (lyophyilized: only serotype 3) |
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avian leukosis virus (incl. lymphoid leukosis)
a. etiology b. relevance c. transmission |
a. RETROVIRUS of leukosis/sarcoma group
b. economic: eradication programs cost each company ~$15M annually research: avian retroviruses were basis for discovery of oncogenes c. VERTICAL: mom --> chick (MOST important) also horizontal |
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avian leukosis virus (incl. lymphoid leukosis)
a. pathogenesis b. clinical signs |
a. most cell types get infected --> bursa (IgM+ B cells TRANSFORMED) --> blood
--> liver, spleen, kidney, other viscera --> intestine, upper respiratory tract --> horizontal infection --> most cell types --> ovary --> vertical transmission --> most cell types transformation occurs b/c of integration of provirus in proximity of cellular oncogene b. non-specific AFFECTS ADULTS > 16 WKS: : takes time for virus to integrate in proximity of cellular oncogene |
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avian leukosis virus (incl. lymphoid leukosis)
a. gross lesions b. histopath lesions |
a. visceral tumors: DOES NOT effect eyes, nerves, rarely skin
+/- bursal lesions -liver & spleen commonly effected b. homogeneous pop’n of lymphoblasts: IgM+ B cells -transformed follicles in bursa -several types of tumors in same bird are NOT UNCOMMON |
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How is Marek's dz transmitted?
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HORIZONTAL: feathers, dander
lung (MPs) --> lymphoid organs (lymphocytes) --> blood (latent in T cells) --> feather follicle epithelium (cells that make feather) --> lungs OR --> skin, eyes, nervous system, viscera --> TUMORS FEATHER FOLLICLE EPITHELIUM is only place where virus exits cell & can infect other chickens |
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avian leukosis virus (incl. lymphoid leukosis)
a. dx b. control |
a. ID of ALV subgroup
ddx: MAREK'S DZ, reticuloendotheliosis b. control: ERADICATION objective: break vertical transmission cycle discard (+) breeders at pedigree level -VERY EXPENSIVE: only way to control dz (NO vaccines available) |
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How would you use the following in differentiating b'twn Marek's dz & lymphoid leukosis?
a. age of animal b. gross lesions |
a. < 16 wks: MD
> 16 wks: MD or LL b. Bursa of Fabricius -affected: most likely LL -not affected: MD or LL eyes & nerves -grey eye or enlarged nerves: MD -no eye or nerve lesions: MD or LL |
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How would you use the following in differentiating b'twn Marek's dz & lymphoid leukosis?
a. histopath lesions b. immunohistochemistry |
a. Bursa of Fabricius
-intrafollicular tumor: LL -interfollicular tumor: MD -no bursal lesions: MD or LL eyes & nerves -lymphoid infiltration in iris or nerves: MD -no lesions in iris or nerves: MD or LL cell morphology -LL tumors composed of homogeneous pop’n of lymphoblasts -MD tumors composed of heterogeneous pop’n of cells: lymphoblasts, small lymphocytes & MPs b. LL tumors: composed of IgM+ B cells MD tumors: composed of T cells |
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How would you differentiate b'twn Marek's dz & lymphoid leukosis at the farm level?
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age: young --> MD
bursa?: yes --> LL (confirm w/ histopath) nerves or eyes?: yes --> MD |
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How would you differentiate b'twn Marek's dz & lymphoid leukosis at the lab level?
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histopath
-homogenous cell pop'n: LL -heterogenous cell pop'n: MD immunohistochemistry -IgM+ B cells: LL -CD4+ T cells: MD |
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botulism (waterfowl)
a. pathogenensis b. clinical signs |
a. spores stable for yrs in environment: heat & drought resistant
hot months --> rotting plant & animal material, anaerobic conditions, fluctuating water levels fly maggots concentrate toxins birds eat maggots birds die & additional toxin production occurs --> major die off b. related to amt. of toxin ingested: don’t all die ascending paralysis: 1st legs, then wings, neck, & nictitans death d/t drowning or respiratory failure |
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botulism (waterfowl)
a. lesions b. dx c. tx d. control |
a. no gross lesions: usually in good flesh
b. presumptive: hx, signs, lack of gross lesions at necropsy definitive: ELISA, PCR, mouse bioassay c. supportive (gavage, fluids, provide shade, +/- antitoxin if available) d. prompt removal & disposal of carcasses during fly season raise water levels, fly control if possible |
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lead toxicosis (waterfowl)
a. sources b. clinical signs c. gross lesions |
a. spent lead shot (banned in US for waterfowl hunting in ’91), fishing sinkers, mine tailings
b. non-specific: weakness, depression, wt. loss, anorexia, PU, diarrhea (bright green) c. usually EMACIATED if chronic green stained feathers around cloaca, GI IMPACTIONS(proventriculus), green stained lining of ventriculus, pale flabby streaked heart, +/- lead shot in ventriculus if chronic: weak, erratic flight or unable to fly, droopy wings, leg weakness |
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lead toxicosis (waterfowl)
a. dx b. tx |
a. ↑ blood lead antemortem (> 0.5 mg/kg warrants tx) or post-mortem in tissue (liver)
b. 1. supportive: fluids, warmth, nutrition, +/- ABs 2. chelation therapy: CaEDTA or DMSA 3. removal of shot or sinkers in ventriculus: oral laxatives, gastric lavage, endoscopy, or sx (last resort) |
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duck virus enteritis
a. etiology b. occurence c. transmission |
a. herpesvirus
b. susceptibilty varies among species adults > juveniles widespread but sporadic: rare in wild c. fecal-contamined water likely also oral secretions, vertical (female --> egg) maybe blood sucking insect vectors carrier state in asymptomatic birds likely |
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duck virus enteritis
a. clinical signs b. gross lesions c. histopath lesions |
a. death in 1-5 d. after acute onset of signs
lethargy, anorexia, photophobia, drooping wings, unable to fly, BLOODY D/C FROM NARES, VENT (classic for DVE), terminal opisthotonus & convulsions b. usually in good flesh HEMORRHAGES on serosa of heart, liver, kidney, pancreas, lung, & GI tract NECROTIC BANDS OR PATCHES in GI, under tongue, esophagus: almost pathognomonic c. extensive necrosis & hemorrhage in lymphoid & reticuloendothelial tissue -EOSINOPHILIC INTRANUCLEAR INCLUSION BODIES: liver, esophagus, gut, pancreas (hallmark) |
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duck virus enteritis
a. dx b. tx c. control |
a. can look similar to avian cholera grossly
-eosinophilic intranuclear inclusion bodies: highly suggestive definitive -VIRUS ISOLATION: liver, spleen -virus neutralization titers: used to monitor progression in flock b. none specific -supportive care for valuable birds -euthanasia of sick birds to prevent spread c. very difficult in wild pop’ns: collect & incinerate carcasses -captive pop’ns: drain & chlorinate ponds +/- depopulation, prevent contact w/ wild waterfowl, attenuated live virus vaccine |
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avian cholera (waterfowl)
a. etiology b. occurence c. transmission |
a. Pasteurella multocida
b. most birds susceptible outbreaks occur during periods of stress chronically infected birds likely carriers wild birds possible source for captive poultry & waterfowl c. mostly fecal-oral: food & water contamined w/ ocular, nasal, & fecal shedding of bacteria -also inhalation or inoculation into feet thru contaminated substrate |
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avian cholera (waterfowl)
a. clinical signs b. gross lesions |
a. classic: many deaths, few clinical signs(death usually rapid: incubation < 24 hrs)
chronic form: variable signs (swollen joints & sinuses, respiratory dz) also anorexia, fluffed feathers, mucous d/c from mouth, diarrhea, tachypnea b. if acute: in good flesh hemorrhage: heart serosa, lungs, gut mucosa, abdominal fat swollen dark liver w/ focal necrosis pneumonia GI tract filled w/ thick yellow or bloody fluid, loaded w/ organisms chronic form: localized infection, caseous abscesses |
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avian cholera (waterfowl)
a. dx b. tx c. control |
a. presumptive: hx, signs, gross lesions, finding G (-) bipolar rods in heart blood or on liver cytology
definitive: bacterial culture & ID must R/O DVE, erysipelas, E. coli, & other bacteremias b. individual birds: broad spectrums ABs killed bacterin or MLV vaccines available for flocks w/ persistent problems c. captive flocks: eliminate carriers, maintain closed flocks, prevent contact w/ wild birds, general sanitation -wild pop’ns: dz spreads very rapidly; collect & incinerate carcasses to remove decoy effect & minimize scavengers OR try to prevent dispersal to other areas using minimal or no disturbance |
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aspergillosis (waterfowl)
a. etiology b. occurence c. transmission |
a. Aspergillus fumigatus or A. flavus
b. young stressed birds & certain species most susceptible opportunistic: often occurs secondary to other stressors or dz c. ubiquitious, worldwide distribution infection by inhalation of spores: NOT transmitted bird to bird warm temps & decompsing organic matter a common source |
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aspergillosis (waterfowl)
a. clinical signs b. gross lesions |
a. may not be apparent until advanced dz
young birds may die peracutely dyspnea, wt. loss, anorexia, weakness, lameness, occ. CNS signs (ataxia, torticollis) b. usually in lungs &/or air sacs, occ. in trachea, eyes, or brain peracute: lung congestion & MF granulomas other: variable lung nodules, small to coalescing granulomas filling air sacs |
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aspergillosis (waterfowl)
a. dx b. tx c. control |
a. antemortem dx difficult: CBC, rads, cultures, endoscopy, serology
-POSTMORTEM DX (most common): gross lesions, histopath, culture b. can be done, but expensive & may take weeks to months options: supportive care + amphotericin B &/or itraconazole or terbinifine killed bacterins used in some collections C. strict sanitation to MINIMIZE CONDITIONS THAT FAVOR SPORE GROWTH: remove wet food, bedding, & other organic matter promptly consider preventive antifungals when treating susceptible species |
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What is vertical integration?
|
2 or more stages of production/marketing combined
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What are advantages of vertical integration for
a. poultry companies b. consumers |
a. known steady supply of products
less long term investment in raising birds/eggs more effective use of resources not exposed to as much market risk can rapidly adopt a new technology & improve quality control b. helps keep cost of poultry products down increased branding programs: can purchase reliable high quality product |
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vertical integration & vets
a. advantages b. disadvantages |
a. technology advances faster --> animals treated more humanely, facilities kept cleaner, safety of product increases
can make genetic changes more quickly, since each hen produces proportionally more offspring b. if disease gets in, it could spread very quickly (many animals on a single farm), more room for error w/ biosecurity |
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CNS diseases in turkeys
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encephalomalacia
encephalomyelitis (less common than in chickens) |
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CNS diseases in chickens
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encephalomalacia
encephalomyelitis |
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musculoskeletal diseases in turkeys
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splay leg
rickets bumblefoot infectious synovitis |
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musculoskeletal diseases in chickens
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splay leg
rickets (less common than in turkeys) bumblefoot infectious synovitis viral arthritis |
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GI diseases in turkeys
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pullorum dz
fowl typhoid paratyphoid crop mycosis coccidiosis coronavirus enteritis poult enteritis & mortality syndrome histomoniasis hemorrhagic enteritis |
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GI diseases in chickens
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pullorum dz
fowl typhoid paratyphoid crop mycosis coccidiosis infectious bursal dz |
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respiratory diseases of turkeys
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colibacillosis
M. gallisepticum M. synoviae AI newcastle dz M. meleagridis bordtella rhinotracheitis chlamydiosis |
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respiratory diseases of chickens
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colibacillosis
M. gallisepticum M. synoviae AI newcastle dz infectious bronchitis |
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infectious diseases of young chicks/poults
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omphalitis
aspergillosis |
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miscellaneous diseases of turkeys
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fowl cholera
turkey pox erysipelas |
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miscellaneous diseases of chickens
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fowl cholera
fowl pox infectious laryngotracheitis avian tuberculosis |
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neoplastic diseases of poultry
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Marek's dz: C > T
lymphoid leukosis: C |
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diseases of waterfowl
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botulism
lead toxicosis duck virus enteritis avian cholera AI aspergillosis |
