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Poultry diseases > Bacterial respiratory diseases in poultry > Flashcards

Bacterial respiratory diseases in poultry Flashcards

1
Q

FC stands for

A

fowl cholera

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2
Q

fowl cholera is also known as

A

pasteurellosis

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3
Q

Pasteurellosis, fowl cholera (FC), is a highly contagious bacterial disease of wild and domesticated birds, characterized by

A

pneumonia, septicemia and sudden deaths.

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4
Q

causative agent of fowl cholera?
genus, family, details?

A

Gram– bacterium Pasteurella multocida

Genus Pasteurella, family Pasteurellaceae

nonmotile, relatively short rod-shaped bacterium

Present in the oral cavity of dogs and cats.
Can stay infectious for several weeks in the environment.

ZOONOSIS

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5
Q

Subspecies of pasteurellosis/fowl cholera

A

Three subspecies:
ssp. multocida,
ssp. septica ja
ssp. gallicida

Present in the oral cavity of dogs and cats.
Can stay infectious for several weeks in the environment.

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6
Q

How are the different pasteurella strains divided?

A

Different strains, divided into serogroups
(A, B, D, E, F) →
different pathogenicity

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7
Q

Host range and age for fowl cholera.

A

Diagnosed in wild and domesticated birds and in most animals too. More often in late summer, autumn and winter.

Chicks and young layers especially sensitive.

Source of infection: sick or latent carrier birds.

Carrier status is for life – excrete the pathogen intermittently.

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8
Q

Explain why fowl cholera is of economic importance. (5)

A

 High mortality
 Losses in weight gain, weight loss and drop in egg production.

 Low quality carcasses
 High cost of treatment

 Prevention is difficult: many ZOONOSIS! serotypes.

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9
Q

Transmission of fowl cholera.

A

Excretion: feces, nasal secretions

Transmission: direct contact, fecal-oral, predatory attacks, alimentary, aerosols.

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10
Q

Course of disease in fowl cholera.

A

either acute pasteurellosis or chronic

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11
Q

Clinical signs of acute pasteurellosis in poultry.

A

Acute septicemia, sudden deaths.

highly morb. + high mort.

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12
Q

Clinical signs of chronic pasteurellosis in poultry.

A

presents as localized infection: joint swelling, or sternal bursa swollen, ears, sinuses or wattle

mucous from the beak, apathy, limping, torticollis, emaciation.

low mort.

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13
Q

Post mortem signs of acute pasteurellosis in poultry.

A

general hyperemia
hematomas, petechiae
organ swelling or enlargement
coagulative necrosis of liver

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14
Q

Post mortem signs of chronic pasteurellosis in poultry.

A

localized purulent inflammation in diff. organs
peritonitis
hepatitis
pneumonia
caseous exudate in middle ear or elsewhere

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15
Q

diagnosis of fowl cholera

A

Material: liver, spleen, lungs, wattles,
joints, feces, blood, nasal secretion.

Methods:
 Bacteriological study → culture from the
carcass or nasal swab.

 Gram staining, ELISA, PCR-based methods

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16
Q

Treatment of fowl cholera.

A

Treatment → based on antibiogram!

Sulfonamides, penicillins, aminoglycosides, tetracyclines, fluoroquinolones.

Multi-resistance can occur!

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17
Q

Prevention of fowl cholera.

A

Prevention: reducing stress, good hygiene, biosecurity.

Avoiding rodents, wild birds and other animals and their feces, avoiding visitors, „all in/all out“ system, buying infection-free
birds.

Vaccination: attenuated live vaccines, with drinking water. However, they do not give full protection.

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18
Q

AIC stands for

A

Avian infectious coryza

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19
Q

Avian infectious coryza is usually an acute infectious disease of chickens, sometimes
pheasants and guinea fowls, characterized by

A

the presence of nasal secretions, swelling of the face, and catarrhal inflammation of
the upper respiratory tract.

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20
Q

Causative agent of avian infectious coryza.
genus, family, +details

A

agent Avibacterium paragallinarum, Av. gallinarum

Genus Avibacterium
family Pasteurellaceae

Gram–, pleomorphic, nonmotile bacterium

Microaerophilic, V-factor is needed for growth.

Catalase negative (important in diagnosing!)

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21
Q

serovariants of AIC

A

Three serovariants: A, B, C (based on Page scheme)

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22
Q

Host range and age demo for AIC.

A

Prevalent all over the world, in chickens of any age.

In developed countries → young birds and layers.

In developing countries → in chicks from 3 weeks of age.

The risk of infection is higher in older birds.

Reservoirs: chronically ill and carrier birds.

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23
Q

Transmission of AIC.

A

Transmission: direct contact, contaminated drinking water, no vertical transmission.

Risk factors: poor biosecurity, poor environment and other diseases.

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24
Q

IP of AIC

A

Incubation period: 1-3 days,
the disease lasts 2-3 weeks.

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25
Q

Mortality of AIC.

A

Mortality 20-50%, usually not more than 20%.

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26
Q

Course of disease in AIC.

A

acute & chronic

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27
Q

Clinical signs of acute AIC.

A

Depend on the severity of the case.

depression, anorexia, epiphora, conjunctivitis, sinus edema, decrease in production, dyspnea, nasal secretions, sneezing, diarrhea

specific to acute: infraorbital sinus swelling/inflammation, gray nasal secretions

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28
Q

Clinical signs of chronic AIC.

A

Depend on the severity of the case.

depression, anorexia, epiphora, conjunctivitis, sinus edema, decrease in production, dyspnea, nasal secretions, sneezing, diarrhea

specific to chronic: thick yellow nasal discharge, rotten smell, secondary infections

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29
Q

Post mortem signs of acute AIC.

A

infraorbital sinus pathology and nothing else, catarrhal inflammation in this site.

gray semifluid nasal exudate

swelling of face and eyes

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30
Q

Post mortem signs of chronic AIC.

A

thick, yellow sinus secretions
conjunctivitis
cerebral edema and petechiae
secondary infections like tracheitis, airsacculitis

31
Q

Diagnosis of avian infectious coryza.

A

Material: secretions (swabs), damaged
tissues, dead bird.

Methods: no suitable serological test
 PCR → fast results, most common
 Isolation → early phase of the acute form
 Hemagglutination inhibition test
 Catalase test → not accurate

Diagnosis is complicated in case of
mixed infection!

32
Q

Treatment & prevention of avian infectious coryza.

A

Early treatment is important.
 Erythromycin, oxytetracycline, fluoroquinolones, macrolides, sulfonamides,
trimethoprim-sulfa.
 Note, they Do not reduce secretion.

Severe cases/delayed treatment → reoccurrence is possible.

Prophylactic treatment + vaccination
 New birds, farms where outbreaks have occurred

Prevention:
„All in/all out“, good keeping and hygiene, biosecurity measures,
isolation/separation/quarantine, testing.

33
Q

Chlamydiosis is a subclinical infection or acute to chronic disease of wild birds and poultry, characterized by

A

respiratory, gastrointestinal or systemic inflammation.

34
Q

Course of disease in chlamydiosis in birds can be (3)

A

subclinical infection or acute to chronic disease

35
Q

PSITTACOSIS = ?
ORNITHOSIS = ?

A

PSITTACOSIS → chlamydiosis of the Psittacines (parrots)

ORNITHOSIS → chlamydiosis of other birds and animals, including humans.

36
Q

Causative agent of chlamydiosis in birds.
genus, family, +details

A

gram neg. bacterium Chlamydia psittaci

Genus Chlamydia
family Chlamydiaceae

Obligatory intracellular, round

Special affinity for reticuloendothelial cells (phagocytic cells), virulence factor: surface
proteins (MAMPs).

Usually causes systemic illness, excreted elementary bodies are resistant to drying.

37
Q

genotypes of chlamydia psittaci

A

9 genotypes
(A-F, E/B, WC, and M56), 7 of them infect birds.

38
Q

Host range and age for chlamydiosis in birds.

A

Prevalent all over the world, in over 450 species of birds → varies greatly.

More common in turkeys, quail, geese, and other poultry species, but also in cattle, pigs, sheep, horses.

Chickens often more resistant.

Sources of the infection: infected or carrier birds and animals.

39
Q

Transmission of chlamydiosis.

A

Excretion: respiratory secretion, feces, intermittent excretion.

Transmission: fecal-oral, inhalation, direct contact, transovarial.

40
Q

IP of chlamydiosis.

A

Incubation period: 3-10 days up to 8 weeks.

Influenced by bird species and age, microbial factors, transmission route and infection dose, other treatments etc.

41
Q

Clinical signs of chlamydiosis.

A

cachexia
eye and nose discharge
resp. distress
diarrhea

42
Q

Post mortem signs of chlamydiosis.

A

lung congestion
enlarged heart & liver, spleen
yellow fibrinous exudate on organs
anemia

43
Q

Diagnosis of chlamydiosis in birds.

A

Material: eye secretion, cloacal swab,
damaged tissues.

Methods: PCR-based methods
 Conventional or real-time
 Staining and microscopy, IHC, IFA, ELISA if
PCR is not available.
 Isolation: eukaryotic cells, chicken embryos, cell cultures, white mice.

44
Q

Treatment of chlamydiosis in birds.

A

Treatment: tetracyclines, tylosin

ADDITIONALLY: patient isolation, stress relief, proper keeping (ventilation!), biosecurity and hygiene.

45
Q

Prevention of chlamydiosis in birds.

A

revention: disinfection, daily sanitation, biosecurity.
- Sensitive to ether and alcohol, ordinary disinfectants work well.
- Resistant to drying.

Avoiding contacts, traffic monitoring, bioaerosol monitoring (ChlamyTrap) etc.

No vaccine!

46
Q

ORT infection stands for?

A

Ornithobacteriosis, ORT infection

47
Q

Ornithobacteriosis, ORT infection is mainly a bacterial disease of chickens and turkeys, characterized by

A

respiratory symptoms, decline in weight gain, egg production and egg quality, and increased mortality.

48
Q

Causative agent of ornithobacteriosis.
genus, family, +details

A

gram neg. Ornithobacterium rhinotracheale

rod-shaped, nonmotile pleomorphic bacterium

  • Grows slowly on culture medium.
    -Acquires resistance to antimicrobials easily.

Does not cause illness in humans!

49
Q

serotypes of ornithobacteriosis + which is most prevalent?

A

18 serotypes, most prevalent is serotype A

50
Q

Host range of ornithobacteriosis.

A

Isolated in many bird species.
Chickens, chukar, turkeys, ostriches, quails, ducks, geese, pigeons, pheasants, etc.

 Prevalent around the world
 Many reservoirs, incl. wild birds

51
Q

Transmission of ORT.

A

Transmission:
 Horizontally: aerosols, contaminated drinkers, direct contact.

 Vertically: eggs

Explains the rapid global spread of the disease.

Usually induces secondary infection.
Causes significant economic losses.

Risk factors: stress, poor housing conditions, low hygiene, other infections.

52
Q

Morbidity, mortality of ORT?

A

Morbidity up to 70%,
mortality up to 20%

53
Q

Clinical signs of ORT infection in young birds versus adult birds?

A

young:
* Respiratory illness and/or nervous
symptoms
* Coryza/rhinitis, sneezing, facial
swelling

adult:
* Drop in egg production and outer quality
* Acute respiratory illness – chickens and
turkeys
* Limping and paralysis – turkeys

54
Q

Post mortem signs of ORT infection in young birds versus adult birds?

A

young:
* Pneumonia: mostly one-sided
* Air sacs contain white foamy
yoghurt-like exudate and clumps of
fibrin

adult:
* Lung consolidation, edema – may be
bloody
* Pleura, peritoneum, air sacs and lung
surface may be covered with fibrinous to
caseous exudate

55
Q

Diagnosis of ORT infection.

A

Impossible to diagnose according to clinical
signs and necropsy findings.

Material: take as early as possible

Live birds: tracheal swab (special medium for
transport is needed)

Dead birds: carcass with head, or internal organs (Lungs, trachea, air sacs, brain, ovary, oviduct)

Methods: bacteriological culture

Due to slow growth, the pathogen may not be discovered.

56
Q

Treatment of ORT infection.

A

Treatment with antimicrobials → antibiogram.

Not always successful → resistance!!!

Doxycycline, enrofloxacin, lincomycin, tylosin and others.

57
Q

Prevention of ORT infection.

A

Prevention: biosecurity, proper hygiene

Organic acids and aldehydes are used for inactivation.

Proper keeping, reducing stress.

Vaccination!

58
Q

Avian tuberculosis is a chronic infectious disease caused by Mycobacterium avium,
characterized by

A

weight loss, decreased activity and production, and the formation of tubercules in the internal organs.

59
Q

Causative agent of avian tuberculosis.
genus, family, +details

A

gram pos. acid-fast Mycobacterium avium

genus Mycobacterium
Family Mycobacteriaceae

  • 4 subspecies:
    subsp. avium,
    subsp. hominissuis,
    subsp. paratuberculosis,
    subsp. silvatucum

 Mb. avium and Mb. intracellulare are often treated as one complex.

Mb. avium-intracellulare (MAC) affects people and pigs.

Mycobacteria are very resistant in the environment.

60
Q

Subspecies of avian mycobacterium.

A

4 subspecies:
Mb. avium subsp. avium,
Mb. avium subsp. hominissuis,
Mb. avium subsp. paratuberculosis,
Mb. avium subsp. silvaticum

Mb. avium and Mb. intracellulare are often treated as one complex.

Mb. avium-intracellulare (MAC) affects people and pigs.

61
Q

Host range and age demo for avian tuberculosis.

A

Worldwide spread

All species are susceptible, in captivity more common.

Mostly in small flocks, older birds, exotic birds in the zoo or at home.

Big differences:
pheasant is very susceptible, turkey resistant.

In chickens and broilers rarely due to short life cycle, disease control programs.

62
Q

Transmission of avian tuberculosis.

A

Excretion: feces, respiratory secretions.

Transmission: alimentary, respiratory.

Also rabbit, pig, cattle, primates and mink are easily infected.

Rare in healthy people.

63
Q

Clinical signs of avian tuberculosis.

A

Symptoms often unclear, visible at the final
stage of the disease:
- Decreased activity
- Sudden weight loss (good appetite)
- Limping, lameness
- Anemia

The comb may become anemic and wrinkly.
Birds can live for several months after getting the infection or die suddenly due to liver or spleen rupture.

Asymptomatic course also possible.

64
Q

Post mortem signs of avian tuberculosis.

A

hanges more often in the liver, spleen, intestine, bone marrow.

The organs are enlarged.

The presence of gray-white or yellowish nodules/granulomas/tubercles that are not mineralized.

Liver or spleen rupture → abdominal cavity filled with blood, organs anemic.

65
Q

Diagnosis of avian tuberculosis.

A

Clinical signs, pathological changes

Tuberculin test: not quite reliable.
- From 6 months of age, into or under the skin. Swelling at the injection site is evaluated after 48 hours.

Bacteriological testing: for confirmation
 PCR
 Seroagglutination tests - differentiation of strains.

66
Q

Treatment & prevention of avian tuberculosis.

A

Birds are not treated → sent to slaughter.

Vaccines are not used.

Eggs can be used in the bread and confectionery industry.

Prevention:
Washing and disinfecting with cresylic substances (are weak acids, e.g. chlorine does not work).

In the breeding flocks 10% of the chickens over two years old are tested during the year.

Zoos: new birds are quarantined > 6 months, valuable and endangered species are kept separately from other birds.

67
Q

Avian mycoplasmosis is an infectious disease caused by Mycoplasma spp.,
characterized by

A

respiratory syndrome in chickens, and
inflammation of infraorbital sinuses, reproductive disorders and skeletal deformities in turkeys.

68
Q

Causative agent of avian mycoplasmosis.
Give details.

A

gram neg. Mycoplasma bacterium spp.

  • Are the smallest identified bacteria, diameter 0.3 μm.
  • Prokaryotic cells, no cell wall.
  • Parasitic or saprotropic lifestyle.
  • Grow on microbiological media.
  • Survive in an oxygen-free environment for a while.

Hundreds of Mycoplasma species are infectious to animals.

WOAH notifiable disease!

69
Q

Avian mycoplasmosis host and age range.

A

Susceptible species: chickens, turkeys, geese, ducks, quail, pheasants, quails and pigeons.

More common in birds of 1-3 months.

Reservoirs: sick and carrier birds.

Birds can carry and excrete the pathogens throughout their lives.

WOAH notifiable disease!

70
Q

Transmission of avian mycoplasmosis.

A

Excretion: feces, respiratory secretions

Transmission:
 Vertical: inside or on the egg, in the egg yolk for longer periods.

 Horizontal: aerosols, direct contact, fomites.

71
Q

Course of the disease in avian mycopalsmosis.

A

acute or chronic or latent

Usually slow and chronic though.

In latent, excretion of a pathogen under stress.

First the chicks, then the young birds get sick.

Long incubation period – up to several months.

Predisposing factors: cold weather, poor air quality, overcrowding, concurrent infections, some live vaccines (viruses).

72
Q

Clinical signs of avian mycoplasmosis.

A

Varies depending on strain, see image.

Signs such as:
- respiratory disease, sinusitis, airsacculitis
- synovitis (lameness)
- chondrodystrophies, growth stunting
- wry neck

73
Q

Diagnosis of avian mycoplasmosis.

A

Material: swabs (nose, sinuses, choanae,
trachea), blood, tissues (lungs, air sacs),
joint fluid, carcass.

Methods:
 Isolation and identification
 Monitoring: agglutination + ELISA
 Diagnosis confirmation: hemagglutination
inhibition.
 PCR
 Specific strain: Mpl. iowae has no serological test.

74
Q

Treatment & prevention of avian mycoplasmosis.

A

Treatment not recommended.

Possibility to use tetracyclines, tylosin, enrofloxacin, egg treatment with tylosin. Penicillins do not work due to no cell wall.

Prevention: biosecurity, sanitation
- New birds from infection-free flock
- Continuous monitoring (especially Mpl. iowae).

Vaccination!
- Mpl. gallisepticum vaccines → no long-term immunity.
- Risk of airsacculitis caused by Mpl. synoviae → preventive treatment when vaccinating against MD and IBR.

Poultry diseases (12 decks)

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