9th lecture • Chlamydiosis • Mycoplasmosis • Coryza • ORT • Anatipestifer disease • Bordetellosis • Clostridial diseases Flashcards

1
Q

Chlamydiosis

Pathogen

A

Other names of the disease:
– psittacosis – ornithosis
• Pathogen: Chlamydia psittaci
– 0,2-0,3 μm diameter, round, IC bacterium (difficult
cultivation!)
– different, virulent & less virulent strains
– often detected in the epithelial cell of intestines & respiratory tract
• All avian species are susceptible
– most often turkey, duck
– chicken is less sensitive
– goose in young age mainly
• Infection: with elementary bodies (EB)
– in the organism turn into reticulate bodies (RB)
– replicate in this form after a transient form (intermediate body, IB)
they become elementary bodies again

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2
Q

Chlamydiosis

Pathogenesis

A
Influential factors: virulence, age, stress, immune status
Main feature of the disease:
– respiratory lesions
– mainly septicaemia
– other disease
• independent conjunctivitis
• independent salpingitis
Pathological lesions (septicaemia)
– acute splenitis and hepatitis
– sero-fibrinous pericarditis, serositis and air sacculitis
• mild to severe
– acute rhinitis
– acute conjunctivitis
• often heterophil granulocytic and lymphocytic
leptomeningitis
– meningitis and/or meningoencephalitis
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3
Q

Chlamydiosis

Diagnosis and Treatment

A
• Incubation time: 5-10 days
• Diagnosis:
– Typical clinical symptoms, lesions
• swelling above the eye (nasal gland adenitis in turkey)
– Serology, IIF, IHC, PCR
– Isolation (cell culture)
– histopath, lenyomat
• Treatment
– Prevention (vaccine Ø)
– AB
– Many countries:
• Reportable disease
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4
Q

Mycoplasmosis

Pathogen

A

Many mycoplasma species
• MG, MS, MM, MI
– In different bird species
– Different diseases
Etiology:
– small (200 nm), bound by single cell membrane
– require complex laboratory background
– no cell wall
• insensitivity to AB degrading cell wall synthesis
• cephalosporins, ß-lactamases
• Other influencing factor:
– Other pathogens (virus, bacteria, fungi, parasites)
– Technopathies, nutritional deficiencies

In chickens: 2 main sp.
– Mycoplasma gallisepticum
– Mycoplasma synoviae

In turkey
– Mycoplasma gallisepticum
• turkey sinusitis
• obligate pathogen
– Mycoplasma synoviae
– Mycoplasma meleagridis
In geese
– Mycoplasma anseris
– Mycoplasma cloacale
– Acholeplasma laidlawi
– M-1220 strain!!!

• In pigeon
– Mycoplasma columbae

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5
Q

Mycoplasmosis pathogenesis

A

mycoplasma sp. usually colonize in the air ways
– cause mainly respiratory disease
– respiratory mycoplasmosis
• Exemptions…….
– independent conjunctivitis
– independent salpingitis
– infertility caused by mycoplasma living in the
testicles and epididymis
• mycoplasmas are usually facultative pathogens
– Exemption in turkey: turkey sinusitis caused by
Mycoplasma gallisepticum

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6
Q

Mycoplasmosis in chickens

A

infection:
– vertical (in ovo), horizontal (with respiratory discharge)
– aerogenous, feed and water contaminated with mycoplasma p.o., through the conjunctiva, other ways……
• develops only after predisposing factors!!!
Specific predisposing factors
– Other respiratory pathogens
•IB, infectious laryngotracheitis
• Avian pox, Newcastle disease
• avian metapneumovirus
• vaccine viruses (fe. Newcastle disease)
• Avibacterium, ornithobacterium
Non specific predisposing factors
• overcrowding, bad climate conditions
• transport, grouping, handling the animals
• immunizations, blood sampling
• malnutrition, husbandry problems

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7
Q

Mycoplasmosis caused by M.

gallisepticum in adult age

A
In layer flocks
– serous rhinitis
– lacrimation
– sneezing
– snuffling
– sinusitis
– drop in egg
production +
– fertility of the layed eggs decreases
Pathological lesions in layer flocks
Respiratory lesions…. +
• pericarditis, perihepatitis
• peritonitis
• salpingitis – sero-fibrinous
•local complication: pneumonia
• In rare cases:
– encephalitis, leptomeningitis

• CRD
– Coryza, sneezing, nasal discharge, coughing
– Dyspnoe (open beak)
– growth rate slowed, rate of lay decreases>10-15 egg/hen
• Turkey: uni- or bilateral sinusitis
– prevents birds from opening the eyes
• Lesions:
– Catarrhal inflammation, fibrinous airsacculitis

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8
Q

Mycoplasmosis caused by

Mycoplasma synoviae in chicken

A

• Infection: as with M. gallisepticum
• Pathogens: they have affinity to synovial membranes!
– some strains have affinity to air ways too!!!
• Two forms exist: the classical and the respiratory
– arthritis, tenosynovitis and bursitis
• appearance:
– in 4-16 week old chicken
• Classic form
– disease of joint, tendon and synovial bursa
• tarsal joints, joints of the toes and the connected tendons
• bursa on the sternal cryst
• Pathological lesions:
– In the above mentioned affexted parts
• serous, sero-fibrinous, sero-purulent
• thick exudate

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9
Q

Mycoplasma melleagridis

A
Susceptible: turkey
airsacculitis, late embrionic death
subclinical disease exists
– stunting, abnormal feathering, bone deformity 
– reduced hatchability
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10
Q

Mycoplasma iowae

A

Susceptible: turkey
– Late embrionic death (between dd 18-24, 5-20%)
• Lesions:
– embryos are small, congested, edematous, hepatitis
– groth retardation, feather abnormalities, leg deformities
– airsacculitis

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11
Q

Mycoplasma melleagridis

Mycoplasma iowae

A
• Diagnosis
– Special laboratory conditions
– identification of colonies (PCR)
– serology
• Treatment
– eradication
• biosecurity
• vaccination
• maybe AB in breeder flocks
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12
Q

Infectious coryza

Pathogen

A

• Haemophilus infection of chickens (+pheasant and guinea fowl)
• Pathogen:
– Avibacterium (Haemophilus) paragallinarum
– different serotypes (A, B, C)
– virulent and less virulent strains
– Av. avium, Av. endocarditis, Av. gallinarum
• disease of broilers and adults (but in every age)
• not often seen, but…
– causes multitudinous disease
– spreads rapidly
– main feature:
• sero-fibrinous inflammation of the upper respiratory airways

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13
Q

Infectious coryza • Pathogenesis:

A

• Spreading:
– Carrier birds (nasal discharge, feces)
• Infection:
– direct contact
– aerosol (through air ways)
– feed/ water contaminated with nasal discharge
• Pathogenesis:
– the pathogen replicates in the air ways• conjunctiva, nasal cavity, trachea
– at the beginning the discharge is serous
– later sero-fibrinous exudate occurs
– fills the nasal cavity too • get stuck there
– incubation period: 1-3 days
– mainly in 8-12 week-old age group
– spreads rapidly
– almost all animals get sick
• Clinical signs:
• at the beginning (in acute phase)
– nasal discharge
– drowsiness because of fever
– lack of appetite
– conjuctivits, lacrimation, oedema of the head
– delayed start of egg production or severly reduced (10-40%)
• scary clinical symptoms, low mortality

– the discharge
becomes thick• fibrinous consistency
–sinuses appear dilated
– edema & cyanosis
of the eyelids, appendixes of the head appear swollen,
bluish-red
– sneezing, snuffling
Infectious coryza
– Chronic case
• abnormal destruction of
the stagnated
inflammatory exudate
• sweet-smelly odor in the
stable
– complications:
• mycoplasmosis
• respiratory inflammation
by Pasteurella sp.
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14
Q

Infectious coryza

Diagnosis & Treatment

A
diagnosis:
– epidemiology of the disease
– clinical signs
– upper respiratory symptoms
– Isolation of the pathogen from nasal discharge
– PCR
• Treatments
– „All in/all out”, vaccination, AB medicated water and/or feed
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15
Q

Ornithobacteriosis

Pathogen

A
• Ornithobacterium rhinotracheale
– Gram -, non-ciliated, pleomorph
– resistance: low
– optionally pathogenous
• different 18 serotypes are known (A-R)
– frequent serotypes: A, B, D, E
– in hens: in 54% of the cases type A infection
• It was identified at the beginning of the ‘90s
– new taxon
– frequent in Hungary
• belongs to the normal flora– in chicken and turkey
• Infection
– horizontal
• aerosol, contaminated
water/feed
– vertical (?)
• the pathogen was found in oviduct, egg or embryo
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16
Q

Ornithobacteriosis

Pathogenesis

A

• the pathogen gets activated when the local
defense mechanisms decrease in the air ways
• causes (secondary) lesions in the air ways
– the lesions become more severe or the type of
pathological processes changes
• Predisposing factors are:
– viral infection in the respiratory tract
– overcrowding
– low ventilation
– high ammonia level

17
Q

Ornithobacteriosis

Pathology

A

Pathology (in broilers)
– Mortality goes up to
– lesions typical for the respiratory disease
• Pathological lesions:
– hyperaemia in the mucous membrane of the air ways
• sometimes small hemorrhages (petechiae)
– discharge in the lumen of the air ways
• rarely fibrinous pseudomembranes
– pneumonia in one or both lungs
– sero-fibrinous air sacculitis
– sometimes fibrinous arthritis (bacteriaemia)
– in most of the cases sero-fibrinous-(purulent) inflammation of the
os parietale
• Clinical signs in broilers
– lacrimation, nasal discharge
– labored breathing (hampered respiration, head shaking)
– swelling of the head
• due to edema of the head and the infraorbital sinus

18
Q

Ornithobacteriosis

A
• In broilers (in 3-4 weeks of age)
– mortality: usually few %
– but it can reach up to 30-60%!!!!
-hot weather/overcrowding
• In adult flocks (between weeks 24-52)
– mortality is low
– decrease in egg production • the eggs are different in size and deformations occur
– nervous symptoms are frequent• because of the inflammation in the parietal bone
• In turkey
– Males >14 weeks
• it can occur in younger age (between 2-8 weeks)
• decrease in egg production
– Mortality: 1-15%
19
Q

Ornithobacteriosis

Diagnosis & Treatment

A
Diagnosis:
– isolation
– PCR, IHC, szerológia
• differential diagnosis:
– coryza
– TRT
– Swollen head disease
– mycoplasmosis
• Treatment:
– desinfection
– AB (after checking sensitivity patterns)
– deal with predisposing factors
– vaccination
20
Q

Anatipestifer-disease

Pathogen

A
• Riemerellosis
• Pathogen: (does not stain according to Gram)
– Bacillus septicaemiae anserum exsudativae
– Pfeiffer influenza bacterium
– Pfeifferella anatipestifer
– Pasteurella anatipestifer
– Schigella septicaemiae
– Haemophilus anserisepticum
– Moraxella anatipestifer
– Riemerella anatipestifer
• Infection
– aerogen (aerosol)
– per os (oro-fecal)
– per cutan (open woulds)
• in case of individual identification (cutting the nails, cutting or clipping
the webbed toes)
21
Q

Anatipestifer-disease Riemerellosis

Pathogenesis

A

(main features):
• the bacteria live together with the birds– facultative pathogens
• after predisposing factors the bacteria enter circulation
• septicaemia develops in the weakened organism
• usually occurs in young age
– In ducklings
– In goslings: between 2-3 week-old age
– (young poults, or chicks)
Riemerellosis
Predisposing factors
• one of the most important is– the young age
• other stressors:
– problems related to husbandry or malnutrition
– long transport, weather fronts, cold
• other concurrent infectious diseases
– Derzsy’s disease
– influenza viruses
– mycoplasmosis
– chlamydophilosis

22
Q

Anatipestifer-disease Riemerellosis

Clinical signs:

A

The main feature of the disease:
• exudative serositis
– sero-fibrinous inflammation of the serous membranes
– with the sero-fibrinous inflammation of the joints and tendonsheaths,
– the leptomeninx
Clinical signs:
• respiratory symptoms
– lacrimation, serous nasal discharge, rhinitis and sinusitis
– well visible in ducks (missing in geese)
• nervous signs
– ataxia, tremor, backing, opistotonus
– listing, lurching, lying on their back and kicking

23
Q

Riemerellosis

Pathology:

A

• sero-fibrinous
– peritonitis, air sacculitis, pericarditis
– leptomeningitis
– arthritis and tenosynovitis
• serous inflammation and hemorrhage in the
subcutaneous connective tissues of the leg
– in prolonged cases: necrotizing dermatitis
• acute catarrhal enteritis
• rhinitis, conjunctivitis, sinusitis in the infraorbital sinus
Histoptahological examination:
• sero-fibrinous inflammation in the leptomeninx
– under the lining ependyma-layer in the cerebral ventricules and
canalis centralis

24
Q

Riemerellosis

• Diagnosis

A
– Bacterium isolation
– plate agglutination
– ELISA
• Differential diagnosis
– Pasteurella, Salmonella, E. coli
• Treatment
– AB
– vaccination
25
Q

Bordetellosis
(turkey coryza)
• Pathogen

A
Bordetella avium
– Gram-, aerobic, motile rod-shaped
– strains with different virulence
• Appearance:
– in 2-6 weeks old turkey flocks
– (Muscovy ducklings, quail, cockatiel, chicken)
• Very contagious disease
– morbidity: 80-100 %, mortality around 10 %
– predisposing factor needed
– direct contact, contaminated water
– Incubation period: 4-10 nap
26
Q

Bordetellosis

• Pathogenesis

A
– bacteria replicate on the mucous membrane
– destruction of the cilia and villi
– increased goblet cell activity (mucus)
• Main feature of the disease:
– catarrhal inflammation of the upper respiratory airways
• Clinical signs:
– lacrimation, nasal discharge, sneezing
– labored breathing
27
Q

Bordetellosis

Pathology:

A
– metaplasia in the epithel
of the airways
– distortion of the cartilage of the trachea
– compression of the
trachea
– sero-mucus content in
the trachea
• secondary bacterial
complications often
occur:
– local and general lesions
– caused mainly by E. coli
28
Q

Bordetellosis

• Diagnosis

A
– Sudden appearance, rapid spread
– IIF, PCR, serology
• Differential diagnosis:
– TRT, ORT, ND, AI
• Treatment
– AB only with limited succesy
– biosecurity
– vaccination
29
Q

Clostridial diseases

A

• Necrotic enteritis (NE)
– Cl. perfringens associated hepatitis (CPH)
• Ulcerative enteritis (UE)
• Gangrenous dermatitis (GD)
– clostridial dermatitis of turkeys (CDT)
• Botulism

30
Q

Necrotic enteritis

Pathogen

A

• Disease of birds kept on a deep-litter system
– Mostly in 2-5-week-old chickens
• But anytime between 2 weeks - 6 months of age
– In young turkey poult
• Pathogen:
– Widely distributed in the environment
– Clostridium perfringens A or C
• C. perfringens A produces alfa-toxin
• C. perfringens C produces alfa- & beta-toxin
• Intestinal coccidiosis often has a role in the
manifestation of the disease
– coccidiostatic drugs in the feed!
• Usually develops due to malnutrition
– Feed containing mycotoxins
– Earlier fish meat was blamed

31
Q

Necrotic enteritis

Pathological lesions:

A

• Small intestine (jejunum and ileum)
– Sometimes in caecum too
– Loose intestinal loops
– Intestinal content is brownish-red, smelly, dentritus material
– Necrosis of the mucous membrane
• dull, dry
• color differs: yellowish-grey, greyish- brown
– Sometimes becomes very thick
– Necrotic area has a sharp edge
• Besides lesions in the intestine
– Cholecystitis because of ascending inflammation
– Necrosis in the liver and around the bile vessels
– Acute cardiomyopathy, degenerations in the liver, kidney and skeletal
muscles
– Circulatory disturbances
– Edema in the subcutaneous connective tissue, hypereamia and edema
in the liver
• Treatment
– AB, change in feed, probiotics, hygiene, acidifying the water

32
Q

Ulcerative enteritis

• Pathogen:

A

Clostridium colinum
– gram-positive, 1 x 3-4 μm, spore-producing, aerob-anaerob
• Infection:
– With the spore form of the pathogen per os
• Via feces, feed, water, litter
• Susceptible species:
– quail (in 4-12-week-old age)
– chicken (young chicks 4-12-week-old)
– turkey (in 3-8-week-old age)
– But also pigeons, pheasant, partridge and guinea fowl
• Predisposing factors (in chicken):
– coccidiosis (E. brunetti, E. necatrix)
– infectious chicken anaemia, infectious bursitis& other stressors
• Dirty litter, malnutrition, sudden change of the feed
• Immunosuppression in the flock

33
Q

Ulcerative enteritis

Pathological lesions

A

• peracute-acute case (mortality 100%):
– hemorrhages in the muscles, under the serous membranes
– hydropericardium
– red ulcers in the intestines
• in the small- and large intestines
– Necrotized mucous membrane borders the ulcers
• Sometimes ulcers are covered with pseudomembranes
• Ulcers are visible through the serous membranes
• Circumscribed fibrinous serositis at the area of ulcers
• Arrodation can occur
– hemorrhages under the hepatic capsule at the edges
– necrotic foci in the liver parenchyma
• yellowish-grey, pinpoint-sized, sharp or irregular shaped

34
Q

Ulcerative enteritis

• Diagnosis of the disease

A
– based on the pathological lesions
– slide smear (liver) with Gram staining
– culturing the pathogen
• from the intestinal ulcers
• from the necrotic foci in the liver
– Identifying the pathogen from the hepatic foci has higher diagnostic value!
• DD: NE, coccidiosis, histomoniasis
• Treatment:
–hygiene, keeping conditions, AB
35
Q

Gangrenous dermatitis

Pathogen(s):

A
Peracute, fatal disease
28-35 days old chicken, 16-18 weeks old turkey
Pathogen(s):
• Staphylococcus aureus (Catalase+), E. coli
• Clostridium perfringens type A
• and/or Clostridium septicum
Predisposing factor needed
• Immunosuppression, skin lesions
Clinical signs:
• sudden increase in mortality (with general symptoms)
• swollen, red, weeping skin lesions
• rapid decomposition
• Dry gangrene or Wet gangrene
36
Q

Gangrenous dermatitis

A
• wing gangrena disease
• blue wing disease
– BWD
• wing rot disease
– WRD
hemorrhages on the wing
Treatment:
– AB
– immunsuppression
– Vitamin E, zinc, selenium
37
Q

Botulism

A

exotoxin of Clostridium botulinum
– Gram+, anaerob, spore-forming rod
– A, C, D, E types (C1 – neurotoxin, C2 – enterotoxin)
• Infection:
– ingestion of preformed toxin
• may proliferate in the dead birds
• cannibalism or eating maggots from carcasses
• in rotting vegetation along shorelines
• litter & feed may be a source as well
• Clinical sign: progressive flaccid paralysis
– reluctant to walk, wings, eyelids, neck drop
– respiratory and cardiac failure

38
Q

Botulism

• Diagnosis

A
Diagnosis
– lack of lesions (eyelid paralysis)
– demonstration of the toxin
• Differential diagnosis:
– Marek disease, ionophor or lead toxicosis
• Treatment
– valuable individuals with antiserum, laxatives
• vitamins, salts, AB, acidified water
– prevent access to the toxins
• biosecurity