9th lecture • Chlamydiosis • Mycoplasmosis • Coryza • ORT • Anatipestifer disease • Bordetellosis • Clostridial diseases Flashcards
Chlamydiosis
Pathogen
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
Chlamydiosis
Pathogenesis
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
Chlamydiosis
Diagnosis and Treatment
• 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
Mycoplasmosis
Pathogen
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
Mycoplasmosis pathogenesis
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
Mycoplasmosis in chickens
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
Mycoplasmosis caused by M.
gallisepticum in adult age
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
Mycoplasmosis caused by
Mycoplasma synoviae in chicken
• 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
Mycoplasma melleagridis
Susceptible: turkey airsacculitis, late embrionic death subclinical disease exists – stunting, abnormal feathering, bone deformity – reduced hatchability
Mycoplasma iowae
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
Mycoplasma melleagridis
Mycoplasma iowae
• Diagnosis – Special laboratory conditions – identification of colonies (PCR) – serology • Treatment – eradication • biosecurity • vaccination • maybe AB in breeder flocks
Infectious coryza
Pathogen
• 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
Infectious coryza • Pathogenesis:
• 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.
Infectious coryza
Diagnosis & Treatment
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
Ornithobacteriosis
Pathogen
• 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
Ornithobacteriosis
Pathogenesis
• 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
Ornithobacteriosis
Pathology
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
Ornithobacteriosis
• 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%
Ornithobacteriosis
Diagnosis & Treatment
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
Anatipestifer-disease
Pathogen
• 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)
Anatipestifer-disease Riemerellosis
Pathogenesis
(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
Anatipestifer-disease Riemerellosis
Clinical signs:
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
Riemerellosis
Pathology:
• 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
Riemerellosis
• Diagnosis
– Bacterium isolation – plate agglutination – ELISA • Differential diagnosis – Pasteurella, Salmonella, E. coli • Treatment – AB – vaccination
Bordetellosis
(turkey coryza)
• Pathogen
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
Bordetellosis
• Pathogenesis
– 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
Bordetellosis
Pathology:
– 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
Bordetellosis
• Diagnosis
– Sudden appearance, rapid spread – IIF, PCR, serology • Differential diagnosis: – TRT, ORT, ND, AI • Treatment – AB only with limited succesy – biosecurity – vaccination
Clostridial diseases
• Necrotic enteritis (NE)
– Cl. perfringens associated hepatitis (CPH)
• Ulcerative enteritis (UE)
• Gangrenous dermatitis (GD)
– clostridial dermatitis of turkeys (CDT)
• Botulism
Necrotic enteritis
Pathogen
• 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
Necrotic enteritis
Pathological lesions:
• 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
Ulcerative enteritis
• Pathogen:
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
Ulcerative enteritis
Pathological lesions
• 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
Ulcerative enteritis
• Diagnosis of the disease
– 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
Gangrenous dermatitis
Pathogen(s):
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
Gangrenous dermatitis
• wing gangrena disease • blue wing disease – BWD • wing rot disease – WRD hemorrhages on the wing Treatment: – AB – immunsuppression – Vitamin E, zinc, selenium
Botulism
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
Botulism
• Diagnosis
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
