Aspergillosis (Mycotic Pneumonia)

Aspergillosis (Mycotic Pneumonia)

Aspergillosis (Mycotic Pneumonia) is also known as Brooder Pneumonia and Pneumomycosis.

Aspergillosis (Mycotic Pneumonia) is primarily an important disease of respiratory system, manifested by granulomatous lesions in lungs.

Aspergillosis (Mycotic Pneumonia) in Birds (Animals)

Mycosis is a fatal disease of man and animals caused by toxins produced by several species of fungus. It is common in commercial poultry. Newly hatched turkeys, chickens and ducks including other avian species are highly susceptible. The Respiratory tract and nervous system of the poultry are commonly infected by fungi.

Etiology

Among 300 species of Aspergillus identified only a few have been considered as potential pathogens for man and animals.

Common species of Aspergillus affecting human and animals are as follows:

  • A. flavus
  • A. parasiticus
  • A. niger
  • A. terreus
  • A. ruber
  • A. wentil
  • A. glaucus
  • A. ostianus
  • A. ocharaceus
  • A. terrus
  • A. nidulans
  • A. tamari
  • A. clavatus
  • A. fumigatus

Aspergillus species are ubiquitous is nature.

In cattle mycotic pneumonia is caused by A. fumigatus and brooders pneumonia in poultry.

Fungi grow rapidly in Saboraud’s agar at 27ºC and sporulated to produce fuzy white colonies and golden brown to greenish colonies.

Fungi have got septate mycelium, the hyphae are 4-6 mm in diameter. The colonial heads are columnar and compact with parallel chains of conidia.

Their growth is inhibited in media containing cyclohexamide. They produce exotoxin.

Fungal hyphae 4-12 µm in diameter and bears conidiophores, produce conidia (spores) of 2-6 µm is diameter.

Epidemiology

Prevalence of infection

  • Avian aspergillosis distributed around the world.
  • Fungal organisms are common soil saprophytes and has worldwide distribution.

Predisposing factors

  • Grow in organic matter in warm (>25ºC) humid condition.
  • They easily spread in air.
  • Cold, stress, high ammonia content of the farm.
  • Dusty environment increase incidence and severity.
  • Adult birds are resistant to new infection. Adults receives infections only when individual birds exposed to high level mycotoxins / immunosuppression / infection or due to nutritional insufficiency.

Source of infection

Aspergillus has been isolated from placenta of aborted cows, uterine discharge of repeat breeder and semen of bull. Mouldy, damp food and moist grains are conducive for growth of Aspergillus.

Spores liberated in large numbers from infected eggs opened at incubation or hatching. Contaminated feed or poultry house litter acts as source of infection Wet litters favour the growth of spores and present in aerosol when litters are dried.

Transmission

Human, animals and birds contract infection through inhalation and ingestion of Aspergillus spores present in the aerosol. Infection occurs by inhalation of spores.

Infection may also spread through abraded skin, mucous membrane and set up lesions in the embedded organs and systems.

Direct transmission from animal to animal and to human is not reported.

Host Affected

Cattle, buffaloes, sheep, goats, birds, and human beings  are affected. All birds are susceptible for infection. Chicken, turkeys, ducks, quails are mainly affected.

Pathogenesis

Aspergillus species are responsible for respiratory infection. In birds, acute Aspergillosis is known as “Brooder pneumonia” and causes heavy mortality in them. Aspergillus is incapable of utilizing keratin, normally they do not establish infection on skin but able to penetrate the skin through epithelial defects and thus capable of establishing infection on subcutaneous tissue to develops chronic suppurative granulomas.

Fungi may disseminate to other organs and systems through haematogeonus route. Even the fungi infects placenta and leading to placentitis and mycotic abortion, skin of some cases may also show gramulomatous changes.Aspergillus are not highly pathogenic and may not produce clinical signs, however, due to some predisposing factors such as prolonged use of antibiotics and corticosteroids, exposure to radiation, neoplastic diseases, malnutrition and tuberculosis makes the animals more prone for infection.

Brooder Pneumonia

Conidia present in aerosol or environment spread through conjunctival, nasal, tracheal, para bronchial and air sac epithelium and form discrete, granulomas of 1-15 mm diameter, containing white plaques or nodules at these sites.

It may have necrotic centre with dichotomous branching septate of 4-7 µm diameter hyphae.

Older lesions contains pleomorphic hyphae upto 12 µm in diameter but is confused with zygomycotic infections. Older lesions in air filled centres appear as green to black due to development of pigmented fungal conidiophores. Fungi tend to proliferate with in the granuloma and rarely invade adjacent tissues in immuno competent birds.

Chronic Infection

In turkeys often pulmonary blood flow impeded by enlarging pulmonary granulomas and this cause right ventricular dilatation or ascites.

In chronically infected birds accumulation of exudate in the trachea or syrinx producing acute respiratory embarrassment .

After inhalation, spores are disseminated rapidly through haematogenous route to other tissues and cause lesions in brain, pericardium, bone marrow and kidneys etc.

Lesions in meninges, leading to large superficial white plaques over the caudal cerebral cortex and in pecten and iris leading to fungal ophthalmitis and iridocyclitis.

Clinical Signs

Pulmonary form

  • Granulomatous pneumonia is the feature of this form in man and animals.
  • High temperature, accelerated shallow breathing, grunting and groaning, nasal discharge and moist type of cough are the signs of pulmonary form.
  • A chronic disease with respiratory complications and not responding to normal therapy should be suspected for aspergillosis.
  • Pneumonia is the cardinal sign.

Myocardial form

  • It is a fatal condition in human beings debilitated by cytotoxic or immuno-suppressive drugs and is rarely seen in animals.

Allergic form

  • Inhalation of spores of A. fumigatus causes high temperature, asthma, malaise and prostration.

Otomycotic form

  • A. fumigatus grow in cerumen and debris of ear canal in human and produces otorrhoea with foul odored exudation.
  • Dogs may also suffer from this form.

Cellulolytic form

  • Found to produce cellulitis of face and corneal region.

Cerebral form

  • Rarely meningitis, meningo-encephalitis and paralysis set up in central nervous system infection.

Abortive form

  • It is more common in adult cow, mare and ewe.
  • From the lungs the fungi traverse the haematogenous route and from there it reaches the gravid uterus in 3rd month of pregnancy.
  • Expulsion of aborted dead fetus, retained placenta and sometimes the aborted fetus born with cutaneous Aspergillosis.

Toxic Form

  • Mycotoxicosis is a very acute, fatal disease of birds, animals, human produce patent toxin known as aflatoxin B1,B2, G1, G2, M1,M2.
  • A. flavus produces a toxins known as “flavotoxins”.
  • Toxins are produced in aspergillus affected corns and cereals. Consumption of these toxins through feed, fodder and forage cause toxicosis in birds, animals, human beings, cattle, sheep, pigs and mortality.
  • Vascular haemorrhages, hepatic necrosis, proliferation of bile duct and diarrhoea.
  • Fungal toxicosis causes the reduction in growth rate and lower feed efficiency.

In Cattle

  • Clinical signs develop in 15 days.
  • Slight cough to laboured breathing.
  • Bloody and foul smelling diarrhoea.

In Horses

  • Infection restricted to nasal sinuses and guturral pouches.

In Sheep

  • Catarrhal pneumonia.
  • Death usually occurs long time after infection.
  • Conidiophores present in sputum and in discrete, calcified nodules (1-7mm dia) in lungs.

In Pigs

  • The aspergillosis is rare in pigs.
  • In affected pigs, persistent cough with lobar pneumonia.

In Wild Animals

  • Pneumonia and respiration problems.

In Brooder Pneumonia

Mortality in infected flocks may be biphasic. Acute respiratory disease cause 5-50% mortality in first 1-3 weeks of age of birds.

Chronic pulmonary insufficiency, ascites, blindness, neurological fungal metastasis causes up to 5% mortality.

At hatchery

In first 3-5 days neonates are dyspnoeic, ploypnoeic, open mouth breathing/gasping due to progressive air way obstruction.

Adult birds

Birds remain sub clinically infected for sometimes. Slow progressive respiratory embarrassment.

Increase body weight, demands on reduced functional pulmonary mass. Asphyxiated due to blockage of syrinx or the trachea.

Necropsy Finding

Thick crusted cutaneous lesions formed on the head, ears and neck.

 In asymptomatic pulmonary aspergillosis a small grey, raised lesions develop in lungs.

Acute mycotic pneumonia will show blood tinged fluid in pleural cavity and fibrinous pneumonia.

The abortive form will produce necrotizing placentitis with yellow grey colored cotyledons.

 Necrotic cotyledons with leathery appearance of placenta showed be suspected for mycotic abortion in cattle.

In Cattle

  • Sub-pleural nodules and interlobular emphysema.
  • Inflammation in small intestine.
  • Generalised interstitial haemorrhage is a typical feature and in lungs centres of heaptization without nodule formation.

In Horses

  • Nodule formation in lungs.
  • Involvement of meninges.
  • Interstitial haemorrhage with caseous nodules in the kidneys.

In Sheep

  • Bluish-grey nodules is surrounded by narrow haemorrhagic zone in lambs (2-3 mm diameter).
  • Bronchitis.
  • Granulomatous lesion in lungs of a day old lamb which indicates the develop of disease in utero.

In Pigs

  • Nodule formation in lungs.
  • Spleen and kidney enlarged and congested.
  • Nodule formation in mesenteric lymph nodes.

In Wild Animals

  • Miliary nodule formation in lungs and through out viscera.
  • Tumor like growths containing hyphae in conchal, ethmoid bones and in lungs.

In Brooder Pneumonia

  • Lesions in meninges, leading to large superficial white plaques over the caudal cerebral cortex and in pecten and iris leading to fungal ophthalmitis and iridocyclitis.

Diagnosis

  • Based on clinical signs, and necropsy findings.
  • Isolation of organism by culture: Direct culture of exudates can be done.
  • Glucose peptone chloramphenicol slants incubating at room temperature.
  • Microscopic examination will reveal presence of Aspergillus mycelia Suspected specimen can also be cultured in Sabouraud’s dextrose agar containing antibiotics but not cyclohexamide Rapidly growing flat white fuzzy colonies will be observedAntigen of A. fumigatus is commercially available and is used in human skin test and several serological tests have been made against invasive and wide spreaded aspergillosis.
  • Bronchi, bronchioles and alveoli of lungs may reveal the presence of mycelia, fibrin, leukocytes, Langhan’s giant cells, exudative cellular inflammation with penetrative mycelia may be present. In the necrotic areas neutrophils may aggregate around clumps of hypae.

Brooder Pneumonia

  • Based on clinical signs and necropsy findings.
  • Identification of organism: Examination of branched septate Aspergillus hyphae.
  • Add one or two drops of 10% KOH in smears taken from lesions and heat it gently and examine under microscope.
  • Routine observation of hyphae stained with H and E. Periodic Acid Schiff special fungal stain, Grocott’s Methenamine Silver (GMS) stain or Calcofluor white.
  • Demonstration of Conidiospore morphology and speciation made from (granuloma or plaques) culture grown in Sabourauds Dextrose Agar with Antibiotics.

Differential Diagnosis

Brooder Pneumonia

  • Other fungal diseases
  • Coliform infection
  • staphylococcal infection
  • Salmonella infection
  • Chronic bacterial pneumonia

Treatment

  • No effective treatment is available against aspergillosis of birds, animals and human.
  • Control depends on reducing exposure to fungus.
  • Eggs should be collected and stored so as to reduce sweating and exposure to spore laden dust.
  • Hatchery equipment and air ducts should be leaned, disinfected and monitored by cultures .
  • Brooding house, wet or previously wet litter or soil, mouldy or dusty feeds avoided.
  • Feed, water lines, soil should be disinfected.
  • Amphotericin B Injectable lotions 3% daily for long treatment.
  • Clinafarm (Griseofulvin, Fulcin, Fulvicin, Griseo 100)- 7.5% Powder feed additive bolus, liquid powder-Foal- 15 mg ⁄ kg ⁄ day 2–4 weeks and for Pony- 10 mg ⁄ kg ⁄ day 1–2 weeks.

Prevention

No successful immunization method has so far been developed against this mycotic problem.

Control

The spores of Aspergilli remain as potential threat to animals.

All attempts should be made to prevent proliferation of aspergilli in animals’ sheds on surroundings.

Methods of sterilization, sanitation and good management practices may be adopted to control this fungal infection.

Richard et al 1984, used a vaccine prepared from spores, germinated spores, mycelium and cultured filtrates of A. fumigatus and injected in birds via aerosol method for immunization was found not sufficient enough for protection.

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