Pneumonia - Sheep And Goats

Other Names

Respiratory Disease


Goats. Sheep.


General information on pneumonia is presented in the previous section (pneumonia - cattle).

In sheep and goats the important infectious agents associated with penumonia include:

  • Viruses: parainfluenza virus type-3 (PI-3), adenovirus, respiratory syncytial virus, and caprine arthritis-encephalitis (CAE) virus (goats).
  • Bacteria: Mannheimia haemolytica, Pasteurella multocida, Haemophilus spp, Chlamydia spss, Salmonella spp., and Mycoplasma spp.

Non-infectious causes of pneumonia include parasitic (lungworms) and aspiration from incorrect drenching.

Many of the causal pathogens (viruses and bacteria including mycoplasma), are normal residents of the upper respiratory tract in most sheep and goat flocks in Australia. The most common sequence of events leading to pneumonia is thought to be initiated by stressors lowering the resistance of the animal and allowing an initial acute virus or mycoplasma infection to commence in the upper respiratory tract or lung. This compromises local defences sufficiently to allow invasion and multiplication of secondary bacteria.

Animals more at risk of viral and bacterial pneumonias are young animals subjected to a range of stressors that are common in the export process including transportation, mixing with new animals, crowding, inadequate ventilation, dust and sudden climatic changes.

Most viral and bacterial pneumonias develop acutely and are highly contagious in susceptible flocks with the potential to cause outbreaks of disease. Survivors often become chronically affected. In goats the pneumonia caused by caprine arthritis-encephalitis (CAE) virus is a chronic progressive pneumonia in adults. Lungworms may be acquired when grazing pastures in temperate climates before entering the export process.

Aspiration pneumonia is caused by incorrect drenching technique and might occur as part of fulfilling a pre-export protocol in an assembly point.

Animals with pneumonia may be more susceptible to heat stress and heat stress may exacerbate clinical signs and disease progression for animals with pneumonia.

Respiratory distress will occur if normal lung function is compromised. Progressive disease may also result in endotoxaemia and septicaemia. If the surface of the lungs and lining of the chest cavity become inflamed (pleurisy) there is severe pain. Death may occur sufficient lung compromise to cause anoxia (usually when more than 70% of lung is affected), or from overwhelming systemic infection including toxaemi

Clinical Signs and Diagnosis

Bacterial pneumonias are often first detected when an animal has died suddenly and is necropsied. Other animals may then be noticed to have signs, including reduced appetite, depression, rapid shallow breathing, coughing and nasal discharge. Dyspnoea (laboured or difficult breathing) may follow minor exertion or rise in temperature as respiratory reserve is reduced.

Nasal and ocular discharge may result from dust, ammonia vapour or fly worry. It can however be a result of viral infection of the upper respiratory tract and a prelude to pneumonia.

Pneumonias that causes persistent forced coughing in young sheep and goats sometimes contributes to prolapse of the rectum.

Most lungworm infections are inapparent. Heavy infections may result in coughing that is reduced following anthelmintic treatment. They are susceptible to most modern drenches.

Necropsy changes have been described in the previous section on pneumonia in cattle.

With bacterial pneumonias the anteroventral lobes are most affected. With viral and mycoplasma pneumonias, all lobes may be involved initially until secondary bacteria invade the anteroventral lobes.

With lungworm the lesions are grey to green nodules scattered throughout the caudal lobes. Sometimes tangles of white threadlike worms up to 5 cm long are found in mucus in the large airways. Lungworm lesions are usually an incidental finding in an animal necropsied for another disease.

Animals that aspirate usually develop severe pneumonia, decline quickly and usually die within a few days of the aspiration occurring. At necropsy the anterior of one lung is usually more affected than the other. There is consolidation, liquefaction and involvement of the pleura. The aspirated material can be difficult to recognise.

In the pneumonia of goats associated with CAE virus the infection becomes clinical only in older goats. At necropsy the lungs are grey and firm.

Laboratory determination of pathogens requires nasal swabs in transport media for virus detection or isolation, and acute and convalescent sera for virus serology. In dead animals, portions of affected lung should be submitted fixed in buffered formalin for histology, and chilled for microbiology and virology.


: When infectious pneumonia is suspected, treat sick animals with antibiotics (oxytetracycline, trimethoprim sulpha). Broad spectrum antibiotics are more likely to be effective than narrow spectrum antibiotics such as procaine penicillin. Non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, tolfenamic acid, or meloxicam) may be warranted in valuable animals. Ensure ready access to feed and water which at sea may require separation from pen mates and movement to hospital pens. Severly affected animals should be euthanased without delay.

Use anthelmintic drenches where lungworm is suspected.


Causative organisms are often ubuiqitous and prevention generally involves management to reduce stressors that may increase likelihood of disease. Options include avoiding mixing sheep of different origins, reducing crowding, ensuring good ventilation, and providing shelter against sudden climatic changes. Early detection, isolation and aggressive treatment with broad spectrum antibiotics may reduce extent and severity of outbreaks of bacterial pneumonia.

Careful drenching on entry to assembly points will eliminate potential for lungworm problems for the remainder of the export process.