Proc 18th Annual Seminar, Society of Dairy Cattle Veterinarians NZVA, 2001 © VetLearn® Foundation (NZ) 2003

Respiratory Disease in New Zealand Dairy Cattle

Respiratory Disease in New Zealand Dairy Cattle

D.P. Twiss, J.J. Vermunt and T.J. Parkinson

Institute of Veterinary, Animal & Biomedical Sciences, Massey University, Palmerston North

Introduction
Currently, lungworm and bovine nasal granuloma (‘nasal catarrh’) are the most significant
respiratory diseases in New Zealand (Fairley, 1996). This reflects our pastoral dairy farm system.
However, with the increased use of supplements to meet the demands of high producing cows,
our pastoral dairy system is beginning to move away from a strictly pastoral system for at least
part of the lactation. Changing management systems in New Zealand dairy herds may result in
respiratory disease having a larger impact on herd production comparable with intensively
managed dairying systems overseas. Supplemental feeds provide opportunity for dairy systems
to increase productivity but they also provide opportunity for pathogens to gain access to cattle.
This is affecting the patterns of diseases that are encountered.

The respiratory system of cattle has a number of defences against invading pathogens. The
beating cilia and the mucous lining of the airways impede the movement of respiratory tract
invaders. (Hjerpe, 1983) In the alveoli of the lower airways, the host defence utilises cellular
immune responses of the alveolar macrophages and antibodies to trap and destroy invaders.
Respiratory pathogens that establish infection in the cow do so because they overwhelm the
barriers of the upper respiratory tract or they are able to gain access to the lungs via the blood
stream and so avoid a confrontation with the first line of defence. Generally, viruses enter the
respiratory tract via inhaled air through the naso-oral route. Bacteria may be inhaled or may
enter the respiratory tract through the circulatory system. Interactions between viruses and
bacteria provide further opportunity for the establishment of respiratory disease. For example,
bovine viral diarrhoea (BVD) virus suppresses the host’s immune system, allowing the
establishment of respiratory infections by other pathogens (Grooms, 1998). Overseas, a similar
relationship occurs between bovine Corona virus and Pasteurella spp. (Storz et al., 2000).

Respiratory disease in adult New Zealand dairy cattle has a limited range of initiating causes.
The disease is usually of infectious or toxic origin, resulting in similar pathologies of the affected
part of the respiratory tract. The resultant anoxia leads to a change in the pH and carbon dioxide
levels in the lung parenchyma that stimulate respiratory reflexes. This causes the outward
clinical signs of dyspnea and increased lung sounds. Respiratory disease is a consequence of
agents causing damage to the lining of the respiratory tract. The severity of the disease is
dependent on the extent of the damage and the ability of the animal to prevent further damage
and repair the damaged tissue. The severity of respiratory disease usually increases with the
degree of compromise to the immune system. Paradoxically, when allergenic agents cause
respiratory insufficiency (e.g. L-tryptophan), it is hyperstimulation of the immune system that
compromises the respiratory system.

The following discussion will focus on respiratory disease in the individual adult New Zealand
dairy cow. The ability to diagnose the cause of the respiratory embarrassment or failure is critical
in determining the value of further treatment. Accurate diagnosis requires an understanding of
the agents that may be present in a respiratory condition and the resultant pathology.

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Aetiological agents causing respiratory disease

Infectious agents

1. Viruses

Viral infection of the epithelial cells lining the respiratory tract causes proliferation and
swelling. In primary viral infections there is no stimulation of the inflammatory cascade to
produce exudative material, which might constrict the bronchial airways. When viral
infections affect the cells of the bronchial alveoli the resultant pulmonary oedema causes an
interstitial pneumonia to develop. Cattle will increase their respiratory effort to compensate
for the reduced perfusion of oxygen across the alveolar membranes. This increase in effort
results in louder lung sounds that can be heard on auscultation of the anterioventral aspect
of the lung fields. Serological surveys indicate that infectious bovine rhinotracheitis (IBR)
virus, parainfluenza 3 (PI-3) virus and bovine respiratory syncytial (BRS) virus occur in
healthy cattle throughout New Zealand (Motha and Hansen, 1998). IBR, PI 3, BRS and BVD
viruses have all been implicated in the development of the bovine respiratory disease
syndrome (Motha et al., 1997).

• Infectious bovine rhinotracheitis (bovine herpesvirus 1)

Infection with bovine herpesvirus 1 (BHV-1) is usually seen during the summer months,
mainly affecting first-calved heifers. The timing of these infections possibly coincides
with the time when first-calved heifers (BHV-1 naïve animals) first come into contact
with older herd animals which are shedding the virus. By contrast, in the North
American situation, the disease is more commonly seen in yearling feedlot cattle and in
6 to 8 month-old, weaned beef calves in the autumn and winter months (Radostits et
al., 2000).

Infection with IBR virus usually results in a mild inflammation of the upper respiratory
tract. The virus may spread to the conjunctivae via the lacrimal ducts. Infection of the
conjunctivae results in inflammation and oedema. Occasionally, severe infections will
result in a drop in milk production. IBR causes clinical disease in only a small number
of herds, suggesting that the virus is not a significant respiratory pathogen in New
Zealand (Horner, 1990). Perhaps the reason we do not commonly see severe clinical
respiratory disease as a result of BHV-1 infection is that the majority of New Zealand
cattle are able to make an effective immune response to the BHV-1 strain present in
herds, and that the strain is not inherently virulent. However, it has been postulated
that there is a genetic component to the response to infection with the virus (Radostits
et al., 2000). Complications arise as a result of secondary bacterial pneumonia
establishing in the face of compromised respiratory defences. The strains of BHV-1
which cause respiratory signs are different to the strains which cause the genital forms
(infectious pustular vulvo-vaginitis / balanoposthitis).

• Parainfluenza 3 (PI-3)
Although surveys have demonstrated the presence of PI-3 infection throughout New
Zealand (Motha and Hansen, 1998), this virus is not considered to be a significant
respiratory pathogen in New Zealand cattle. The survey conducted by Motha and
Hansen in 1998 showed that the prevalence of antibodies to PI-3 is relatively high
compared with those of IBR and BRS. Infections with paramyxoviruses such as PI-3 are

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usually of short duration, so there is little time for a significant immune response by the
infected animal. This would allow reinfection of the respiratory tract supporting the
suggestion that PI-3 is a common respiratory tract inhabitant of New Zealand cattle.
Persistent infections do sometimes occur, in which the virus may stimulate an
eosinophilic response in the nasal epithelium. This may be of importance in the
development of bovine nasal granuloma (Oliver et al., 1976). It is possible that PI-3,
together with bacteria such as Haemophilus somnus and Pasturella multocida, is
responsible for some cases of acute pneumonia in calves.

• Malignant catarrhal fever (MCF)

In New Zealand, MCF is believed to be the result of infection with ovine herpesvirus 2.
Sheep and goats would therefore act as reservoirs of infection for cattle. The disease is
characterised by a mucopurulent ocular and nasal discharge, bilateral corneal opacity,
and high fever. Encephalitis frequently occurs, resulting in neurological, as well as
respiratory, signs. Necrotic erosions of the nasal, oral and gut mucosa occur as a result
of the MCF virus damaging vascular tissues. Peracute cases of disease have been
reported in New Zealand (James et al., 1975). Generally, all ages of cattle are affected,
but there is a higher morbidity in younger animals, but affected animals always die.
The time from the appearance of the first clinical signs to death varies from 1-5 days.
The disease course may be drawn out in the development of encephalitis.
Confirmation of MCF can be obtained in the live animal by the use of polymerase
chain reaction (PCR) using lymphocytes (EDTA blood). Submit fresh lymphoid tissue
(lymph node or spleen) from an animal, which has died. Post mortem examination will
reveal histological findings of fibrinoid necrosis around blood vessels (vasculitis) of the
brain, kidneys, lungs and the portal triads of the liver.

• Bovine viral diarrhoea virus

BVD virus may act synergistically with Mannheimia (formerly Pasturella) haemolytica
to cause a severe fibrinopurulent bronchopneumonia in North American feedlot cattle
(Grooms, 1998), although there is not a clear concensus on the role of BVD virus as a
risk factor in bovine respiratory disease. Serological surveys in a small number of herds
in New Zealand have shown the prevalence of antibodies to IBR and BVD virus to be
higher in herds with a known respiratory disease problem compared with herds that
did not have a respiratory disease problem (Durham and Forbes-Faulkner, 1975). More
recently, it has been shown that 60% to 80% of cattle in New Zealand have got
antibodies against BVD virus (Pérez et al., 1995). BVD virus may be playing a role in
the development of respiratory disease by compromising the immune system. Hence,
the potential exists for BVD virus to modify (albeit indirectly) the severity of respiratory
disease that occurs in young (6 to18 month-old) New Zealand cattle.

• Bovine respiratory syncytial virus

Although BRSV is widespread in the New Zealand cattle population (Motha and
Hansen, 1998), it has not been implicated in severe respiratory disease. BRSV can
cause rhinitis, tracheitis, bronchitis and interstitial pneumonia in North American and
European feedlot cattle (Radostits et al., 2000).

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2. Bacteria

The lobulated compartmentalisation of the bovine lung decreases oxygen perfusion in the
ventral aspects of the lung parenchyma. As pathogens are not effectively eliminated by the
cellular defence mechanisms of the body in conditions of anoxia, lung infections often
establish in the anterioventral lung lobes (Radostits et al., 2000).

• Mannheimia haemolytica
Infection of the alveolar epithelial cells with M. haemolytica results in a fibrinous
pleuropneumonia. M. haemolytica acts synergistically with BVD virus and
Haemophilus somnus in the development of the bovine respiratory disease complex.
Mannheimia is not considered a significant pathogen, but with the increasing use of
feed pads to supply supplementary feed to large numbers of dairy cows, this species
of bacterium may increase in significance.

• Haemophilus somnus
H. somnus is a commensal organism found in the mucous membranes of the upper
respiratory and genital tracts of healthy cattle. (Corstvet et al., 1973; Howell, 1991).
Like MCF virus, H. somnus infection can result in systemic disease and vasculitis
resulting in disseminated intravascular coagulation (Radostits et al., 2000). This
disturbance to blood vessels can result in meningoencephalitis, myocarditis and
respiratory disease.

H. somnus infection of lung parenchyma is rare in adult cattle in New Zealand.

Respiratory infection is more commonly seen in weaned calves. Adult cattle are likely
to act as reservoirs of infection for calves. Serological surveys in North America
(Corstvet et al., 1973) indicate that an increased prevalence of clinical respiratory
disease due to H. somnus occurs in autumn born calves, implying that the time of
year is a factor in the development of the disease. However, New Zealand studies
describe H. somnus infections occurring in spring (Howell, 1991; Hooper et al.,
2000). This suggests that management factors associated with the exposure of young
stock to bacteria at a time of stress are important in the development of
haemophilosis. Infection of young stock probably occurs through inhalation of
aerosols originating from the respiratory tract and from discharges from the
reproductive tract.

Pleurisy and fibrinosuppurative bronchopneumonia, similar to those seen with

Mannheimia spp. infection, are the commonly recognised pathologies of H. somnus
disease in young calves. The severity of the infection may be increased with
concurrent infection with M. haemolytica (Janzen, 1997). Numerous small abscesses
are present in the anterioventral lobes of the lungs. In chronic bronchopneumonia,
H. somnus may be isolated in conjunction with A. pyogenes and Pasteurella
multocida.

• Acarnobacterium pyogenes and Fusobacterium necrophorum

Ruminal acidosis associated with the feeding of lush pasture to achieve high milk
production may be an important factor in the development of caudal vena caval
syndrome (Hutton2 et al., 2000). This acidosis can compromise the rumen wall,
allowing bacteria to seed through the circulation of the host animal. Circulating

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bacteria normally localise in the liver (Radostits et al., 2000) to form abscesses. The
seeding of bacteria-laden emboli from those abscesses result in embolic pneumonia,
pulmonary abscesses and aneurysms. If such an aneurysm ruptures, the
pathognomonic signs of haemoptysis and bilateral epistaxis occur. The presence of
exudate partially obstructing the trachea and bronchi causes increased respiratory
noise that can be heard on auscultation (rhonchi). Death is a predictable sequel to
these events (Vermunt et al., 2000). Anaemia, weight loss, and thoracic pain on
respiration may be evident in animals that do not die from acute blood loss.

• Mycobacterium bovis
With the current programme of detection and eradication it is highly unlikely that
clinical respiratory disease due to M. bovis would occur in New Zealand dairy cattle.
In the interest of public health testing for M. bovis was made compulsory for all dairy
herds in New Zealand in 1970 (O’Neil and Pharo, 1995). M. bovis can spread to
humans though the consumption of unpasteurised milk from infected animals and
through the inhalation of M. bovis aerosols.

3. Fungi

• Mortierella wolfii and Aspergillus fumigatus

The processing and storage of supplemental feed can provide fungi such as
Aspergillus spp. and Mortierella wolfii with a suitable substrate for growth. These
fungal pathogens are saprophytes which thrive in poorly stored/fermented silage
where the pH is >5. When ingested by pregnant cattle, the Mortierella fungus may
spread haematogenously to the uterus and cause a mycotic placentitis and abortion.
In some cases, a fatal mycotic pneumonia may develop following the abortion.
Animals may present with laboured breathing and increased respiratory effort. A
diagnosis of fungal pneumonia can usually be made of the basis of an appropriate
history (abortion following the feeding of spoiled silage or hay).

Besides causing placentitis and abortion, A. fumigatus can also cause lesions in
various organs, such as the lungs, brain, lymph nodes and udder.

4. Parasites

• Dictyocaulus viviparus
This parasite may become more important in adult cattle as current anthelmintic
programmes reduce the exposure of young stock to natural lungworm infections. As
well as effective drench control programmes management practices have moved
away from rearing stock in one dedicated paddock to rotational grazing (Bisset,
1995). This further reduces the exposure of young stock to lungworm burdens.
Lungworm infections have been reported in adult cattle, with concurrent Pasturella
infection (Fairley et al., 1996).
D. viviparus larvae stimulate an eosinophilic reaction as they congest the bronchioles.
This stimulation causes the animals to cough. If left untreated the larvae will mature
and produce eggs. This congestion and antigenic stimulation of the lungs causes
pulmonary oedema and interstitial emphysema to develop. As a result of the increase
in exudate in the lung, crackles and loud breath sounds can be heard over the
bronchi. Death may result from acute infection where there are large areas of

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collapsed lung and haemorrhagic bronchitis; or the animal may show ill-thrift as a
result of severe, permanent damage to the cells lining the alveoli.

Non-infectious agents

1. Toxic agents stimulating an allergic response

• L-tryptophan
Ingestion of lush pastures with high levels of L-tryptophan may result in the
development of an acute interstitial pneumonia (atypical bovine pulmonary
emphysema and oedema; ABPEE). The L-tryptophan is converted to 3-methyl-indole,
which prevents the vasoconstriction of pulmonary blood vessels and damages the
type I alveolar septal cells. Fluid exudes into the alveoli and alveolar walls as a result
of the toxic damage to the interstitial cells and the blood vessels. Up to this stage, the
damage is thought to be reversible. However, when the type II cells of the alveolar
septum start proliferating, the damage becomes irreversible. The interstitial tissues
become thickened with lymphocytes and fibrous tissue.
The thickened septa and interstitial oedema reduce the perfusion of oxygen across the
alveolar membrane. Hence, these animals present with an extended head and are
mouth breathing in an attempt to compensate for the hypoxia. Mortality is reported at
30% in outbreaks of ABPEE.

• Pollen, fungal spores and pasture mites

Chronic allergic inflammation stimulated by pollen, fungal spores or pasture mites
results in a chronic granular rhinitis (bovine nasal granuloma or ‘nasal catarrh’). Small
raised nodules are present at the entrance of the nares extending 5-8 cm into the
nostrils. The allergic inflammation results in a bilateral nasal and ocular discharge and
swelling of the nasal mucosa. The affected animals exhibit pruritus, often attempting
to alleviate the irritation by scratching on fibrous material. This can result in animals
having plant stalks broken off inside their noses. This condition is more prevalent in
Jersey than Friesian cattle and occurs most frequently during the summer months. The
condition is chronic and progressive, and severely affected animals will have a
marked decrease in milk production.

2. Toxic agents causing traumatic injury to the respiratory tract

• Inhalation of rumen fluid in recumbent cattle.

• Human error in the delivery of liquid drenches.

The placement of small volumes of liquid into the bronchi results in the development of a
suppurative pneumonia (aspiration pneumonia). In cases where death does not supervene,
bacteria introduced with the noxious substance localise in abscesses within the damaged
lung tissue. Consolidation of the lung tissue and pleuritis develop. The animals have an
increased respiratory rate and cough with a putrid breath. The progression of aspiration
pneumonia depends on the bacterial species involved, the amount and type of fluid inhaled
and whether antibiotic treatment has been instituted early and aggressively.

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Correlation between Respiratory Sounds and Lung Pathology

Diagnosis of respiratory disease in the individual animal requires thorough auscultation of both
the left and right lung fields. The results of the auscultation may reveal the likely disease process
occurring in the respiratory system (see Table II)

Treatment
Therapy for respiratory disease is aimed at reversing pathology before the changes are
irreversible. Treatment may seek to clear the infecting agent from the respiratory tract or
minimise the damage caused by the pathogen. Damage to the respiratory tract may be a direct
effect of the infection or the result of the host immune system responding inappropriately to the
noxious stimuli. In case of severe infection therapy is often unrewarding. A summary of
therapies that are indicated for various respiratory diseases is given in Table III.

The therapeutic agents to be considered in the treatment of respiratory disease are antibiotics,
anti-inflammatories, brohcnodilators, expectorants and cough suppressants. Fluid therapy may
be indicated in the presence of dehydration (refer to Forsyth’s paper in the 1995 DCV
Proceedings for a detailed discussion of fluid therapy in the bovine patient). Antibiotics address
the inciting cause of the pneumonia, while the other therapeutic agents provide support in
relieving the aspects of respiratory insufficiency.

Antibiotics

The antibiotics selected for therapy of bacterial infections should be active in the presence of
excessive proteinaceous material that may be present in the bronchi. Often the bacterial
infection will decrease the pH of the tissue, which encourages more ionisation of antibiotics,
which are weak bases. The increased polarity of the antibiotic allows the antibiotic to move
across the bacterial cell membrane. Generally, the sporadic nature of respiratory disease in adult
cattle implies that parenteral route of drug administration is the most practical. If there is severe
consolidation of the lungs, the intravenous route should be considered to maximise the rate
penetration of the antibiotic into the lung. Drugs that are administered via the percutaneous
route must have good lipid solubility to aid transport across the endothelial cells into the alveoli.
Therapy often requires a minimum of seven days of antibiotics at therapeutic levels. The milk
and meat withholding time of the drug should also be considered in drug selection.

Extracellular, gram negative, facultative anaerobic bacteria cause most of the bacterial
pneumonias seen in cattle lungs (Langston, 1989). A successful response to treatment requires
early accurate diagnosis of the bacterial disease and prompt institution of antibiotic therapy. If
treatment is commenced early in the disease process, the animal should show a response to
treatment in 12 to 24 hours.

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Anti-inflammatory agents

1. Corticosteroids

The mechanism of action of corticosteroids as anti-inflammatory agents is largely unknown,

despite long-standing evidence of their effectiveness in such a role. One proposed
mechanism of action of corticosteroids is preventing the breakdown of phospholipids. Such
phospholipids are precursors of arachidonic acid, from which the main effectors of
inflammation such as thromboxanes, prostaglandins and leukotrienes are produced (Van de
Weerdt and Lekeux, 1997). Corticosteriods are contra-indicated in the presence of
microbial infection (when host immune responses are important in clearing the infection),
since they depress the host’s immune system. They are likely to cause abortion in cows,
which are beyond the middle of gestation.

2. Non steroidal anti-inflammatory drugs (NSAIDs)

There are a number of NSAIDs that inhibit various stages of the cyclooxygenase pathway,
which prevents the production of prostaglandins and thromboxanes. The NSAIDs used in
cattle practice are ketoprofen (Ketofen®), tolfenamic acid (Tolfedine®) and flunixin
(Finadyne®). The NSAIDs differ in the selectivity of the parts of the cyclooxygenase cascade
that they inhibit and, consequently, the potency of their respective anti-inflammatory
actions.

3. Antihistamines

Antihistamines inhibit respiratory secretions, and may relieve some respiratory distress in
the acute phase of disease.

Bronchodilators

Products such as clenbuterol bind to ß adrenergic receptors in the lung to increase lung
compliance through bronchiolar dilation.

Expectorants

Secretolytic agent (e.g. bromhexine; Bisolvon ®) can be used in cases of moist exudative
bronchopneumonia. Oral administration of ammonium and potassium salts may be useful
in painful, tacky, exudative pneumonia to suppress the cough reflex. Such treatment may
relieve some of the respiratory distress whilst the inciting cause is being treated.

Prevention

Environmental modification
For housed, unweaned calves, isolating sick animals, controlling dust and providing adequate
ventilation are management practices that reduce the level of pathogen exposure.

Vaccination
Vaccination may provide some protection against IBR (Hutton1 et al., 2000). IBR vaccination
may also reduce the prevalence of bovine nasal granuloma, suggesting a possible link between
IBR and this condition.

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Conclusion

Currently, bovine respiratory disease is generally of a sporadic nature in the adult New Zealand
dairy cow. Where treatment is attempted, it should aim to kill bacterial pathogens (or
contaminants) and to alleviate respiratory insufficiency. The prevalence of respiratory disease is
sufficiently low that specific control measures are seldom indicated.

References

Bisset SA. Epidemiology of internal parasites of dairy cattle. Proceedings of the 12th Seminar for
the Society of Dairy Cattle Veterinarians of the NZVA, 135-52, 1995
Corstvet RE, Panciera RJ, Rinker HB, Starks BL, Howard C, Survey of tracheas of feedlot cattle for
Hemophilus somnus and other selected bacteria. Journal of the American Veterinary
Medical Association 163, 870-3, 1973
Durham PJK, Forbes-Faulkner JC. The prevalence of antibodies to bovine virus diarrhoea and
infectious bovine rhinotracheitis viruses in diagnostic sera from New Zealand cattle. New
Zealand Veterinary Journal 23, 226-9, 1975
Fairley R, Houston N, Davidson P. Lungworm infestation in adult cattle. The Society of dairy
Cattle Veterinarians of the NZVA Newsletter 14(1), 9, 1996
Fairley R. Respiratory diseases of New Zealand cattle. Surveillance 23(4), 15-6, 1996
Forsyth S. Bovine Fluid therapy. Proceedings of the 12th Seminar for the Society of Dairy Cattle
Veterinarians of the NZVA, 53-62, 1995
Grooms DL. Role of bovine viral diarrhoea virus in the bovine respiratory disease complex. The
Bovine Practitioner 32(2), 7-12, 1998
Hjerpe CA. Clinical management of respiratory disease in feedlot cattle. Veterinary Clinics of
North America: Large Animal Practice 5(1), 119-42, 1983
Hooper C, Harvey C, Williamson C, Fraser T, Julian A, Bastianello A, Hill F, Thompson J,
McKenna P. Quarterly review of diagnostic cases –October to December 1999 AgriQuality
laboratory network cattle. Surveillance 27(1), 11-2, 2000
Horner GW. Infectious bovine rhinotracheitis in New Zealand. Surveillance 17(2), 25-6, 1990
Howell J. Haemophilus somnus infections in cattle. Surveillance 18(2), 10, 1991
Hutton1 J, Arthur D, Bailey K. Quarterly review of diagnostic cases –July to September 2000
labworks animal health ltd. Surveillance 27(4), 19-20, 2000
Hutton2 J, Arthur D, Bailey K. Quarterly review of diagnostic cases –January to March 2000
labworks animal health ltd. Surveillance 27(2), 20-1, 2000
James MP, Neilson FJA, Stewart WJ. An epizootic of malignant catarrhal fever. New Zealand
Veterinary Journal 23, 9-12, 1975
Janzen ED. The role of Haemophilus somnus in bovine respiratory disease (BRD). The Bovine
Practitioner 31(1), 39-45, 1997
Langston AC, Davis LE. Factors to consider in the selection of antimicrobial drugs for therapy.
The Compendium 11, 270-6, 1989
Motha MXJ, Hansen MF. Prevalence of IBR, PI 3, BRS and BCV infections in the dairy cattle
population of New Zealand. New Zealand Veterinary Journal 46, 239-40, 1998
Motha J, Hansen M, Orr D. Viral aetiologies for bovine respiratory disease. New Zealand
Veterinary Journal 45, 40, 1997
O’Neil BD, Pharo HJ. The control of bovine tuberculosis in New Zealand. New Zealand
Veterinary Journal 43, 249-55, 1995

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Oliver RE, Horner GW, Hunter R, Niederer W. Parainfluenza type 3 virus in cattle with upper
respiratory disease. New Zealand Veterinary Journal 24, 135-7, 1976
Pérez MJ, Wilks CR, Vermunt JJ, West DM. Observations on BVD virus infection in New
Zealand beef herds. New Zealand Veterinary Journal 43, 85-6, 1995
Radostits OM, Gay C, Blood DC, Hinchcliff KW (eds). Veterinary medicine a textbook of the
diseases of cattle, sheep, pigs, goats and horses. 9th ed, Harcourt Brace Limited, London.
2000
Storz J, Purdy CW, Xiaoqing L, Burrell M, Truax RE, Briggs RE, Frank GH, Loan RW. Isolation of
respiratory bovine coronavirus, other cytocidal viruses and Pasteurella spp from cattle
involved in two natural outbreaks of shipping fever. Journal of the American Veterinary
Medical Association 216, 1599-604, 2000
Van de Weerdt ML, Lekeux P. Modulation of lung inflammation in the control of bovine
respiratory disease. The Bovine Practitioner 31(1), 19-31, 1997
Vermunt J, Collett M, Burbidge H. The caudal vena cava syndrome. Vetscript 13(7), 6-7, 2000
Whittem T, and Hanlon D. Rational use of antibacterial drugs. Proceedings of the 12th Seminar
for the Society of Dairy Cattle Veterinarians of the NZVA, 125-34, 1995

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 Table I
Summary of Agents that may have a Role in Causing Respiratory Disease in Adult New Zealand Dairy Cattle
Agent Site of Infection Respiratory Disease
Viruses Bovine herpesvirus 1 Upper respiratory tract Infectious bovine rhinotracheitis
Parainfluenza 3 Upper respiratory tract ? probably supports development of bacterial
Ovine herpesvirus 2 Nasal mucosa, lymph nodes, upper bronchopneumonia
alimentary tract Malignant catarrhal fever: necrosis and erosion of the nasal
Pestivirus: Bovine viral diarrhoea virus and oral mucosa.
Bovine respiratory syncytial virus Upper respiratory tract/alimentary tract May predispose cattle to secondary bronchopneumonia
Upper respiratory tract Uncertain
Bacteria Mannheimia haemolytica Infection of the lower respiratory tract Fibrinous pleuropneumonia
results in release of bacterial toxins that
damage leukocytes and endothelial cells of
pulmonary arterioles
Haemophilus somnus Systemic infection from respiratory or
reproductive tract Meningoencephalitis, pleuropneumonia and myocarditis
Fusobacterium necrophorum Liver, caudal vena cava and pulmonary
Acarnobacterium pyogenes blood vessels Caudal vena caval thrombosis and pulmonary embolism,
suppurative pneumonia and interstitial pneumonia
Parasites Dictyocaulus viviparus Bronchioles, trachea and diaphragmatic Parasitic bronchitis and atelectasis, interstitial emphysema in
lung lobe dorsal aspect and consolidation and bronchitis in ventral
aspect
Fungi Mortierella wolfii Infection centred around bronchioles Severe fibrinous pneumonia, with small granulomatous
Aspergillus spp. abscesses in the lungs
Allergenic Lush pasture (tryptophan) Interstitial type I alveolar septal cells. Interstitial pneumonia, atypical bovine pulmonary
Toxins emphysema and oedema and thickening of the alveolar
septum.
Pollen, fungal spores, pasture mites Nasal cavity Bovine nasal granuloma
Toxins Liquid drenches (esp. oil based) Aspiration pneumonia
Causing Inhalation of rumen fluid by recumbent
Trauma cattle
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Table II
Relationship between Respiratory Sounds and Lung Pathology

Sound Pathogenesis Condition

Rub Friction of dry pleural surfaces rubbing against each Acute pleurisy
other
Crackle Airways suddenly opening, allowing the pressure Emphysematous conditions
between the distal and proximal portions of the where expiration is forced.
airway to equalise. In cases of parasitic infection, Acute phase of parasitic
crackles and wheezes are heard in the bronchopneumonia and
caudal/diaphragmatic lung lobes, c.f. anterior/ventral interstitial pneumonia
lobes in other causes of bronchopneumonia
Wheeze Air being forced through a narrowed passage, usually Chronic interstitial pneumonia
auscultated in the anterioventral aspects of the lung or chronic bronchopneumonia
Absence of No sounds will be heard in the bronchi when the Aspiration pneumonia,
sound in bronchial lumen is filled with exudate, or when the pneumothorax,
the bronchi pleural pressure is equal to the alveolar pressure (so
there is no movement of air into the alveoli)
Stridor Inhalation over an upper airway obstruction. Laryngeal abscess, laryngeal
Granulomatous reaction in nasal mucosa. oedema
Cellulitis and abscessation. Pharyngeal trauma
Calf diphtheria, actinobacillosis,
bovine nasal granuloma, IBR.
Increased Collapse and filling of lung alveoli Consolidation of lung
loudness of parenchyma
breath
sounds
Grunt Indication of thoracic pain on inhalation, Pleurisy
Must be differentiated from non-thoracic pain. Interstitial pneumonia
Cough Initiated by stimulation of respiratory tract sensors, Inflammation such as infectious
with feed back to the medulla oblongata bronchopneumonia, M. bovis
infection;
parasitic bronchopneumonia;
lung abscesses, caudal vena
caval syndrome

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