Respiratory Disease


On the basis of current knowledge, the following overview and information should prove useful in the management of canine respiratory disease.


Canine respiratory disease is essentially split into two syndromes, one of simple upper respiratory infection (URT) caused by viruses or bacteria, and one of lower respiratory tract infection caused by bacterial invasion of the lower airways.

Simple URT infections are loosely grouped as “kennel cough” and are caused by several respiratory pathogens. These are self-limiting and rarely more than a nuisance. The morbidity is high, due to the number of agents behind kennel cough, with over 50% affected.

The far more serious lower respiratory tract infection usually manifests as an acute rapidly fatal pneumonia – this is canine haemorrhagic pneumonia (CHP). The disease appears very rapidly and can be fatal within 6-8 hours, and usually follows 24-36 hrs after period of stress. It is thought that the primary stressor allows invasion of the lower respiratory tract by bacteria, which commonly include Streptococcus equi zooepidemicus or E.coli, but can include Strep. canis, Klebsiella, Bordetella and Pasteurella. The streptococci may act as primary agents.



Most cases of CHP develop within 24-36 hours of a stressful event, e.g. transport or racing, with very few warning signs. Stress and/or high-speed air flow allows the agents to gain access to the lower respiratory tract.

The morbidity due to CHP is typically only one case in a group of greyhounds, but mortality varies between 50% and 100%. It is thought that Str. zooepidemicus is now endemic on the greyhound population via tonsillar carriers (up to 30% of greyhounds may be carriers); thus many greyhounds may be immune. No data is available for E. coli carrier states, but it assumed to be an opportunistic pathogen. It would appear that naïve greyhounds meeting the agent during a period of stress succumb to CHP, but since they are in a group of immune greyhounds no further cases are seen. In rare instances second or even third cases are seen, but these always occur within 48 hours of the index case.

The appearance of CHP is not necessarily linked with KC, since the two diseases are clinically distinct syndromes. Therefore cases of CHP can, and do, appear independently of any other disease.


These include, but are not limited to:


  • Racing.
  • Long distance transport.
  • Close contact with other dogs with respiratory disease.
  • Shared air spaces.

Other risk factors that may be involved are:


  • Humans with streptococcal sore throats.
  • Unpasteurized milk.
  • Raw horse meat.
  • Poor food handling hygiene.
  • Close contact with horses with Str. zooepidemicus respiratory disease.



The primary phase may be missed, but is limited to malaise of 1-2 days with occasional coughing. This progresses rapidly to depression, inappetance, tachypnoea and a marked pyrexia (>40 C). A muco-purulent nasal discharge with some blood may be seen. There is little coughing since this is a true pneumonia, not a bronchopneumonia.

Therefore cases of CHP present as peracute collapse, circulatory compromise and marked pyrexia: they are medical emergencies. The pyrexia may be absent later because of the hypotensive effects of the bacterial exotoxins. The typical features of pyrexia and depression with tachypnoea allow a clinical diagnosis to be made.



The clinical signs of CHP are enough to warrant immediate treatment without a specific diagnosis. Differential diagnoses include aspiration pneumonia and foreign body pneumonia. In the unfortunate case of a sudden death, the body may be submitted for post mortem examination only AFTER being reported to the GBGB.


Post mortem findings reveal a markedly haemorrhagic lung field, affecting all of the lobes, with bleeding into the airways and pleural cavities. Samples for bacteriology may be taken from the bronchi or the lung parenchyma. The rest of the body shows signs of toxaemia / hyperaemia.



The GBGB area stipendiary steward, or the GBGB on 0207 822 0900, must be informed at the earliest opportunity, as it is a GBGB Rule of Racing for trainers to report cases of disease.

The 24-hour line for reporting a suspected case of CHP or any sudden death in GBGB-licenced racing greyhounds is 0207 822 0929.



The level of treatment is governed by the severity of the clinical signs. The two most important treatments are:


  • Intravenous antibiotics.
  • Intravenous fluids.

with non-steroidal anti-inflammatory drugs for the pyrexia.

Good first choice antibiotics are augmented amoxycillin, enrofloxacin or marbofloxacin[1]. Intravenous antibiotics are essential in treating CHP and are available for use in dogs over 12 months. The human augmented penicillin preparation “Augmentin®” may be used via the cascade route. Oral or subcutaneous administration of antibiotics in acute cases is rarely successful and is to be avoided. Response to treatment is rapid where treatment has been started without delay, with significant improvements seen within 12 hours, after which oral medication should be used for 7-10 days. Non-responders decline quickly over a several hours despite treatment, and should be euthanased to prevent further suffering.


The actual antibiotics used are to be decided by the attending veterinary surgeon, but should be directed against streptococci and coliforms. A range of sensitivities is listed below.



Proportion of isolates sensitive



Augmented amoxycillin

100 %

96 %


Not tested

80 %


96 %

100 %


98 %

100 %


98 %

95 %


98 %

59 %


Not tested

21 %


Table 1: Antibiotic sensitivities for Str. zooepidemicus and E. coli retrieved from cases of CHP.


Cases which recover from CHP appear to make a full recovery and are able to return to racing. No long term sequelae have been identified.


Isolation and good biosecurity procedures must be used. In-contacts should be treated as well, although not necessarily as intensively as acute cases. All cases should be treated with antibiotics at the recommended dosage for a minimum of seven days.

Until the attending veterinary surgeon is satisfied that no further significant risk is involved, all greyhounds within the affected kennel are to be quarantined at that kennel. As a guide, the anticipated quarantine period is about three weeks for KC, but only seven days for CHP, assuming one initial outbreak. Obviously if new cases are appearing, the quarantine period must be extended.

Although it is counter-intuitive to have a much shorter quarantine period for CHP, this is because the causal agents are endemic and because to date all second/third cases of CHP have occurred within 48 hours of the index case. Counter this, with KC there is much more coughing and therefore airborne contamination, and also the coughing lasts 10-14 days or more.


Extra vigilance is required at the tracks where possible contact has occurred, in addition to the routine biosecurity procedures already detailed in a previous document. These biosecurity guidelines are also on the GBGB website (


It is not believed that there is a greater risk for the kennel of origin when a greyhound is found to be diseased after being moved to a destination kennel. The attending veterinary surgeon may wish to inform the kennels of origin, but attention should remain focussed on the destination kennel where the disease is evident.

As a general rule, all new entrants to a kennel should be quarantined for a minimum of seven days, and not presented at a race track, nor worked hard, during this time. Antibiotic prophylaxis is not advised nor required.


Broadly speaking, the track vet should be concerned with protecting the well-being of the healthy greyhounds at the track. Any greyhound that is presented as off-colour and/or coughing repeatedly should be examined away from the other greyhounds.


If the veterinary surgeon suspects that the greyhound may be suffering from contagious respiratory disease, then it must be removed from the paddock without delay, and sent home. The other greyhounds from the same trainer's kennels should also be examined for similar signs. If there are other greyhounds that give cause for concern, then the entire cohort from that trainer's kennel should be withdrawn and sent home. The track vet should try to resolve logistical problems on a pragmatic case-by-case basis, being mindful of the risks of contagion and pre-clinical disease states.

There is a similar, if not greater risk, from greyhounds from larger kennels, and as such they should all be handled in the same way, regardless of the impact of a mass withdrawal on the race card.

The track vet must be mindful of the duty to prevent the spread of disease to healthy greyhounds. As such, the track vet should ideally not be involved in the diagnosis nor treatment of acutely ill greyhounds. The duty of care of veterinary surgeons must take precedence, however, and any cases which need immediate therapy should receive appropriate care and treatment, prior to referral. In such cases strict biosecurity must be applied.

Although to date no cases of CHP have been identified at stadia, if a case of acute severe respiratory disease becomes apparent at the track, then that greyhound should be referred to a suitable veterinary practice without delay, where proper facilities for barrier nursing and intensive care are available. The Transport of Injured Greyhounds certificates can easily be used to aid the receiving practice, and to impress on the trainers the need for urgent treatment.

In order to be vigilant for CHP cases, direct in-contact greyhounds should be monitored closely for signs of disease over the next 48-72 hours. Any off-colour and/or pyrexic dogs should be treated without delay.

Bodily discharges must be dealt with to prevent contamination of the environment, as per the biosecurity and deep cleaning guidelines.


Updates and advice can be obtained from the GBGB. This document is subject to modification as further facts become available.