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RESPIRATORY DISEASE IN FOALS Slide 1 Slide 2 Prior to the foal being born the placenta serves as the primary site for oxygen and carbon dioxide exchange. The lungs are fluid filled and collapsed whilst the foal is in the uterus. Whilst in the uterus the foal makes breathing movements at some stages but no gas exchange takes place through the lungs. Slide 3 The birthing process in the horse is explosive and quick. Since the lungs are fluid filled in-utero, successful transition to breathing air requires the expulsion and absorption of fluid from the lungs. As the foal is born, the stimulus to begin spontaneous breathing or ventilation relies on adequate external stimulation of the central nervous system to create chest expansion. Slide 4 Hypoxia or a lack of oxygen due to dystocia, cold or hypothermia , and surfactant deficiency can all result in this initial stimulus to breathe being compromised.
Slide 5 Critical respiratory compromise at birth usually results in a foal presenting with what we call APNOEA which means basically no breathing. At this stage quick thinking is required and the very first thing that is vital is to assess whether or not there is a heartbeat. If that is positive then rapid institution of therapy is critical and initially external stimulation by vigorous rubbing, stimulating nasal mucosa or ear canal with a straw, and flexion and extension of the limbs may be used in an attempt to initiate ventilatory efforts. SLIDE 6 If that fails after 30-60 seconds then check the airway, if there is a large amount of fluid then attempt to drain it (place foal on incline, use 60ml bute syringe for suction) then begin mouth to nose resuscitation . This is done by closing the foals mouth and lips, occluding one nostril with the hands, and blowing into the other nostril. Look for expansion of the rib cage to ensure that you are blowing hard enough. Unfortunately this will only provide short term support, and ideally these little guys need an endotracheal or nasotracheal tube placed and an oxygen supply. There is a drug called DOPRAM (consisting of doxapram) which is a pharmacological stimulant that initiates breathing but it is better to initially start external resuscitation as there is a pretty variable response to this drug. SLIDE 7 Immediately following delivery a foals respiratory rate is rapid, as high as 60-80 breaths per minute. As all the liquid in the lungs is absorbed and the alveoli (end airway) are expanded the respiratory rate decreases to 20-40 breaths/minute in the first week of life. SLIDE 8 Pneumonia in neonatal foals (< 2wks) is usually associated with generalized sepsis and has a high mortality rate. Bacteria that cause neonatal pneumonia are the same that cause septicaemia eg E. coli, etc Treatment for pneumonia is only part of the intensive care necessary to save these septic foals. SLIDE 9 The majority of bacterial pneumonias involve older foals and are caused by opportunistic pathogens that are either environmental contaminants or normal inhabitants of the equine upper respiratory tract. E. coli, Pasteurella, Bordetella, Actinobacillus, Streptococcus , can all be implicated in foal pneumonia. Rhodococcus equi is the most devastating cause of foal pneumonia and can be endemic on some breeding farms. It is important to remember that Rhodococcus is not the only bacteria that can cause foal pneumonia. The majority of pneumonia cases are seen in foals between the ages of 6 weeks and 4months. High ambient temperatures Dusty, dry conditions Overcrowding Poor ventilation in stables, (ammonia) All predispose to the development of foal pneumonia. SLIDE 10 Most infections leading to foal pneumonia are acquired by inhalation of aerosolised dust. The defence mechanisms in the lungs that work to prevent infection occurring can be compromised by a pre existing viral infection or the exposure to excessive ammonia. In the face of overwhelming challenge these defence mechanisms are also impeded. SLIDE 11 SLIDE 12 Rhodococcus equi is a soil inhabitant. It is a very resistant bacteria and can survive in soil containing manure for at least 12 months. Foals become exposed to Rhodococcus through aerosolised dust and also from ingestion from coprophagy (manure eating). SLIDE 13 Once an infection has been established ( usually due to overwhelming challenge) Rhodococcus lives within the cells in the lungs and causes massive abcessation and fibrosis in the lungs. SLIDE 14 The process of abscess development occurs very slowly and gradually and clinical signs may not be present until several weeks to a month after infection. SLIDE 15 Foals are initially protected against Rhodococcus by antibody they receive in the colostrum from their mother. This protection lasts around 2 months. The foal does not produce sufficient amounts of its own antibody against Rhodococcus until 5-6 months of age. As you can see there is a vital gap in protection from 2 5/6mths of age and it is for this reason that we see foals affected at this time. SLIDE 16 Clinical signs include increased resting respiratory rate, flaring nostrils, and apparent difficulty breathing (dyspnoea) Elevated temperature Exercise intolerance Coughing sometimes Unthriftiness, lethargy, dull coat SLIDE 17 Diagnosis ULTRASOUND gives an excellent picture of periphery of lung but not more internal areas BLOODS normally show an increased white cell count and elevated fibrinogen
SLIDE 18 Treatment long term, usually 6-8 weeks of antibiotics. Erythromycin/Rifampin Treatment of choice. Side effects and expensive For subclinical and early infections neomycin has good efficacy. Prevention again is key. SLIDE 19 PREVENTION Reduce dust water/sprinkle tracks, yards, if running mares and foals in. Avoid leaving mares and foals in yards (usually waiting for the vet). Move feeders around frequently. Remove manure from yards and paddocks where possible. SLIDE 20 Observe foals in early morning for those with subtle nostril flaring and increased respiratory rate. Ultrasound chests routinely. SLIDE 21 Use hyperimmune plasma as a preventative SLIDE 22 STRANGLES Is an acute, contagious disease of horses caused by STREPTOCOCCUS equi. It affects predominantly young horses. Is characterized by mucopurulent inflammation of the nasal and pharyngeal mucous membranes with enlargement and subsequent abcessation of lymph nodes. SLIDE 23 Is a centuries old disease Is still a major cause of economic loss to the horse industry worldwide since current control measures are not completely effective in preventing this disease. SLIDE 24 The most common source of infection is the introduction of a horse incubating, clinically ill with or recovering from strangles. Spread is by DIRECT NOSE OR MOUTH CONTACT WITH PURULENT NASAL DISCHARGE OR DRAINING PUS FROM ABSCESS Aerosol spread occurs but is not the most important mode of infection Feeders, waterers, flies, halters, stables handlers mechanically transfer Strep equi all around the farm. It is extremely contagious. SLIDE 25 Incubation period 2 days 2weeks. Clinical signs temperature elevation, depression, bilateral nasal discharge, enlarged lymph nodes which eventually form large abscesses that can STRANGLE the horse SLIDE 26 Not all enlarged lymph nodes are caused by Strep equi but always be suspicious. Most weanlings at some stage develop some form of upper respiratory tract disease. The best approach is to get some nasal swabs from the earlier affected weanlings. Sometimes these can be hard to interpret. Swabs directly from a freshly drained abscess are usually very diagnostic. SLIDE 27 TREATMENT Immediate and strict isolation of affected weanling. Good nursing care, soft moist palatable feeds Pain killers and anti inflammatories eg Phenyl butazone often helps appetite Lance abscesses when soft, drain and flush with dilute antiseptic, be patient! And poultice if not ready Protect area around incision with Vaseline SLIDE 28 PENICILLIN- to do or not to do that is the question! Use after abscess is draining Must be continued for at least 10 14 days twice daily If given at initial temperature rise when there is not lymph node involvement can stop progression of disease again 10-14 days twice daily Not effective when abscess is forming SLIDE 29 CONTROL OF INFECTION Isolation- clothes, boots, hands, halters, stable, buckets FOR ONE MONTH AFTER COMPLETE RESOLUTION OF SIGNS Fly control Steam clean stable. Remove all organic material. Boiling water and heat kills Strep . equi. Follow with disinfectant eg phenol, glutaraldehyde, povidone iodine or chlorhexidine. Bleach is not effective. Allow to dry . Leave empty for one month.! Pastures empty for one month. Maximise exposure of soil to sunlight and heat slash/mow. |