Review: Depm Ment of Vete Na D, Pathology, The University of Sydn, New South Wales 2006, Australia

B~: va.~ (1995).
151,233
REVIEW
EQUINE PLEUROPNEUMONIA:
SHARANNE L. RAIDAL
Depmment of Vete~naD, Pathology, The University of Sydn~, New South Wales2006,
Australia
SUMMARY
Pleuropneumonia is a clinically, important equine disease, predisposed by
a number of identifiable factors. Successful management is largely dependent on early identification and prompt initiation of appropriate treatment strategies. Rapid resolution of the disease process is associated with
appropriate treatment commenced within 48 h of the causative insult.
Lower airway contamination by oropharyngeal organisms and subsequent
extension into the puhnonary parenchyma results in respiratory dysfunction and systemic toxaemia. Acute disease is associated with the isolation
of facultatively anaerobic organisms, especially [3-haemolytic Streptococcus
spp. and Pasteurellaceae. Delayed or inappropriate treatment is likely to
result in chronic disease characterized by the involvement of anaerobic
bacteria and a poor response to therapy. The primary mode of treatment
for anaerobic infection of the human thorax is surgical drainage and
resection of necrotic tissue but whilst such techniques have been
described for the management of equine pleuropneumonia, the size of
the equine thoracic cavity hinders accurate diagnostic evaluation and successful completion of such intervention. The chronic nature and cost of
ongoing treatment and limitations on choice of antimicrobial agents
warrant a poor prognosis for sin-viral and a poorer prognosis for return to
athletic endeavour.
KE.'~,ORBS:Equine; pleuropneumonia; horses; pneumonia.
INTRODUCTION
Bacterial pneumonia develops following bacterial colonization of the pulmonary
parenchyma (Sweeney et al., 1991a; Chaffin & Carter, 1993). Extension of the
disease process to the visceral pleural surface and pleural space is common
(Spurlock, 1991) and in such cases the condition may be more appropriately
termed 'pleuropneumonia' (Raphael & Beech, 1982; Byars and Becht, 1991). In
adult horses, bacterial pleuropneumonia' is usually the result of polymicrobial
0007-1935/95/030233-30/$08.00/0
1995Bailli6re Tindall
234
BRITISH VETERINARY JOURNAL, 151, 3
infection (Sweeney et aL, 1985, 1991a; Bailey, 1989; Racklyeft, 1990; Collins et al.,
1994). Acute disease follows a predisposing factor (Racklyeft, 1989) which permits
aspiration of oropharyngeal contaminants (Mansmann, 1983a; Bailey, 1989;
Racklyeft, 1990; Racklyeft & Love, 1990; Bailey & Love, 1991).or causes inhibition
of pulmonary defence mechanisms (Bayly et aL, 1986). Aspirated fluid may conrain 105-107 organisms ml -~ (Slocombe, 1989), with anaerobes outnumbering
aerobic organisms by 10 to one (Gorbach & Bartlett, 1974a).
Equine pleuropneumonia has been divided into four stages (subacute, acute,
chronic and end-stage) based on the duration of the disease process, clinical signs
and associated prognosis (Mansmann, 1983a; Bernard-Strother & Mansmann,
1985). Ideally, recognition of a predisposing event should alert the clinician to the
possibility of pleuropneumonia and treatment within 48 h of an insult, the 'subacute' or 'peracute' phase, should prevent establishment or arrest the development of the disease process; controlled studies on the development of disease and
retrospective analysis of clinical cases indicate that the multiplication of facultatively anaerobic organisms, especially ~-haemolytic Streptococcus spp. and Pasteurellaceae, is responsible for acute stage disease. Anaerobic organisms are usually isolated from disease of greater than 5 days duration and have been associated with a
poor prognosis for survival. While Enterobacteriaceae have been isolated from
cases of equine pleuropneumonia, they are not normal oropharyngeal inhabitants
and, thus, their involvement in the initiation of pulmonary disease is uncertain. As
the majority of published reviews on organisms isolated from equine pleuropneumonia are based on cases treated at university teaching hospitals, there is an
emphasis on chronic disease, where animals had received prior antibiotic treatment. Therefore, isolation of Enterobacteriaceae may reflect superinfection following antibiotic treatment or other derangement of oropharyngeal microbiota.
Chronic disease has been defined as a disease of >2 weeks duration and is associated with a greatly reduced prognosis possibly due to established anaerobic
disease and the presence of organisms resistant to available antibiotics. End-stage
disease is reached after a protracted course of illness which results in irreversible
structural damage to pulmonary parenchyma such as bronchopleural fistulae,
abscessation and scarring.
PATHOGENESIS
Predisposing factors and causes of pleuropneumonia

The involvement of aspiration of oropharyngeal organisms in the development
of thoracic sepsis has been demonstrated in people (Huxley et al., 1978), cats
(Love et al., 1989, 1990) and horses (Bailey & Love, 1986; Bailey et al., 1988; Bailey,
1989; Racklyeft, 1990). Disease occurs following bacterial colonization of the bronchiolar epithelium when pulmonary defence mechanisms are overwhelmed by
massive challenge or otherwise compromised (Wilson, 1992b). Mucociliary-transport of tracheobronchial secretions and pulmonary alveolar macrophage phagocytosis have been suggested as the two most important clearance mechanisms in
the equine lung (Bayly et al., 1986; Robinson, 1991). Derksen (1991c) indicates
that protective mechanisms, such as coughing and bronchospasm, are poorly
EQUINE PLEUROPNEUMONIA
235
developed in the horse. Predisposing factors have been identified in many retrospective studies of equine pleuropneumonia (Raphel & Beech, 1982; Sweeney et
al., 1984, 1985; Bernard-Strother & Mansmann, 1985; Bailey, 1989; Mair & Lane,
1989; Racklyeft, 1989, 1990; Collins et al., 1994) and include long distance transportation, strenuous exercise (usually racing), general anaesthesia, exerciseinduced pulmonary haemorrhage, dysphagia and systemic illnesses (such as
enteritis). Such events are associated with increased aspiration of oropharyngeal
organisms a n d / o r impaired clearance of such organisms.
Transportation.
Leadon et al. (1990) reported that seven of 12 horses on a 39 h
flight between London, England, and Sydney, Australia, developed clinical evidence of respiratory disease within 1-2 days of arrival. Aspiration of oropharyngeal organisms and defective postural drainage associated with elevated head positions, as occur during transportation, result in reduced clearance of
contaminants and the accumulation of mucopurulent exudate (Racklyeft, 1990;
Racklyeft & Love, 1990; Raidal et al., unpublished). Bacterial products and factors
released by the host's phagocytic defences present in these exudates may impair
mucociliary beating (Denny, 1974; Johnson & Inzana, 1986; Wilson et aL, 1986;
Sykes et al., 1987; Wilson & Cole, 1988) or interfere with phagocyte function
(Caruso & Ross, 1990; Dom et al., 1992). Road transportation of calves (Murata &
Hirose, 1991a, b) and goats (Sanhouri et aL, 1992) has been associated with
impaired leucocyte function mediated by hypothalamic-pituitary-adrenal
responses to transit stress (Zavy et al., 1992) and increases in inflammatory
mediators such as haptoglobin (Murata & Miyamoto, 1993). Traub-Dargatz et al.
(1988) demonstrated delayed inflammatory response in transported horses, but
failed to demonstrate altered alveolar macrophage function or changes in
microbial contamination of bronchoalveolar lavage-derived samples. Dehydration,
associated with reduced fluid consumption prior to or during transportation, may
reduce mucociliary clearance (Dixon, 1992).
Exercise. Aspiration of track debris and oropharyngeal secretions during
strenuous exercise may cause significant bacterial contamination. Endoscopic
examination after racing has demonstrated aspiration of track debris, dirt and turf
into the lower airways (Arthur, 1983; Sweeney et al., 1991b). Environmental contaminants, however, have not been found to be associated with the development
of pleuropneumonia. Studies in this laboratory have demonstrated contamination
of the lower respiratory tract by oropharyngeal organisms following single bouts of
strenuous treadmill exercise (Raidal et al., unpublished). Exercise-induced pulmonary haemorrhage, which may occur in up to 90% of Thoroughbred racehorses (McKane et al., 1993), creates an ideal environment for the development of
bacterial infections (Raphel & Beech, 1982; Clarke, 1987).
Human studies have demonstrated immunosuppressive effects of intensive exercise (Budgett, 1990; Sharp & Koutedakis, 1992; Weidemann et al., 1992), possibly
mediated by increased production of glucocorticoids and opioids (Smith &
Weidemann, 1990; Weidemann et al., 1992). Studies in horses have shown elevations in adrenaline, noradrenaline, cortisol, adrenocorticotrophin and [3-endorphin associated with exercise (Thornton, 1985; Church et al., 1986; Freestone et
al., 1991; McCarthy et al., 1991). Huston et al. (1986) demonstrated increased cor-
236
tisol concenn'ations in bronchoalveolar lavage fluid, decreased alveolar macrophage viability and impaired phagocytic function following single bouts of strenuous
exercise. Wong et al. (1990) found a profound suppressive effect on alveolar macrophage chemiluminescence which persisted for 3 days after a single episode of
strenuous exercise.
Viral disease. Viral infection may predispose to bacterial colonization of ain.vays
by species such as Pasteurella spp. or haemolytic Streptococcus spp. (McChesney,
1975). In calves, viral infection has been associated with disease due to Paste~crella
haemolytica or P. multocida (Hamdy et al., 1963; Baldwin et al., 1967; Jericho &
Langford, 1978). Compromise of host defences may occur due to impairment of
mucociliary clearance associated with viral damage to respiratory epithelium or
cilia (Loosli, 1968; Camner et al., 1973; Lopez et al., 1976; Sakakura, 1983), facilitation of airway colonization or bacterial growth and extension into pulmonary
parenchyma (Halfford et al., 1949; Harford & Hara, 1950; Frank et al., 1986, 1989;
Briggs & Frank, 1992), and defects in leucocyte and phagocyte response (Jakab &
Green, 1972, 1973; Nickerson &Jakab, 1990; Adair et al., 1992). Viral pathogens of
the equine respiratory tract include equine" influenza virus (Coggins, 1975;
McChesney, 1975; Burrell, 1985), equine herpesviruses 1 and 4 (Burrell, 1985;
Mason et al., 1990), parainfluenza virus (Coggins, 1975), rhinoviruses (Coggins,
1975; Thorsen, 1991), adenoviruses (McChesney, 1975) and equine arteritis virus
(Coggins, 1975). Equine influenza virus has been associated with deciliation and
erosion of the respiratory mucosa (McChesney, 1975). Willoughby et al. (1992)
demonstrated impaired mucociliary clearance in horses infected with equine
influenza and equine herpesvirus 4. Alterations in cell content of bronchoalveolar
lavage fluid and changes in pulmonary alveolar macrophage function have been
reported in transport-stressed horses with viral respiratory infection (Anderson et
al., 1985).
General anaesthesia or surgety. The mechanisms by which general anaesthesia
predisposes equine patients to pleuropneumonia have not been elucidated. Endotracheal intubation may inta-oduce oropharyngeal contaminants to the lower trachea (Racklyeft, 1989). Positioning in dorsal or lateral recumbency and anaesthetic drug-induced depression of respiratory functions, including compromised
mucociliary clearance, may exacerbate respiratory infections (Slocombe, 1989).
McDonell et al. (1979) and Nyman el al. (1990) demonstrated compression atelectasis and vascular congestion associated with general anaesthesia, which could
lead to regional ischaemia and/or necrosis within the pulmonary mass. This may
proxdde local conditions suitable for bacterial multiplication or impair the phagocytic function of pulmonary alveolar macrophages (Bayly, 1989). The inhalation
of dry anaesthetic gases has been associated with damage to the ciliated respiratory epifllelium (Burton, 1962; Chalon et al., 1972) and may impair mucociliary
clearance. Immune suppression may be associated with the stress of anaesthesia
and/or surgery due to specific inhibition of cellular defence mechanisms (Muir,
1990). Profound increases in adrenocorticotrophic hormone, cortisol, adrenaline
and cytokine levels have been found in human patients associated with anaesthetic
reversal and recovery (Udelsman et al., 1987; Naito et al., 1992). The magnitude of
the apparent stress response may be related to the type or duration of surgery
237
(Udelsman et al., 1987). Minor surgical stress in humans has been associated with
negligible hormonal changes (Chernow et al., 1987). Studies of circulating metabolites and hormones following arthroscopic surgery in horses demonstrated only
minor changes which were unlikely to influence the convalescence of the patient
(Robertson et al., 1990).
Bacterial isolates
Bacterial species isolated from clinical cases of equine pleuropneumonia have
been shown phenotypically (Bailey, 1989; Racklyeft, 1990; Bailey & Love, 1991)
and genetically (Bailey, 1989; Bailey & Love, 1991) to resemble species present in
the oral ca~4ty. Aerobic and facultatively anaerobic bacteria most commonly isolated from .equine pleuropneurnonia cases include [3-haemolytic Streptococcus spp.,
(especially S. equi ss. zooepidemicus), members of the Pasteurellaceae family
( Pasteurella and ActinobaciUus spp.), Enterobacteriaceae (including Escherichia coli,
Klebsiella spp. and Enterobacter spp.), ~Pseudomonas spp., Staphylococcus spp. and BordeteUa ko'onchiseptica (Naglic et al., 1982; Raphel & Beech, 1982; Sweeney et al., 1984,
1985, 1991a; Bailey, 1989; Racklyeft, 1990; Collins et al., 1994). Single species are
uncommonly isolated from cases of equine pleuropneumonia (Bailey, 1989;
Racklyeft, 1990; Sweeney et al., 1991a; Collins et al., 1994). Almost exclusively, S.
zooepidemicus, PasteureUa/Actinobacilhts spp. or E. coli are the species reported as
single isolates.
Anaerobic bacteria commonly isolated from equine cases include Bacteroides
spp. (at the time of isolation identified as B. oralis, B. melaninogenicus and B.
fiagilis), Eubacterium spp. and Fusobacterium spp. (Sweeney et al., 1984, 1985, 1991a;
Bailey, 1989; Racklyeft, 1990; Collins et al., 1994). In agreement with human
studies (Bartlett & Finegold, 1972, 1974; Bartlett, 1993; Marina et al., 1993), obligate anaerobes were almost invariably isolated from samples in which facultatively
anaerobic organisms were present also (Bailey, 1989; Racklyeft, 1990; Sweeney et
aL, 1991a; Collins et al., 1994). This may reflect synergy between species, with facultatively anaerobic or aerobic organisms required to render the local environment more suitable for anaerobic growth by reducing the oxygen-reduction
potential or supplying growth factors (Gorbach & Bartlett, 1974b; Kohn, 1978).
Anaerobic bacteria may impair the host leucocyte response (Hofstad et al., 1993;
Rotstein, 1993). In human pneumonia (Bartlett & Finegold, 1972, 1974; Bartlett,
1993) and equine pleuropneumonia (Bernard-Strother & Mansmann, 1985;
Bailey, 1989; Carlson & O'Brien, 1990; Racklyeft, 1990; Sweeney et al., 1991a)
anaerobic isolates are most commonly associated with disease of greater than 5-7
days duration.
Stages of p l e u r o p n e u m o n i a
Although subjective, staging may aid an understanding of the disease process
and provide an insight into various therapeutic strategies required. Studies on animal models of mixed aerobic-anaerobic infections have demonstrated distinct
stages in the development of illness (Onderdonk et al., 1979; Dunn & Simmons,
1984). Facultative organisms tend to be responsible for initial acute diseases and
greater systemic toxicity. Subsequent anaerobic involvement is characterized by
abscess formation and chronic disease.
238
BRITISH VETERINARYJOURNAL, 151, 3
A possible mechanism for the development of equine pleuropneumonia following oropharyngeal contamination is illustrated in Fig. 1. Studies in this laboratory
using head elevation to impair mucociliary clearance of aspirated organisms have
shown that oropharyngeal contamination results in rapid multiplication of Streptococcus spp. and Pasteurellaceae and the accumulation of inflammatory exudate in
the lower airways (Racklyeft & Love, 1990; Raidal et al., unpublished). Pre-existent
epithelial damage, virulence factors liberated by these bacteria or inflammatory
mediators in the accumulated exudate may allow colonization of pulmonary tissue
and subsequent extension of the disease process into the pleural space.
Acute disease. One hemithorax, usually the right, is often more severely affected than the other (Arthur, 1983; Mansmann, 1983a,b; Racklyeft, 1990). This is
presumably due to the more direct route of the right main stem bronchus
(Sweeney et al., 1984). Pulmonary lesions are usually cranioventral in distribution
(Racklyeft, 1990) and characterized by areas of mottling due to varying degrees of
congestion, hyperaemia, leucocyte infiltration, oedema and atelectasis (Yates,
Subacute stage
(pre-existent)
Epithelial ~
damage
~
Clearance ~
Aspiration of
oropharyngealorganisms
(facultativelyanaerobic
and anaerobic organisms)
Proliferation of oropharyngea] organisms

(airway inflammation)
Acute stage
Invasion of p(flmonary"/"
tissue Pneumofiia,
-. . . . .
/:~~ ,E~.t~nsibn into pleural ":

space'Pleuritis "
damage.to']p ~.az.~nc~ym.a,
endotoxa~ia7 e~:"
(auaer6~eSi~_!eSent
in 10,-w~numbers)... ,
Redox potential
$ Phagocytefunction
Resolution
D
eath
I Mixed F/A and I

anaerobic disease ] Chronicstage
Fig. I. Schematicrepresentation of the development of pleuropneumonia. Contamination of
the lower airways by oropharyngeal organisms, usually due to impaired clearance or increased
aspiration, is associated with preferential muhiplication of Streptococcus spp. and
Pasteurellaceae; if the respiratory epithelium is damaged, bacterial infection extends to the
pulmonary parenchyma and hence to the pleura. Progression of the disease process results in
conditions suitable for the multiplication of anaerobic bacteria.
239
1988). Mucopurulent or fibrinous exudate is usually present in airways. Extension

of the inflammatory process to the visceral pleura produces reddening, roughening and accumulation of yellow-grey fibrinous or fibrinopurulent exudate
(Dungworth, 1988). Accumulation of large volumes of fibrin-rich, haemorrhagic
fluid (often up to 60 1) occurs within the pleural space. Compression atelectasis of
pulmonary tissue is usual to the dorsal extent of the pleural fluid (Racklyeft,
1990). The formation of fibrinous adhesions between the parietal and visceral
pleural is common. Morbidity and mortality are associated with impaired pulmonary function (and resultant hypoxaemia) and systemic toxaemia and, at this stage
of infection, facultatively anaerobic bacteria are most likely responsible for
pathological changes. Resistant species may emerge associated with inadequate
antibiotic dosage or prolonged administration. Parenchymal damage caused by
facultatively anaerobic species present, especially reduced redox potential and
impaired phagocyte function, renders the local environment progressively more
suited to anaerobic organisms.
Chronic disease. Inadequate treatment of acute disease or failure to respond to
therapy may result in the development of a primarily anaerobic disease process.
Post-mortem features of anaerobic pleuropneumonia include pulmonary or subpleural abscessation, extensive pulmonary necrosis and liquefaction, bronchopleural fistulae and the accumulation of foul smelling pus and pleural fluid (Racklyeft,
1990).
In equine (Reimer et aL, 1989; Sweeney et aL, 1991a) and human patients
(Gorbach & Bardett, 1974a) the isolation of anaerobic bacteria has been associated with increased mortality. Anaerobic bacteria possess a number of pathogenic
mechanisms (reviewed by Finegold, 1979) which may account for the increased
mortality, chronicity and poor response to treatment of anaerobic disease. Among
the most important of these are virulence factors such as proteases (e.g.
collagenase), elastase, hyaluronidase, fibrinolysin, heparinase, lecithinase, DNase
and RNase, neuroaminidase, glucuronidase, lysozyme and endotoxin. Short chain
fatty acids generated by anaerobic bacteria have been shown to impair macrophage phagocytic capacity (Eftimiadi et al., 1990) and reduce neutrophil
microbicidal activity (Rotstein, 1993). A capsular polysaccharide present on B.
fragilis and some Gram-negative anaerobes has been shown to be responsible for
abscess formation (Onderdonk et al., 1979). Anaerobic bacteria may further contribute to the disease process by reducing the efficacy of appropriate organisms
are able to produce a l$-lactamase (Finegold, 1979); B. fragilis and Clostridium
perfringens are able to reduce chloramphenicol to inactive derivatives (Onderdonk
et al., 1979).
DIAGNOSIS
Pleuropneumonia may be confirmed by the combination of physical examination,

haematology, transtracheal aspiration a n d thoracocentesis, thoracic radiography
and ultrasonography. The identification of factors predisposing to pleuropneumonia in the patient's history may aid early diagnosis.
240
Observation
Clinical signs of acute disease include lethargy, depression, anorexia, shallow
guarded respiratory movements and hyperpnoea (Semrad & Byars, 1989). Pleural
pain (pleurodynia), when present, is usually most obvious in the initial stages of
disease (Mansmann, 1983a) and may manifest as reluctance to move or lie down,
abducted elbows, grunting while walking or defaecating, intercostal muscle spasm
or flinching, or guarded escape manoeuvres when pressure is applied to the thoracic wall (Semrad & Byars, 1989). These observations may be confused with signs
of colic, laminitis, forelimb lameness or rhabdomyolysis (Mansmann, 1983a). As
the disease progresses, coughing and nasal discharge may become apparent. In
chronic cases ventral or limb oedema and weight loss may be evident (Mansmann,
1983a,b).
Physical examination
The physical examination should begin rostrally. The presence and character of
nasal discharge should be noted. Malodorous breath, especially after coughing, is
an important prognostic factor, as it often accompanies disease due to anaerobic
infections (Sweeney et al., 1985; Reimer et al., 1989). Mild to moderate pyrexia is a
frequent finding (Purdy, 1985; Semrad & Byars, 1989; Spurlock, 1991; Collins et
aL, 1994). Heart and respiratory rates may be increased due to pain or anxiety
(Derksen, 1991a), ventilation-perfusion mismatching and resultant hypoxaemia
and hypercapnia (Beadle, 1991), or vagally-mediated bronchospasm. Dyspnoea is
often evident and associated with the expiratory phase of respiration (Derksen,
1991a).
Thoracic and tracheal auscultation should include use of a rebreathing bag to
detect subtle changes early in the course of disease (Murray, 1989; Hoffman et al.,
1992). Auscuhatory findings vat3, depending on parenchymal involvement and the
volume of fluid present (Spurlock, 1991). Low-pitched wheezes, often associated
with secretions in airways, and coarse crackles are the most commonly described
airway and adventitious sounds in pneumonic conditions (Roudebush, 1982;
Derksen, 1991a). Pleural friction rubs may also be produced by inflamed parietal
and visceral pleural surfaces rubbing together. Pulmonary consolidation or pleural effusion may result in dullness of the ventral thorax and loss of air movement
evident on auscultation (Purdy, 1985; Sweeney et al., 1985) or cardiac sounds may
be auscultated over a wider area of the thorax (Semrad & Byars, 1989). Percussion
may aid the differentiation of consolidation or abscessed areas from effusion
(Roudebush & Sweeney, 1990; Wilson, 1992a), but may elicit a painful response
(Spurlo ck, 1991 ).
Haematology and biochemistry
Venous blood should be collected and submitted for haematological evaluation.
In acute cases, non-specific changes reflecting the degree of accompanying toxaemia or inflammatory disease are to be expected (Semrad & Byars, 1989).
Marked leucocytosis due to greatly increased neutrophil numbers (leukaemoid
response) or neutropaenia with a left shift with or without toxic neutrophils may
be observed in peracute disease (Tyler et al., 1987; Beadle, 1991). Monitoring of
systemic white cell counts is generally not beneficial (Mansmann, 1983b), but the
241
type of response may aid determination of prognosis (Coles, 1986). A mild to

moderate decrease in packed cell volume (PCV) may be present due to the
anaemia of inflammatory disease (Tyler et al., 1987; Morris, 1989; Collins et al.,
1994), although PCV may not fall outside the normal clinical range. In experimental disease in dogs and cats, red blood cell numbers have been shown to
decline within 3-5 days of illness (Feldman et al., 1981; Weiss et al., 1983; Weiss &
McClay, 1988).
Ahnost half of affected horses will have increased total plasma protein (Beech,
1988) due to increased globulins and acute phase reactant proteins. Hypoalbuminaemia and hypoproteinaemia may be associated with protein sequestration in the
pleural cavity (Pearson, 1990), especially as the condition progresses. Biochemical
findings are frequently of little consequence in the diagnosis or management of
pleuropneumonia, but are usually included in the initial database (Semrad &
Byars, 1989). Monitoring of renal function is wise if treatment involves administration of potentially nephrotoxic agents. Blood gas analysis may be useful in formulating a prognosis or in evaluating responses to treatment (Derksen, 1991c).
Bacteriology a n d cytology
Samples for cytological evaluation and bacterial culture are essential for the
establishment of a definitive diagnosis and the isolation of causative organisms.
Serial sampling may be required if an appropriate response to treatment is not
obtained. Appropriate samples must be collected in a manner that bypasses the
tipper airway (Pecora, 1963; Bartlett & Finegold, 1974; Jordan et aL, 1976).
Samples collected via fibreoptic endoscopy and tracheal wash or bronchoalveolar
lavage (BAL) are of limited value (Sweeney et al., 1984; Mair et al., 1987; Mair &
Sweeney, 1990; Racklyeft, 1990; Moore, 1993). Contamination of the inner channel of the endoscope with nasal secretions during passage through the upper airway leads to difficulties in interpretation of culture results (Bartlett et al., 1976;
Whitwell & Greet, 1984). Attempts have been made to obtain uncontaminated
endoscopic samples from the lower respiratory tract by passage of a guarded endoscope (Hoffman et al., 1991), guarded swab (Sweeney et al., 1989b), protected
catheter brush (Grandguillot et al., 1991) or protected aspiration catheter (Darien
et al., 1990; Racklyeft, 1990). Triple lumen protected aspiration catheters
(Racklyeft, 1990) were unable to reliably prevent contamination of samples in
standing horses. BAL samples may fail to demonstrate abnormalities where focal
lesions are present, as is frequently the case in pleuropneumonia because only a
small segment of lung is sampled (Mair & Sweeney, 1990; Rossier et al., 1991).
The preferred techniques for the collection of suitable samples for bacterial culture and cytology are transtracheal aspiration and thoracocentesis (Arthur, 1983;
Sweeney et al., 1985, 1991a). Transtracheal aspiration was introduced to human
medicine by Pecora (1959) to provide uncontaminated lower airway samples and
adapted for use in the horse by Mansmann and Knight (1972). The technique has
been described in the veterinary literature (Beech, 1981; Rose, 1983; Derksen,
1987; Edwards, 1988; Beadle, 1991). Complications of transtracheal aspiration are
few and of limited clinical significance (Ka.linske et al., 1967; Farrow, 1976; Mair et
al., 1987; Racklyeft, 1990).
Where pleural exudate is present, samples should be obtained by bilateral thor-
242
acocentesis (Rose, 1983; Cowell et al., 1987; Derksen, 1987; Schott & Mansmann,
1990; Beadle, 1991) because pleural inflammation may be associated with
occlusion of small mediastinal fenestrations by fibrin and cellular debris, resulting
in the mediastinum becoming functionally complete (Schott & Mansmann, 1990).
Bacterial samples obtained from each hemithorax may differ. Anaerobes are more
commonly isolated from the side which is clinically the more severely affected
(Sweeney et al., 1984; Racklyeft, 1990). Samples should be submitted for aerobic
and anaerobic bacterial culture. Collection and handling of suitable samples has
been described (Sweeney et al., 1985, 1991a; Racklyeft, 1990; Bailey & Love, 1991),
as have anaerobic culture techniques (Berkhoff & Redenberger, 1977; Walker et
al., 1983; Moore, 1993). Capped plastic syringes ~vith excess air expelled are
acceptable for collection and transportation of specimens. The time between collection and culturing should be minimized because facultatively anaerobic bacteria multiply more quickly than obligately anaerobic bacteria (Dow & Jones,
1987). All specimens should be held at room temperature until culture.
Samples obtained should be examined grossly for colour, turbidity and odour
(Schott & Mansmann, 1990). The presence of a putrid odour in the pleural fluid
or transtracheal aspirate fluid is significantly associated with the isolation of anaerobic bacteria from affected horses and offers a poorer prognosis for survival
(Sweeney et al., 1984, 1985, 1991a; Semrad & Byars, 1989; Reimer et al., 1989). A
putrid odour is considered a reliable indicator of anaerobic infection because facultatively anaerobic and aerobic bacteria do not tTpically produce such a characteristic odour of putrefaction (Sweeney et al., 1985) which arises primarily due to
the end products of anaerobic metabolism (Bartlett & Finegold, 1972). However,
the absence of a putrid odour does not exclude the possibility of anaerobic infection (Sweeney et al., 1985). The use of gas liquid chromatography for the rapid
presumptive diagnosis of anaerobic infection has been described (Gorbach el al.,
1976; Hunter et al., 1985; van den Bogaard et al., 1989) and is currently being
evaluated in our laboratory. The accurate identification of anaerobic involvement
is an important determinant of prognosis, choice of antibiotic and likely cost and
duration of treatment.
Cytological evaluation of samples obtained by transtracheal aspiration, endoscopic tracheal wash, BAL or thoracocentesis has been reviewed (Cowell et al.,
1987; Murray, 1989; Schott & Mansmann, 1990; Rossier et al., 1991). Smears of all
samples should be prepared and examined for determination of the individual
morphotypes present and their Gram reactions (Berkhoff, 1978; Sweeney et al.,
1991a).
Diagnostic imaging
Ultrasonography and radiography may provide complementary information

(Mackey, 1983; Rantanen, 1986; Sande, 1986). Pleural diseases and pulmonary
parenchymal diseases affecting the periphery of the lung can be characterized by
diagnostic ultrasonography (Rantanen, 1981, 1986; Rantanen et al., 1981). I'n the
adult horse, ultrasonography is often easier than radiographical evaluation but
will fail to demonstrate deep parenchymal lesions if the overlying lung is normally
aerated (Powis, 1986). Radiography is generally superior in detecting diffuse parenchymal disease and mediastinal or deep parenchymal abscessation, but may fail
243
to demonstrate pulmonary lesions that are obscured by the cardiac silhouette

(Riemer, 1990). An appropriate ultrasound technique has been described
(Rantanen, 1986; Riemer et al., 1989; Riemer, 1990; Byars et aL, 1991).
As demonstrated in Fig. 2, pleural effusion is characterized ultrasonographically
by an anechoic-space between the lung and the thoracic wall (Lamb, 1989), the
lung is displaced axially and dorsally (Rantanen, 1981, 1986; Stowater & Lamb,
1989). The character of fluid visualized may be determined by its sonographic
appearance (Reef et al., 1991); highly cellular material (effusion fluid) is more
echogenic than a transudate which is typically anechoic (Rantanen, 1986; Reimer,
1990). In the acute stages of pleurifis, pleural effusion may be absent or minimal
(Arthur, 1983). The presence of gas echoes in pleural or abscess fluid has been
correlated with the presence of anaerobic infection (Reimer et aL, 1989). Fibrinous adhesions may be apparent as echogenic strands or separations in the pleural fluid between the lung and the body wall (Fig. 2) and the lung surface may
appear thickened and rough if it is covered with fibrinous material. Regions of
consolidated lung have a homogenous, grey echogenicity, of similar sonographic
appearance to liver. Bronchi and blood vessels are often visualized within regions
of consolidated lung (Reimer, 1990).
Serial ultrasound examinations may offer an effective way of monitoring the
efficacy of thoracic drainage and response to treatment (Rantanen, 1981). Ultra-
Fig. 2. Ultrasound image of left hemithorax (5th intercostal space). Pleural effusion is
indicated by substantial widening of the pleural space and the presence of relatively anechoic
fluid. Fibrin tags are readily demonstrable within the pleural space and adherent to the pleural
surface.
244
BRITISH \rETERINARY .JOURNAL, 151, 3
sonographic guided drainage of pleural fluid and/or aspiration of abscess contents has also been r e c o m m e n d e d (Mackey, 1983; Rantanen, 1986; Lamb &
O'Callaghan, 1989; Reimer, 1990).
Thoracic radiography of adult horses is becoming more widely used (Lamb &
O'Callaghan, 1989) due to increased availability of high output radiographical
equipment and the advent of faster (rare-earth) intensifying screens. Techniques
for systematic radiographical evaluation of the adult equine thorax have been
described utilizing four projections (King et al., 1981; Farrow, 1981a,b; Mair &
Gibbs, 1990a) or two projections (Sanderson & O'Callaghan, 1983). A 200 cm
focus-film distance has been recommended to reduce distortion and magnification but requires greatly increased exposure factors (Feeney el al., 1982). Radiographs taken from each side may be required to examine both hemithoraces
adequately. All air-gap between the thorax and cassette is usually unavoidable due
to positioning difficulties and may be useful in reducing the amount of scattered
radiation incident upon the film (King et al., 1981).
Radiographical patterns recognized in small animals (Owens, 1982; Watters,
1986) are described in equine radiographical interpretation (Kkngstr6m, 1968;
Farrow, 1981c; King, 1981; Lamb, 1989; Lamb & O'Callaghan, 1989; Mair &
Gibbs, 1990b). However, the correlation between radiographical signs and underlying puhnonary pathology is less easily demonstrated than in small animals
(Wisher et al., 1993). Many pulmonary diseases confirmed by other means are
associated with normal radiographs (Farrow, 1981a) and abnormal lung sounds
may precede radiographical changes by several days (Mackey, 1983). Radiographical changes tend to be non-specific because various causative factors can
stimulate a similar inflammatory response in the lungs (Lamb & O'Callaghan,
1989). Pleural fluid may be detected as a uniform opacity with an ill-defined dorsal border obscuring the cardiac silhouette, ventral lung field and diaphragm
(Lamb & O'Callaghan, 1989). A fluid line will be evident only if there is free gas
present within the pleural space. Minimally, 1-21 of fluid are required in either
hemithorax for detection in a 450 kg patient (Sande, 1986). Other abnormalities
which may be detected radiographically include abscessation (Fig. 3) and
pneumothorax (I~ngstr6m, 1968; Farrow, 1976, 1981c; Mansmann & BernardStrother, 1985; Mair & Gibbs, 1990b). Pneumothorax is usually associated with
transtracheal aspiration, thoracocentesis, thoracic drainage or pleuroscopy, but
will occasionally be evident in cases of chronic pleuropneumonia where horses
have not been subjected to these interventions, probably due to the presence of
gas-producing organisms or due to bronchopleural fistulae (Mackay, 1983).
Other techniques
Endoscopy. This may allow visualization of tracheal exudates, but is usually of
limited value (Derksen, 1991a; Hoffman et al., 1992).
Pleuroscopy. This may be useful to evaluate the extent of pleural involvement,
and to determine the presence of subpleural or superficial pulmonary abscesses or
bronchopleural fistulae (Spurlock, 1991). It has also been used to evaluate healing, or to determine if further drainage is required (Mansmann, 1983b). The
technique is invasive, however, and should be reserved for the evaluation of horses
245
Fig. 3. Radiographic image of the dorsocaudal lung field. Increased opacity of pulmonary
tissue is evident (arrows) due to abscessation. A diffuse interstitial pattern can be seen in more
peripheral areas as evidenced by the reticular pattern of the more peripheral lung fields.
with chronic pleuritis and extensive areas of organized fibrin in the pleural space
(Beadle, 1991). Various pleuroscopic techniques have been described (Mackey,
1983; Mackey & Wheat, 1985; Mansmann & Bernard-Strother, 1985; Rossier et al.,
1990).
Lung biopsy. This has been described (Raphel & Gunson, 1981), but is an
invasive procedure indicated only when a histological diagnosis or microbial
evaluation is required for management or therapy. It should only be undertaken
after less hazardous techniques have been performed (Derksen, 1991a).
TREATMENT
A favourable response to therapeutic intervention is most often related to early
identification and aggressive treatment. In many circumstances, the duration of
therapy, associated costs and questionable prognosis make the eventual outcome a
decision based on economic rather than medical considerations. Retrospective
studies indicate an overall survival rate of between 42-75% (Raphel & Beech,
1982; Sweeney et aL, 1984, 1991a; Racklyeft, 1990; Collins et al., 1994). Survival is
improved if treatment is initiated early in the clinical course of the disease process
(Mansmann, 1983a; Racklyeft, 1990). Ideally, treatment should be initiated within
48 h of a predisposing event to prevent significant invasion of pulmonary tissue. A
good-to-guarded prognosis may be given to horses which present with clinical
246
signs suggestive of pleuropneumonia after some predisposing factor, such as transportation or racing, and in which progressive pulmonary or pleural inflammation
fails to develop (Arthur, 1983; Mansmann, 1983a). The prognosis deteriorates
with increased duration of illness due to the involvement of anaerobic bacteria
and the development of complicating factors such as pulmonary or subpleural
abscesses, pleural adhesions, pulmonary necrosis and fibrosis, and bronchopleural
fistulae. Other serious complications, such as venous thrombosis, disseminated
intravascular coagulation, laminitis and acute diarrhoea, may develop during the
course of treatment (Bernard-Strother & Mansmann, 1985; Racklyeft, 1990).
Antibiotic treatment
The first line of treatment of pleuropneumonia is appropriate antimicrobial
therapy (Spurlock, 1989). In most circumstances, this is initiated prior to the availability of bacterial culture and sensitivity results. Antibiotic selection should be
guided by cytological evaluation (especially Gram-stained preparations), a knowledge of the most common bacterial isolates and their sensitivity patterns, and the
duration of disease. Dosage guidelines for antibiotics commonly used in the treatment of equine pleuropneumonia are available (Love et aL, 1983; Brumbaugh,
1987, 1990b; Spurlock, 1989, 1991; Beadle, 1991). Combination antibiotic u-eatment has frequently been recommended for the management of pleuropneumonia. Penicillin, combined with an aminoglycoside, usually gentamicin, has been
regarded as an acceptable empirical choice (Sweeney et al., 1991a), due to the frequent isolation of Gram-negative enteric bacteria. However, early in the disease
when Streptococcus spp. and Pasteurellaceae predominate, the logical antibiotic
choice is penicillin. Penicillin-resistant species are uncommonly present in the
normal oropharynx. Mean inhibitory concentrations of PasteureUa isolates to penicillin G have been found to be well below serum levels following recommended
dosages (Bailey, 1989). Streptococcus spp. and the majority of anaerobic isolates,
with the exception of B. fi'agilis and some species identified as B. melaninogenicus,
(Anderson & Sykes, 1973; Weinrich & del Bene, 1976; Hirsh et al., 1985), are
responsive to therapeutically achievable serum concentrations of penicillin G
(Hirsh &Jang, 1987).
The empirical use of aminoglycoside antibiotics should be re-evaluated in the
management of equine pleuropneumonia. Firstly, Enterobacteriaceae are not normal inhabitants of the equine oropharynx and members of this family have no
known virulence factors which would aid colonization of the respiratory tract.
Hence, the role of these organisms in the initiation of pleuropneumonia is questionable. Bailey (1989) found that Enterobacteriaceae were isolated only from
cases of pleuropneumonia which had received prior antibiotic therapy and other
equine studies have not documented the stage of disease at which these organisms
were isolated. Therefore, it has been suggested that Enterobacteriaceae play at
most a minor role in the initiation of lower respiratory tract infection, assuming
numerical significance only following institution of antimicrobial treatment.This
contention is supported by the work of Wood et al. (1993) who found that isolation of ~-haemolytic Streptococcus spp and PasteureUa/ActinobaciUus spp. from
horses with respiratory disease was significantly associated with lower airway
inflammation, whereas Enterobacteriaceae were not. Human swdies have found
EQUINE PLEUROPNEUMON1A
247
an increased likelihood of isolating Gram-negative enteric bacteria from patients

with nosocomial pneumonia (Bartlett et al., 1974; Saito et al., 1984), possibly
reflecting superinfection or a stress-induced change in oropharyngeal microbiota.
The efficacy of aminoglycosides may be reduced by local conditions at the site of
infection; they are most effective in an alkaline environment (Langston & Davis,
1989) while pleural fluid is usually acidic in cases of pleuropneumonia (Schott &
Mansmann, 1990); they are also highly bound by intracellular components present in purulent fluids, especially nucleic acids and possibly acidic proteins
(Aronson & Brownie, 1978). Since the uptake of aminoglycoside agents by bacteria is an oxygen-dependent process, lowered oxygen tension and the presence of
anaerobic bacteria will limit their efficacy. Finally, anaerobic bacteria are
inherently resistant to aminoglycosides. Thus, use of aminoglycoside antibiotics
may inhibit growth of some facultatively anaerobic organisms while selectively permitting multiplication of obligately anaerobic organisms. For these reasons, aminoglycosides are unlikely to be effective once the disease process has become established. They are likely to be of use only very early in the disease process, at which
stage the significance a n d / o r contribution of Gram-negative bacteria resistant to
penicillin has not been established.
Ceftiofur sodium, a broad-spectrum cephalosporin antibiotic, has been evaluated for the treatment of equine pleuropneumonia (Folz et al., 1992; Foreman,
1992). The use of ceftiofur would allow for treatment of a broader spectrum of
Gram-negative facultatively anaerobic species, including most Enterobacteriaceae,
with less selection pressure for anaerobic species. In conditions where the presence of Gram-negative enteric organisms is possible, ceftiofur may be a more
judicious choice than penicillin. Other second and third generation cephaloporins, especially cefotetan and cefoxitin, also have good activity against Gram-negative bacilli and have been useful as single agent treatments of aspiration pneumonia in people (Dow & Papich, 1991). The use of most agents in this class of
antibiotics has been prohibitively expensive for the routine management of
equine pleuropneumonia. Ceftiofur, developed and used in the treatment of bovine and porcine respiratory infections (Gustin el al., 1990), may offer an affordable alternative. However, due to the rapid development of resistance observed in
Gram-negative enteric organisms and the relative lack of information available on
the efficacy of this agent against equine isolates, antibiotic sensitivity testing of
clinical isolates is recommended before its use as a first choice empiric antibiotic
for equ!ne pleuropneumonia can be justified.
Routine testing of clinical anaerobic isolates is not usually attempted since most
of the clinically relevant anaerobes have predictable susceptibilities to antimicrobial agents (Hirsh et al., 1985; Indiveri & Hirsh, 1986; Hirsh & Jang, 1987;
Racklyeft, 1990). Most anaerobic bacteria resident in the oropharynx are highly
sensitive to penicillin. However, penicillin-resistant anaerobic species formerly
identified as B. melaninogenicus (now Porphryomonas and PrevoteUa spp.) are among
the resident microbiota of the equine oropharynx and are frequently isolated
from cases of equine (Sweeney et al., 1985; Jang & Hirsh, 1991) and human
(Bartlett et al., 1974; Gorbach & Bartlett, 1974a; Saito et al., 1984; Bartlett, 1993;
Marina et al., 1993) anaerobic pleuropneumonia. Early in the disease process,
anaerobic species are of little significance and do not warrant specific therapeutic
248
intmwention. If the disease progresses, resulting in conditions suitable for extensive multiplication of anaerobes, strategies must address these penicillin-resistant
organisms. Protracted disease may also result in the emergence of other penicillinresistant species, including B. fi'agilis which, like Enterobacteriaceae, are not oropharyngeal residents.
Metronidazole is highly effective against penicillin-resistant anaerobic species
(Bartlett, 1993; Marina et al., 1993) and has been recommended for use in equine
patients (Sweeney et al., 1986, 1991c; Mair & Yeo, 1987, Specht et al., 1992). The
addition of metronidazole to the treatment regimen has been responsible for
clinical improvement in horses with conditions refractory to penicillin and aminoglycoside treatment (Sweeney et al., 1991a). Anaerobic reduction to a biologically
active compound may enhance the spectruln of activity of this drug in mixed aerobic-anaerobic infections to include some facultatively anaerobic species
(Onderdonk et aL, 1979). However, metraonidazole should be used in combination with a drug, such as penicillin, effective against facultatively anaerobic
organisms that may be present.
Most anaerobic bacteria, including B. fi'ag~lis, are susceptible to cefoxitin and
cefotetan (second and third generation cephalosporins, respectively) but have
variable susceptibility to other cephalosporins (Mandell & Sande, 1985). The efficacy of ceftiofur against [3-1actamase producing anaerobes has not been assessed.
Extended spectrum penicillins, such as ticarcillin, piperacillin and carbenicillin,
have been evaluated for the management of human anaerobic infections
(Heseltine et al., 1984) and equine respiratory disease (Spurlock, 1989), but are
expensive and offer little or no advantage over penicillin and metronidazole. Clindamycin is frequently used in the management of human mixed aerobic and
anaerobic puhnona D, infections (Bartlett et al., 1972; Haldane & van Rooyen,
1972; Gorbach & Thadepalli, 1974) but cannot be used in horses (Moore, 1993).
Chloramphenicol is active against a wide range of anaerobic bacteria (Gorbach &
Bartlett, 1974b) and has been recommended for the management of equine
anaerobic infection (Moore, 1993) although it is not registered for use in horses
in Australia or the European Union. Obligately anaerobic organisms are reportedly susceptible to trimethoprim-sulphamethoxazole combinations (Indiveri &
Hirsh, 1986), although clinical response has been disappointing (Sweeney et aL,
1991a). This may be due to the presence of tissue breakdown products, such as
thymidine, in purulent exudates that may inhibit the effect of trimethopriln or sulphonamide (Indiveri & Hirsh, 1986) or reduced susceptibility of bacterial pathogens to this combination (Baggot, 1989).
Drainage, lavage a n d surgical intervention
The removal of excessive pleural fluid is mandatory. Accumulation of fluid and
fibrin within the pleural space may allow the development of plaques on the surfaces of the lung and thoracic wall which protect bacteria from antimicrobial
agents, and form loculations of fluid that inhibit proper drainage and resutt in
adhesions of the lung to the pleural wall (Mackey, 1983; Lamb & O'Callaghan,
1989; Beadle, 1991). Methods of removal of excessive fluid have been described
(Schott & Mansmann, 1990; Beadle, 1991; Spurlock, 1991). Intermittent chest
drainage performed at 2-3 day intervals is adequate if fluid accmnulation is slow
249
(Spurlock, 1991) but indwelling chest tubes may be required if rapid accumulation of large volumes of fluid occurs (Arthur, 1983). Lavage through indwelling
tubes may be attempted in associated with thoracic drainage (Arthur, 1983;
Schott & Mansmann, 1990). Antibiotics (Schott & Mansmann, 1990) and
fibrinolytic enzymes (Burbidge, 1982) have been added to lavage fluid, although
their value is uncertain.
Aggressive surgery (drainage and debridement) to improve tissue oxygenation
and circulation, thereby creating a less favourable environment for anaerobes, is
usually the primary treatanent strategy for anaerobic infections (Dow & Jones,
1987). This is often difficult to implement in equine patients although Byars et al.
(1991) have described drainage of cranial mediastinal abscesses and standing
thoracotomy has been described as a salvage procedure (Bernard-Strother &
Mansmann, 1985; Carter et al., 1986). Partial lung resection has also been utilized
in the management of recurrent equine pleuropneumonia (Boulton et al., 1986).
Anti-inflammatory medication
Non-steroidal anti-inflammatory agents (NSAIDs) or opioids may be used for
analgesia (Purdy, 1985) and are useful in stimulating the animal to move about,
maintaining appetite and decreasing the inflammatory response. If signs of endotoxaemia are evident, flunixin meglumine is the preferred drug (BernardStrother & Mansmann, 1985). Minimal NSAID administration reduces the risk of
renal or gastrointestinal damage and enables monitoring of body temperature as a
guide to the therapeutic efficacy of selected antibiotics.
In toxaemi~: horses, aspirin (Cambridge et al., 1991) or heparin (Arthur, 1983;
Beadle, 1991) may reduce the incidence of thrombus formation, decrease fibrin
formation in the pleural space and protect from laminitis. Dimethylsulphoxide
(DMSO) is reported to reduce fibrous adhesions associated with infections and
inhibit platelet aggregation (Alsup, 1984) and may have an inhibitory effect on
bacterial growth (Blythe et al., 1986). Although not registered for systemic administration, DMSO has been used ill the management of equine pleuropneumonia
(Purdy, 1985; Blythe et al., 1986; Brayton, 1986; Sojka et al., 1990) but controlled
trials demonsta'ating the benefit of this drug have not been reported.
Inhalation therapy
Nebulization is commonly used in human medicine in the management of pulmgnary " disease (Rossing, 1983). Such therapy has been described in small numbers of cases of equine pleuropneumonia (Purdy, 1985) but its usefulness may be
limited in the horse due to plugging of airways with mucus or exudate and patient
non-compliance (Derksen, 1991b). The benefits attributed to inhalation treatment in horses may be effected via systemic drug absorption.
Bronchodilators
Bronchodilators are used in management of human pleuropneumonia
(Rossing, 1983), although it has been suggested that infectious conditions such as
pneumonia may not respond well to bronchodilator treatment because these
drugs do not reverse the pathophysiology of the disease process. Bronchoconstriction may occur due to activation of pulmonary receptors by oedema, cellular infil-
250
tration of submucosal tissues, intraluminal debris and sputum or extraluminal

compression (Brumbaugh, 1990a; Derksen, 1991c). Agents commonly used
include ]3~.agonists, anticholinergics and phosphodiesterase inhibitors; ~2 agonists, adrenaline isoproterenol, clenbuterol, metaproterenol, albuterol and terbutaline, cause bronchodilation by interaction with receptors on bronchiolar smooth
muscles (Brumbaugh, 1990a). Isoproterenol use has been advocated in cases of
acute airway obstruction (Derksen, 1991b) and [32 agonists may also be effective in
augmenting clearance of tenacious pulmonary secretions (Melville et al., 1976;
Boothe, 1988). Improved mucociliary clearance has been demonstrated following
clenbuterol adminisu-ation (Turgut & Sasse, 1989), although the efficacy of this
drug as a bronchodilator in horses has been questioned (Derksen, 1991b).
Atropine or the newer synthetic parasympathomimetics, such as glycopyrrolate
and ipratropium, have been r e c o m m e n d e d for the management of inflammatory
lung disease (Derken, 1991b), but they are infrequently used in the management
of pleuropneumonia. Anticholinergic agents block parasympathetic-induced
bronchoconstriction, produce decongestion and reduce bronchiolar secretions
(Ziment, 1978; Rau, 1984). Atropine reduces mucociliary clearance in man
(Yeates et al., 1975) and its prolonged administration to horses is not reco m m e n d e d because of side-effects such as tenacious bronchiolar secretions, tachycardia, ileus and neurological derangements (Brumbaugh, 1990a). Insufficient
clinical data on glycopyrrolate or ipratropium usage in the horse precludes
specific recommendations.
Phosphodiesterase inhibitors, such as caffeine, theobromine and theophylline,
have been used in equine medicine (Brumbaugh, 1991a), although therapeutic
doses approach toxic levels. Theophylline treatment of inflammatory airway disease has shown benefits related to reduced bronchoconstriction, improved pulmonary dynamic compliance and easier breathing (Beech, 1989; McKiernan et al.,
1990).
Mucolytics
Mucokinetic therapy is indicated when the horse has inefficient removal of
secretions from pulmonary airways. The efficacy of mucociliary clearance depends
on mucociliary activity and on the rheological properties of the mucus in which
the ciliary action takes place (Turgut & Sasse, 1989). Hence, mucolytics may have
a beneficial role in reducing the tenacity of pulmonary secretions and thus aid
expectoration. The use of iodide, citrate or chloride salts, guafenesin and acetyleysteine have been suggested, but not evaluated (Brumbaugh, 1990a). Dembrexine has been shown to mobilize sputum from the lower airways (Sasse, 1981) and
to expedite the resolution of nasal discharge and coughing in horses with acute
upper respiratory tract viral infection and post-viral small airway disease (Matthews
et al., 1988). The pharmacokinetics of this drug in the horse, and the possible beneficial effects in the management of bacterial pneumonia, have not been documented. Similarly, bromhexine has been shown to have a beneficial effect on
mucus characteristics in horses with chronic obstructive pulmonary disease (Sasse,
1981); pharmacokinetics of this drug have been investigated (de Backer et al.,
1980) but its value in the management of equine pleuropneumonia has not been
evaluated.
251
Topical administration of water by aerosolation, direct instillation or inhalation

of vapour has been suggested as an effective means of adding water to tenacious
sputum and hence aiding its clearance (Brumbaugh, 1990a). In dogs (Parks et aL,
1971) and horses (Sweeney et aL, 1989a) normal saline and water aerosols have
been shown to be largely ineffective. Systemic fluid administration may be more
beneficial (Derksen, 1991b; Dixon, 1992).
General
Good supportive care of horses with pleuropneumonia is important. Fluid therapy should be considered in toxaemic or dehydrated horses and may be required
following pleural drainage. Plasma transfusion or colloid administration should be
considered jf the horse becomes hypoproteinaemic. B vitamins and anabolic steroids may be of value in the stimulating anorectic horses (Bernard-Strother &
Mansmann, 1985). Postural drainage to help clear airway secretions should also be
encouraged by feeding from ground level to ensure lowering of the head. Modest
exercise (i.e. hand walking) may encourage airway drainage by stimulating greater
depth of respiration, thereby dilating airways (Derksen, 1991b), but should be
avoided in severely ill, toxaemic or dyspnoeic horses.
CONCLUSIONS
Pleuropneumonia usually follows a predisposing event which increases oropharyngeal contamination of the lower respiratory tract or inhibits pulmonary
defence mechanisms. Recognition of such an insult and treatment within 48 h of
contamination is frequently associated with rapid resolution of the disease process. If disease progresses, accurate evaluation and staging is an important determinant of the nature and likely outcome of treatment. A diagnosis of pleuropneumonia can usually be made following consideration of the patient's history and
clinical evaluation. Confirmation involves various imaging methods (radiography,
ultrasonography) and collection of appropriate samples from the lower respiratory tract and pleural spaces. As the oropharynx is the likely source of organisms,
samples must be obtained without contamination from the upper airways
(transtracheal aspiration a n d / o r thoracocentesis). Collection, transport and processing methods must facilitate isolation of obligately anaerobic bacteria.
Treatment is often expensive and prolonged. The decision to proceed with
tfierapy must be based on the clinical stage of disease and the individual's future
use. Treatment should be directed at oropharyngeal organisms, especially [3-haemolytic Streptococcus spp. and Pasteurellaceae. Penicillin is highly effective against
these organisms and is also effective against most anaerobic organisms present as
contaminants from the oropharynx. Current understanding of the disease process
would suggest that the early presence of penicillin-resistant species, such as
Enterobacteriaceae and B. fragilis, should be considered unlikely unless the
patient has a history of prior antibiotic therapy or recent hospitalization. Treatment of Enterobacteriaceae should be undertaken on the basis of laboratory culture and sensitivity tests, bearing in mind that aminoglycoside agents are unlikely
to achieve therapeutic levels within affected tissue and are completely ineffective
252
against anaerobes. Metronidazole is very effective against penicillin-resistant anaerobes, and may be r e q u i r e d in the m a n a g e m e n t o f a n a e r o b i c disease.
Thoracic drainage is r e q u i r e d if significant pleural effusion is present. More
radical procedures, such as abscess drainage or t h o r a c o t o m y should be c o n s i d e r e d
if anaerobic bacteria and a chronic disease process are present. Flunixin meglumine is usually r e q u i r e d for the m a n a g e m e n t o f systemic toxaemia. Aspirin or heparin may be useful to r e d u c e fibrin formation in the pleural space and to r e d u c e
t h r o m b u s formation. Bronchodilatory or mucolytic agents may be o f value,
although c o n t r o l l e d studies on the efficacy o f these agents in the m a n a g e m e n t o f
e q u i n e p l e u r o p n e u m o n i a are lacking.
T h e prognosis for c o m p l e t e recovery is g o o d if early recognition is
a c c o m p a n i e d by p r o m p t , aggressive therapy. Delayed diagnosis, i n a p p r o p r i a t e
t r e a t m e n t or a p o o r response to U'eatment is frequently associated with a protracted disease course, untoward sequelae and a p o o r prognosis for future athletic
endeavour.
ACKNOWLEDGEMENTS
T h e help o f Dr J. D. Wright (University o f Q u e e n s l a n d ) , Professor R e u b e n Rose
and Associate Professor Daria Love (University o f Sydney) in the p r e p a r a t i o n and
review o f this manuscript are gratefully acknowledged.
REFERENCES
ADAIR, B. M., BRADFORD,H. E. L., MACrUE,D. P. & McNuLT',', M. S. (1992). Effect of macrophages and in vitro infection with parainfluenzatype 3 and respiratory syncytial viruses on
the mitogenic response of bovine lymphocytes. American Journal of Veterinary Research 53,
255-9.
ALSUP,E. M. (1984). Dimethyl sulfoxide. Journal of the AmeT~can Vetelinary Medical Association
185, 1011-14.
ANDERSON, D.J. & SYKES,R. B. (1973). Characterisation of a I~-lactamase obtained from a
strain of Bacteroidesfragilis resistant to 13-1actam antibiotics. Journal of Medical Microbiology
6, 201-6.
ANDERSON,V., D E B o ~ , R. M., N~xov, IC A. & DAVrON,A. D. (1985). Mononuclear phagocytes of transport-stressed horses with viral respiratory tract infection. American Journal of
Veterinary Research 46, 2272-7.
ARoysoy, A. L. & BROWNIE, C. (1978). Clinical pharmacology of antibacterial drugs in
horses. Proceedings of the 2nd Equine Phmvnacology Symposium, eds J. D. Powers & T. E.
Powers, pp. 115-25.
ARTHUR,R. M. (1983). Subacute and acute pleuritis. Proceedings of the American Association of
Equine Practitioners, 29, 65-9.
BACGOT,J. D. (1989). Antimicrobial drug selection and dosage. II: Pharmacological considerations. Proceedings of the Bain-FaUon Lectures 11, 82-90.
B~Jczv, G. D. (1989). Studies on oral-associated bacterial infections in horses. PhD Thesis,
University of Sydney.
BAILEY,G. D. & LOVE,D. N. (1986). Eubacteriumfossor sp.. n~ov., an agar-corroding organism
from normal pharynx and oral and respiratory tract/lesions of horses. International Jourhal of Systematic Bacteriology 36, 383--7.
BARLEY,G. D. & LovE, D. N. (1991). Oral-associated bacterial infection in horses: studies on
253
the normal anaerobic flora from the pharyngeal tonsillar surface and its association with
lower respiratory tract and paraoral infections. Veterinary Microbiology 26, 367-79.
BArnEY, G. D., MOORE, L. V. H., LOVE, D. N. &JOHNSON,J. L. (1988). Bacteroides heparinolyticus:
deoxyribonucleic acid relatedness of strains from the oral cavity and oral-associated disease conditions of horses, cats and humans. International Journal of Systematic Bacteriology
38, 42--4.
BALDWIN,D. E., MARSHALL,R. G. & WESSMAN,G. E. (1967). Experimental infection of calves
with myxovirns parainfluenza-3 and Pasteurella haemolytica. American Journal of Veterinary
Research 28, 1773-82.
BARTLETT,J. G. (1993). Anaerobic bacterial infections of the lung and pleural space. Clinical
Infectious Diseases 16 (Suppl. 4), $248-55.
BARTLETT,J. G. & FINEC.OLt),S. M. (1972). Anaerobic pleuropulmonary infections. Medicine
51,413-50.
BARTt.ETT J. G. 8c FINEC.OLD,S. M. (1974). Anaerobic infections of the lung and pleural
space. Ame~ican Review of Respiratory Disease 110, 56-77.
BARTI.ETT J. G., GORBACH,S. L. gc FINEC;Ot.D,S. M. (1974). The bacteriology of aspiration
pneumonia. The American Journal of Medicine 56, 202-7.
BARTLE'Iq"J. G., SLITTER,V. L. ~ FINEGOLD,S. M. (1972). Treatment of anaerobic infections
with lincomycin and clindamycin. The New England Journal of Medicine 287, 1006-10.
BARTLETI',J.G., ALEXANDER,J., MA~IEW,J., SULLIVAN-SIGLER,N. & GORBACH,S. L. (1976). Should
fiberoptic bronchoscopy aspirates be cultured? American Review of Respiratory Disease 114,
73-8.
BAYLY,W. M. (1989). Pulmonary mucosal defences and the development of infectious respiratory disease. Australian Equine Veterinarian 7, 24-30.
BAVLV,W. M., LIGC.tT,H. D., HUSTON,L.J. & LAEC,REID,W. W. (1986). Stress and its effect on
equine pulmonary mucosal defences. Proceedings of the American Association of Equine Practitioners 32, 253-62.
BEADLE,R. E. (1991). Diseases of the pleura, mediastinum, diaphragm and thoracic wall. In
Equine Medfdne and Surgery 4th Edn, eds P. T. Colahan, I. G. Mayhew, A. M. Merritt &
J. N. Moore, pp. 456-62; Goleta, California: American Veterinary Publications.
BEECH,J. (1981). Technique of tracheobronchial aspiration in the horse. Equine Veterinary
Journal 13, 136-7.
BEECH,J. (1988). Pleuritis. Proceedings of the Bain-Fallon Lectures, 10, 15-21.
BEECH, J. (1989). Drug therapy of respiratory disorders. Veterinary Clinics of North
America--Equine Practice 5, 59-80.
BERKHOVV,G. A. (1978). Recovery and identification of anaerobes in veterinary medicine: a
2 year experience. Veterinary Microbiology 2, 237-52.
BEP,mJOVE, G. A. & REDENBERCER,G. L. (1977). Isolation and identification of anaerobes in
the veterinary diagnostic laboratory. American Journal of Veterinary Research 38, 1069-74.
BERNARD-STROTHER,B. & MANSMANN,R. A. (1985). Diagnosis and treatment of anaerobic bacterial pleuropneumonia in six horses. Compendium of Continuing Educationfar the Practicing Veterinarian 7, $341-9.
BLVrHE,L. L., CP,AIG,A. M., AePELL,L. H. & LASSEN,E. D. (1986). Intravenous use of dimethyl
sulfoxide (DMSO) in horses: Clinical and physiologic effects. Proceedings of the American
Association of Equine Practioners 32, 441-6.
BOOTHE, D. M. (1988). The effect of clenbuterol on tracheal mucociliary transport rate in
healthy horses. Research Abstracts. Proceedings of the 6th Annual Veterinary Medical Forum,
American College of Veterinary Internal Medicine. p. 764.
BOULTON, C. H., MODRANSKY,P. D., GRANT,B. D., LEATHERS,C. W., GALLAGHER,L. V. & BAYLY,
W. M. (1986). Partial equine lung resection using a stapling instrument. Veterinary Surgery
15, 93-8.
Be.AVrON,C. F. (1986). Dimethyl sulfoxide (DMSO): A review. Cornell Veterinarian 76, 61-90.
BmGc,s, R. E. & FRANK,G. H. (1992). Increased elastase activity in nasal mucus associated
with nasal colonisation by Pasteurella haemolytica in infectious bovine rhinotracheitis virusinfected calves. American Journal of Veterinary Research 53, 631-5.
BRUMRAUGH,G. W. (1987). Rational selection of antimicrobial drugs for treatment of infections of horses. Veterinary Clinics of North America--Equine Practice 3, 191-220.
254
BRUMBAUGH,G. W. (1990a). Respiratory therapy: clinical applications of bronchodilatory

and expectorant medications in horses. American Association of Equine Practitioners 36,
133--9.
BRt:MBAUGH,G. W. (1990b). Antimicrobial therapy for the emergency equine patient. American Association of Equine Practitioners 36, 247-54.
BUDGETT,R. (1990). Overtraining syndrome. B~itishJournal of Sports Medicine 24, 231-6.
BURBIDGE,H. M. (1982). Peneu'ating thoracic wound in a Hackney mare. Equine Veterina~
Journal 14, 94-5.
BUR~LL, M. H. (1985). Endoscopic and virological observations on respiratory disease in a
group of young Thoroughbred horses in training. Equine l:eteT4natyJou~a117, 99-103.
BURTON,J. D. K. (1962). Effects of dry anaesthetic gases on the respiratory mucous membrane. Lancet i, 235-8.
B~u~s, T. D. & BECHT, J. L. (1991). Pleuropnenmonia. Veterinary Clinics of North
B~RS, T. D., D~aNlS, C. M., SELTZEg,K. L. & 1L~TANEN,N. W. (1991). Cranial thoracic masses
in the horse: a sequel to pleuropneumonia. Equine Vete~7;na~yJourna123, 22-4.
CAMBRIOGE,H., LEES, P., HOOKE, R. E. & RUSSEt.L, C. S. (1991). Antithrombotic actions of
aspirin in the horse. Equine VetelTnao,Journa123, 123-7.
CAMNER, P., JARSTI~\'D, C. 8c PIJILII'SON,K. (1973). Tracheobronchial clearance in patients
x~fith influenza. American Reviezo of Respiratory Diseases 108, 131-5.
CARLSON, G. P. & O'BRIEN, M. A. (1990). Anaerobic bacterial pneumolaia with septicaemia
in two racehorses.Jou~vml of the Ame14can Vete~qnaO, Medical Association 196, 941-3.
CARTER,G. K., WARD,D. S. & TA~ZOR,T. S. (1986). Thoracotomy in the treatment of chronic
eqtfine pleuropneumonia. Veterinary Surgery 15, 115-16.
CARUSO,J. P. & Ross, R. F. (1990). Effects of Mycoplasma hyopneumoniae and ActinobaciUus
(Haemophihts) pleuropneumoniae infections on alveolar macrophage functions in swine.
American Journal of Vete~4naO, Research 51,227-31.
CHAVVIN,M. K. & CARTER,G. K. (1993). Equine bacterial pleuropneumonia. Part I. Epidemiology, pathophysiology and bacterial isolates. The Compendium of Continuing Education for
the Practicing Vetelinm~an 15, 1642-50.
CHALON,J., LOEW,D. A. Y. & M_~LE~Z~NCHE,J. (1972). Effects of dry anaesthetic gases on tracheobronchial ciliated epithelium. Anesthesiology 37, 338--43.
CHEr~OW, B., At.E~'DER, R., SM,~LmDGE,R. C. et al. (1987). Hormonal responses to graded
surgical stress. Archives ofbT.ternal Medicine 147, 1273-8.
CHURCH, D. B., EX'ANS,D. L., LEwls, D. R. & ROSE, R.J. (1986). The effect of exercise on
plasma adrenocorticotrophin, cortisol and insulin in the horse and adaptations with
la-aining. Second International Conference on Equine Exercise Physiology, pp. 506-15.
C L ~ , A. F. (1987). A review of environmental and host factors in relation to equine respiratory disease. Equine VeterinaryJournal 19, 435--41.
COGGINS,L. (1975). Viral respiratory infections of horses: some specific viruses affecting the
horse.Journal of the American Vetelina~), Medical Association 166, 80-3.
CoLas, E. H. (1986). Interpretation of leucocyte alterations. In Veterinary Clinical Pathology
4th Edn, p. 70. Philadelphia: W, B. Saunders Company.
COLLINS,M. B., HODGSO~,D. R. & HuTc:mYS,D. R. (1994). Pleuropneumonia in adult horses:
a review of 43 cases in Ausu'alia. Journal of the American Veterinary Medical Association (in
press).
COWbeLL,R. L., T~tER, R. D., CLt~KE~B~D, K. S. & MACALUSTE~,C. G. (1987). Collection and
evaluation of equine peritoneal and pleural effusions. Veterinary Clinics of North
A meffca--Equine Practice 3, 543-61.
DA~E~, B.J., BRO~, C. M., WAL~, R. D., W~LHAMS,M. A. & DEm~SEN,F.J. (1990). A tracheoscopic technique for obtaining uncontaminated lower airway secretions for bacterial.culture in the horse. Equine Vete~na~yJou~'nfl,l 2'~, 170-3.
DE BACKER, P., VANDE~TEEL-THIENPON~/L.M. R., JONCKI-IEERE,J. A. A., BELeAmE, F. M.,
DEKACKERE,M. 8 DE LEENHEER,A./P. (1980). Bioavailability of bromhexine in the horse.
Zentralblattfiter Vete~nacrmedizin, Reihe A27: 740-5.
DENNY,F. W. (1974). Effect of a toxin produced by Haemophilus influenzae on ciliated respiratory epithelium. 7~heJournal of Infectious Diseases 129, 93-100.
255
DERKSEN,F.J. (1987). Evaluation of the respiratory system: diagnostic techniques. In Current

Therapy in Equine Medicine, 2nd Edn, ed. N. E. Robinson, p. 580. Philadelphia: Lea &
Febiger.
DERKSEN, F.J. (1991a). Examination of the respiratory system. In Equine Medicine and Surgery, 4th Edn, eds P. T. Colahan, I. G. Mayhew, A. M. Merritt &J. N. Moore, pp. 353-61.
Goleta, California: American Veterinary Publications.
DERKSEN,F.j. (1991b). Medical respiratory therapy. In Equine Medicine and Surgery, 4th Edn,
eds P. T. Colanan, I. G. Mayhew, A. M. Merritt & J. N. Moore, pp. 374-7. Goleta, California: American Veterinary Publications.
DERKSEN,F.J. (1991c). Aspiration pneumonia. In Equine Medicine and Surgery, 4th Edn, eds
P. T. Colanan, I. G. Mayhew, A. M. Merritt &J. N. Moore, pp. 431-2. Goleta, California:
American Veterinary Publications.
DIXON, P. M. (1992). Respiratory mucociliary clearance in the horse in health and disease,
and its pharmaceutical modification. Veterinary Record 131,229-35.
DoM, P., HAESEBROUCK,F. & D~; BAETSELIER,P. (1992). Stimulation and suppression of the
oxygenation activity of porcine ptdmonary alveolar macrophages by Actinobacillus p~tropneumonia and its metabolites. American Journal of Veterinary Research 53, 1113-18.
Dow, S. W. &JONES, R. L. (1987). Anaerobic infections. Part II. Diagnosis and treatment.
Compendium of Continuing Education for the Practicing Veterinarian 9, 827-39.
Dow, S. W. & PAPICH, M. G. (1991). Keeping current on developments in antimicrobial
therapy. Veterinary Medicine 86, 600-9.
DUNGWORTH,J. L. (1993). Lungs. In Pathology of Domestic Animals, 4th Edn, eds K. V. F. Jun,
P. C. Kennedy & N. Palmer, pp. 591-7. New York: Academic Press.
DUNN, D. L. & SIMMONS,R. L. (1984). The role of anaerobic bacteria in intraabdominal
infections. Reviews of Infectious Diseases 6 (Suppl. 1), $139--46.
EDWARDS,D.J. (1988). Transu-acheal aspiration--a technique using reusable materials. Australian Equine Veterinary Association Newsletter 6, 34-5.
EvnMl,U31, C., TONErn, M., CAVALLERO,A., SACCO,O. & Rossl, G. A. (1990). Short-chain fatty
acids produced by anaerobic bacteria inhibit phagocytosis by human lung phagocytes.
The Journal of Infectious Diseases 161,138-42.
FARROW, C. S. (1976). Pneumomediastinum in the horse: A complication of transtracheal
aspiration. Journal of the American Vetel~nary Radiology Society 17, 192-5.
FARROW,C. S. (1981a). Equine thoracic radiology. Journal of the American Veterinary Medical
Association 179, 776-81.
FARROW,C. S. (1981b). Radiography of the equine thorax: anatomy and technique. Veterinary Radiology 22, 62-8.
FARROW,C. S. (1981c). Radiographic aspects of inflammatory lung disease in the horse. Vete~nary Radiology 22, 107-14.
FEENEV,D. A., GORDON,B.J.,JOHNSTON, G. R., McCt.ANAI-IAN,S. L. &JESSEN, C. R. (1982). A 200
centimetre focal spot-film distance (FFD) teclmique for equine thoracic radiography.
Veterinary Radiology 23, 13-19.
FELD~'4, B. F., KANEKO,J.J. & FaRVER,T. B. (1981). Anaemia of inflammatory disease in the
dog: clinical characterization. American Journal of Vetednary Research 42, 1109-15.
FrYEGOL~, S. M. (1979). Taxonomy, enzymes and clinical relevance of anaerobic bacteria.
Reviews of lnfectious Disease 1,248-52.
FOLZ, S. D., HANSON,B.J., GRIVrIN,A. K. el al. (1992). Treatment of respiratory infections in
horses with ceftiofur sodium. Equine VeterinaryJournal 24, 300--4.
FORE~V~,J. H. (1992). Practical aspects of the use of ceftiofur sodium in the treatment of
equine respiratory infections. Proceedings of the American Association of Equine Practitioners
38, 307-10.
FRANK,G. H., BRIeeS, R. E. & GIw:rrE, IL G. (1986). Colonisation of the nasal passages of
calves with PasteureUa haemolytica serotype 1 and regeneration of colonisation after experimentally induced viral infection of the respiratory tract. American Journal of Veterinary
Research 47, 1704-7.
FRANK,G. H., NELSON,S. L. & BRICtS, R. E. (1989). Infection of the middle nasal meatus of
calves with Pasteurella haemolytica serotype 1. American Journal of Veterinary Research 50,
1297-301.
256
FREESTONt~,J. F., WOt.FSHEI,~t~R,K.J., KAMEm.fNG,S. G., Ctlt'RCH, G., Hh,~ma, J. & BAC.WEH, C.
(1991). Exercise induced laormonal and metabolic changes ill T h o r o u g h b r e d horses:
effects of conditioning and acepromazine. Equine Velerinao,Journa123, 219-23.
GOR~ACH,S. L. & B..xRvI.Eaq',J. G. (1974a). Anaerobic infections--Part II. New England Journal
of Medidne 290, 1237-45.

GORa:XCH,S. L. & B,-~RTI.EI-r,J. G. (1974b). Anaerobic infections--Part III. NeTvEngland Jour-
hal of Medidne 290, 1289-94.

GORBACH,S. L. & THADH'At.t.t, H. (1974). Clindamycin in pure and ,nixed anaerobic infections. Archives of lnternal Medicine 134, 87-92.
Go~:XCH, S. L., MA~-tEW,J. W., BAR'rt.Ea-r,J. G., TllADEVAt.t.I, H. & ONDEROONK,A. B. (1976).
Rapid diagnosis of anaerobic infections by direct GLC of clinical specimeqs..]ournal of
Clinical Investigation 57, 478-84.
GP~XNDGVU.t.OT,L., FAmI~ROTHER,J. M. & VRtNS, A. (1991). Use of a protected catheter brush
for culture of the lower respiratol 3, tract in horses witla small ailavay disease. Canadian
Jou~7lal of Veterinary Research 55, 50-5.
GvsrJN, P., L~NDSER,F.J., Lo~mA, F. & LEKt.:VX,P. (1990). Assessment of respiratol T disease
and therapeutic intervention by the forced oscillation technique in feedlot cattle.
Research in Vete~4na~3,Sdence 49, 319-22.
HAI.DANI:.,E. V. & VAN ROO'~EN,C. E. (1972). Treatment of severe Bactemides infection with
parenteral clindamycin. Canadian Medical AssociationJournal 107, 1177-81.
HAxIDv, A. H., Tr~-\PP, A. L., GALE, C. & I'b,~c., N. B. (1963). Experimental transmission of
shipping fever in calves. AmericanJournal of VeterinaO, Research 24, 287-94.
HARVO~D, C. G. & HA~-\, M. (1950). Pulmonal T oede,na in influenzal pneumonia of the
mouse and the relation of fluid in the htng to the inception of pneumococcal pneumonia. Journal o]Expel4mental Medicine 91,245-58.
HAaFORO, C. G., LHI)I.I:.R,V. & HAI~..\,M. (1949). Effect of the lesion due to influeqza virus oq
resistance of mice to inhaled pneumococci..]om77al of Experimental Medidne 98, 53-68.
HESELrlsF, P. N. R., API'I.I-M.-~,N,M. D. & LI-EDoXI,J.M. (1984). EpidemiologT and susceptibility
of resistant Bacteroidesfiagilis group organisms to new I]-lactam antibiotics. Revimvs of
Infectious Disec~ws6, (Suppl. 1 ), $254-9.
HIRsC:ll, D. C., INDIVt-RI,M. C.,JAN(;, S. S. & BII',I.ZRSTEIN,E. L. (1985). Changes in prevalence
and susceptibility of obligate anaerobes in clinical vete,'ina~T practice. Journal of the
AmetTcan Veterina~),Medical Association 186, 1086--9.
H~Rs~I, D. C. &.].-~.',~., S. S. (1987). Antimicrobial susceptibility of bacterial pathogens ti'om
horses. Vete~4naO, Clinics of North A me~4ca--Equine Practice3, 181-90.
How:xtAx, A. M., VH~I.,L., Mt'c~.z, C. A. & Tt-s..\Rows~, D. B. (1991). Evaluation of a guarded
bronchoscopic method fo,- microbial sampling of the lower airways in foals. Canadian
.Journal of l"ete~qna~3.'Research 55, 325-31.
Hovv,~?,~, A. M., V~_~, L. & PRt-S~:O-H,J. F. (1992). Clinical endoscopic study of lower respirato~T-tract infections in foals on Ontario breeding fal-llls. Proceedings of the A met4can Association of Equine Practitioners38, 191-2.
HOVSTAI~,T., Sg..xv(;, N. & Sv~zy, K. (1993). Stimulation of B lymphocytes by lipopolysaccharides fi'om anaerobic bacteria. Clinical Infectious Diseases 16 (Suppl. 4), $200-2.
HU.N"FER,J. v., CHADWICK,M., HURCIIINSON,G. 8 HODSON, M. E. (1985). Use of GLC in the
clinical diagnosis of anaerobic pleuropulmona~ 3, infection. BritishJournal of Diseases of the
Chest 79, 1-8.
Hus-rox, L.J., B..~a.v, W. M., L~(.Grrq, H. D. & MA(;.~IVSSON,N. S. (1986). Alveolar ,nacrophage
function in Thoroughbreds after strenuous exercise. Proceedings of lhe 2rid Inlernational
Conference of Equine ExercisePhysiology, pp. 243-52.
Huxt.EV, E.J., V~os~_~w,J., Gr~.~, W. R. & P~EaCE,A. K. (1978). Pharyngeal aspiration in normal adults and patients with depressed consciousness. American Journal of Medicin(, 64,
564-8.
IM)WZR~,M. C. & HmscH, D. C. (1986). Susceptibility of obligate anaerobes to trimethoprimsulfamethoxazole. Journal of the American Veterinmy Medical Association 188, 486-8.
JA~..x~, G.J. & GR~N, G. M. (1972). The effect of Sendai virus infection o,a bactericidal and
transport mechanism of the m urine lung. Journal of Clinical Investigation 51, 1989-98.
257
JAKAB, G. J. & GREEN, G. M. (1973). hnmune enhancement of pulmonary bactericidal

activity in routine virus pneumonia. Journal of Clinical Investigation 52, 2878-84.
JANC,, S. S. & HmSH, D. C. (1991). Identity of Bacteroides isolates and previously named Bacteroides spp. in clinical specimens of animal origin. American Journal of Veterinary Research 52,
738-41.
JERICrXO,K. W. F. & LANCFOm),E. V. (1978). Pneumonia in calves produced with aerosols of
boxdne herpesvirus 1 and PasteureUa haemolytica. Canadian Journal of Comparative Medicine
42, 269-77.
JOHNSON,A. P. & INZaNA,T.J. (1986). Loss of ciliary activity in organ cultures of rat trachea
treated with lipooligosaccharide from Haemophilus influenzae. Journal of Medical Microbiology 22, 265-8.
JORDAN, G. W., WON(;, G. A. & HOEPRICH,P. D. (1976). Bacteriology of the lower respirator),
tract as deternained by fibreoptic bronchoscopy and transtracheal aspiration. Journal of
Infectious Diseases 134, 428-35.
K-XLINS~, R. W., PAmOZR,R. H., BP.~.,Dr, D. & HOEPRmVl,P. D. (1967). Diagnostic usefulness
and safety of transtracheal aspiration. New England Journal of Medidne 276, 604-8.
KaN~S'rR6,Xl, L. E. (1968). The radiological diagnosis of equine pneumonia. Journal of the
American Veterina~),Radiolo~, Society,9, 80-8.
IZ~Y(., G. K. (1981). Equine thoracic radiography. Part 2: Radiographic patterns of equine
puhnonary and pleural diseases using air-gap rare-earth radiograph),. Compendium of Continuing Education for the Practicing Veterinarian 3, $283-7.
IZ~NC;,G. K., rvLu~vZNS,R.J. & McC:u.c, V. H., (1981). Equine thoracic radiography. Part 1:
Air-gap rare-earth radiography of the normal equine thorax. Compendium of Continuing
Education for the Practidng Veterinarian 3, $278-81.
KoIIN, C. (1978). Management of anaerobic infections. Proceedings of the 2rid Equine Pharmacolo~, Symposium, pp. 109-13. Colorado: Golden.
L~m, C. R. (1989). Aspects of diagnostic imaging in equine pulmonary disease. Vetedna73,
Annual 29, 127-35.
L.xxm, C. R. & O'C..xH..~ta-t.\N, M. W. (1989). Diagnostic imaging of equine pulmonary disease. Compendium of Continuing Education for the Practicing Veterina~qan 11, 1110-19.
L-v~.svox, V. C. & D-wls, L. E. (1989). Factors to consider in the selection of antimicrobial
drugs for therapy. Compendium of Continuing Education for the Practicing Veterinarian 11,
355-60.
L.~a,DON, D. P., D.,\51IN,J., BACKHOUSi~.,W., FRANK,C. 8 ATOCK, M. A. (1990). Environmental
haematological and blood biochemical changes in equine transit stress. Proceedings of the
American Association of Equine Practitioners 36, 485-90.
LoosH, C. G. (1968). Synergism between respiratory viruses and bacteria. YaleJourn.al of
Biolo~, and Medicine 40, 522-40.
LoPEz, A., Tvlo,xlSON,R. G. & S..way, M. (1976). The pullaaonary clearance of Pasteurella haemolytica in calves infected with bovine parainfluenza-3 virus. Canadian Journal of Comparative Medicine 40, 385-91.
Lox% D. N., Rosy., R.J., NL\R'I'IN,C. A. &: B.aH.Ev,M. (1983). Serum concentrations of penicillin in the horse after adnainistration of a variety of penicillin preparations. Equine Vetelqn auJdurna115, 43-8.
Lovz, D. N., JOHNSON,J. L. & MOORt-, L. V. H. (1989). Bacteroides spp. fi-om the oral cavity
and oral associated diseases of cats. I/eterinan, Microbiolo~, 19, 275-81.
Lox% D. N., VI:'KEt.STt.'IN,R. & COLLIN;S,S. (1990). The obligate and facultatively anaerobic
bacterial flora of the normal feline gingival margin. Veterinary Mio'obiology 22, 267-75.
MAttEr, V. S. (1983). Equine pleuropneumonia: radiology--diagnostic ultrasound-pleuroscopy. Proceedings of the American Assodoation of Equine Practitioners 29,
75-80.
MacKt.:v, V. S. & WIm~v, J. D. (1985). Endoscopic examination of the equine thorax. Equine
Vete~4naryJourna117, 140-2.
Mare, T. S. & Gml~s, C. (1990a). Thoracic radiography in the horse. In Practice 12, 8-10.
Mare, T. S. & Gm~s, C. (1990b). The radiographic evaluation of pulmonary disease in the
horse. Veterinmy Annual 30, 181-9.
258
M,u~, T. S. &LANE,J. G. (1989). Pneumonia, lung abscesses and pleuritis in adult horses: a
review of 51 cases. Equine VeterinaryJou~zal 2 l, 175-80.
MAIR, T. S. & SV,'EENEV,C. R. (1990). Advances in the diagnosis of equine lung disease: sampling from the lower airways. Equine Veterinao,Journa122, 147-8.
MAIR, T. S., STOKES,C. R. & BOURNE,F.J. (1987). Celhdar content of secretions obtained by
lavage from different levels of the equine respiratory tract. Equine VetefinaTyJournal 19,
458-62.
M.~'qDELL,G. L. & DA,'qOE,M. A. (1985). Cephalosporins. Goodman and Gibnan's The Pharmacological Basis of Therapeutics, 7th Edn, eds A. G. Gilman, L. S. Goodman, T. W. Rall& F.
Murad, pp. 1137--44. New York: MacMillan Publishing Company.
~JIANSMANN, R. A. (1983a). The stages of equine pleuropneunaonia. Proceedings of the
M_~'~SMANN,R. A. (1983b). Chronic pleuropneumonia. Proceedings of the American Association
of Equine Practitioners 29, 71-3.
MANS~'L-kNN,R. A. & BERNARD-STROTHER,S. (1985). Pleuroscopy in horses. Modern Veterinary
Practice 66, 9-17.
MANSMANN,R. A. & IG'4W,HT, H. D. (1972). Transtracheal aspiration in the horse.JouT~zal of the
American 1/eteHna~yMedical Association 160, 1527-9.
MAmNA, M., STRONC,,C. A., CWEN, R., MOHTOmS,E. & FINE(;Ot.D,S. M. (1993). Bacteriology of
anaerobic pleuropuhnonary infections: preliminary report. Clinical hTfectious Diseases 16,
(Suppl. 4), $256-62.
MASON, D. K., WATKINS,K. L., McNIE, J. T. & LUK, C. M. (1990). Haematological measurements as an aid to early diagnosis and prognosis of respirator), viral infections in
thoroughbred horses. Veterinary Record 126, 359-63.
MATrHEWS,A. G., HAcKErr, I.J. & L~wroN, W. A. (1988). The mucolytic effect of Sputolysin
in horses with respiratory disease. Veterinary Record 122, 106-8.
McCARTm, R. N., JEVFCOrr, L. B., FUNOER,J. W., FULLERTON,M. & CL~KE, I.J. (1991). Plasma
beta-endorphin and adrenocorticotrophin in young horses in training. Australian VeterinaryJournal 68, 359-61.
McCHESNE~, A. E. (1975). Viral respiratory infections of horses: structure and function of
lungs in relation to viral infection. JoulTzal of the Amet~can l/eteHnaly Medical Assodation
166, 76-7.
McDONEt.L, W. N., HALe, L. W. & JEvvCorr, L. B. (1979). Radiographic evidence of impaired
pulmonary function in laterally recumbent, anaesthetised horses. Equine VeteHnaTyJourhal 11, 24--32.
MctGtNE, S. A., CANnELD, P. J. & ROSE, R. J. (1993). Equine BAL cytology: survey of
Thoroughbred racehorses in training. Australian VeterinaryJournal 74, 401-4.
MCtOE~'~AN, B. C., KOmTZ, G. D., Scorr, J. S., BEr~NEV,C. & ROmNSON, N. E. (1990). Plasma
theophylline concentration and lung function in ponies with recurrent obstructive lung
disease. Equine Vetefina~yJourna122, 194--7.
MELVmLE,G. N., HOP,ST~WNN,G. & IP~aVANt,J. (1976). Adrenergic compounds and the respiratory tract: a physiological and electron-microscopical study. Respiration 33, 261-9.
MOORE, R. M. (1993). Diagnosis and treatment of obligate anaerobic bacterial infections in
horses. Compendium on Continuing Education for the Practicing Veterinarian 15, 989-94.
MoP.ms, D. (1989). Review of anaemia in horses. Part 2. Pathophysiologic mechanisms,
specific diseases and treatment. Equine Practice 11, 34--46.
MLqr(, W. W. (1990). The equine stress response to anaesthesia. Equine Veterina~yJou~za122,
303-5.
MUR~TA, H. & HmOSE, H. (1991a). Suppression of bovine neutrophil function by sera fiom
cortisol-treated calves. British VeterinaryJournal 147, 63-70.
MURaTA, H. & HIROSE, H. (1991b). Suppression of bovine lymphocyte and macrophage
functions by sera from road-transported calves. British Vetelina~yJourna1147, 455-62.
MtJRATA,H. & MWAMOTO,T. (1993). Bovine haptoglobin as a possible immunomodulator in
the sera of transported calves. British VeterinaryJournal 149, 277-83.
MURRAY,M.J. (1989). Respiratory problems in horses: dealing with lower airway disease. Veterinary Medicine 84, 105-12.
259
NAGLIC,T., HERCEG,M., H~\ISIG,D. & BAMBIR,S. (1982). Bacteria in equine pneumonia. Veterinarski Arhiv 52, 107-13.
Narro, Y., T ~ , S., SmNGU, K. et aL (1992). Responses of plasma adrenocorticotropic hormone, cortisol and cytokines during and after upper abdominal surgery. Anesthesiology
77, 426-31.
NICKERSON,C. L. & JAgAB, G.J. (1990). Pulmonary antibacterial defences during mild and
severe influenza virus infection. Infection and Immunity 58, 2809-14.
NYMAN,G., FUNKQUIST,B., KVART,C. et al. (1990). Atelectasis causes gas exchange impairment
in the anaesthetised horse. Equine VeterinaryJournal 22, 317-24.
OYDERDON~;,A. B., KASPER,D. L., MANSHEIM,B.J., LOUIE,T.J., GORBAGH,S. L. & BARTLErr,J. G.
(1979). Experimental animal models for anaerobic infections. Reviews of Infectious Disease
1,291-301.
O~NS, J. M. (1982). The lung. In Chapter 6: The Chest. In Radiographic Interpretation for the
Small Animal Clinician, pp. 95-115. ed. D. N. Biery. St Louis, Missouri: Ralston Purina
Company.
PARKS,C. R., WOODRUM,D. E., GRAHAM,C. B., CHENEY,F. W. & HODSON,W. A. (1971). Effect of
water nebulisation on canine pulmonary mucociliary clearance. American Review of Respirator3,Disease 104, 99-106.
PEARSON,E. G. (1990). Hypoalbuminaemia in horses. Compendium of Continuing Education for
the Practicing Vetelqnarian 12, 555-60.
PECO~, D. V. (1959). A method of securing uncomtaminated tracheal secretions for bacterial examination. Journal of Thoracic Surgery 37, 653-4.
PECORA, D. V. (1963). A comparison of transtracheal aspiration with the methods of
determining the bacterial flora of the lower respiratory tract. New England Journal of Medicine 267, 664-6.
Powls, R. L. (1986). Ultrasound science for the veterinarian. Veterinary Clinics of North
PURDV, C. M. (1985). Septic pleuritis in horse. Compendium of Continuing Education for the
Practicing Veterinarian 7, $361-3.
RAc~vsrr, D.J. (1989). Lower respiratory tract infections in horses. Australian Equine Veterinarian 7, 33-6.
ILxcKtm~vr,D.J. (1990). Studies on bacterial infections of the equine lower respiratory tract.
PhD Thesis, University of Sydney.
R A c ~ v r , D.J. & Lo~q~, D. N. (1990). Influence of head posture on the respiratory tract of
healthy horses. Australian VeterinaryJournal 67, 402-5.
RANT~'4EN,N. W. (1981). Ultrasound appearance of normal lung borders and adjacent viscera in the horse. Veterinmy Radiology 22, 217-19.
P~.N'rANEN, N. W. (1986). Diseases of the thorax. Veterinary Clinics of North America--Equine
Practice 2, 49-66.
RANTANEN,N. W., GAGE, L. & PARADIS,M. R. (1981). Ultrasonography as a diagnostic aid in
pleural effusion of horses. Vete~qnaryRadiology 22, 211-16.
RAPHEL, C. F. & BEECH,J. (1982). Pleuritis secondary to pneumonia or lung abcessation in
90 horses. Journal of the Amelican Veterinary Medical Association 181,808-81.
R~W]-tEL,C. F. 8c GUNSON,D. E. (1981). Percutaneous lung biopsy in the horse. Cornell Veterinarian 71,439-48.
RAU, J. L. (1984). Parasympatholytic and xanthine bronchodilators. In Respirator3, Therapy
and Pharmacology, 2nd Edn, ed. I. Zimmert, pp. 93-11. Chicago: Year Book Medical
Publishers.
REEF, V. B., BoY, M. G., RZID, C. F. & EkSER,A. (1991). Comparison between diagnostic ultrasonography and radiography in the evaluation of horses and cattle with thoracic disease:
56 cases. Journal of the American Veterinary Medical Association 198, 2112-18.
REIMER,J. M. (1990). Diagnostic ultrasonography of the equine thorax. Compendium of Continuing Education f m the Practicing Veterinarian 12, 1321-7.
REIMER,J. M., REEF, V. B. & SPENCER,P. A.. (1989). Ultrasonography as a diagnostic aid in
horses with anaerobic bacterial pleuropneumonia a n d / o r pulmonary abscessation: 27
cases (1984-1986). Journal of the American Veterinary Medical Association 194, 278--82.
260
ROBERTSON, S. A., STEELE,C.J. & CHEN, C. L. (1990). Metabolic and hormonal changes
associated with arthroscopic surgery in .the horse. Equine VeterinaryJournal 22, 313-16.
ROmNSON,N. E. (1991). Pulmonary physiology and pathophysiology. In Equine Medidne and
Surgery, 4th Edn, eds P. T. Colahan, I. G. Mayhew, A. M. Merritt & J. N. Moore,
pp. 362-72. Goleta, California: American Veterinary Publications.
ROSE, R . J . (1983). Respiratory system. In Vade Mecum number 1--Horses; University of
Sydney Post-graduate foundation in veterinary science, pp. 28-9.
ROSSlER,Y., SWEENEY,C. R., HEYER,G. & HAIVIIR,A. N. (1990). Pleuroscopic diagnosis of disseminated haemangiosarcoma in a horse. JmLrnal of the American VeterinaryMedical Assodation 196, 1639-40.
ROSSlER,Y., SX~ENEV,C. R. & ZIEMER,E. L. (1991). Bronchoalveolar lavage fluid cytologic findings in horses with pneumonia or pleuropneumonia. Journal of the American Veterinary
Medical Assodation 198, 1001-4.
ROSSING,T. H. (1983). Supportive measures in the treatment of pneumonia. In Respiratory
Infections: Diagnosis and Management, ed. J. E. Pennington, pp. 455-60. New York: Raven
Press.
ROTSTEIN,O. D. (1993). Interactions between leucocytes and anaerobic bacteria in polymicrobial surgical infections. Clinical Infectious Diseases 16 (Suppl. 4), $190-4.
ROUDEBUSH,P. (1982). Lung sounds. Journal of the American VeterinaryMedical Association 181,
122-6.
ROUDEaUSH,P. & S~qEENEV,C. R. (1990). Thoracic percussion. Journal of the American Veterinary Medical Association 197, 714-18.
S~vo, A., HARA,IC, YA~IAGUCHI,IL & Usul, T. (1984). Pulmonary infection due to anaerobes
in a hospital survey. Reviews on Infectious Diseases6 (Suppl. 1), S 128-31.
SAgAKURA,Y. (1983). Changes of mucociliary function during colds. European Journal of Respiratory Disease64 (Suppl. 128), 348-54.
S~DE, R. D. (1986). The pleural space. In Textbook of Veterinary Diagnostic Radiology, ed. D.
E. Thrall, pp. 333-8. Philadelphia: W. B. Saunders Company.
SANDERSOn,G. N. & O'CALLAGHAN,M. W. (1983). Radiographic anatomy of the equine thorax as a basis for radiological interpretation. New Zealand VeterinaryJournal 31, 127-30.
SAYHOUPa,A. A.,Joy~, R. S. & DOBSON,H. (1992). Effects of xylazine on the stress response
to transport in male goats. British VeterinaryJournal 148, 119-28.
SASSE, W. (1981). Efficacy of the new expectorant Na 1523 (hydroxycyclohexyl-hydroxy
dibromobenzyl amine) in horses with chronic obstructive bronchitis. Inaugural Dissertation, Tier~rztliche Hochschule, Hannover.
ScnoTr, H. C. & MANS~m, R. A. (1990). Thoracic drainage in horses. Compendium of Continuing Education for the Practicing Veterinarian 12, 251-61.
SEMRAD,S. D. & BVARS,T. D. (1989). Pleuropneumonia and pleural effusion: diagnosis and
treatment. VeterinaryMedicine 84, 627-35.
SnAP.P, N. C. C. & KOUTEDA~aS,Y. (1992). Sport and the overtraining syndrome: immunological aspects. British Medical Bulletin 48, 518-33.
SLOCOMBE,R. (1989). Respiratory system defences. Australian Equine Veterinarian 7, 20-4.
SMITH,J. A. & WEmE~NN, M.J. (1990). The exercise and immunity paradox: a neuroendocrine/cytokine hypothesis. Medical Science and Research 18, 749-53.
Soj~,J. E., BRISSON-IZaMMICK,S. V., CARLSOn,G. P. & CopPoc, G. L. (1990). Dimethyl sulfoxide
update--new applications and dosing methods. Proceedings of the American Association of
Equine Practitioners36, 683-90.
SPECHT,T. E., BROWN,M. P., GRONWALL,R. R., RJa, W.J. & HOUSTON,A. E. (1992). Pharmacokinetics of metronidazole and its concentration in body fluids and endometrial tissues of
mares. AmericanJournal of Veterinary Research 53, 1807-12.
SPURLOCK,S. L. (1989). Antimicrobial use in equine respiratory disease. Equine Practice 11,
6-12.
SPURLOCn,S. L. (1991). Pleuropneumonia in the horse. Equine Practice13, 10-11.
STOWATER,J. L. & LAMa, C. R. (1989). Ultrasonography of noncardiac thoracic diseases in
small animals.Journal of the American VeterinaryMedical Association 195, 514-20.
S~V~T, B. & GORaACU,S. L. (1989). Recent developments in the understanding of the patho-
261
genesis and treatment of anaerobic infections. Part I. New England Journal of Medicine
321,240-6.
SX~ENEV, C. R., DWERS, T. J. & BENSON, C. E. (1984). Diseases of the lung: diagnostic
approach and management of horses with anaerobic pleuropneumonia. Proceedings of the
SWEENEV,C. R., Dr~Rs, T. J. & BENSON, C. E. (1985). Anaerobic bacteria in 21 horses with
pleuropneumonia. Journal of the American Veterinary Medical Association 187, 721---4.
SWEENEV,R. W., S~ENEV, C. R., SOMA,L. R., WOODWARD,C. B. & CHARLTON,C. A. (1986). Pharmacokinetics of metronidazole given to horses by intravenous and oral routes. American
Journal of Veterinary Research 47, 1726-9.
SWEENEV,C. R., LEARV,H.J., ZIE~IER,E. L. & SPENCER,P. A. (1989a). Effect of water vapoursaturated air therapy on bronchoalveolar lavage and tracheal mucus transport rate in
clinically normal horses. American Journal of Veterinary Research 50, 276-9.
SWEENEV, C. R., SWEENEV,R. W. & BENSON, C. E. (1989b). Comparison of bacteria isolated
from specimens obtained by use of endoscopic guarded tracheal swabbing and percutaneous tracheal aspiration in horses. Journal of the American Veterinary Medical Association
195, 1225-9.
SWEENEV,C. R., HOLCOMBE,S.J., BARNING~L~I,S. C. & BEECH,J. (1991a). Aerobic and anaerobic bacterial isolates from horses with pneumonia or pleuropneumonia and antimicrobial susceptibility patterns of the aerobes. Journal of the American Veterinary Medical
S~ENEV, C. R., MAXSON,A. D. & So,x, L. R. (1991b). Endoscopic findings in the upper respiratory tract of 678 Thoroughbred racehorses. Journal of the American Veterinary Medical
SWEENEV,R. W., SWEENEV,C. R. & WEIHER,J. (1991C). Clinical use of metronidazole in horses:
200 cases (1984-1989). Journal of the American Veterinary Medical Association 198, 1045--8.
Svv,Es, D. A., WtLSON, R., GREENSTONE,M., CURRIE,D. C., STEINFORT,C. 8~ COLE,P.J. (1987).
Deleterious effects of purulent sputum sol on human ciliary function in vitro: at least two
factors identified. Thorax 42, 256-61.
THORSEN,J. (1991). Equine rhinoviruses. Equine Practice 13, 19-22.
THORNTON,J. R. (1985). Hormonal responses to exercise and training. Veterinary Clinics of
North America--Equine Practice 1,477-96.
TRAuB-DARGATZ,J. L., McKINNON, A. O., BRUYNINCKX,W. J., THRALL, M. A., JONES, R. L. &
BLANCQUAERT,A-M. B. (1988). Effect of transportation stress on bronchoalveolar lavage
fluid analysis in female horses. American Journal of Veterinary Research 49, 1026-9.
TURGUT, K. & SASSE,H. H. L. (1989). Influence of clenbuterol on mucociliary transport in
healthy horses and horses with chronic obstructive pulmonary disease. Veterinary Record
125, 526-30.
TYLER,R. D., COW~LL,R. L., CUN~NBEARD,tC D. & MACALLlSTER,C. G. (1987). Haematologic
values in horses and interpretation of haematologic data. Veterinary Clinics of North
America---Equine Practice 3, 461-84.
UDELSMAN,R., NORTON,J. A., JELENICH,S. E. et aL (1987). Responses of the hypothalamic-pituitary-adrenal and renin-angiotensin axes and the sympathetic system during controlled surgical and anaesthetic stress. Journal of Clinical Endocrinology and Metabolism 64,
986-94.
VANDENBOGnAP.~,A. E.J.M., HAZENING, M.J. & MAES,J. H. (1989). Rapid presumptive diagnosis of anaerobic infections in animals by GLC. American Journal of Veterinary Research 50,
1454-9.
WALmR, R. D., RIC~P.DSON, D. C., BRYANT,M.J. & DRAPER,C. S. (1983). Anaerobic bacteria
associated with osteomyelitis in domestic animals. Journal of the American Veterinary Medical Association 182, 814-16.
WATI~RS,J. W. (1986). The Lungs (companion animals). In Textbook of Veterinary Diagnostic
Radiology, ed. D. E. Thrall, pp. 306-17. Philadelphia: W. B. Saunders Company.
WEmE~u~NN,M.J., SMXTH,J. A., G~Y, A. B., Pv~, D. B., KOLBUCH-BP.ADDON,M. & TELFORD,R. D.
(1992). Exercise and the immune system. Life Science4, 24-33.
WEIN~UCH,A. E. & DEL BENE,V. E. (1976). fl-lactamase activity in anaerobic bacteria. Antimicrobial Agents and Chemotherapy 10, 106-11.
262
WEIss, D.J. & McCI.AV,C. B. (1988). Studies on the pathogenesis of the erythrocyte desta'uction associated with the anaemia of inflammatory disease. Veterinary Clinical Pathology 17,
90-3.
WEIss, D.J., KREHBIEL,J. D. & LUND,J. E. (1983). Studies of the pathogenesis of anaemia of
inflammation: mechanism of impaired erythropoiesis. American Journal of Veterinary
Research 44, 1832-5.
WHITE,WALL,K. E. & GREET,T. R. C. (1984). Collection and evaluation of tracheobronchial
washes in the horse. Equine VeterinmyJourna116, 499-508.
WILLOUGHBY,R., ECKER,G., McKEE, S. et al. (1992). The effects of equine rhinovirus, influenza virus and herpesvirus infection on tracheal clearance rate in horses. Canadian Jourhal of Veterinary Research 56, 115-21.
WILSON,J. H. (1992a). Tips for assessment of the respiratory tract: percussion of the upper
and lower respiratory tracts and guttural pouch catheterisation. Proceedings of the American
Association of Equine Practitioners 38, 489-94.
WILSON, W. D. (1992b). Foal pneumonia: an overview. Proceedings of the American Association
of Equine Practitioners 38, 203-29.
WILSON, R. & COLE, P.J. (1988). The effect of bacterial products on ciliary function. American Review of Respiratory Disease 138, $49-53.
WILSON,R., S~Es, D. A., CURRIE,D. & COLE, P.J. (1986). Beat frequency of cilia from sites of
purulent infection. Thorax 41,453-8.
WISNER, E. R., O'BRIEN, T. R., L~waxz, j. R., WILSON,D. W. & TYLER,W. 8. (1993). Radiographic and microscopic correlation of diffuse interstitial and bronchointerstitial pulmonary patterns in the caudodorsal lung of adult Thoroughbred horses in race training.
Equine VeterinaryJournal 25, 293-8.
WoNe, C. W., THOMPSON,H. L., THONG,Y. H. & THORNTON,J. R. (1990). Effect of strenuous
exercise styess on chemiluminescence response of equine alveolar macrophages. Equine
VeterinaryJournal 22, 33-5.
WooD, J. L. N., BURRELL,M. H., ROBERTS,C. A., CHANTER,N. & SHAW,Y. (1993). Streptococci
and Pasteurella spp. associated with disease of the equine lower respiratory tract. Equine
VeterinaryJournal 25, 314-18.
YATES,W. D. G. (1988). Respirator), System. In Special Veterinary Pathology, ed. R. G. Thomson, pp. 92-4, Toronto: B. C. Decker Inc.
Y~TES, D. B., ASPIN,N., LEVlSON,H.,JoNES, M. T. & BRYAN,A. C. (1975). Mucociliary tracheal
transport rates in man. Jou~zal of Applied Physiology 39, 487-95.
ZAVV,M. T., JUNIEWlCZ,P. E., PHILLIPS,W. A. & VON TUNGELN,D. L. (1992). Effect of initial
restraint, weaning, and transport stress on baseline and ACTH-stimulated cortisol
responses in beef calves of different genotypes. American Journal of Veterinary Research 53,
551-7.
ZIMENT, I. (1984). General pharmacology of respiratory drugs. In Respirator3, Pharmacology
and Therapeutics, pp. 1-40. Philadelphia: W. B. Saunders.
(Acceptedfor publication 27 May 1994)

Review: Depm Ment of Vete Na D, Pathology, The University of Sydn, New South Wales 2006, Australia

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Review: Depm Ment of Vete Na D, Pathology, The University of Sydn, New South Wales 2006, Australia

Uploaded by

Copyright:

Available Formats

B~: va.~ (1995).

BRITISH VETERINARY JOURNAL, 151, 3

Predisposing factors and causes of pleuropneumonia

BRITISH VETERINARY JOURNAL, 151, 3

BRITISH VETERINARYJOURNAL, 151, 3

Proliferation of oropharyngea] organisms

/:~~ ,E~.t~nsibn into pleural ":

I Mixed F/A and I

1988). Mucopurulent or fibrinous exudate is usually present in airways. Extension

Pleuropneumonia may be confirmed by the combination of physical examination,

BRITISH VETERINARY JOURNAL, 151, 3

type of response may aid determination of prognosis (Coles, 1986). A mild to

BRITISH VETERINARY JOURNAL, 151, 3

Ultrasonography and radiography may provide complementary information

to demonstrate pulmonary lesions that are obscured by the cardiac silhouette

BRITISH \rETERINARY .JOURNAL, 151, 3

BRITISH VETERINARY JOURNAL, 151, 3

an increased likelihood of isolating Gram-negative enteric bacteria from patients

BRITISH VETERINARY JOURNAL, 151, 3

BRITISH VETERINARY JOURNAL, 151, 3

tration of submucosal tissues, intraluminal debris and sputum or extraluminal

Topical administration of water by aerosolation, direct instillation or inhalation

BRITISH VETERINARYJOURNAL, 151, 3

BRITISH VETERINARY JOURNAL, 151, 3

BRUMBAUGH,G. W. (1990a). Respiratory therapy: clinical applications of bronchodilatory

DERKSEN,F.J. (1987). Evaluation of the respiratory system: diagnostic techniques. In Current

BRITISH VETERINARYJOURNAL, 151, 3

of Medidne 290, 1237-45.

hal of Medidne 290, 1289-94.

JAKAB, G. J. & GREEN, G. M. (1973). hnmune enhancement of pulmonary bactericidal

BRITISH VETERINARYJOURNAL, 151, 3

BRITISH VETERINARYJOURNAL, 151, 3

BRITISH VETERINARYJOURNAL, 151, 3

(Acceptedfor publication 27 May 1994)

You might also like