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The Veterinary Journal 179 (2009) 163–170

TheVeterinary Journal

Review

Feline pyothorax – New insights into an old problem:Part 1. Aetiopathogenesis and diagnostic investigation

Vanessa R. Barrs *, Julia A. Beatty

Valentine Charlton Cat Centre, Faculty of Veterinary Science, University of Sydney, Sydney NSW 2006, Australia

Accepted 19 March 2008

Abstract

Feline pyothorax is a life-threatening emergency commonly encountered by the small animal clinician. Historically, thoracic wall pen-etration from a bite wound has been postulated to be a major route of infection. New information has challenged this dogma and indi-cated that aspiration of oropharyngeal flora is the usual route of infection of the pleural space in cats. A role for unusual pathogens,including gastrointestinal flora and fungal agents, has been identified in some cases, particularly in kittens. In the first of a two-partreview, the clinical findings in feline pyothorax are discussed with a focus on an improved understanding of the aetiopathogenesis ofthe disease and subsequent implications for diagnostic investigation.� 2008 Elsevier Ltd. All rights reserved.

Keywords: Thoracic empyema; Pleural fluid; Infection; Cat

Introduction

Pyothorax, or thoracic empyema, describes infection ofthe pleural space characterised by accumulation of a puru-lent exudate. Some of the earliest descriptions of pyothoraxin humans were made by Hippocrates in the 4th centuryBC (Miller, 2000). Reports of pyothorax affecting domesticcats have been available in the veterinary literature for halfa century (Wilkinson, 1956; Holzworth, 1958) but,although it is encountered commonly in small animal prac-tice, there are no data on the incidence of pyothorax in thecat. Much of the published literature exists as descriptiveaccounts, including individual case reports, book chaptersor non-peer-reviewed articles.

Ten retrospective case series have provided useful infor-mation on aetiologies, clinical presentation, diagnostics,treatment, outcome, risk factors and prognostic indicatorsfor the disease (Hayward, 1968; Crane, 1976; Gruffydd-

1090-0233/$ - see front matter � 2008 Elsevier Ltd. All rights reserved.

doi:10.1016/j.tvjl.2008.03.011

DOI of original article: 10.1016/j.tvjl.2008.03.019.* Corresponding author. Tel.: + 61 2 9351 3437; fax: + 61 2 9351 4261.

E-mail address: vbarrs@vetsci.usyd.edu.au (V.R. Barrs).

Jones and Flecknell, 1978; Pidgeon, 1978; Jonas, 1983;Davies and Forrester, 1996; Walker et al., 2000; Demetriouet al., 2002; Waddell et al., 2002; Barrs et al., 2005). Ourunderstanding of the aetiopathogenesis of pyothorax hasbeen further informed by improved techniques for anaero-bic culture (Walker and Richardson, 1981; Dow and Jones,1987b). Available evidence suggests that para-pneumonicspread is currently the most common route of infectionof the pleural space. However, this may not have alwaysbeen the case. The relative frequencies with which differentroutes of infection of the pleural space occur may havealtered with changes in husbandry. For example, increasedneutering, confinement and routine treatment with antibi-otics after a cat fight may have reduced the incidence ofpyothorax due to penetrating trauma. Improved prophy-laxis and management for viral upper respiratory tract(URT) and lungworm infections and improved nutritionmay also have had an impact.

In this first part of a two-part review we focus on theclinico-pathological findings and the advances in theunderstanding of the aetiopathogenesis and diagnosticinvestigation of feline pyothorax. Subsequent recommen-

164 V.R. Barrs, J.A. Beatty / The Veterinary Journal 179 (2009) 163–170

dations for treatment and prophylaxis based on currentlyavailable evidence are presented in the second part (Barrsand Beatty, in press).

Signalment

Pyothorax predominantly affects young cats (mean age4–6 years), although cats of any age can be affected (Pid-geon, 1978; Davies and Forrester, 1996; Walker et al.,2000; Demetriou et al., 2002; Waddell et al., 2002; Barrset al., 2005). No breed or gender predisposition has beenidentified.

Aetiopathogenesis

An understanding of aetiopathogenesis underpins rec-ommendations for investigation, treatment and prophy-laxis. Information on the mechanisms of infection of thepleural space has remained elusive since it is often notdetermined in individual cases either ante- or post-mortem(Sherding, 1979; Bauer, 1986; Sherding, 1994; Demetriouet al., 2002; Waddell et al., 2002). Given the protractedcourse of the disease, by the time clinical signs of pyotho-rax develop, evidence of any inciting cause may no longerbe present. Possible routes of infection include extensionfrom an adjacent structure (bronchopneumonia, para-pneumonic spread, oesophageal rupture, mediastinitis orsub-phrenic infection), direct inoculation (penetratingtrauma, migrating foreign body, thoracocentesis or tho-racic surgery) or haematogenous or lymphatic spread froma distant site (systemic sepsis).

Oropharyngeal flora

Bacterial isolates from the majority of cases of pyotho-rax are polymicrobial and similar in composition to thenormal feline oropharyngeal flora (Love et al., 1982,1989, 1990, 2000). Isolates include obligate and facultativeanaerobic bacteria; Bacteroidaceae (Bacteroides spp., Por-phyromonas spp., Prevotella spp.), Fusobacterium spp.,Peptostreptococcus spp., Clostridium spp., Actinomyces

spp., Eubacterium spp., Propionibacterium spp., Filifactor

villosus, Pasteurella multocida, Streptococcus spp. andMycoplasma spp. (Pidgeon, 1978; Thompson et al., 1992;Walker et al., 2000; Gulbahar and Gurturk, 2002; Wegnerand Pablo, 2006). The question is: ‘How do these oropha-

ryngeal flora reach the pleural space?’

Aspiration versus bite wounds

Oropharyngeal flora could gain access to the pleuralspace by aspiration, direct penetration from a bite woundor by haematogenous spread from a distant wound. Manysources, including most standard texts, list penetratingwounds, migrating foreign bodies and oesophageal tearsahead of parapneumonic spread as common causes ofpyothorax (Prevot et al., 1961; Hayward, 1968; Sherding,

1994; Hawkins, 2003; Mertens et al., 2005; Greene andReinero, 2006). However, available evidence suggests thataspiration of oropharyngeal flora is the most significantroute.

A recent retrospective study demonstrated that aspira-tion of oral flora was the most likely mechanism of pleuralspace infection in 15/18 (78%) cats in which probablemechanisms of pleural space infection were identified (Bar-rs et al., 2005). Aspiration of oropharyngeal flora, subse-quent colonisation of the lower respiratory tract anddirect extension of infection from the bronchi and lungsis the most common cause of human anaerobic pyothoraxand equine pleuropneumonia (Bartlett, 1993; Racklyeftet al., 2000; Schiza and Siafakas, 2006). In human anaero-bic lung infections, tissue necrosis results in abscess forma-tion and/or bronchopleural fistula with subsequentextension to the pleural space (Bartlett, 1993).

Pleuropneumonia is a common sequel to transportationin horses. Mucociliary clearance of lower respiratory secre-tions is impaired when horses are restrained with theirheads elevated; this results in accumulation of aspiratedoropharyngeal flora and increased risk of pleuropneumo-nia (Racklyeft et al., 2000). Viral URT infection may alsotemporarily impair the mucociliary escalator in cats,humans and horses (Carson et al., 1985; Willoughbyet al., 1992; Gaskell et al., 2004), predisposing them topleuropneumonia.

In necropsies of cats with pyothorax, pneumonia orfocal pulmonary abscessation was identified in 7/15 (47%)cats in two studies (Hayward, 1968; Davies and Forrester,1996) and 4/7 cats in another (Brady et al., 2000). Diffuseor focal pulmonary lesions have been noted in numerousother reports (Wilkinson, 1956; Malik et al., 1991; Waddellet al., 2002; Doyle et al., 2005; Wegner and Pablo, 2006).These lesions support a pathomechanism of para-pneu-monic spread. Cats with pyothorax are 3.8 times as likelyto have come from multi-cat households compared to con-trol cats (Waddell et al., 2002). The authors suggested thatinter-cat aggression may account for the increased risk inthis environment. However, behavioural studies do notsupport the notion of significant aggression in multi-cathouseholds at least when these populations are stable (Cro-well-Davis et al., 2004). If fight wounds were a significantcause of pyothorax, then free-roaming males would belikely to be overrepresented among cats with pyothorax.However, neither outdoor access nor sex was identified asrisk factors for pyothorax (Waddell et al., 2002). An alter-native explanation for the increased risk of pyothorax inmulti-cat environments may be related to the greater riskof developing viral URT infections (Binns et al., 2000).Antecedent URT infection has been recognised as a predis-posing event in 15% and 26% of cases of feline pyothorax(Jonas, 1983; Barrs et al., 2005) and in individual casereports (Malik et al., 1991).

Direct inoculation of oral flora into the thorax from abite wound is likely to be the initiating event in somecases of pyothorax and could result in pleuritis without

V.R. Barrs, J.A. Beatty / The Veterinary Journal 179 (2009) 163–170 165

pulmonary involvement. Para-pneumonic spread of infec-tion could occur if inoculation of the lung occurred duringbiting. Where thoracic wounds have been identified in nec-ropsy studies, it is not clear what proportion of cats hadconcurrent pulmonary abscessation (Jonas, 1983; Waddellet al., 2002). However, in cases where pulmonary abscessa-tion has been identified, concurrent thoracic wounds wereuncommon (Hayward, 1968; Pidgeon, 1978; Davies andForrester, 1996; Brady et al., 2000; Waddell et al., 2002).

In a case series of feline pyothorax reported 25 yearsago, 8/20 cats had evidence of thoracic wounds, includingfive bite wounds and three wounds of unknown origin(Jonas, 1983). In this study, 9/20 cats (45%) were entiremales. It is not known whether intact males, more likelyto exhibit territorial aggression, were overrepresented inthis population compared to the normal hospital popula-tion at that time. Interestingly, the study by Waddellet al. (2002) demonstrated a greater proportion of entirecats, both male and female, in the pyothorax group com-pared with controls. Whether this attained statistical signif-icance is not clear. If neuter status is identified as a riskfactor in future studies, it would be interesting to determinewhether entire animals with pyothorax are free-roaming,and thus more likely to fight, or whether they are part ofstable breeding colonies where viral URT infections mayimpact. More recently, two case series have identified tho-racic puncture wounds in 4% (Barrs et al., 2005) and 16%of cases at post mortem examination (Waddell et al.,2002). It may be that, given changes in pet ownership hab-its in the last 25 years – including more neutered cats withrestricted territories, this route of infection is now less com-mon (Baldock et al., 2003; Clancy et al., 2003).

Non-oropharyngeal flora

Less than 20% of cases of feline pyothorax are caused byinfectious agents other than oropharyngeal flora includingStaphylococcus spp., Rhodococcus equi, Nocardia spp.,enteric Gram-negative organisms (Escherichia coli, Salmo-nella spp., Klebsiella spp., Proteus spp.) non-entericGram-negative organisms (Pseudomonas spp.) and proto-zoa (Toxoplasma gondii) (Gruffydd-Jones and Flecknell,1978; Sherding, 1979; Barrs et al., 1999; Walker et al.,2000; Demetriou et al., 2002; Anfray et al., 2005; Barrset al., 2005). Fungal causes of feline pyothorax are rareand include Cryptococcus spp., Candida albicans and Blas-

tomyces dermatitidis (McCaw et al., 1984; Sherding, 1994;Barrs et al., 2005).

Mechanisms of infection of the pleural space with non-oropharyngeal flora include penetrating thoracic traumanot associated with a cat bite. However, if environmentalcontamination of thoracic wounds were a common mecha-nism, a higher isolation rate of saprophytic bacteria such asNocardia spp., Pseudomonas spp. and Mycobacteria spp.would be expected. In contrast to dogs, Nocardia spp. areuncommonly isolated from feline septic pleural effusions.Infection can occur secondary to inhalation of aerosols,

including dust (Greene and Reinero, 2006; Malik et al.,2006). Other routes of infection with non-oropharyngealflora include haematogenous spread from a septic focus(Davies and Forrester, 1996; Demetriou et al., 2002; Barrset al., 2005), perforation of the oesophagus, trachea, orbronchi (Harai et al., 1995; Barrs et al., 2005), migratingplant material (Jonas, 1983; Pidgeon, 1978) and parasiticmigration (Wilkinson, 1956; Hayward, 1968; Barrs et al.,1999).

Pyothorax and/or pneumonia caused by Salmonella spp.has been documented in cats with concurrent Aelurostron-

gylus abstrusus infestation (Barrs et al., 1999; Foster et al.,2004). Migrating lungworm or ascarid larvae may act ascarriers for intestinal bacteria. Non-oropharyngeal patho-gens were more likely to be isolated from kittens in onestudy (Barrs et al., 2005) but this may be because of age-related infectious or parasitic conditions such as ascaridor lungworm infections.

History and clinical signs

Historical and physical examination findings can beattributed to either the presence of a pleural effusion orto systemic illness, the latter being non-specific. Dyspnoea,inappetence and lethargy are the most commonly reportedfindings, affecting approximately 80% of cases (Jonas,1983; Demetriou et al., 2002; Waddell et al., 2002; Barrset al., 2005). Pleural effusion and pulmonary atelectasiscause a restrictive pattern of respiration characterised byan increase in respiratory rate and inspiratory effort andshallow respiratory excursions (Sherding, 1994). Cats typi-cally adopt a crouched, sternally recumbent posture withelbows abducted (Hayward, 1968; Piermattei and Gowing,1964; Crane, 1976; Sherding, 1979). Poor body condition,dehydration and abnormalities on auscultation (abnormallung sounds or muffled heart sounds) are also common(Jonas, 1983; Demetriou et al., 2002; Waddell et al.,2002; Barrs et al., 2005). A fluid line may be detected onthoracic percussion (Sherding, 1979). Coughing is reportedin 14–30% of cases, reflecting pleuritis and/or concurrentpneumonia (Jonas, 1983; Sherding, 1994; Demetriouet al., 2002; Barrs et al., 2005). Pyrexia has been reportedin 28–50% of cases, although some cats in these serieshad received prior antibiotic treatment (Demetriou et al.,2002; Barrs et al., 2005). Thus, pyrexia at initial presenta-tion may be more common than these figures suggest.

Hypothermia, present in 15% of cats (Waddell et al.,2002), should alert the clinician to the possibility of severesepsis, particularly when accompanied by bradycardia(Brady et al., 2000). In the largest retrospective study of80 cats with pyothorax, bradycardia was significantly morecommon in cats that were hypothermic (Waddell et al.,2002). These authors also found that non-survivors hadsignificantly lower heart rates when compared with survi-vors, although not all of these cats were bradycardic, limit-ing the clinical utility of this observation (Waddell et al.,2002).

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Pyothorax progresses insidiously. The duration of clini-cal signs prior to diagnosis is typically 1–2 weeks, but itmay be months (Jonas, 1983; Davies and Forrester, 1996;Demetriou et al., 2002; Barrs et al., 2005). A protractedcourse is also supported by the demonstration of granula-tion tissue on the pleura and the formation of adhesionswith subsequent loculation of fluid (Hayward, 1968; Dowand Jones, 1987a). Such is the propensity of the cat to com-pensate for gradual onset respiratory compromise byreduced activity that signs may be noted only acutely ornot at all by the owner. That the dyspnoea can be surpris-ingly subtle is evidenced by the fact that it had not beenobserved by 40% of owners in one study (Barrs et al.,2005). Coupled with the non-specific nature of many ofthe presenting signs, many cats are presented late in thecourse of the disease. By the time clinical signs of respira-tory compromise become obvious in feline patients, mini-mal respiratory reserve remains. Pyothorax should beconsidered as a cause of sudden death (Brodrick, 1983;Gulbahar and Gurturk, 2002).

Diagnostic investigation

In many cases, clinical examination findings will beindicative of pleural space disease making the diagnosticinvestigation straightforward. The non-specific nature ofsigns in some cases, including normothermia in at least35% of cases and the absence of dyspnoea in 20% of thecats examined supports the use of thoracic imaging in catswith non-specific signs. The relatively subtle changesobserved in presenting signs may partially explain why10–33% of pyothorax cases examined at post-mortem hadnot been diagnosed ante-mortem (Jonas, 1983; Daviesand Forrester, 1996; Waddell et al., 2002).

Minimum database

While the results of haematology, biochemistry, urinaly-sis and retrovirus testing are not crucial for the diagnosis ofpyothorax, they should form part of the minimum data-base to guide management of the patient.

Haematology

A neutrophilic leucocytosis with a left shift is the mostcommon haematological finding (36–73%), but the absenceof these changes does not preclude the diagnosis of pyotho-rax (Demetriou et al., 2002; Barrs et al., 2005). A neutrope-nia with a degenerative left shift will occur with advancedsepsis and sequestration of neutrophils in the pleural space.One study found that the white cell count was significantlyhigher in cats that survived (Waddell et al., 2002). Toxicchanges in neutrophils are usually identified on examina-tion of the peripheral blood film (Ottenjann et al., 2006).Mild to moderate anaemia is seen in <20% of cases (Jonas,1983; Demetriou et al., 2002; Barrs et al., 2005).

Biochemistry

The most common abnormalities observed in serum bio-chemistry are hypoalbuminaemia, hyperglobulinaemia,hypo- or hyper-glycaemia, hyponatraemia, hypochlora-emia, hypocalcaemia and mild elevations of aspartate ami-notransferase (AST) and bilirubin (Demetriou et al., 2002;Waddell et al., 2002). Hypoalbuminaemia is a commonfinding in sepsis, attributed to increased vascular perme-ability and decreased hepatic synthesis due to a shifttowards synthesis of positive acute phase proteins (Bradyet al., 2000; Paltrinieri, in press). In one study, cholesterolconcentrations were significantly lower in survivors than innon-survivors, although the significance of this finding wasunclear (Waddell et al., 2002).

Retrovirus testing

Data on the feline leukaemia virus (FeLV) and felineimmunodeficiency virus (FIV) status of cats with pyotho-rax are limited. Even in large retrospective studies, retrovi-rus status has not been obtained consistently andconsequently the population tested is likely to be biasedtowards cases where a clinical suspicion of retrovirus infec-tion existed. Interpretation of the data for FeLV is furthercomplicated since it spans a 30 year period during whichtime testing methodologies improved (Hardy and Zucker-man, 1991) and the prevalence of the virus declined world-wide (Louwerens et al., 2005).

Overall, when data are combined, 3/68 (4.4%) of catswith pyothorax tested for FeLV were positive (Pidgeon,1978; Thompson et al., 1992; Demetriou et al., 2002; Wad-dell et al., 2002; Barrs et al., 2005). Of these cats, one diedand two were euthanased. Where persistent FeLV infectionis identified in the diagnostic investigation of cats with pyo-thorax, euthanasia is recommended because of the poorprognosis (Jarrett and Hosie, 2004). Of 51 cats with pyo-thorax tested for FIV, three (5.8%) were seropositive(Thompson et al., 1992; Demetriou et al., 2002; Waddellet al., 2002 Barrs et al., 2005). All three survived, at leastin the short term. One cat was treated for recurrence ofpyothorax, which is seen in 5–14% of all cases managedmedically (Gruffydd-Jones and Flecknell, 1978; Jonas,1983; Waddell et al., 2002; Barrs et al., 2005), but remainedwell at follow up 3 months later.

The prevalence of FIV worldwide ranges from 1–14% inasymptomatic cats and up to 44% in sick cats (Hartmann,1998). Notwithstanding the limitations discussed above,the currently available data do not support an associationbetween FIV infection and pyothorax, either as a predis-posing event or a prognostic indicator. Interestingly, sincethe major route of transmission of FIV is believed to bebiting (Pedersen et al., 1989), these data similarly do notsupport biting as a major mechanism of infection of thepleural space. Prospective studies will provide useful infor-mation on any association between retroviruses andpyothorax.

V.R. Barrs, J.A. Beatty / The Veterinary Journal 179 (2009) 163–170 167

Diagnostic imaging

Thoracic ultrasonography is an expedient, non-invasivetechnique for confirmation of a moderate to large volumepleural effusion in the dyspnoeic patient. In contrast totransudates, which are anechoic, the exudate in pyothoraxis hypoechoic or complex echoic. The effusion is often sep-tate due to fibrinous or fibrous tags extending between theparietal and visceral pleura (Yang et al., 1992; Mattoonand Nyland, 2002). Pulmonary abscesses and restrictivepleuritis can also be identified ultrasonographically. Wheresonography is not available, a single dorso-ventral radio-graphic view will confirm the presence of a large volumepleural effusion while requiring minimal restraint. Effusionsare bilateral in 70–90% of cases (Gruffydd-Jones and Flec-knell, 1978; Demetriou et al., 2002; Waddell et al., 2002;Barrs et al., 2005). Severe hypoxemia may occur if cats withlarge volume effusions are placed in lateral recumbency forradiography. Alternatively, horizontal beam radiographymay be used to detect pleural effusion in the standingpatient (Myer, 1978).

Thoracic radiography is more sensitive than ultrasonog-raphy in detecting small volume pleural effusions. On aventrodorsal radiographic view, small volumes of fluidresult in rounding or filling of the costophrenic angles(Myer, 1978). Other radiographic signs of pleural effusioninclude retraction of the lobar borders from the thoracicwall together with pulmonary atelectasis, accentuation oflobar edges and accentuation of interlobar fissures. A com-plete set of thoracic radiographs should be obtained afterdrainage of pleural effusion to assess for underlying bron-chopulmonary disease.

Thoracocentesis

Needle thoracocentesis facilitates collection of diagnosticspecimens and therapeutic stabilisation of the patient. Sickcats usually tolerate thoracocentesis without sedation.Diagnostic thoracocentesis is performed, preferably underultrasound-guidance, at the ventral third of the sixth, sev-enth or eighth intercostal space with the cat positioned insternal recumbency. Care should be taken to avoid intercos-tal vessels and nerves located near the caudal rib margin.Prior subcutaneous instillation of 1 mL of local anaesthetic(e.g. 2% lignocaine) at the thoracocentesis site helps facili-tate the procedure. A 21- or 23-gauge butterfly needle withextension tubing and three-way-tap is attached to a syringefor this purpose. Once a sample has been obtained for diag-nostics, thoracocentesis is continued to remove as muchpleural exudate as possible prior to general anaesthesia.Unless imaging indicates a unilateral effusion, initial thora-cocentesis should be carried out bilaterally.

Pleural fluid characteristics

Gross characteristics: The gross characteristics of the fluidare usually sufficient to direct the clinician towards a diag-

nosis of pyothorax. In particular, the fluid should beassessed for odour since mixed anaerobic infections aretypically malodorous (Dow and Jones, 1987a). While afoul-smelling pleural effusion almost certainly indicatesanaerobic infection, a lack of odour does not rule out pyo-thorax. Rather, it should arouse suspicion for an unusualpathogen (e.g. aerobes, yeast or Mycoplasma spp.) or alter-native disease process, such as feline infectious peritonitisor a malignant effusion. Septic exudates are usually turbidto opaque and flocculent material can often be appreciated.The colour is usually creamy, but can be pink, green-tingedor sanguinous (Gruffydd-Jones and Flecknell, 1978; Sherd-ing, 1979; Jonas, 1983).

Complete diagnostic investigation, including fluid anal-ysis, cytology and culture as outlined below, should be car-ried out in all suspected cases of pyothorax, even when thegross characteristics are highly suggestive. This will confirmthe diagnosis, identify unusual infections, non-septic pro-cesses or concurrent problems (e.g. lungworm), and directappropriate antimicrobial treatment (Barrs and Beatty, inpress).

Fluid analysis: Results of laboratory analysis are consistentwith an exudate, including protein >30 g/L, total nucleatedcell count >7000/lL and specific gravity P1.025 (Greeneand Reinero, 2006). Neutrophils predominate in septic effu-sions (>85% of total nucleated cell count) (Gruffydd-Jonesand Flecknell, 1978; Padrid, 2000). Occasionally, othereffusions such as those associated with neoplasia or effusivefeline infectious peritonitis, may need to be differentiatedfrom the septic exudate of pyothorax. The measurementof lactic dehydrogenase (LDH), glucose and pH has beenadvocated to assist in the classification of feline pleuraleffusions. In septic effusions, LDH is typically >200 IU/L,pH is 66.9 and glucose is usually <1.68 mmol/L and lessthan a concurrent blood glucose measurement (Padrid,2000). Neoplastic exudates typically have a normal or highpH (P7.4), low neutrophil count (<30%) and glucose of0.5–4.5 mmol/L (Padrid, 2000). In effusive FIP, the proteincontent is high (>35 g/L) consistent with an exudative pro-cess, whereas the nucleated cells count is low, consistentwith a modified (<5000 cells/lL) or even a pure transudate(<1000/lL) (Hartmann, 2005; Addie and Jarrett, 2006).

Cytology: Cytological evaluation of pleural fluid smears ishighly recommended to identify the presence and morphol-ogy of bacteria or other infectious organisms (Gruffydd-Jones and Flecknell, 1978; Jonas, 1983; Walker et al.,2000; Demetriou et al., 2002; Barrs et al., 2005). Infectiousagents may not be identified in cases where prior antimicro-bial therapy has been administered or due to non-staining(e.g. Mycoplasma spp.). Cytological findings should becompared with culture results to identify discrepancies incausation. Cytology could enable detection of polymicrobi-al infections if, for example, the culture is negative or ifonly one bacterial species is isolated. Pleural fluid culturewill be negative in obligate anaerobic infections if laborato-

168 V.R. Barrs, J.A. Beatty / The Veterinary Journal 179 (2009) 163–170

ries use only routine aerobic culture techniques. In mixedinfections, only the aerobic component of the infection willbe cultured. Further, isolation rates of anaerobes aredecreased when primary incubation periods are too short(Love et al., 1982).

The Gram stain is the most important tool for rapidassessment of bacteria in pleural fluid. Acid-fast stainsaid in differentiation of Nocardia spp. from Actinomyces

spp. and Filifactor spp., since the former are partiallyacid-fast. In actinomycosis and Filifactor villosus infec-tions, other oropharyngeal bacterial species are likely tobe identified in pleural fluid. Nocardia spp. infections usu-ally occur as a single isolate (Malik et al., 2006).

In-house cytological examination of pleural fluid is use-ful to determine empiric antimicrobial therapy prior to cul-ture and susceptibility results. Modified Wright–Giemsastains (e.g. ‘Diff-Quik’; Dade Shearing) are readily avail-able in a practice setting. Polymicrobial infections of obli-gate anaerobes and facultative bacteria typically featurelarge numbers of degenerate neutrophils, a small propor-tion of mononuclear inflammatory cells and large numbersof pleomorphic, intracellular and/or extracellular bacteria.Cell types less commonly identified include erythrocytes,mesothelial cells and epithelial cells. Any combination offilamentous bacteria (e.g. Filifactor villosus), cocci (e.g.Peptostreptococcus spp.) or rods may be present. Bacterialrods may be non-enteric facultative bacteria (e.g. Pasteu-

rella spp.), enteric facultative bacteria (e.g. E. coli) or obli-gate anaerobes (e.g. Bacteroides spp., Prevotella spp.,Porphyromonas spp. or Fusobacterium spp.) (Love et al.,1982; Walker et al., 2000).

Sample handling for culture

Careful attention should be paid to sample handling.Pleural fluid should be collected in ethylene diaminetetraacetic acid (EDTA) for cell counts and cytology, whilea sterile container should be used for culture. Aerobic andanaerobic culture should be requested. For reliable anaero-bic culture results, oxygen must be excluded from the trans-port specimen. Commercial anaerobic specimen collectorsare available (e.g. Vacutainer Anaerobic Specimen collector,BD Diagnostics). This device allows collection and transportof liquid specimens with 72 h viability of fragile anaerobicspecimens. A built-in oxygen-eliminating system convertsoxygen and hydrogen to water within the system to producean anaerobic environment and an indicator changes colourto signal when anaerobiosis has been achieved within thedevice. Failure to exclude oxygen from the specimenreceptacle will result in false negative culture results in somecases (Love et al., 1982). The organisms isolated from casesof feline pyothorax have been discussed earlier.

Conclusions

Pyothorax is predominantly a disease of young cats.Although the disease is likely to have progressed insidi-

ously, most patients present acutely. Pyothorax in cats ismost often caused by obligate and facultative anaerobesof oropharyngeal origin. Para-pneumonic spread of infec-tion after colonisation and invasion of lung tissue by oro-pharyngeal flora seems to be the most frequent cause offeline pyothorax and contests the widespread belief thatdirect inoculation of pleural cavity by bite wounds is morecommon. Around 20% of cases of feline pyothorax, partic-ularly in kittens, are caused by unusual bacterial, fungal orprotozoal pathogens, emphasising the need for pleural fluidcytology and culture. Cytology, including Gram and,where appropriate, acid-fast stains, should be requested,in addition to aerobic and anaerobic culture, since thesetechniques are complimentary. In-house cytology of diag-nostic samples obtained by thoracocentesis provides usefulinformation for the clinician while laboratory results arepending.

Conflict of interest statement

None of the authors of this paper has a financial or per-sonal relationship with other people or organisations thatcould inappropriately influence or bias the content of thepaper.

Acknowledgements

The authors thank Dr Katherine Briscoe for assistancein preparation of the manuscript.

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