Feline pyothorax - new insights into an old problem_part 1. Aetiopathogenesis and diagnostic investi

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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 penetration from a bite wound has been postulated to be a major route of infection. New information has challenged this dogma and indicated 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-part review, the clinical findings in feline pyothorax are discussed with a focus on an improved understanding of the aetiopathogenesis of the disease and subsequent implications for diagnostic investigation. Ó 2008 Elsevier Ltd. All rights reserved.

Keywords: Thoracic empyema; Pleural fluid; Infection; Cat

Introduction Pyothorax, or thoracic empyema, describes infection of the pleural space characterised by accumulation of a purulent exudate. Some of the earliest descriptions of pyothorax in humans were made by Hippocrates in the 4th century BC (Miller, 2000). Reports of pyothorax affecting domestic cats have been available in the veterinary literature for half a century (Wilkinson, 1956; Holzworth, 1958) but, although it is encountered commonly in small animal practice, there are no data on the incidence of pyothorax in the cat. Much of the published literature exists as descriptive accounts, including individual case reports, book chapters or non-peer-reviewed articles.

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

*

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).

1090-0233/$ - see front matter Ó 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.tvjl.2008.03.011

Jones and Flecknell, 1978; Pidgeon, 1978; Jonas, 1983; Davies and Forrester, 1996; Walker et al., 2000; Demetriou et al., 2002; Waddell et al., 2002; Barrs et al., 2005). Our understanding of the aetiopathogenesis of pyothorax has been further informed by improved techniques for anaerobic culture (Walker and Richardson, 1981; Dow and Jones, 1987b). Available evidence suggests that para-pneumonic spread is currently the most common route of infection of the pleural space. However, this may not have always been the case. The relative frequencies with which different routes of infection of the pleural space occur may have altered with changes in husbandry. For example, increased neutering, confinement and routine treatment with antibiotics after a cat fight may have reduced the incidence of pyothorax due to penetrating trauma. Improved prophylaxis and management for viral upper respiratory tract (URT) and lungworm infections and improved nutrition may also have had an impact.

In this first part of a two-part review we focus on the clinico-pathological findings and the advances in the understanding of the aetiopathogenesis and diagnostic investigation of feline pyothorax. Subsequent recommen-

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

Signalment Pyothorax predominantly affects young cats (mean age 4–6 years), although cats of any age can be affected (Pidgeon, 1978; Davies and Forrester, 1996; Walker et al., 2000; Demetriou et al., 2002; Waddell et al., 2002; Barrs et al., 2005). No breed or gender predisposition has been identified.

Aetiopathogenesis An understanding of aetiopathogenesis underpins recommendations for investigation, treatment and prophylaxis. Information on the mechanisms of infection of the pleural space has remained elusive since it is often not determined in individual cases either ante- or post-mortem (Sherding, 1979; Bauer, 1986; Sherding, 1994; Demetriou et al., 2002; Waddell et al., 2002). Given the protracted course of the disease, by the time clinical signs of pyothorax develop, evidence of any inciting cause may no longer be present. Possible routes of infection include extension from an adjacent structure (bronchopneumonia, parapneumonic spread, oesophageal rupture, mediastinitis or sub-phrenic infection), direct inoculation (penetrating trauma, migrating foreign body, thoracocentesis or thoracic surgery) or haematogenous or lymphatic spread from a distant site (systemic sepsis).

Oropharyngeal flora Bacterial isolates from the majority of cases of pyothorax are polymicrobial and similar in composition to the normal feline oropharyngeal flora (Love et al., 1982, 1989, 1990, 2000). Isolates include obligate and facultative anaerobic bacteria; Bacteroidaceae (Bacteroides spp., Porphyromonas spp., Prevotella spp.), Fusobacterium spp., Peptostreptococcus spp., Clostridium spp., Actinomyces spp., Eubacterium spp., Propionibacterium spp., Filifactor villosus, Pasteurella multocida, Streptococcus spp. and Mycoplasma spp. (Pidgeon, 1978; Thompson et al., 1992; Walker et al., 2000; Gulbahar and Gurturk, 2002; Wegner and Pablo, 2006). The question is: ‘How do these oropharyngeal flora reach the pleural space?’

Aspiration versus bite wounds Oropharyngeal flora could gain access to the pleural space by aspiration, direct penetration from a bite wound or by haematogenous spread from a distant wound. Many sources, including most standard texts, list penetrating wounds, migrating foreign bodies and oesophageal tears ahead of parapneumonic spread as common causes of pyothorax (Pre´vot et al., 1961; Hayward, 1968; Sherding,

1994; Hawkins, 2003; Mertens et al., 2005; Greene and Reinero, 2006). However, available evidence suggests that aspiration of oropharyngeal flora is the most significant route.

A recent retrospective study demonstrated that aspiration of oral flora was the most likely mechanism of pleural space infection in 15/18 (78%) cats in which probable mechanisms of pleural space infection were identified (Barrs et al., 2005). Aspiration of oropharyngeal flora, subsequent colonisation of the lower respiratory tract and direct extension of infection from the bronchi and lungs is the most common cause of human anaerobic pyothorax and equine pleuropneumonia (Bartlett, 1993; Racklyeft et al., 2000; Schiza and Siafakas, 2006). In human anaerobic lung infections, tissue necrosis results in abscess formation and/or bronchopleural fistula with subsequent extension to the pleural space (Bartlett, 1993).

Pleuropneumonia is a common sequel to transportation in horses. Mucociliary clearance of lower respiratory secretions is impaired when horses are restrained with their heads elevated; this results in accumulation of aspirated oropharyngeal flora and increased risk of pleuropneumonia (Racklyeft et al., 2000). Viral URT infection may also temporarily impair the mucociliary escalator in cats, humans and horses (Carson et al., 1985; Willoughby et al., 1992; Gaskell et al., 2004), predisposing them to pleuropneumonia.

In necropsies of cats with pyothorax, pneumonia or focal 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). Diffuse or focal pulmonary lesions have been noted in numerous other reports (Wilkinson, 1956; Malik et al., 1991; Waddell et al., 2002; Doyle et al., 2005; Wegner and Pablo, 2006).

These lesions support a pathomechanism of para-pneumonic spread. Cats with pyothorax are 3.8 times as likely to have come from multi-cat households compared to control cats (Waddell et al., 2002). The authors suggested that inter-cat aggression may account for the increased risk in this environment. However, behavioural studies do not support the notion of significant aggression in multi-cat households at least when these populations are stable (Crowell-Davis et al., 2004). If fight wounds were a significant cause of pyothorax, then free-roaming males would be likely to be overrepresented among cats with pyothorax.

However, neither outdoor access nor sex was identified as risk factors for pyothorax (Waddell et al., 2002). An alternative explanation for the increased risk of pyothorax in multi-cat environments may be related to the greater risk of developing viral URT infections (Binns et al., 2000).

Antecedent URT infection has been recognised as a predisposing event in 15% and 26% of cases of feline pyothorax (Jonas, 1983; Barrs et al., 2005) and in individual case reports (Malik et al., 1991).

Direct inoculation of oral flora into the thorax from a bite wound is likely to be the initiating event in some cases of pyothorax and could result in pleuritis without

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

pulmonary involvement. Para-pneumonic spread of infection could occur if inoculation of the lung occurred during biting. Where thoracic wounds have been identified in necropsy studies, it is not clear what proportion of cats had concurrent pulmonary abscessation (Jonas, 1983; Waddell et al., 2002). However, in cases where pulmonary abscessation has been identified, concurrent thoracic wounds were uncommon (Hayward, 1968; Pidgeon, 1978; Davies and Forrester, 1996; Brady et al., 2000; Waddell et al., 2002).

In a case series of feline pyothorax reported 25 years ago, 8/20 cats had evidence of thoracic wounds, including five bite wounds and three wounds of unknown origin (Jonas, 1983). In this study, 9/20 cats (45%) were entire males. It is not known whether intact males, more likely to exhibit territorial aggression, were overrepresented in this population compared to the normal hospital population at that time. Interestingly, the study by Waddell et al. (2002) demonstrated a greater proportion of entire cats, both male and female, in the pyothorax group compared with controls. Whether this attained statistical significance is not clear. If neuter status is identified as a risk factor in future studies, it would be interesting to determine whether entire animals with pyothorax are free-roaming, and thus more likely to fight, or whether they are part of stable breeding colonies where viral URT infections may impact. More recently, two case series have identified thoracic 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 habits in the last 25 years – including more neutered cats with restricted territories, this route of infection is now less common (Baldock et al., 2003; Clancy et al., 2003).

Non-oropharyngeal flora Less than 20% of cases of feline pyothorax are caused by infectious agents other than oropharyngeal flora including Staphylococcus spp., Rhodococcus equi, Nocardia spp., enteric Gram-negative organisms (Escherichia coli, Salmonella spp., Klebsiella spp., Proteus spp.) non-enteric Gram-negative organisms (Pseudomonas spp.) and protozoa (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; Barrs et al., 2005). Fungal causes of feline pyothorax are rare and include Cryptococcus spp., Candida albicans and Blastomyces dermatitidis (McCaw et al., 1984; Sherding, 1994; Barrs et al., 2005).

Mechanisms of infection of the pleural space with nonoropharyngeal flora include penetrating thoracic trauma not associated with a cat bite. However, if environmental contamination of thoracic wounds were a common mechanism, a higher isolation rate of saprophytic bacteria such as Nocardia spp., Pseudomonas spp. and Mycobacteria spp. would be expected. In contrast to dogs, Nocardia spp. are uncommonly isolated from feline septic pleural effusions.

Infection can occur secondary to inhalation of aerosols,

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including dust (Greene and Reinero, 2006; Malik et al., 2006). Other routes of infection with non-oropharyngeal flora include haematogenous spread from a septic focus (Davies and Forrester, 1996; Demetriou et al., 2002; Barrs et al., 2005), perforation of the oesophagus, trachea, or bronchi (Harai et al., 1995; Barrs et al., 2005), migrating plant material (Jonas, 1983; Pidgeon, 1978) and parasitic migration (Wilkinson, 1956; Hayward, 1968; Barrs et al., 1999).

Pyothorax and/or pneumonia caused by Salmonella spp. has been documented in cats with concurrent Aelurostrongylus abstrusus infestation (Barrs et al., 1999; Foster et al., 2004). Migrating lungworm or ascarid larvae may act as carriers for intestinal bacteria. Non-oropharyngeal pathogens were more likely to be isolated from kittens in one study (Barrs et al., 2005) but this may be because of agerelated infectious or parasitic conditions such as ascarid or lungworm infections.

History and clinical signs Historical and physical examination findings can be attributed to either the presence of a pleural effusion or to systemic illness, the latter being non-specific. Dyspnoea, inappetence and lethargy are the most commonly reported findings, affecting approximately 80% of cases (Jonas, 1983; Demetriou et al., 2002; Waddell et al., 2002; Barrs et al., 2005). Pleural effusion and pulmonary atelectasis cause a restrictive pattern of respiration characterised by an increase in respiratory rate and inspiratory effort and shallow respiratory excursions (Sherding, 1994). Cats typically adopt a crouched, sternally recumbent posture with elbows abducted (Hayward, 1968; Piermattei and Gowing, 1964; Crane, 1976; Sherding, 1979). Poor body condition, dehydration and abnormalities on auscultation (abnormal lung 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 on thoracic percussion (Sherding, 1979). Coughing is reported in 14–30% of cases, reflecting pleuritis and/or concurrent pneumonia (Jonas, 1983; Sherding, 1994; Demetriou et al., 2002; Barrs et al., 2005). Pyrexia has been reported in 28–50% of cases, although some cats in these series had received prior antibiotic treatment (Demetriou et al., 2002; Barrs et al., 2005). Thus, pyrexia at initial presentation 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 severe sepsis, particularly when accompanied by bradycardia (Brady et al., 2000). In the largest retrospective study of 80 cats with pyothorax, bradycardia was significantly more common in cats that were hypothermic (Waddell et al., 2002). These authors also found that non-survivors had significantly lower heart rates when compared with survivors, although not all of these cats were bradycardic, limiting the clinical utility of this observation (Waddell et al., 2002).

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Pyothorax progresses insidiously. The duration of clinical signs prior to diagnosis is typically 1–2 weeks, but it may be months (Jonas, 1983; Davies and Forrester, 1996; Demetriou et al., 2002; Barrs et al., 2005). A protracted course is also supported by the demonstration of granulation tissue on the pleura and the formation of adhesions with subsequent loculation of fluid (Hayward, 1968; Dow and Jones, 1987a). Such is the propensity of the cat to compensate for gradual onset respiratory compromise by reduced activity that signs may be noted only acutely or not at all by the owner. That the dyspnoea can be surprisingly subtle is evidenced by the fact that it had not been observed by 40% of owners in one study (Barrs et al., 2005). Coupled with the non-specific nature of many of the presenting signs, many cats are presented late in the course of the disease. By the time clinical signs of respiratory compromise become obvious in feline patients, minimal respiratory reserve remains. Pyothorax should be considered as a cause of sudden death (Brodrick, 1983; Gulbahar and Gurturk, 2002).

Diagnostic investigation In many cases, clinical examination findings will be indicative of pleural space disease making the diagnostic investigation straightforward. The non-specific nature of signs in some cases, including normothermia in at least 35% of cases and the absence of dyspnoea in 20% of the cats examined supports the use of thoracic imaging in cats with non-specific signs. The relatively subtle changes observed in presenting signs may partially explain why 10–33% of pyothorax cases examined at post-mortem had not been diagnosed ante-mortem (Jonas, 1983; Davies and Forrester, 1996; Waddell et al., 2002).

Minimum database While the results of haematology, biochemistry, urinalysis and retrovirus testing are not crucial for the diagnosis of pyothorax, they should form part of the minimum database to guide management of the patient.

Haematology A neutrophilic leucocytosis with a left shift is the most common haematological finding (36–73%), but the absence of these changes does not preclude the diagnosis of pyothorax (Demetriou et al., 2002; Barrs et al., 2005). A neutropenia with a degenerative left shift will occur with advanced sepsis and sequestration of neutrophils in the pleural space.

One study found that the white cell count was significantly higher in cats that survived (Waddell et al., 2002). Toxic changes in neutrophils are usually identified on examination 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 biochemistry are hypoalbuminaemia, hyperglobulinaemia, hypo- or hyper-glycaemia, hyponatraemia, hypochloraemia, hypocalcaemia and mild elevations of aspartate aminotransferase (AST) and bilirubin (Demetriou et al., 2002; Waddell et al., 2002). Hypoalbuminaemia is a common finding in sepsis, attributed to increased vascular permeability and decreased hepatic synthesis due to a shift towards synthesis of positive acute phase proteins (Brady et al., 2000; Paltrinieri, in press). In one study, cholesterol concentrations were significantly lower in survivors than in non-survivors, although the significance of this finding was unclear (Waddell et al., 2002).

Retrovirus testing Data on the feline leukaemia virus (FeLV) and feline immunodeficiency virus (FIV) status of cats with pyothorax are limited. Even in large retrospective studies, retrovirus status has not been obtained consistently and consequently the population tested is likely to be biased towards cases where a clinical suspicion of retrovirus infection existed. Interpretation of the data for FeLV is further complicated since it spans a 30 year period during which time testing methodologies improved (Hardy and Zuckerman, 1991) and the prevalence of the virus declined worldwide (Louwerens et al., 2005).

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

The prevalence of FIV worldwide ranges from 1–14% in asymptomatic cats and up to 44% in sick cats (Hartmann, 1998). Notwithstanding the limitations discussed above, the currently available data do not support an association between FIV infection and pyothorax, either as a predisposing event or a prognostic indicator. Interestingly, since the major route of transmission of FIV is believed to be biting (Pedersen et al., 1989), these data similarly do not support biting as a major mechanism of infection of the pleural space. Prospective studies will provide useful information on any association between retroviruses and pyothorax.

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Diagnostic imaging Thoracic ultrasonography is an expedient, non-invasive technique for confirmation of a moderate to large volume pleural effusion in the dyspnoeic patient. In contrast to transudates, which are anechoic, the exudate in pyothorax is hypoechoic or complex echoic. The effusion is often septate due to fibrinous or fibrous tags extending between the parietal and visceral pleura (Yang et al., 1992; Mattoon and Nyland, 2002). Pulmonary abscesses and restrictive pleuritis can also be identified ultrasonographically. Where sonography is not available, a single dorso-ventral radiographic view will confirm the presence of a large volume pleural effusion while requiring minimal restraint. Effusions are bilateral in 70–90% of cases (Gruffydd-Jones and Flecknell, 1978; Demetriou et al., 2002; Waddell et al., 2002; Barrs et al., 2005). Severe hypoxemia may occur if cats with large volume effusions are placed in lateral recumbency for radiography. Alternatively, horizontal beam radiography may be used to detect pleural effusion in the standing patient (Myer, 1978).

Thoracic radiography is more sensitive than ultrasonography in detecting small volume pleural effusions. On a ventrodorsal radiographic view, small volumes of fluid result in rounding or filling of the costophrenic angles (Myer, 1978). Other radiographic signs of pleural effusion include retraction of the lobar borders from the thoracic wall together with pulmonary atelectasis, accentuation of lobar edges and accentuation of interlobar fissures. A complete set of thoracic radiographs should be obtained after drainage of pleural effusion to assess for underlying bronchopulmonary disease.

Thoracocentesis Needle thoracocentesis facilitates collection of diagnostic specimens and therapeutic stabilisation of the patient. Sick cats usually tolerate thoracocentesis without sedation.

Diagnostic thoracocentesis is performed, preferably under ultrasound-guidance, at the ventral third of the sixth, seventh or eighth intercostal space with the cat positioned in sternal recumbency. Care should be taken to avoid intercostal 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 facilitate the procedure. A 21- or 23-gauge butterfly needle with extension tubing and three-way-tap is attached to a syringe for this purpose. Once a sample has been obtained for diagnostics, thoracocentesis is continued to remove as much pleural exudate as possible prior to general anaesthesia.

Unless imaging indicates a unilateral effusion, initial thoracocentesis should be carried out bilaterally.

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

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nosis of pyothorax. In particular, the fluid should be assessed for odour since mixed anaerobic infections are typically malodorous (Dow and Jones, 1987a). While a foul-smelling pleural effusion almost certainly indicates anaerobic infection, a lack of odour does not rule out pyothorax. Rather, it should arouse suspicion for an unusual pathogen (e.g. aerobes, yeast or Mycoplasma spp.) or alternative disease process, such as feline infectious peritonitis or a malignant effusion. Septic exudates are usually turbid to opaque and flocculent material can often be appreciated.

The colour is usually creamy, but can be pink, green-tinged or sanguinous (Gruffydd-Jones and Flecknell, 1978; Sherding, 1979; Jonas, 1983).

Complete diagnostic investigation, including fluid analysis, cytology and culture as outlined below, should be carried out in all suspected cases of pyothorax, even when the gross characteristics are highly suggestive. This will confirm the diagnosis, identify unusual infections, non-septic processes or concurrent problems (e.g. lungworm), and direct appropriate antimicrobial treatment (Barrs and Beatty, in press).

Fluid analysis: Results of laboratory analysis are consistent with an exudate, including protein >30 g/L, total nucleated cell count >7000/lL and specific gravity P1.025 (Greene and Reinero, 2006). Neutrophils predominate in septic effusions (>85% of total nucleated cell count) (Gruffydd-Jones and Flecknell, 1978; Padrid, 2000). Occasionally, other effusions such as those associated with neoplasia or effusive feline infectious peritonitis, may need to be differentiated from the septic exudate of pyothorax. The measurement of lactic dehydrogenase (LDH), glucose and pH has been advocated to assist in the classification of feline pleural effusions. In septic effusions, LDH is typically >200 IU/L, pH is 66.9 and glucose is usually <1.68 mmol/L and less than a concurrent blood glucose measurement (Padrid, 2000). Neoplastic exudates typically have a normal or high pH (P7.4), low neutrophil count (<30%) and glucose of 0.5–4.5 mmol/L (Padrid, 2000). In effusive FIP, the protein content is high (>35 g/L) consistent with an exudative process, whereas the nucleated cells count is low, consistent with 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 is highly recommended to identify the presence and morphology of bacteria or other infectious organisms (GruffyddJones and Flecknell, 1978; Jonas, 1983; Walker et al., 2000; Demetriou et al., 2002; Barrs et al., 2005). Infectious agents may not be identified in cases where prior antimicrobial therapy has been administered or due to non-staining (e.g. Mycoplasma spp.). Cytological findings should be compared with culture results to identify discrepancies in causation. Cytology could enable detection of polymicrobial infections if, for example, the culture is negative or if only one bacterial species is isolated. Pleural fluid culture will be negative in obligate anaerobic infections if laborato-

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

The Gram stain is the most important tool for rapid assessment of bacteria in pleural fluid. Acid-fast stains aid in differentiation of Nocardia spp. from Actinomyces spp. and Filifactor spp., since the former are partially acid-fast. In actinomycosis and Filifactor villosus infections, other oropharyngeal bacterial species are likely to be identified in pleural fluid. Nocardia spp. infections usually occur as a single isolate (Malik et al., 2006).

In-house cytological examination of pleural fluid is useful to determine empiric antimicrobial therapy prior to culture and susceptibility results. Modified Wright–Giemsa stains (e.g. ‘Diff-Quik’; Dade Shearing) are readily available in a practice setting. Polymicrobial infections of obligate anaerobes and facultative bacteria typically feature large numbers of degenerate neutrophils, a small proportion of mononuclear inflammatory cells and large numbers of pleomorphic, intracellular and/or extracellular bacteria.

Cell types less commonly identified include erythrocytes, mesothelial cells and epithelial cells. Any combination of filamentous bacteria (e.g. Filifactor villosus), cocci (e.g.

Peptostreptococcus spp.) or rods may be present. Bacterial rods may be non-enteric facultative bacteria (e.g. Pasteurella spp.), enteric facultative bacteria (e.g. E. coli) or obligate anaerobes (e.g. Bacteroides spp., Prevotella spp., Porphyromonas spp. or Fusobacterium spp.) (Love et al., 1982; Walker et al., 2000).

ously, most patients present acutely. Pyothorax in cats is most often caused by obligate and facultative anaerobes of oropharyngeal origin. Para-pneumonic spread of infection after colonisation and invasion of lung tissue by oropharyngeal flora seems to be the most frequent cause of feline pyothorax and contests the widespread belief that direct inoculation of pleural cavity by bite wounds is more common. Around 20% of cases of feline pyothorax, particularly in kittens, are caused by unusual bacterial, fungal or protozoal pathogens, emphasising the need for pleural fluid cytology and culture. Cytology, including Gram and, where appropriate, acid-fast stains, should be requested, in addition to aerobic and anaerobic culture, since these techniques are complimentary. In-house cytology of diagnostic samples obtained by thoracocentesis provides useful information for the clinician while laboratory results are pending.

Sample handling for culture

Addie, D.D., Jarrett, O., 2006. Feline coronavirus infections. In: Greene, C.E. (Ed.), Infectious Diseases of the Dog and Cat, third ed. Saunders Elsevier, Philadelphia, pp. 88–104.

Anfray, P., Bonetti, C., Fabbrini, F., Magnino, S., Mancianti, F., Abramo, F., 2005. Feline cutaneous toxoplasmosis: a case report.

Veterinary Dermatology 16, 131–136.

Baldock, F.C., Alexander, L., More, S.J., 2003. Estimated and predicted changes in the cat population of Australian households from 1979 to 2005. Australian Veterinary Journal 81, 289–292.

Barrs, V.R., Beatty, J.A., in press. Feline pyothorax – new insights into an old problem: Part 2. Treatment recommendations and prophylaxis.

The Veterinary Journal 179 (2), 171–178.

Barrs, V.R., Swinney, G.R., Martin, P., Nicoll, R.G., 1999. Concurrent Aelurostrongylus abstrusus infection and Salmonellosis in a kitten.

Australian Veterinary Journal 77, 229–232.

Barrs, V.R., Martin, P., Allan, G.S., Beatty, J.A., Malik, R., 2005. Feline pyothorax: a retrospective study 27 cases in Australia. Journal of Feline Medicine and Surgery 7, 211–222.

Bartlett, J.G., 1993. Anaerobic bacterial infections of the lung and pleural space. Clinical Infectious Diseases 16, S255–S428.

Bauer, T., 1986. Pyothorax. In: Kirk, R.W. (Ed.), Current Veterinary Therapy IX. WB Saunders Co, Philadelphia, pp. 292–295.

Binns, S.H., Dawson, S., Speakman, A.J., Cuevas, L.E., Hart, C.A., Gaskell, C.J., Morgan, K.L., Gaskell, R.M., 2000. A study of feline upper respiratory tract disease with reference to prevalence and risk factors for infection with feline calicivirus and feline herpesvirus.

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Brady, C.A., Otto, C.M., Van Winkle, T.J., King, L.G., 2000. Severe sepsis in cats: 29 cases (1986–1998). Journal of the American Veterinary Medical Association 217, 531–535.

Careful attention should be paid to sample handling.

Pleural fluid should be collected in ethylene diamine tetraacetic acid (EDTA) for cell counts and cytology, while a sterile container should be used for culture. Aerobic and anaerobic culture should be requested. For reliable anaerobic culture results, oxygen must be excluded from the transport specimen. Commercial anaerobic specimen collectors are available (e.g. Vacutainer Anaerobic Specimen collector, BD Diagnostics). This device allows collection and transport of liquid specimens with 72 h viability of fragile anaerobic specimens. A built-in oxygen-eliminating system converts oxygen and hydrogen to water within the system to produce an anaerobic environment and an indicator changes colour to signal when anaerobiosis has been achieved within the device. Failure to exclude oxygen from the specimen receptacle will result in false negative culture results in some cases (Love et al., 1982). The organisms isolated from cases of feline pyothorax have been discussed earlier.

Conclusions Pyothorax is predominantly a disease of young cats.

Although the disease is likely to have progressed insidi-

Conflict of interest statement None of the authors of this paper has a financial or personal relationship with other people or organisations that could inappropriately influence or bias the content of the paper.

Acknowledgements The authors thank Dr Katherine Briscoe for assistance in preparation of the manuscript.

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