Small Animal Medicine, Faculty of Veterinary Science, The University of Sydney, NSW, Australia
Infectious agents of the lower respiratory tract (LRT) of cats include bacteria, parasites (lungworm, heartworm, toxoplasmosis), fungi (cryptococcosis, aspergillosis) and viruses (FHV-1, virulent systemic FCV, coronavirus, H1N1). Common bacterial and parasitic causes are addressed in this review.
Mycoplasmas, prokaryotic organisms without a cell wall, are commensals of the upper respiratory tract (URT) of cats. Their role as ocular/URT pathogens is well characterised. Mycoplasmas are also an important cause of LRT infection in cats. However, whether they act as primary pathogens or secondary pathogens only capable of colonizing diseased airways is less clear. Mycoplasmas (M. felis, M. gateae, M. feliminutum) have been detected by culture or PCR in 15 to 22% of cats with LRT disease in the USA, Australia and UK.1-3 They have been reported to cause bronchopneumonia, focal pulmonary abscessation and pyothorax spontaneously in owned cats2,4 and pneumonia after experimental inoculation in kittens. Evidence is mounting for a pathogenic role of mycoplasmas (M. pneumoniae) in triggering acute exacerbations in humans with chronic asthma. It has been speculated that mycoplasmas could be a similar trigger for feline bronchitis/asthma, although evidence is lacking.
Mycoplasmas have fastidious growth requirements and are short-lived outside the host. They are cultured from bronchoalveolar (BAL) fluid infrequently at commercial laboratories, because of loss of viability during transport and the need for specialized media. Mycoplasmas can be detected in BAL fluid by PCR. However, detection by culture or by PCR must be interpreted together with BAL cytology and culture results. The presence of squamous epithelial cells and light, mixed bacterial growth suggests URT contamination, while the finding of numerous inflammatory cells and absence of mixed bacterial growth suggests a pathogenic role for mycoplasmas.
Mycoplasma spp. are generally susceptible to doxycycline, macrolides and fluoroquinolones. Doxycycline is an appropriate empirical first-choice antimicrobial. Minimum effective treatment durations for Mycoplasma LRT infections have yet to be established. Extrapolating from URT infections, a treatment period of six weeks is recommended (10 mg/kg q 24 h PO or 5 mg/kg q 12 h PO).
Bordetella bronchiseptica, a small gram-negative coccobacillus, is shed in oral and nasal secretions of infected cats. It is a primary pathogen in cats or an URT co-pathogen with respiratory viruses/mycoplasmas.5-6 It also causes chronic respiratory infections in dogs, rabbits and pigs and is a rare cause of zoonotic infection in humans, especially if immunosuppressed. After oronasal exposure mucosal surfaces are colonised, bacteria attach to airway cilia causing stasis, lysis and failure of mucociliary clearance favoring further colonization and chronic infection. Risk factors for infection in cats include multiple-cat environments (catteries/shelters), poor hygiene, young age/immunosuppression and contact with dogs with respiratory disease.
Clinical disease ranges from sneezing, ocular discharge and mild cough to severe LRT disease (dyspnoea, respiratory distress), which can be fatal. Bronchopneumonia is most common in kittens less than 10 weeks of age but can occur in adult cats. Diagnosis is by detection of B. bronchiseptica using PCR (oropharyngeal swabs) and/or culture (BAL fluid). Sensitivity of detection is affected by short survival and fastidious growth requirements. BAL cytology is characterised by neutrophils, macrophages, bacteria and epithelial cells. Where cultured, treatment should be based on antimicrobial susceptibility testing. It is usually susceptible to doxycycline, the antibiotic of choice for first-line therapy. Isolates are also usually susceptible to marbofloxacin and the long, postantibiotic effect of this drug could improve in vivo efficacy.7 Resistance to ampicillin and trimethoprim is common. Amoxicillin-clavulanate is not recommended due to poor distribution into respiratory secretions. Minimum effective duration of therapy has not been determined. Early treatment of URT infections is recommended to prevent LRT involvement. Long courses of therapy may be required to resolve LRT infections.
Other LRT Bacterial Pathogens - Pneumonia and Pyothorax
The most common bacteria associated with feline LRT infections, other than B. bronchiseptica and mycoplasmas, are Pasteurella spp., Streptococcus spp. and E. coli. Other bacterial pathogens less commonly involved include obligate anaerobes, Salmonella typhimurium, Pseudomonas spp. and mycobacteria.8 Bacterial infection of the LRT in cats often results in pleuropneumonia and pyothorax. Similar to cat-bite abscesses the majority of cases of pyothorax in cats are polymicrobial infections caused by obligate and facultative anaerobic bacteria derived from the feline oropharynx, including Pasteurella spp.9 Pyothorax occurs mainly in cats aged 4–6y, although cats of any age can be affected. There is no breed, nor sex predisposition. Oropharyngeal microbiota can gain access to the pleural space by aspiration, direct penetration from a bite wound or by haematogenous spread from a distant wound. The evidence suggests that aspiration of oropharyngeal microbiota, subsequent colonisation of the lower respiratory tract and direct extension of infection from the bronchi and lungs is the most common cause of feline pyothorax, as it is for human pyothorax and equine pleuropneumonia.9 Viral URTI can impair mucociliary clearance of respiratory secretions and predispose to accumulation of aspirated oropharyngeal secretions, resulting in colonisation of the lower respiratory tract then pleuropneumonia.
Lungworm - Aelurostrongylus abstrusus
The prevalence of A. abstrusus in stray/feral cats in Europe, USA and Australia ranges from 15 to 25%. Prevalence is lower in owned cats. Most infections are self-limiting and subclinical, although disease may be misdiagnosed as feline bronchial disease (FBD)/asthma. An understanding of the life cycle of this parasite informs the choice of diagnostic tests. Adult lungworms live in terminal bronchioles, alveolar ducts and small pulmonary artery branches.
Eggs shed into alveoli hatch into first stage larvae (L1), ascend the airways and are swallowed and shed in faeces 5 to 6 weeks postinfection. Development to infective third-stage larvae (L3) occurs in intermediate hosts (IH) (e.g., snails, slugs). After ingestion of L3 in IH or paratenic hosts (e.g., birds, rodents), L3 migrate to the lungs from the gastrointestinal tract via the circulatory system within 24 h. Adult worms can survive 2 years or longer.
Clinical disease is more likely in kittens and immunosuppressed adult cats. Signs range from mild coughing to severe respiratory distress and pneumothorax. Complications include bacterial bronchopneumonia and pyothorax from A. abstrusus larvae coated with enteric bacteria (e.g., Salmonella, E. coli) during migration from the gastrointestinal tract.2,10 Clinical signs are most severe 6 to 13 weeks after infection when large numbers of eggs and L1 are produced. Clinical signs and faecal larval shedding often cease within two to three months but can recur with stress or immunosuppression.
Peripheral eosinophilia is a common hematological finding, while radiographic findings depend on chronicity of infection and include small, poorly defined, nodules, most numerous in the caudal lobes, severe alveolar infiltrates, bronchial and interstitial patterns, lobar pulmonary arterial enlargement, pleural effusion and pneumothorax. The faecal Baermann sedimentation test detects L1 and is frequently used for diagnosis, and in one study comparing it with bronchoalveolar lavage (BAL) examination, faecal sedimentation-flotation and histologic examination for detection of A. abstrusus infection, the Baermann technique was most sensitive (86%).11 Submission of three consecutive faecal samples is recommended to increase sensitivity of L1 detection. BAL cytology should not be relied upon to rule out infection due to low sensitivity (36%).11 Molecular testing using PCR performed on pharyngeal swabs to detect A. abstrusus rDNA is highly sensitive (96.6%) and specific (100%)12 and is a recommended noninvasive diagnostic test where available.
Single administration of topical "spot-on" imidacloprid 10%/moxidectin 1% (Advocate, Bayer)13 or emodepside 2.1%/praziquantel 8.6% (Profender, Bayer)14 or treatment with fenbendazole administered (50 mg/kg q 24 h PO for 3 consecutive days) were 99–100% efficacious in eliminating faecal L1 shedding 28 +/- 2 days post-treatment. In some cases longer coursers of fenbendazole (10 to 15 days) are necessary to eliminate infection. Supportive therapies in cats that do not have bacterial bronchopneumonia include oral corticosteroids (prednisolone 2 mg/kg/day) to reduce the inflammatory response during worm death, and bronchodilators (e.g., oral terbutaline 0.3–1.25 mg/cat PO q 12 h).
Lungworm - Eucoleus aerophilus (Previously Capillaria aerophila)
The prevalence of E. aerophilus worldwide is somewhat lower than A. abstrusus ranging from 3–6% in domestic and stray cats. The life cycle is direct, although earthworms may act as paratenic hosts. Adult worms reside embed in the epithelium of the trachea, bronchi and bronchioles. Eggs are coughed up, swallowed and passed in the faeces. Infective larvae develop within the egg in 30–45 days and can survive in the environment for up to one year. Ingested ova hatch in the intestine and larvae migrate to the lungs haematogenously within a week. The prepatent period is 6 to 8 weeks and infections remain patent for 8 to 11 months.
Infections are often subclinical although clinical disease may be more common than previously thought. E. aerophilus ova were detected in the faeces of 11 of 200 feline convenience faecal samples and respiratory signs were present in 8/11 cases.15 Clinical signs include coughing, wheezing and sneezing. Heavy worm burdens cause severe bronchitis and bronchopneumonia and can be fatal. E. aerophilus is zoonotic and can cause pulmonary capillariasis in humans. Diagnosis is by detection of ova in faecal flotation. Adult nematodes are detected occasionally in bronchoalveolar lavage fluid (Barrs et al.).16 Care should be taken to differentiate the double-operculated ova of E. aerophilus from intestinal Trichuris spp. Specific treatment protocols have not been evaluated, but fenbendazole and abamectin (AVOMEC®; Merial) 300 µg/kg SC, two weeks apart) have been used successfully.16
Heartworm-Associated Respiratory Disease (HARD)
Cats are at risk of Dirofilaria immitis infection wherever disease is endemic in dogs.17 Due to natural resistance of cats to D. immitis infection, there is a low rate of maturation of heartworm larvae to adult worms. However, a unique syndrome of bronchointerstitial inflammation and pulmonary arteriolar hypertrophy known as HARD, can develop in the absence of adult worms approximately three months postinfection. Clinical signs include dyspnoea, coughing and wheezing. Histologic changes persist after death of immature adults (L5). Cats with HARD are heartworm-antigen negative, usually heartworm-antibody positive and have a bronchointerstitial pattern on thoracic radiographs. Optimal treatments for HARD are not known. Adulticide therapy is contraindicated in cats with adult heartworm infections due to treatment toxicity and high risk of mortality associate with worm death. Use of heartworm prophylaxis eliminates larvae in the L3–L4 stages, preventing the development of HARD.
See Toxoplasmosis notes in these Proceedings, also by the author.
1. Randolph JF, et al. Am J Vet Res. 1993;54:897.
2. Foster SF, et al. J Feline Med Surg. 2004;6:167.
3. Reed N, et al. J Feline Med Surg. 2012: Epub before print.
4. Foster SF, et al. Aust Vet J. 1998;76:460.
5. Speakman AJ, et al. J Small Anim Pract. 1999;40:252.
6. Egberink H, et al. J Feline Med Surg. 2009;11:610.
7. Carbone M, et al. Vet Microbiol. 2001;81:79.
8. Foster SF, Martin P. J Feline Med Surg. 2011;13:313.
9. Barrs VR, Beatty JA. Vet J. 2009;179:163.
10. Barrs VR, et al. Aust Vet J. 1999;77:229.
11. Lacorcia L, et al. J Am Vet Med Assoc. 2009;235:43.
12. Traversa D, et al. J Clin Microbiol. 2008;46:1811.
13. Traversa D, et al. Parasitol Res. 2009;105:S55.
14. Traversa D, et al. Parasitol Res. 2009;105:S83.
15. Traversa D, et al. Res Vet Sci. 2009;87:270.
16. Barrs VR, et al. Aust Vet J. 2000;78:154.
17. Lee AC, Atkins CE. Topic Companion Anim Med. 2010;25:224.