LAPORAN KASUS

PENYAKIT RESPIRASI

BRONCHOLITHIASIS PADA KUCING

Oleh:

DHARMA AUDIA SAMSURI

NIM: 2009611034

KELOMPOK 17G

LABORATORIUM ILMU PENYAKIT DALAM VETERINER

PENDIDIKAN PROFESI DOKTER HEWAN

FAKULTAS KEDOKTERAN HEWAN

UNIVERSITAS UDAYANA

2021
 PENDAHULUAN

Bronkolitiasis didefinisikan sebagai adanya material yang terklasifikasi atau mengeras

dalam lumen bronkial. Pada manusia, ini adalah kelainan langka dengan kejadian 0,1-0,2%
dari semua penyakit paru (Anwer dan Venkantram., 2011). Broncholithiasis adalah kondisi
yang tidak umum, yang harus dianggap sebagai diagnosis banding untuk kucing dengan
penyakit pernapasan kronis. Kucing yang terkena dapat mengembangkan bronkolitiasis
sekunder akibat penyakit saluran napas bawah inflamasi difus dengan mineralisasi sekresi di
saluran udara.
Bronkolitiasis miliaris telah dikaitkan dengan penyakit pernapasan saluran napas
bawah kucing kronis dan progresif pada kucing, yang awalnya didiagnosis dengan infeksi
spesies Mycoplasma dan tidak memiliki bukti radiografi dari bronkolitiasis ini (Baral., 2010).
Peradangan tanpa bukti infeksi juga hadir dalam dua kasus lain yang dilaporkan. Berdasarkan
kasus kami dan laporan tersebut, adanya bronkolitiasis pada kucing mungkin menunjukkan
adanya peradangan saluran napas bagian bawah, dan penyelidikan untuk hal ini akan
direkomendasikan.

REKAM MEDIK
1. Signalement dan Anamnesa
Pada kasus yang dilaporkan, pasien yang diperiksa yaitu kucing dengan berbagai jenis
(Domestic Shorthair, Cornish Rex, Persia). Pada kasus kucing ras Domestic shorthair
betina berumur 12 tahun, dilaporkan mengalami batuk yang semakin parah selama 2 bulan
terakhir. Kucing tersebut divaksinasi setiap tahun dan diberikan obat cacing secara teratur
(Sanchez et al., 2017). Pada kasus kucing ras Cornish Rex jantan berumur 9 tahun yang
sudah dikebiri, dilaporkan mengalami penurunan berat badan dan tanda-tanda pernapasan
yang semakin memburuk, termasuk batuk dan sesak nafas (Byrne et al., 2016). Pada kasus
kucing ras Persia jantan berumur 14 tahun yang sudah dikebiri dengan berat 5 kg dengan
eksaserbasi batuk kronis selama 2-3 tahun (Talavera et al., 2008).
2. Pemeriksaan Fisik
Pada kasus kucing Domestic shorthair, pemeriksaan fisik menunjukkan takipnea
ringan (frekuensi pernapasan 48 napas per menit) dengan pola pernapasan normal dan
mengi saat inspirasi ringan pada auskultasi paru (Sanchez et al., 2017). Pada kasus kucing
Cornish Rex, pada pemeriksaan fisik kucing memiliki berat badan 4,88 kg dan dalam
kondisi tubuh yang baik. Denyut jantung (180 denyut per menit), laju pernapasan (28 napas
 per menit), dan suhu rektal (37,5°C) normal, tetapi ada upaya peningkatan inspirasi. Pada
auskultasi, suara paru cukup meningkat disemua bidang paru (Byrne et al., 2016). Pada
kasus kucing Persia, pada pemeriksaan fisik kucing dalam keadaan gizi yang baik dan
terlihat waspada dan ceria. Mukosa mulut normal dan CRT kurang dari 2 detik. Pola
pernafasan normal dan saat palpasi laring dan trakea tidak ada tanda-tanda
ketidaknyamanan. Setelah palpasi, muncul 4-6 batuk non-produktif yang parah. Auskultasi
toraks mengungkapkan suara napas yang menonjol di semua bidang paru-paru (Talavera et
al., 2008).
3. Pemeriksaan Penunjang
Pemeriksaan penunjang yang dilakukan pada ketiga kasus menggunakan radiografi
thoraks, kasus pertama menambahkan pemeriksaan bronkoskopi, kasus kedua
menambahkan pemeriksaan CT scan. Pada kasus kucing Domestik shorthair, Cornish Rex,
dan Persia, radiografi thorax menunjukkan adanya kekeruhan mineral pada jaringan paru-
paru dan diseluruh bidang paru-paru serta penebalan dinding bronkial. Pada pemeriksaan
bronkoskopi kucing Domestik shorthair menunjukkan material padat berwarna kuning
muda yang menghalangi sebagian besar lumen bronkus. Pada pemeriksaan CT scan kucing
Cornish Rex menunjukkan adanya peningkatan umum dalam opasitas dinding bronkial di
seluruh toraks.

A
B

Gambar 1. (A) Radiografi ventrodorsal toraks. Banyak kekeruhan mineral tidak

teratur dengan diameter 3-6 mm ditemukan di seluruh bidang paru-paru; (B)
Radiografi lateral toraks. Banyak kekeruhan tidak teratur dengan diameter 3-6 mm
ditemukan di seluruh bidang paru-paru (Sanchez et al., 2017).
 A B

Gambar 2. (A) Gambar bronkoskopi menunjukkan material pada berwarna

kuning muda yang menghalangi sebagian besar lumen bronkus; (B) Gambar
bronkoskopi menunjukkan adanya material kuning pucat di lumen bronkus
(Sanchez et al., 2017).

Gambar 3. Tampilan lateral dan ventrodorsal dari radiografi toraks. Terdapat

pola interstitial retikuler dengan peningkatan opasitas dinding bronkial. Nodul
jaringan lunak dengan bentuk tidak teratur terdapat di dalam bidang belakang
paru-paru, yang terbesar di dalam lobus paru-paru belakang kanan bawah
(Byrne et al., 2016).

Gambar 4. Pada bidang dorsal terdapat focus pelemahan mineral di lobus

paru-paru caudal kanan dan kiri yang terkait dengan cabang segmental
bronkus batang utama caudal. Pada bidang transversal area fokus campuran
mineral dan jaringan lunak atenuasi di lobus paru kaudal kiri tersusun dalam
bentuk tubular yang bersinggungan dengan lobar bronkus (Byrne et al.,
2016).
 A B

Gambar 5. Gambaran radiografi toraks lateral (A) dan dorsoventral (B)

dari kucing Persia jantan berumur 14 tahun (5kg) yang sudah dikebiri,
menunjukkan adanya beberapa kekeruhan mineral yang didistribusikan
secara difus ke seluruh bidang paru-paru (Talavera et al., 2008).

4. Diagnosa
Berdasarkan gejala klinis, pemeriksaan klinis, dan pemeriksaan penunjang pada ketiga
kasus mengalami bronkolitiasis, dan pada kasus pertama bersamaan dengan penyakit
radang saluran napas bawah kronis.
5. Prognosis
Berdasarkan pemeriksaan, pemeriksaan penunjang, dan diagnosa pada ketiga kasus ini
menunjukkan prognosis dubius.
6. Treatment
Pada kasus kucing Domestik shorthair, kucing tersebut diobati dengan
amoksisilin/klavulanat (20 mg / kg IV q8h) dan deksametason (0,1 mg / kg IV sekali),
diikuti dengan prednisolon (0,5 mg / kg PO q12h) karena dicurigai adanya penyakit radang
saluran napas bawah kucing dan ini adalah pendekatan terapeutik standar untuk kondisi ini
oleh tim klinis yang terlibat. Kucing tersebut awalnya diberi antibiotik sambil menunggu
hasil BAL dan terus digunakan sebagai tindakan pencegahan karena pneumotoraks
iatrogenik dan risiko infeksi pleura sekunder dan perbaikan klinis yang sedang
berlangsung. Drain toraks diangkat 3 hari setelah penempatan. Kucing dipulangkan 6 hari
setelah presentasi dengan amoksisilin/klavulanat (20 mg / kg PO q12h) selama 2 minggu
berikutnya, prednisolon (0,5 mg / kg PO q12h) dan nebulisasi dengan saline steril isotonik
selama 5-10 menit setiap 8 jam.
Pada kasus kucing Cornish Rex, pengobatan menggunakan doksisiklin 5 mg/kg q12h
dan prednisolone 2 mg/kg q24h (keduanya per oral). Pada pemeriksaan ulang 1 minggu
kemudian, pemilik melaporkan penurunan frekuensi batuk yang nyata. Pengobatan dimulai
 dengan metered dose inhaler (MDI) yang mengandung salbutamol dan fluticasone dua kali
sehari. Dosis prednisolone dikurangi selama lima hari dan kemudian dihentikan. Pada
pemeriksaan ulang 4 tahun setelah presentasi awal, pemilik melaporkan bahwa ada
perbaikan pada tanda-tanda pernafasan setelah pengobatan awal, tetapi dyspnea dan batuk
sporadic masih terjadi.
Pada kasus kucing Persia dilakukan percobaan pengobatan dengan prednison oral (1
mg/kg/bid selama 2 minggu) dan doksisiklin (5 mg/kg q24h selama 2 minggu) yang
diusulkan. Dua minggu kemudian, frekuensi batuk berkurang secara signifikan. Kemudian
doksisiklin ditarik dan dosis prednisone diturunkan secara perlahan (1 mg/kg 48 jam) dan
ditarik dua minggu kemudian. Pemberian terbutaline intermiten (0,625 mg bid)
direkomendasikan untuk meredakan akut eksaserbasi batuk akut. Selama eksaserbasi,
pemilik percaya terbutaline bermanfaat untuk meredakan batuk. Pada pemeriksaan fisik,
kucing tampak lesu dan depresi. Parameter kardiovaskular dan pernapasan ada di dalam
batas normal. Bidang paru-paru terlihat tidak berubah dibandingkan dengan pemeriksaan
awal, tetapi dengan mineralisasi paru yang lebih luas. Namun kucing tersebut di eutanasi.

PEMBAHASAN
Broncholithiasis adalah kondisi yang tidak umum, yang harus dianggap sebagai
diagnosis banding untuk kucing dengan penyakit pernapasan kronis. Kucing yang terkena
dapat mengembangkan bronkolitiasis sekunder akibat penyakit saluran napas bawah inflamasi
difus dengan mineralisasi sekresi di saluran udara. Bronkolitiasis pada kucing dapat terjadi
akibat penyakit radang saluran napas kronis.
Dalam kasus ini, bronkolitiasis dicurigai secara radiografis dan didiagnosis dengan
adanya sumbatan intraluminal kuning, bahan padat di beberapa bronkus pada bronkoskopi,
konsisten dengan bronkolit. Kasus ini menggambarkan bronkoskopi pertama yang dilaporkan
pada kucing dengan bronkolitiasis. Pada kasus kucing domestic shorthair dimana histopatologi
mengungkapkan hyperplasia dan hipertrofi kelenjar mukosa peribronchiolar dan dua kasus
lainnya hanya menggunakan radiografi thoraks dan CT scan. Dalam pengobatan manusia, CT
scan toraks atau bronkoskopi diperlukan untuk memastikan bronkolitiasis. Pada manusia,
bronkoskopi memiliki sensitivitas rendah 50%; Namun, kemungkinan memvisualisasikan
bronkolit mungkin lebih tinggi pada kucing karena kucing tampaknya memiliki penyakit yang
lebih menyebar dengan beberapa bronkolit. Komposisi kimiawi yang tepat dari bronkolit tidak
ditentukan, tetapi pewarnaan von Kossa dari bahan di lumen bronkial menegaskan bahwa
bronkolit yang dicurigai mengandung bahan kalsifikasi.
 Perawatan optimal untuk bronkolitiasis pada kucing masih belum diketahui. Jika
bronkolitiasis dicurigai sebagai akibat peradangan saluran napas bawah kucing, pengobatan
untuk kondisi ini dianjurkan. Pengobatan jangka panjang dengan steroid sering dibutuhkan
pada pasien ini. Pengobatan jangka panjang dengan steroid inhalasi seperti flutikason telah
dilaporkan efektif pada kucing dengan penyakit inflamasi saluran napas bagian bawah.

DAFTAR PUSTAKA
Anwer M and Venkatram S. Broncholithiasis: ‘incidental finding during bronchoscopy’ –
case report and review of the literature. J Bronchol Intervent Pulmonol 2011; 18:
181–183.
Baral RM. Lower respiratory tract diseases. In: Little SE (ed). The cat, clinical medicine and
management. St Louis, MO: Elsevier, 2010, pp 861–891.
Byrne P, Berman JS, Allan GS, et al. CT findings in two cats with broncholithiasis. JFMS
Open Rep 2016; 2: 1–6.
Sanchez V.F, Stewart J, Bovens C, Puig J. Broncholithiasis associated with lower airway
inflammation and subsequent pyothorax in a cat. Journal of Feline Medicine and
Surgery Open Reports 2017; 1-6.
Talavera J, Fernandez del Palacio MJ, Bayon A, et al. Broncholithiasis in a cat: clinical
findings, long-term evolution and histopathological features. Journal of Feline
Medicine and Surgery 2008; 10: 95–101.
746798
research-article2017
JOR0010.1177/2055116917746798Journal of Feline Medicine and Surgery Open ReportsValls Sanchez et al

Case Report
Journal of Feline Medicine and Surgery Open

Broncholithiasis associated with Reports

1­–6
© The Author(s) 2017
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subsequent pyothorax in a cat https://doi.org/10.1177/2055116917746798

DOI: 10.1177/2055116917746798
journals.sagepub.com/home/jfmsopenreports
This paper was handled and processed
by the European Editorial Office (ISFM)
for publication in JFMS Open Reports

Ferran Valls Sanchez1*, Jennifer Stewart2,

Catherine Bovens1† and Jordi Puig1‡

Abstract
Case summary  A 12-year-old female spayed domestic shorthair cat presented with history of a long-term chronic
cough that had worsened during the previous 2 months. Thoracic radiographs revealed numerous mineral opacities
throughout the lung fields. Multiple bronchial plugs of pale yellow material were present on bronchoscopy, consistent
with broncholithiasis. Bronchoalveolar lavage cytology revealed a mild neutrophilic inflammation and bacterial
culture was negative. The cat was diagnosed with chronic inflammatory lower airway disease and broncholithiasis,
suspected to be due to mineralisation of secretions in the bronchial lumen. The cat was treated for 6 years with oral
prednisolone and responded well to treatment. Six years later, the cat developed severe respiratory distress and died.
Post-mortem examination identified chronic multifocal broncholithiasis, pulmonary abscessation and pyothorax.
Relevance and novel information Broncholithiasis is a very rare condition in feline medicine; however, we are
reporting a new case and it should be considered as a differential diagnosis for chronic coughing in cats, especially
when other common causes have been ruled out and the radiographic findings are suggestive of it. We hypothesise
that pathogenesis of the pulmonary abscessation and pyothorax in our patient was, at least partially, due to
broncholithiasis. Pleural disease should be considered a complication of broncholithiasis.

Accepted: 11 November 2017

Introduction
Broncholithiasis is defined as the presence of calcified or
ossified material within the bronchial lumen.1,2 In
humans, it is a rare disorder with an incidence of 0.1–0.2%
of all lung diseases.3 To the authors’ knowledge, only
four cases of broncholithiasis in cats have been reported
in the veterinary literature.4–7 This condition is not
reported in dogs. This case report describes a new case of
feline broncholithiasis (including the first report of bron-
choscopic appearance of the broncholiths), its long-term
outcome and its association with pleural disease.
Case description
A 12-year-old female neutered domestic shorthair cat
was referred to the Animal Health Trust for a worsen-
ing cough over the past 2 months. The cat was vacci-
On presentation, physical examination demonstrated
a mild tachypnoea (respiratory rate was 48 breaths
per minute) with a normal respiratory pattern and
mild inspiratory wheezes on pulmonary auscultation.
Haematology and biochemistry were unremarkable.
Thoracic radiographs revealed the presence of numerous
clusters of cauliflower-like, mineral opacity structures of
3–6 mm diameter throughout the lung fields affecting all
1Department of Small Animal Internal Medicine, UK
2Department of Pathology, Animal Health Trust, Kentford, UK
*Current address: Dick White Referrals, Cambridgeshire, UK
†Currentaddress: Veterinary Referral Hospital, Princes Highway,
Australia
‡Current address: Hospital Ars Veterinaria, Barcelona, Spain

nated yearly (for feline calicivirus, feline herpesvirus,

Corresponding author:
feline panleukopaenia and feline lekaemia), was Ferran Valls Sanchez DVM, Dick White Referrals, Station Farm,
wormed regularly (praziquantel + emodepside) and London Road, Six Mile Bottom, Cambridgeshire CB8 0UH, UK
was an outdoor cat. Email: fvs@dwr.co.uk

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use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and
Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
2 Journal of Feline Medicine and Surgery Open Reports 
Figure 1  Ventrodorsal radiograph of the thorax. Numerous
irregular mineral opacities of 3–6 mm diameter were present
throughout the lung fields
Figure 2  Lateral radiograph of the thorax. Numerous
irregular mineral opacities of 3–6 mm diameter were present
throughout the lung fields
pulmonary lobes but more severe in the right cranial and
middle lung lobes (Figures 1 and 2). Differential diagno-
ses were mucous gland calcifications, dystrophic calcifi-
cations, inhaled mineral foreign bodies, broncholithiasis,
neoplasia, hypervitaminosis D or granulomatous disease.
Thoracic radiographs also showed a 1.7 cm diameter
Figure 3  Bronchoscopic image showing light yellow solid
material obstructing most of the lumen of a bronchus
soft tissue circular nodule in the cranial thorax and a 2 cm
soft tissue nodule cranial to the cardiac silhouette.
Thoracic ultrasound revealed a 1.3 cm diameter nodule,
heterogeneous nodule in the left cranial lung field, con-
sistent with one of the soft tissue nodules. The other nod-
ule seen on radiography could not be seen on
ultrasonography. On bronchoscopy, the interbronchial
septae appeared rounded and the mucosa was diffusely
erythematous. An excessive amount of mucus was pre-
sent in the lower airways. Light yellow plugs of solid
material were present in numerous bronchi, either par-
tially or completely obstructing their lumen, depending
on the case, consistent with broncholithiasis (Figures 3
and 4). Mineral material was not retrieved during
bronchoalveolar lavage (BAL). BAL cytology revealed
moderate cellularity with mild neutrophilic inflamma-
tion (red blood cells: 30/µl; nucleated cells: 230/µl).
Microorganisms were not seen on cytology, and a Ziehl–
Neelsen stain was negative. Bacterial aerobic and anaero-
bic cultures were negative. Investigations were consistent
with feline inflammatory lower airway disease and mul-
tifocal broncholithiasis.
During the bronchoscopy, an iatrogenic pneumo-
thorax developed as a result of perforation of an air-
way. It was drained immediately and a unilateral
small-bore wire guided thoracostomy tube was placed.
The cat was treated with amoxicillin/clavulanate (20
mg/kg IV q8h) and dexamethasone (0.1 mg/kg IV
once), followed by prednisolone (0.5 mg/kg PO q12h)
as feline inflammatory lower airway disease was sus-
pected and this was the standard therapeutic approach
Valls Sanchez et al 3
Figure 4  Bronchoscopic image showing the presence of pale
yellow material in the lumen of a bronchus
of this condition by the clinical team involved. The cat
was initially started on antibiotics while waiting for
the results of the BAL and kept on them as a preventive
measure because of the iatrogenic pneumothorax and
risk of secondary pleural infection and ongoing clinical
improvement. The thoracic drain was removed 3 days
after placement. The cat was discharged 6 days after
presentation with amoxicillin/clavulanate (20 mg/kg
PO q12h) for a further 2 weeks, prednisolone (0.5 mg/
kg PO q12h) and nebulisations with isotonic sterile
saline for 5–10 mins q8h.
The cat was managed at the first-opinion veterinary
practice for the following 6 years. According to the first-
opinion practice, the cat was reported to have received
prednisolone at a dose of 0.34 mg/kg PO q12–24h dur-
ing the 6 years, depending on the severity and frequency
of the coughing, and was asymptomatic on this dose.
Further tapering of the prednisolone dose was attempted
but resulted in relapse of dyspnoea. An episode of
tachypnoea occurred 5 years after referral, at which time
a right-sided grade III/VI systolic heart murmur was
reported by the primary practice. No diagnostic investi-
gations were performed at that stage and the cat was
started on furosemide (1.7 mg/kg PO q12h) and
benazepril (0.8 mg/kg PO q24h).
The cat presented with acute respiratory distress to
the first-opinion practice 6 years after the initial diagno-
sis. It was treated with oxygen therapy, intravenous
furosemide and dexamethasone. There was a clinical
improvement and the cat was discharged on oral furo-
semide (1.6 mg/kg PO q12h) and telmisartan (dose for a
3 kg cat). It died at home 24 h later.
Figure 5  Macroscopic appearance of the lungs.
Accumulations of yellow-green, thick, pasty pus are
expanding multiple bronchioles
Post-mortem examination was performed at the
Animal Health Trust. At gross necropsy, the thoracic cav-
ity was filled with 50 ml watery-grey turbid fluid and
the pleural surface of the ribs had multiple slightly
raised, 2 mm white lesions. The lungs had an irregular
nodular appearance. The nodules were up to 7–10 mm in
diameter, and many contained light-green purulent
material on cut surface (Figure 5). The heart showed
mild left ventricular hypertrophy. The remaining organs
were macroscopically normal. Cytology of the pleural
fluid and suspected pulmonary abscessation revealed
neutrophilic inflammation with intracellular bacteria.
Neither bacterial culture nor special stains of these sam-
ples were performed.
Histology identified numerous bronchi and bron-
chioli severely distended by large quantities of calci-
fied proteinaceous material, with mucus and
neutrophils also present within the lumen. A von Kossa
stain of the lumen contents was positive, confirming
calcification (Figure 6). No bacteria were seen. Severe
hyperplasia and hypertrophy of the peribronchiolar
mucous glands were present. The histopathologic
diagnosis was chronic purulent bronchitis and bron-
chiolitis with pulmonary abscessation, severe chronic
bronchiectasis and moderate miliary broncholithiasis,
and secondary pyothorax and pleuritis.
Discussion
The pathogenesis of feline broncholithiasis has not been
determined. The most common aetiology in humans is
granulomatous lymphadenitis (most commonly due to
fungal infection in the US and mycobacterial infection
in the rest of the world), with erosion of the bronchus
by a calcified lymph node which then extrudes into
the lumen.1–3,8 Chronic pneumonia by Mycobacterium
4 Journal of Feline Medicine and Surgery Open Reports 
Figure 6  Von Kossa stain. Histology of lung sample.
Intraluminal brown–black concretions, confirming the
presence of mineralised material. Bar = 10 μm
thermoresistibile has been associated with pulmonary
mineralization in a cat.9 Other causes include silicosis,
aspiration of mineral material, in situ calcification of
mucus or aspirated foreign material or erosion/extru-
sion of calcified bronchial cartilage plates.1–3
There was no evidence of a bacterial airway infection
in our case or most of the previously reported feline
cases; however, an infectious agent could have played a
trigger role for chronic inflammation in two reported
cases.9,10 BAL bacterial culture was negative in our case
and two other cases.6 In our case, an underlying myco-
bacterial infection was considered unlikely considering
the clinical presentation and negative Ziehl–Neelsen
stain on BAL sample cytology at initial diagnosis; how-
ever, the sensitivity of this test can be low and one of the
limitations of this case report is that no other tests were
performd to rule this condition completely out. Fungal
infection was considered unlikely in the absence of fun-
gal organisms on cytology and because pulmonary fun-
gal infections are very rare in the UK. The appearance of
the intraluminal material on bronchoscopy and on post-
mortem examination results did not support foreign
body inhalation.
A common feature in all the feline reported cases has
been the presence of multiple broncholiths, whereas in
human medicine the number of broncholiths is smaller
and the disease is localised. This might be because in cats
a generalised lower airway disease is causing the bron-
cholithiasis, contrary to a local injury as in humans.
In the previously reported cases of broncholithiasis in
cats, mineralisation of inspissated bronchial secretions
was considered the likely cause for the broncholiths.4–6
We suspect that this was also the cause for the broncho-
lithiasis in our case. Histopathology revealed hyperpla-
sia and hypertrophy of the peribronchiolar mucous
glands in our case and the two other cases in which his-
topathology was performed.4,5 This would have predis-
posed to the production of excessive secretion in the
airways and supports the aforementioned theory.
Intraluminal material (along with broncholiths) of a dif-
ferent nature was described histologically in our case
and two of the previously reported cases.4,5 In two cases
where a CT scan of the thorax was performed, the bron-
choliths were embedded in soft tissue density material
in the bronchial lumen.7 Hyperplasia and hypertrophy
of the bronchial mucous glands is a non-specific response
to injury, and may be initially triggered by an inflamma-
tory or infectious event and the excessive production of
airway mucus become self-perpetuating.5 In the present
case, feline inflammatory lower airway disease may
have caused the excessive production of mucus in the
lower airways, which could have undergone a process of
mineralisation and consequent formation of broncho-
liths. Miliary broncholithiasis has been associated with
chronic and progressive feline lower airway respiratory
disease in a cat, which was initially diagnosed with
Mycoplasma species infection and had no radiographic
evidence of this broncholithiasis.10 Inflammation with-
out evidence of infection was also present in two other
reported cases.4,6 Based on our case and those reports,
the presence of broncholithiasis in a cat may suggest the
presence of lower airway inflammation, and investiga-
tion for this would be recommended.
In our case, broncholithiasis was radiographically
suspected and diagnosed in the light of the presence of
intraluminal plugs of yellow, solid material in multiple
bronchi on bronchoscopy, consistent with broncholiths.
Our case describes the first reported bronchoscopy in a
cat with broncholithiasis. In human medicine, a thoracic
CT scan or bronchoscopy are required to confirm bron-
cholithiasis.1,3 In humans, bronchoscopy has a low sensi-
tivity of 50%;1,2 however, the likelihood of visualising
broncholiths may be higher in cats as they appear to
have more diffuse disease with multiple broncholiths.
The exact chemical composition of the broncholiths was
not determined, but the von Kossa stain of the material
in the bronchial lumen confirmed that the suspected
broncholith contained calcified material.
Therapeutic options in affected humans include mon-
itoring and conservative management, bronchoscopic
removal of broncholiths or surgery.1–3 Conservative
management and monitoring can be recommended in
asymptomatic patients.1,6 In our cat, bronchoscopic or
surgical removal of the broncholiths was considered not
Valls Sanchez et al 5
feasible because of the large number and diffuse distri-
bution of the broncholiths. The optimal treatment for
broncholithiasis in cats remains unknown. If the bron-
cholithiasis is suspected to be secondary to feline lower
airway inflammation, treatment for this condition is rec-
ommended. Long-term treatment with steroids is fre-
quently needed in these patients.11 Long-term treatment
with inhaled steroids such as fluticasone has been
reported as effective in cats with inflammatory lower air-
way disease.11 However, at the time of the presentation,
the use of inhaled corticosteroids was not as widespread
as it is currently and, furthermore, it was hypothesised
by the clinical team that the efficacy of inhaled steroids
may be impaired in cats with broncholithiasis as physi-
cal obstruction of the lumen by the broncholiths may
impair complete delivery of inhaled drugs. Systemic
treatment was therefore elected for in the present case.
However, current published data has reported the long-
term treatment with inhalations of fluticasone and salbu-
tamol to be successful in one case of broncholithiasis,
with no clinical signs for 3 years.7
Potential complications of broncholithiasis described
in human medicine are recurrent infections, haemopty-
sis, bronchiectasis and bronchial fistulas.2,3,8 In our case,
reported complications were iatrogenic pneumothorax,
development of pulmonary abscessation and pyotho-
rax. The cat in this report may have been predisposed
to the development of an iatrogenic pneumothorax
during bronchoscopy due to inflamed or more rigid
lower airway walls12 or, this may be a genuine iatro-
genic damage. Pneumothorax is considered a possible
complication of a bronchoscopy and it was reported to
occur in 3% of cats undergoing a bronchoscopy accord-
ing to one study.13 In our patient, post-mortem findings
revealed a pyothorax, most likely secondary to pulmo-
nary abscessation. We suspect that the pulmonary
abscessation could have been due to the large number
of broncholiths. A predisposition to infection may be
possible due to the broncholiths acting as a nidus for
bacteria. A similar case has been reported in a human
patient suffering from broncholithiasis, who developed
a secondary intraparenchymal pulmonary abscess
associated with Histoplasma capsulatum and pyotho-
rax.14 Investigation for possible respiratory or pleural
infections would be recommended in cats with bron-
cholithiasis with clinical deterioration. However, in the
present case, the chronic administration of corticoster-
oids could also have played a role and predisposed the
patient to secondary infections.
Regarding the prognosis, the first reported cat with
broncholithiasis was euthanased within 12 months of
diagnosis due to worsening respiratory signs.4 The sec-
ond reported cat was euthanased owing to an unrelated
condition 3 years following diagnosis; the cat was treated
initially with doxycycline and prednisolone but only
received intermittent terbutaline after that and no other
treatments.5 Two other reported cats were alive 3 and 4
years after initial diagnosis, respectively, and were
treated long-term with inhalations of salbutamol and
fluticasone.7 In the present case, the cat remained asymp-
tomatic on oral prednisolone for 6 years after the initial
diagnosis of broncholithiasis.
Conclusions
Broncholithiasis is an uncommon condition, which
should be considered as a differential diagnosis for cats
with chronic respiratory disease. Affected cats may
develop broncholithiasis secondary to a diffuse inflam-
matory lower airway disease with mineralisation of
secretions in the airways. Consequently, investigation
for underlying lower airway inflammation is recom-
mended. The optimal treatment of broncholithiasis in
cats is unknown but may involve treatment for underly-
ing airway inflammation if present. Local treatment
(endoscopical or surgical removal) in the absence of
available data, seems unlikely to be indicated because of
the diffuse distribution of the disease in cats; however,
further research is necessary in that regard. Iatrogenic
pneumothorax (while performing the bronchoscopy),
secondary pulmonary abscessation and pyothorax are
possible complications of the disease, but good long-
term prognosis is possible.
Conflict of interest  The authors declared no potential con-
flicts of interest with respect to the research, authorship, and/
or publication of this article.
Funding  The authors received no financial support for the
research, authorship, and/or publication of this article.
References
1 Seo JB, Song KS, Lee JS, et al. Broncholithiasis: review of
the causes with radiologic-pathologic correlation. Radio-
graphics 2002; 22: S199–S213.
2 Lim SY, Lee KJ, Jeon K, et al. Classification of broncholiths
and clinical outcomes. Respirology 2013; 18: 637–642.
3 Anwer M and Venkatram S. Broncholithiasis: ‘incidental
finding during bronchoscopy’ – case report and review
of the literature. J Bronchol Intervent Pulmonol 2011; 18:
181–183.
4 Allan GS and Howlett CR. Miliary bronchiolithiasis in a
cat. J Am Vet Med Assoc 1973; 162: 214–216.
5 Brummer DG. Microlithiasis associated with chronic
bronchopneumonia in a cat. J Am Vet Med Assoc 1989; 194:
1061–1064.
6 Talavera J, Fernandez del Palacio MJ, Bayon A, et al. Bron-
cholithiasis in a cat: clinical findings, long-term evolution
and histopathological features. J Feline Med Surg 2008; 1:
95–101.
7 Byrne P, Berman JS, Allan GS, et  al. CT findings in two
cats with broncholithiasis. JFMS Open Rep 2016; 2: 1–6.
6 Journal of Feline Medicine and Surgery Open Reports 
8 Ungprasert P, Srivali N, Bauer MA, et al. Broncholithiasis:
an uncommon cause of chronic cough. J Bronchol Intervent
Pulmonol 2014; 21: 102–103.
9 Foster SF, Martin P, Davis W, et al. Chronic pneumonia
caused by Mycobacterium thermoresistibile in a cat.
J Small Anim Pract 1999; 40: 433–438.
10 Baral RM. Lower respiratory tract diseases. In: Little SE
(ed). The cat, clinical medicine and management. St Louis,
MO: Elsevier, 2010, pp 861–891.
11 Padrid P. Chronic bronchitis and asthma in cats.
In: Bonagura JD and Twedt DC (eds). Kirk’s current
veterinary therapy XV. St Louis, MO: Elsevier, 2014,
pp 673–680.
12 Mooney ET, Rozansky EA and King RGP. Spontaneous
pneumothorax in 35 cats (2001–2010). J Feline Med Surg
2012; 14: 384–391.
13 Johnson LR and Drazenovich TL. Flexible bronchoscopy
and bronchoalveolar lavage in 68 cats (2001–2006). J Vet
Intern Med 2007; 21: 219–225.
14 Summers SM. Broncholithiasis with post-obstruc-
tive pneumonia and empyema. J Emerg Med 2013; 45:
612–614.
676176
research-article2016
JOR0010.1177/2055116916676176Journal of Feline Medicine and Surgery Open ReportsByrne et al

Case Series
Journal of Feline Medicine and Surgery

CT findings in two cats with Open Reports

1­–6
© The Author(s) 2016
broncholithiasis Reprints and permissions:
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DOI: 10.1177/2055116916676176
jfmsopenreports.com

This paper was handled and

Patrick Byrne1, James S Berman1, Graeme Sutcliffe Allan2, processed by the European Editorial
Office (ISFM) for publication in JFMS
Jennifer Chau1 and Vanessa R Barrs1 Open Reports

Abstract
Case series summary  Chronic inflammatory airway disease with secondary broncholithiasis was diagnosed
in two cats from CT and bronchoalveolar lavage cytological findings. In one cat with progressively worsening
lower respiratory tract signs, more than 80 discrete, highly attenuating endobronchial opacities were detected on
thoracic CT. The broncholiths were distributed throughout the right middle, and left and right caudal lung lobes,
and the caudal part of the left cranial and accessory lobes. In the other cat broncholithiasis was an incidental
finding on thoracic radiographs taken during diagnostic investigation of inappetence. On thoracic CT, 25 calcified
endobronchial opacities were detected in the left caudal lung lobe in secondary and tertiary bronchi. CT features
of chronic inflammatory airway disease were present in both cases, including bronchiectasis, atelectasis, flattening
of the diaphragm and bronchial wall thickening.
Relevance and novel information  This is the first report to document CT features of broncholithiasis in cats. Feline
broncholithiasis should be considered as a differential diagnosis in any case where calcified endobronchial material
is evident on thoracic radiographs or CT.

Accepted: 3 October 2016

Introduction
Broncholithiasis, the presence of mineralised material
within the bronchial lumen, is a well-documented condi-
tion in humans and was first reported by Aristotle (384–
322 BC), who described the ‘spitting of stones’ (lithoptysis).1
In humans, broncholiths are formed from extrusion of a
calcified lymph node through an eroded bronchial wall
into the bronchial lumen.1–3 In contrast, feline broncholithi-
asis has only been described in two cats.2,4 The proposed
aetiology of the broncholiths in both cases was dystrophic
mineralisation of intraluminal bronchial secretions sec-
ondary to chronic inflammatory airway disease. In this
report, we describe two further cases in cats, as well as the
CT features of feline broncholithiasis.
the referring veterinarian 2 months before referral, after
which there was a transient improvement in signs.
On physical examination at referral the cat weighed
4.88 kg and was in good body condition (body condition
[BCS] score 3/5). Heart rate (HR; 180 beats per min
[bpm]), respiratory rate (RR; 28 breaths per min) and rec-
tal temperature (37.5°C) were normal, but there was
increased inspiratory effort. On auscultation lung sounds
were moderately increased over all lung fields, and a
grade IV/VI left parasternal systolic heart murmur was
detected. Three-view thoracic radiographs were per-
formed (Figure 1). Several calcific aggregations were

Case series description 1Faculty of Veterinary Science, School of Life and Environmental
Case 1 Sciences, University of Sydney, Sydney, Australia
A 9-year-old, male, neutered Cornish Rex was referred to the 2Veterinary Imaging Associates, St Leonards, Australia

Valentine Charlton Cat Centre (VCCC) for a 3 month his-

Corresponding author:
tory of inappetence, weight loss and progressively worsen- Vanessa Barrs BVSc, PhD, MVetClinStud, FANZCVS, Faculty of
ing respiratory signs, including cough and dyspnoea. A Veterinary Science, University of Sydney, NSW 2006, Australia
short course of oral prednisolone had been prescribed by Email: vanessa.barrs@sydney.edu.au

Creative Commons Non Commercial CC-BY-NC: This article is distributed under the terms of the Creative Commons
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use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and
Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
2 Journal of Feline Medicine and Surgery Open Reports 

Figure 1  Case 1: lateral and ventrodorsal view thoracic radiographs. There is a reticular interstitial pattern with increased
opacity of the bronchial walls. Multiple mineralised soft tissue nodules with irregular margins are present within the caudal lung
fields, the largest of which lies within the dorsal right caudal lung lobe

present within the right middle and both caudal lung
lobes. Clearly marginated soft tissue opacities sur-
rounded 5/8 larger aggregates, with diameters ranging
from 6–18 mm. The diameter of the calcific material
itself ranged between 1 and 12 mm. Calcification
appeared to be within the bronchial walls in some places.
It was difficult to determine definitively whether intra-
luminal calcifications were also present. A reticular inter-
stitial pattern of the remaining pulmonary parenchyma
and bronchiectasis of the right cranial lobar bronchus
was evident. Pulmonary vasculature was normal. On
echocardiography there was evidence of mild left ven-
tricular free wall hypertrophy in diastole, and there
was mild tricuspid valve regurgitation (peak velocity
2.5 m/s). All other parameters, including atrial size,
were within reference limits. Systolic blood pressure was
normal (130 mmHg, Doppler method).
Thoracic CT was performed under general anaesthe-
sia using contiguous 0.8 mm helical slices (Philips
Brilliance, 16 Slice; Philips Medical Systems). There was
a generalised increase in opacity of bronchial walls
throughout the thorax. Approximately 80 discrete 2–9
mm diameter, ellipsoid-to-linear mineralised endobron-
chial concretions were present embedded in soft-tissue
opacity intraluminal bronchial material, generally adja-
cent to the bronchial wall (Figure 2). Opacity of the con-
cretions ranged from 981–1850 HU. There was minimal
to no enhancement (10–20 HU) post-contrast adminis-
tration. Broncholiths were predominantly distributed
throughout the right middle, left and right caudal lung
lobes, and, to a lesser extent, in the caudal part of the left
cranial and accessory lobes. The bronchial lumen diam-
eter in affected lung lobes was greater than that of
accompanying pulmonary vessels. Bronchiectasis was
present in the right cranial lung lobe. Flattening of the
diaphragm was apparent in the sagittal projections.
Cytological preparations of bronchoalveolar lavage
(BAL) fluid collected by unguided BAL comprised 77%
neutrophils, 15% eosinophils and 8% macrophages.
Circular aggregates of mineralised spicules were present
throughout the sample. No infectious agents were
detected. Cytological findings were consistent with
chronic, active airway inflammation with mineralised
airway deposits. A presumptive diagnosis of chronic
feline bronchial disease with secondary broncholithiasis
was made. Empirical treatment using doxycycline 5 mg/
kg q12h and prednisolone 2mg/kg q24h (both PO), was
initiated pending culture and susceptibility results from
the BAL.
A very light mixed bacterial growth on aerobic culture
was consistent with contamination by oropharyngeal
flora. At a recheck examination 1 week later, the owner
reported a marked reduction in the frequency of cough-
ing. Treatment was commenced with a metered dose
inhaler (MDI) containing salbutamol (25 μg) and flutica-
sone (125 μg) twice daily (Seretide; GlaxoSmithKline
Australia). The prednisolone dose was tapered over
5 days and then discontinued.
The cat returned to the primary care veterinarian for
follow-up care. At a recheck examination, 4 years after
Byrne et al 3

Figure 2  CT images of case 1 reformatted as a maximum intensity projection in dorsal plane and single-slice image in
transverse plane displayed in a bone window (window level −300, window width 1500). In the dorsal plane there are mineral
attenuating foci in the right and left caudal lung lobes that are associated with the segmental branches of the caudal main stem
bronchi. These mineral-attenuating foci are surrounded by a small region of soft tissue attenuation. In the transverse plane
the focal area of mixed mineral and soft tissue attenuation in the left caudal lung lobe is arranged in a tubular shape that is
confluent with the lobar bronchus. There is mild generalised thickening of the bronchial walls

initial presentation, the owner reported that there was
improvement in respiratory signs following initial treat-
ment, but that sporadic episodes of dyspnoea and cough-
ing still occurred. Compliance with MDI therapy had
been low. Physical examination findings included body
weight 4.48 kg, tachycardia (HR 240 bpm) and a grade
III/VI systolic heart murmur, mild tachypnoea (RR 36
breaths per min) with normal respiratory effort, and
mild-to-moderately increased lung sounds in all lung
fields on thoracic auscultation. Haematology was unre-
markable and serum biochemistry revealed mild eleva-
tions in urea (17.7 mmol/l; reference interval [RI] 5–15
mmol/l) and creatinine (0.24 mmol/l; RI 0.08–0.2
mmol/l) and a normal total thyroxine (T4; 23 nmol/l; RI
10–60 nmol/l). Urine specific gravity was 1.018, urine
sediment was benign and there was no proteinuria
(urine protein:creatinine ratio 0.1), and systolic blood
pressure was normal (130 mmHg). The cat was diag-
nosed with IRIS stage II chronic kidney disease (CKD)
and referred back to the primary care veterinarian
for ongoing management of CKD and inflammatory
airway disease, with a recommendation to re-institute
MDI therapy using fluticasone/salmeterol.
Case 2
A 14-year-old, female, spayed domestic shorthair cat
was presented to the VCCC for further investigation of
several mineralised discrete miliary nodules that were
detected on routine thoracic radiographs taken 3 weeks
previously when the cat had presented for acute onset
lethargy and inappetence. There was no history of res-
piratory signs.
The owner, a veterinarian, had performed a complete
blood count and serum biochemistry, which were unre-
markable. Serology for feline immunodeficiency virus
antibody and feline leukaemia virus antigen was nega-
tive. Thoracic radiographs revealed several discrete min-
eralised miliary nodules in the left caudal lung lobe
(Figure 3). An unguided BAL was performed to further
investigate this finding. On cytology of BAL fluid there
were 58% macrophages, 5% lymphocytes and 37% eosin-
ophils. No microorganisms were detected, and bacterial
culture was negative.
On physical examination at referral the cat weighed
3.57 kg and was in good body condition (BCS 3.5/5). HR
(196 bpm), RR (36 breaths per min) and rectal tempera-
ture (38.6°C) were normal. Increased tracheal sensitivity
was noted on palpation. Both thyroid lobes were mildly
enlarged and rounded (left 4 mm, right 5 mm diameter)
on palpation. Total T4 was high normal (52 nmol/l;
RI 6–52 nmol/l) and in-house heartworm antigen test
was negative.
Three-view thoracic radiographs were performed.
Associated with consolidation of the left caudal lung
lobe were approximately 25 linearly distributed mineral
opacities measuring up to 2 mm, which followed the line
4 Journal of Feline Medicine and Surgery Open Reports 

Figure 3  Case 2: lateral and ventrodorsal view thoracic radiographs. There are multifocal, somewhat linearly distributed
mineral opacities within the left caudal lung lobe along the line of the main lobar bronchus. Linear soft tissue margins are
associated with the mineralised opacities, and there is a generalised increase in bronchial wall opacity

of the main lobar bronchus (Figure 3). Linear soft tissue
margins were associated with the mineralised opacities
and there was a generalised increase in bronchial wall
opacity. Thoracic CT, performed as for case 1, revealed
mixed mineralised and soft tissue attenuating material
linearly distributed within the lumen of the ventral
branches of the left caudal bronchi, with hyperattenua-
tion of surrounding pulmonary parenchyma (Figure 4).
Circular, nodular mineral opacities (954–2187 HU) up to
4 mm in diameter were present within the bronchial
lumen of secondary and tertiary bronchi. Affected
bronchi were air-filled and expanded with peripheral
branches measuring up to 8 mm in diameter. There was
bronchiectasis and failure of tapering of the right middle
lung lobe with the bronchus measuring 3 mm in diame-
ter peripherally with no associated abnormality of the
pulmonary parenchyma. Some degree of flattening of
the diaphragm was present.
A presumptive diagnosis of chronic inflammatory air-
way disease with secondary broncholithiasis was made
based on CT and BAL cytology. The cat was prescribed
MDI therapy with salbutamol (25 μg) and fluticasone
(125 μg) q12h (Seretide; GlaxoSmithKline Australia) and
doxycycline 5 mg/kg q12h PO for 3 weeks. Repeat serum
total T4 was recommended, as concurrent hyperthyroid-
ism was suspected. Frequency of MDI therapy was
reduced to q24h 1 month post-discharge. At last contact
by telephone, 3 years after initial presentation, the cat
had no respiratory signs and at the time of writing is
maintained on MDI therapy. Hyperthyroidism had
been confirmed on a repeat total T4 and treatment with
radioiodine was curative.
Discussion
The two cats in this report had evidence of chronic
inflammatory airway disease on thoracic radiographs,
CT and BAL cytology. Dystrophic mineralisation of
inspissated airway exudates was the likely cause of
broncholithiasis in both cases, similar to the mechanism
described in the only other two cases of broncholithiasis
reported in cats.2,4 Consistent with this putative mecha-
nism, in one of our cases aggregates of mineralised mate-
rial were detected on BAL cytology. Unlike humans with
broncholithiasis, where pulmonary tuberculosis and his-
toplasmosis are the most common causes of bronchial
lymph node calcification and extrusion, there was no
evidence of bacterial or mycotic pneumonia in any of the
feline cases.5–7
While not proven, the presence of broncholithiasis is
likely suggestive of a chronic time course for the inflam-
matory airway disease in these two cats. Interestingly,
respiratory signs had only been detected by the owner
in the 3 months before presentation in case 1, and not at
all in case 2, in which broncholiths were an incidental
radiological finding. However, clinical signs can go
unnoticed by owners, even in cats with severe respira-
tory disease, as evidenced in a series of feline pyotho-
rax cases where 40% of owners of affected cats did not
notice respiratory signs before presentation for acute
respiratory decompensation.8 Thus, chronic inflamma-
tory airway disease and broncholithiasis cannot be
excluded, even in cats with no history of lower respira-
tory tract disease.
By contrast, it is possible that broncholithiasis as an
incidental finding is not clinically relevant in cases where
Byrne et al 5

Figure 4  CT images of case 2 reformatted as a maximum-intensity projection in dorsal plane and transverse plane displayed
in a bone window (window level −250, window width 1600). In the dorsal plane, the periphery of the left caudal main stem
bronchus contains multiple mineral-attenuating foci surrounded by soft tissue attenuation. In the transverse plane, obstruction
of the bronchial lumen with mixed mineral and soft tissue attenuation is evident. The bronchial wall is mildly thickened and
irregular, compatible with regional bronchiectasis

cats have no lower respiratory tract signs historically or
on physical examination. A recent study comparing tho-
racic CT findings in cats with and without respiratory
signs found 77% of asymptomatic cats had abnormalities
of thoracic structures,9 with 24% of these cats having
evidence of bronchial disease. Bronchial changes
were mainly wall thickening and mucus plugging.
Interestingly, broncholiths were noted in one cat; how-
ever, no details were provided and it was not clear if this
cat had respiratory signs or was asymptomatic. Given
the suspected pathogenesis of feline broncholithiasis,
their presence likely suggests the presence of lower air-
way inflammation and investigation for this would be
prudent, even in an asymptomatic cat.
The two previously reported cases of feline broncho-
lithiasis were confirmed at necropsy where broncholiths
were present alongside intraluminal plugs of eosino-
philic2 or mucopurulent4 and cellular debris. The CT
findings in our cases were also consistent with this find-
ing, with mineralised opacities embedded in soft tissue
opacity intraluminal bronchial material. The distribution
of the broncholiths was linear, following the arboreal
pattern of the bronchi in both left and right lung lobes,
and reflecting areas of bronchial secretion accumulation.
In the previously reported cases, histological findings at
necropsy showed evidence of severe diffuse chronic
inflammatory airway disease with bronchiectasis,
atelectasis, pulmonary fibrosis, goblet cell hyperplasia,
bronchial gland hyperplasia and hypertrophy, and
lymphocytic inflammation of affected bronchial lamina
propria.2,4 In our cases, there was CT and radiographic
evidence of diffuse lower respiratory tract airway
involvement. Evidence of chronic inflammatory airway
disease included bronchiectasis of the right cranial lung
lobe (case 1) or the right middle lung lobe (case 2), atelec-
tasis, flattening of the diaphragm and bronchial wall
thickening.
Neutrophilic and/or eosinophilic inflammation in
BAL fluid is typical but not pathognomonic for feline
chronic inflammatory airway disease.10,11 A limitation in
the current study was the absence of comprehensive
testing for heartworm and lungworm, which was
declined by the owners, but could result in similar cyto-
logical findings.
The clinical significance of broncholithiasis in cats is
uncertain, with both cats in this report alive 4 years after
diagnosis. Bronchoscopic broncholithectomy was not
performed in either cat owing to the relative inaccessibil-
ity of many affected small airways. In human broncho-
lithiasis, conservative management is indicated if clinical
signs are minimal.5 If more severe signs are present, such
as bronchiectasis, haemoptysis or broncho-oesophageal
fistulae, or where there is uncertainty about the diagno-
sis, surgery or bronchoscopy is indicated.3,5
6 Journal of Feline Medicine and Surgery Open Reports 
Conclusions
Broncholithiasis in cats can occur secondarily to
chronic inflammatory airway disease. Radiographic
features of nodular mineralisation and bronchial
changes are seen. Definitive diagnosis can be readily
established on thoracic CT to confirm the location
of mineralised material within the bronchial lumen
and presence of features of chronic inflammatory
airway disease such as bronchiectasis, flattening
of the diaphragm, atelectasis and bronchial wall
thickening.
Funding  The authors received no financial support for the
research, authorship, and/or publication of this article.
Conflict of interest  The authors declared no potential con-
flicts of interest with respect to the research, authorship, and/
or publication of this article.
References
1 Craig K, Keeler T and Buckley P. Broncholithiasis: a case
report. J Emerg Med 2002; 23: 359–363.
2 Talavera J, del Palacio MJF, Bayon A, et al. Broncholithiasis
in a cat: clinical findings, long-term evolution and histo-
pathological features. J Feline Med Surg 2008; 10: 95–101.
3 Olson E J, Utz JP and Prakash UB. Therapeutic bronchos-
copy in broncholithiasis. Am J Respir Crit Care Med 1999;
160: 766–770.
4 Allan GS and Howlett CR. Miliary broncholithiasis in a
cat. J Am Vet Med Assoc 1973; 162: 214–216.
5 Menivale F, Deslee G, Vallerand H, et al. Therapeutic man-
agement of broncholithiasis. Ann Thorac Surg 2005; 79:
1774–1776.
6 Seo JB, Song KS, Lee JS, et al. Broncholithiasis: review of
the causes with radiologic-pathologic correlation. Radio-
graphics 2002; 22: 199–213.
7 Yeo CD, Baeg MK and Kim JW. A case of endobronchial
aspergilloma presenting as a broncholith. Am J Med Sci
2012; 20: 1–3.
8 Barrs VR, Allan GS, Beatty JA, et al. Feline pyothorax:
a retrospective study of 27 cases in Australia. J Feline Med
Surg 2005; 7: 211–212.
9 Lamb CR and Jones ID. Associations between respiratory
signs and abnormalities reported in thoracic CT scans of
cats. J Small Anim Pract 2016; 57: 561–567.
10 Moise NS, Wiedenkeller D, Yeager AE, et al. Clinical,
radiographic, and bronchial cytologic features of cats
with bronchial disease: 65 cases (1980–1986). J Am Vet Med
Assoc 1989; 194: 1467–1473.
11 Reinero C. Advances in the understanding of pathogen-
esis, and diagnostics and therapeutics for feline allergic
asthma. Vet J 2011; 190: 28–33.
Journal of Feline Medicine and Surgery (2008) 10, 95e101
doi:10.1016/j.jfms.2007.06.012

CASE REPORT
Broncholithiasis in a cat: clinical findings, long-term
evolution and histopathological features
1
Jesus Talavera DVM, PhD *, Marı́a Josefa Fernandez del Palacio DVM, PhD,
1 1 2
Dipl ECVIM-CA (Cardiology) , Alejandro Bayon DVM, PhD , Antonio J Buendia DVM, PhD ,
Joaquin Sanchez DVM, PhD, Dipl ECVP2

1
Cardiorespiratory Service,
Veterinary Teaching Hospital,
University of Murcia, 30100
Espinardo, Murcia, Spain
2
Pathology Service, Veterinary
Teaching Hospital, University of
Murcia, 30100 Espinardo, Murcia,
Spain
Date accepted: 22 June 2007
A 14-year-old neutered male Persian cat was evaluated because of an acute
exacerbation of a chronic cough of 2e3 years of duration. Physical examination
was normal except for the auscultation of accentuated breath sounds and
wheezes cranially on both sides of the chest. Complete blood count, biochemical
parameters and urinalysis were normal. Thoracic radiographs showed
a generalised nodular pattern with multiple mineral opacities. Oral prednisone
and doxycycline were prescribed. Two weeks later, the frequency of the cough
was significantly reduced. Terbutaline was recommended for relief of acute
exacerbations. Three years later the cat was evaluated again due to a non-related
disease that led to the euthanasia of the cat. Concerning its respiratory disease,
the cat had experienced nearly asymptomatic periods of 3e6 weeks of duration
punctuated by acute exacerbation periods of 7e10 days, during which
terbutaline was useful to relieve the cough. Thoracic radiographs showed
a mild increase in the size and extent of the pulmonary mineralisation.
Histopathologically, mild bronchitis and bronchiectasis were evident,
accompanied by calcified bronchial plugs and marked hyperplasia and
hypertrophy of the seromucinous glands. Based on clinical and pathoanatomical
findings, a final diagnosis of miliary broncholithiasis and bronchiectasis was
made. Broncholithiasis should be considered in differential diagnosis of
pulmonary mineralisation in cats. When no concomitant diseases are present,
this rare disease appears to have a slowly progressive evolution that does not
appear to carry a bad prognosis and may be satisfactorily managed with
combinations of bronchodilators and corticosteroids.
Ó 2007 ESFM and AAFP. Published by Elsevier Ltd. All rights reserved.

A
14-year-old neutered male Persian cat
(5.0 kg) was presented to the Cardiore-
spiratory Service of the Veterinary
Teaching Hospital of the University of Murcia
with an exacerbation of a 2e3-year history of
a chronic cough. Symptomatology consisted of
non-productive daily coughing (1e2 times/day)
with episodic exacerbations 2e3 times/year.
The cat was kept exclusively indoors, in a flat
in an urban environment. Annual polyvalent
vaccination (Fel-O-Vax Lv-K IV, Fort Dodge
*Corresponding author. Departamento de Medicina y Cirugı́a
Animal, Facultad de Veterinaria, Universidad de Murcia, Cam-
pus de Espinardo, 30100 Espinardo, Murcia, Spain. Tel: þ34-
968367156; Fax: þ34-968364737. E-mail: talavera@um.es
Animal Health) and internal deparasitation sta-
tus were current. Before presentation, the respi-
ratory problem had not received any clinical
investigation or specific treatment. Except during
the most serious coughing paroxysms, the owner
had not observed respiratory distress or exercise
intolerance.
On physical examination, the cat showed good
nutritional condition (body condition score, 3/5)
and appeared alert and playful. The mucous
membranes were normal and the capillary refill
time was less than 2 s. Respiratory pattern was
normal, with a respiratory rate of 45 breaths/
min. Gentle laryngeal and tracheal palpation
were well tolerated without signs of discomfort.

1098-612X/08/010095+07 $32.00/0 Ó 2007 ESFM and AAFP. Published by Elsevier Ltd. All rights reserved.
96 J Talavera et al
After strong tracheal palpation/compression,
a series of 4e6 profound non-productive coughs
were elicited. Thoracic auscultation revealed ac-
centuated breath sounds in all lung fields and in-
spiratory and expiratory wheezes in the cranial
regions of both hemithorax. Cardiac auscultation
was normal, with a heart rate of 160 beats/min.
Results of complete blood count, biochemical
parameters and urinalysis were within normal
limits (Table 1). Thoracic radiographs showed
a generalised nodular pattern characterised by
the presence of multiple (1e10 mm) mineral
opacities (Fig 1). Moreover, bronchial wall thick-
ening was also evident. At this point, differential
diagnosis included broncholithiasis, pulmonary
alveolar microlithiasis, chronic pneumonia,
chronic bronchitis/asthma and bronchopulmo-
nary neoplasia with calcification. Bronchoscopy,
bronchoalveolar lavage, pulmonary biopsy and
high resolution computed tomography were sug-
gested as useful ancillary tests, but the owner de-
clined these investigations. A treatment trial
consisting of oral prednisone (1 mg/kg/bid for
2 weeks) and doxycycline (5 mg/kg q24 h for 2
weeks) was proposed. Two weeks later, the fre-
quency of the cough was significantly reduced.
Doxycycline was withdrawn and the dose of
prednisone was slow tapered (1 mg/kg/48 h)
and withdrawn 2 weeks later. Intermittent ad-
ministration of terbutaline (0.625 mg bid) was
recommended for acute relief of acute exacerba-
tions of the cough.
Three years later, the cat was presented again
because of a large mass on its back. Concerning
respiratory disease, the owner indicated that
the cat had alternated between nearly asymp-
tomatic periods of 3e6 weeks with exacerbation
periods of 7e10 days with increasing frequency
and intensity of the cough. During exacerbations,
the owner believed terbutaline was useful at re-
lieving the cough. On physical examination, the
cat appeared lethargic and depressed. Cardio-
vascular and respiratory parameters were within
normal limits. A solid, round mass (11 cm diam-
eter) was present on the back caudally to the
interscapular area. Cytological examination ob-
tained by fine needle aspiration was consistent
with neoplasia. Blood count, biochemical param-
eters and urinalysis were unremarkable (Table 1).
In thoracic radiographs, the mass appeared be-
tween T8 and L4 vertebral bodies without signs
of bone involvement (Fig 2). Lung fields ap-
peared unchanged compared to 3 years ago,
but with more extensive pulmonary mineralisa-
tion (Fig 2). Surgical excision of the mass was
recommended. The cat was, however, eutha-
nased a week later, at the owner’s request.
On post-mortem examination, the mass ap-
peared white, hard and well delineated, extend-
ing to subcutaneous tissue. In the lungs,
multiple, yellowish, hard nodules (1e10 mm)
were distributed throughout the lung paren-
chyma. No lesions were seen in any of the other
organs examined. Samples of the mass and lungs
were obtained, fixed in 10% buffered formalin
and embedded in paraffin wax at 56 C. Haema-
toxylineeosin staining was used for initial histo-
pathological analysis. Later, Gram and Grocott
stains were carried out to investigate the pres-
ence of bacteria or fungi, respectively, in the
bronchial secretions and broncholiths. In order
to test bacterial colonisation in the lesions,
a broad range polymerase chain reaction (PCR)
technique was carried out on the paraffin em-
bedding samples. Primer design was based on
the highly conserved regions of the eubacterial
16S rRNA gene that has been used previously
in veterinary medicine (Pille et al 2007). The
technique was performed following the method
described by (Ortega et al 2007). A previously di-
agnosed salmonella abortion in an ewe served as
positive control. Characterisation of the lym-
phoid infiltration in the lung was carried out
using polyclonal antibodies against CD3 (T cells)
and CD79 (B cells) antigens (Dako Corp, Califor-
nia, USA). An avidinebiotin-peroxidase com-
plex (ABC) method was used and positive
reaction was demonstrated by the precipitation
of diaminobenzidine tetrahydrochloride.
Histopathological study of the mass led to a di-
agnosis of a grade I fibrosarcoma. With regard to
the lung samples, both bronchi and bronchioli
displayed marked dilation (bronchiectasis), coex-
isting with intraluminal plugs of eosinophilic
material containing cell debris and multiple ag-
gregations of calcified concretions forming bron-
choliths (Fig 3). Gram and Grocott stains failed to
identify the presence of bacteria or fungi in the
broncholiths. The negative results of the PCR
analysis with universal bacterial primers dis-
missed the presence of bacteria in the bronchial
lesions at the time of the death. The epithelium
of ectatic bronchi displayed areas of atrophy,
small areas of necrosis, and marked hyperplasia
of globet cells (Fig 4). Hyperplasia and hyper-
trophy of the bronchial glands were consistent
findings, with expanded lumen containing an
eosinophilic material that was secreted and accu-
mulated to the ectatic airways (Fig 5). Mild to
moderate lymphoid infiltration was observed in
 Broncholithiasis in a cat 97

Table 1. Complete blood count and serum biochemical parameters in a 14-year-old (5 kg) neutered male
Persian cat at first presentation (day 0) and 3 years later
Day 0 3 Years later Reference range
Haematocrit (%) 34 35 24e45
Red blood cell count (cells/ml) 8.12  106 8.33  106 5e10  106
Haemoglobin (g/dl) 11.2 10.7 8e15
White blood cell count (cells/ml) 8.6  103 7.8  103 5.5e19.5  103
Neutrophils (cells/ml) 6.8  103 6.87  103 2.5e12.5  103
Lymphocytes (cells/ml) 1.5  103 0.62  103 1.4e7  103
Eosinophils (cells/ml) 0.16  103 0.16  103 0.1e1  103
Monocites (cells/ml) 0.16  103 0.16  103 0.1e0.8  103
Basophiles (cells/ml) 0 0 0
Platelets (cells/ml) 380  103 323 175e500  103
Total proteins (g/dl) 7.1 7.2 5.4e7.8
Alanine aminotransferase (UI/l) 34 26 <50
Asparate aminotransferase (UI/l) 30 25 <50
g-Glutamyl transferase (UI/l) 0.8 0.3 1e6.5
Alcaline phosphatase (UI/l) 18 8 20e63
Creatine kinase (UI/l) 110 114 50e450
Sodium (mmol/l) 145 148 140e154
Potassium (mmol/l) 4.2 4.0 4.1e5.3
Chloride (mmol/l) 112 113 105e116
Calcium (mmol/l) 9.8 9.5 9e10.2
Phosphorus (mmol/l) 4.8 4.6 4e8
Albumin (g/dl) 2.7 2.4 2.3e3.4
Urea (mg/dl) 48 55 20e50
Creatinin (mg/dl) 1.4 1.5 0.5e1.5
Total bilirubin (mg/dl) 0.12 0.10 <1
Cholesterol (mg/dl) 175 150 100e300
Triglycerides (mg/dl) 45 43 50e200
Blood glucose (mg/dl) 145 136 70e110

the lamina propria of the ectatic bronchi, mainly
composed of T cells and a scarce number of B
cells among them. Occasionally, small aggregates
of neutrophils were observed in the wall of the
airways. Findings of atelectasia in the alveoli sur-
rounding ectatic airways alternating with areas
of emphysema were also present (Fig 3). Based
on clinical and pathoanatomical findings, a final
diagnosis of miliary broncholithiasis and bron-
chiectasis was made.
Broncholithiasis is defined as a pathological
condition in which calcified or ossified material
is present within the bronchial lumen (Olson et al
1999, Seo et al 2002). In humans, the most com-
mon cause of broncholithiasis is erosion by and
extrusion of a calcified adjacent lymph node
into the bronchial lumen, a finding usually asso-
ciated with tuberculosis or histoplasmosis (Seo
et al 2002). Other causes include aspiration of for-
eign material, in situ calcification, erosion and
extrusion of calcified bronchial cartilage plates
and migration of stones via nephrobronchial or
tracheobronchial fistula (Olson et al 1999, Craig
et al 2002, Seo et al 2002). The most common
symptoms of broncholithiasis in humans are
non-productive cough frequently associated
with haemoptysis and, less commonly, lithopty-
sis (expectoration of calcified material). The
most common radiographic findings include
the presence of a calcified nodule and signs of
airway obstruction (bronchiectasis, air trapping)
(Seo et al 2002). In the author’s knowledge,
only a single clinical case describing miliary
broncholithiasis in a cat has been reported (Allan
and Howlett 1973). In that case, broncholithiasis
was postulated to be associated with a chronic
intrapulmonary infection, although a specific
agent was not isolated and signs of terminal con-
gestive heart failure were also found at necropsy.
The cat had a 2-year history of progressive
fatigue associated with moderate to severe dysp-
noea on exertion and the progressive worsening
of the condition resulting ultimately in euthana-
sia. Radiographic findings consisted of multiple
98 J Talavera et al
Fig 1. Lateral (A) and dorsoventral (B) thoracic radio-
graphic views of a 14-year-old (5 kg) neutered male Persian
cat with broncholithiasis, showing the presence of multiple
mineral opacities distributed diffusely throughout all lung
fields.
miliary opaque masses throughout the entire
lung field and evidence of fluid in the ventral
third of the thorax. Histological examination of
the lungs showed marked bronchiectasis, promi-
nent fibrosis of the bronchial walls, calcified
bronchiolar plugs and marked hyperplasia and
hypertrophy of the seromucinous glands of the
ectatic airways. In the present clinical case,
Fig 2. Lateral (A) and dorsoventral (B) thoracic radiographic
views 3 years after initial presentation. A round mass extend-
ing between T8 and L4 vertebral bodies can be seen. Lung
fields’ appearance is similar to 3 years ago, with a mild inten-
sification and mild increased extension of pulmonary
mineralisation.
respiratory signs were mild and showed a
benign long time evolution. In fact, the cat
was euthanased at 17 years of age because of
a non-related disease. The respiratory disease
 Broncholithiasis in a cat
Fig 3. Panoramic view of an ectatic airway with a large
bronchiolith (BL) within the lumen. The bronchial wall
(BW) shows a marked hyperplasia of the glands. Surround-
ing areas of lung parenchyma show atelectasis (AT) and
compensatory emphysema (EN). Haematoxylin and eosin
5. Bar ¼ 500 mm.
was relatively stable over a 6-year period and
did not significantly affect the cat’s quality of
life. No signs of cardiac failure or other cardio-
pulmonary disease were found. Radiographic
findings were consistent with miliary broncholi-
thiasis. Histopathologically, mild inflammation
was found. In contrast, the most constant find-
ings were bronchiectasis, the presence of
Fig 4. Detail of the bronchial wall (BW) and a bronchiolith
(BL) in the bronchial lumen. Note the marked hyperplasia of
the glands in the bronchial wall and the histological struc-
ture of the bronchiolith, with the presence of cell debris,
an eosinophilic material from glandular secretion (*) and
multiple small basophilic crystals of calcium (arrows). There
is atrophy of the epithelium in the area of contact between
the bronchial wall and the bronchiolith. Haematoxylin and
eosin 20. Bar ¼ 50 mm.
99
Fig 5. Detail of the wall of an ectatic airway showing hy-
perplasia (*) and dilation (#) of the bronchial glands contain-
ing eosinophilic material. Peribronchial fibrosis (PF) and
images of atelectasis (AT) are also present. Haematoxylin
and eosin 20. Bar ¼ 50 mm. BLU ¼ bronchial lumen.
calcified bronchial plugs and marked hyperpla-
sia and hypertrophy of the seromucinous glands.
Pathological soft tissue mineralisation is con-
sidered to occur through three basic mechanisms:
dystrophic, metastatic and idiopathic (Chan et al
2002, Berry and Tyson 2004). In dystrophic miner-
alisation, deposition of calcium salts occurs in
previously injured, degenerating, or necrotic soft
tissues with normal plasma levels of calcium
and phosphorus, and in the absence of derange-
ments of calcium metabolism (Berry and Tyson
2004). The most common causes of dystrophic
mineralisation in small animals are previous in-
flammation, degeneration, infection or neoplasia
(Berry and Tyson 2004). Pulmonary mineralisa-
tion in a cat in the last period of a chronic pneu-
monia caused by Mycobacterium thermoresistible
has been reported (Foster et al 1999). Metastatic
mineralisation implies previous abnormalities in
plasma calcium and phosphorus concentrations;
when plasma calcium and phosphorus product
concentrations exceed 70, calcification of normal
soft tissue can ensue (Chan et al 2002, Berry and
Tyson 2004). Causes of metastatic mineralisa-
tion can include primary hyperparathyroidism,
vitamin D toxicity, bone tumours (multiple mye-
loma), and chronic renal failure with hyperphos-
phataemia (Berry and Tyson 2004). Idiopathic
mineralisation designs a type of soft tissue miner-
alisation in which an underlying pathological
cause or abnormalities of serum calcium or
phosphorus cannot be determined (Berry and
Tyson 2004). Idiopathic mineralisation in the
lung occurs in alveolar microlithiasis, a rare
100 J Talavera et al
disease characterised by intra-alveolar calcium
deposits (Brummer et al 1989, Brix et al 1994,
Chan et al 2002). Its pathophysiology is not well
understood although several theories have been
proposed. One of these postulates that an inap-
propriate immune response leads to the forma-
tion of the calculi (Brix et al 1994). Microliths
begin as inspissated masses of intrabronchial
mucus, which act as nuclei for precipitation,
with subsequent accumulation of calcium salts
(Brummer et al 1989). Another theory about
formation of alveolar microliths suggests that an
inborn error of metabolism (enzymatic abnormal-
ity) leads to excessive alkalinity and decreased
solubility of calcium phosphate within the lumen
of alveoli (Brix et al 1994). Pulmonary alveolar
microlithiasis has been described in a cat with
chronic bronchopneumonia, and microliths’ for-
mation was considered secondarily to inspissa-
tion and mineralisation of mucinous exudates
(Brummer et al 1989).
In the only reported case of feline broncholi-
thiasis, the formation of the broncholiths was at-
tributed to dystrophic mineralisation secondarily
to chronic bronchopneumonia and the conse-
quent accumulation of bronchial secretions
(Allan and Howlett 1973). However, with the
exception of pulmonary alveolar microlithiasis,
both dystrophic and metastatic forms of pulmo-
nary mineralisation usually occur in well-
perfused tissue (such as pulmonary interstitial
or peribronchial tissues). In the present clinical
case, mineralisation was only located in bron-
chial intraluminal plugs. Thus, serum calcium
and phosphate levels were within normal range
and no features of diseases predisposing to met-
astatic mineralisation were found.
Bronchiectasis is uncommon in cats, and has
been reported mainly in older males secondary
to disorders such as neoplasia, chronic bronchitis
and asthma (Norris and Samii 2000). In the pres-
ent clinical case, although the presence of T cells
could point to a relationship with chronic bron-
chitis and asthma (Padrid 2000, Bay and Johnson
2004), other typical findings of asthma, such as
eosinophilic infiltrate, airway smooth muscle
thickening or contracted bronchioli, were absent.
In contrast, the hyperplasia of the bronchial sero-
mucinous glands was a consistent finding, but
glandular hyperplasia is an unspecific mucosal
strategy in response to external injury. In the
present clinical case, the origin of the mucosal
plug could be related with an abnormal exacer-
bated glandular response to a previous bacterial,
viral or fungal infection that triggered the
process and then becomes self-perpetuating. In
that case, bronchiectasis could have been second-
ary to the chronic presence of broncholiths in the
airways.
In human medicine, patients with symptom-
atic broncholithiasis must be specifically treated
to avoid complications such as massive hae-
moptysis, bronchial fistula, bronchiectasis, and
recurrent infections (Olson et al 1999). Therapeu-
tic options include observation, bronchoscopic
broncholithectomy, and surgery (Olson et al,
1999, Seo et al 2002). In the only previously
reported case of feline broncholithiasis, no
therapeutic intervention was detailed by the
authors. In the present clinical case, broncho-
scopic broncholithectomy or surgery was not
considered as a suitable option because of the
miliary distribution of the broncholiths. Based
on in vivo clinical data available to us, a trial
with corticosteroids and doxycycline was consid-
ered appropriate in order to treat an underlying
inflammation and possible bacterial infections.
Considering that airway hyperreactivity and
bronchoconstriction could be implicated in the
clinical exacerbations, terbutaline was also pre-
scribed. Acute response to corticoids and doxy-
cycline trial was satisfactory. Also, the owner’s
impression was that terbutaline was useful dur-
ing exacerbations to reduce the duration, inten-
sity and frequency of the cough.
In conclusion, broncholithiasis should be con-
sidered in differential diagnosis of pulmonary
mineralisation in cats. When no concomitant dis-
eases are present, this rare disease looks to have
a slowly progressive evolution that does not
appear to carry a bad prognosis and may be
satisfactorily managed with combinations of
bronchodilators and corticosteroids. The exact
pathogenesis and the meaning of feline broncho-
lithiasis remain to be established and further
studies of a possible inciting infectious aetiology
are justified.
Acknowledgements
The authors would like to thank Nieves Ortega
and Maria C. Gallego from the Department of
Animal Health, University of Murcia for perfom-
ing PCR analysis on paraffin-embedded samples.
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