J. Comp. Path. 2021, Vol. 189, 59e71 Available online at www.sciencedirect.

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INFECTIOUS DISEASE

Causes and Lesions of Fatal Pneumonia in

Domestic Cats
M^onica Slaviero, Luiza P Ehlers, Fernando F Argenta, Caroline Savi,
Bruna C Lopes, Saulo P Pavarini, David Driemeier and Luciana Sonne
Department of Veterinary Pathology, College of Veterinary Medicine, Universidade Federal do Rio Grande do Sul, Porto
Alegre, Brazil

Summary
Pneumonia in cats may cause severe lung injury and consequent death. We describe the post-mortem findings
and aetiologies of naturally fatal pneumonia in 78 domestic cats, using gross and histopathological examina-
tions, immunohistochemistry and microbiological techniques. Morphological patterns found were broncho-
pneumonia (27/78), interstitial (15/78), bronchointerstitial (13/78), granulomatous (8/78), aspiration (8/78)
and pyogranulomatous (5/78) pneumonia, and pleuropneumonia (2/78). Bacterial pneumonia was identified
as the most common cause (32/78), followed by viral (15/28 feline calicivirus, 10/28 felid alphaherpesvirus 1
and 3/28 both viruses), aspiration (8/78), fungal (5/78) and parasitic pneumonia (5/78). Co-infection with fe-
line immunodeficiency virus and feline leukaemia virus was found in 54 cats. Viral infections involved cats of all
ages, indicating the importance of investigating viral causes in cats with respiratory diseases, including in adult
and ageing cats.

Ó 2021 Elsevier Ltd. All rights reserved.

Keywords: bacterial pneumonia; cats; feline retroviruses; viral pneumonia

Introduction Pneumonia in cats may result in severe lung injury

Pneumonia in cats can be caused by infectious agents,
such as bacteria, viruses, fungi or parasites, or by
inhaling toxic or irritating substances (Foster and
Martin, 2011; Caswell and Williams, 2016; Dear,
2020). The feline caudal respiratory tract (Nomina
Anatomica Veterinaria, 2017) is most commonly
affected by infections in young cats (Bart et al, 2000;
Chvala-Mannsberger et al, 2009; Monne Rodriguez
et al, 2014, 2018). In adult cats, pneumonia is less
common and usually related to predisposing factors
and systemic immunosuppression. These conditions
include co-infections by feline leukaemia virus
(FeLV) and feline immunodeficiency virus (FIV),
endocrine or metabolic diseases, or immunosuppres-
sive chemotherapy or corticosteroid therapy (Foster
and Martin, 2011).
Correpondence to: M Slaviero (e-mail: monicaslav.vet@gmail.com).
and consequent death. Although case reports on res-
piratory tract diseases in cats are common, there is lit-
tle information regarding feline fatal pneumonia. In
addition to post-mortem examination, recognition
of clinical patterns of pneumonia is a crucial tool in
reaching a specific aetiological diagnosis or, at least,
for refining the differential diagnosis (Maxie and
Miller, 2016).
Although more frequent in cranial respiratory tract
infections, primary respiratory viral agents such as fe-
line calicivirus (FCV) and felid alphaherpesvirus 1
(FeHV 1) may occasionally be involved in interstitial
pneumonia (Chvala-Mannsberger et al, 2009; Monne
Rodriguez et al, 2014, 2017). However, viral diagnosis
using only histopathological analysis is a challenging
process and often requires ancillary diagnostic tests
such as immunohistochemistry (IHC), which has
rarely been carried out in studies on pneumonia in

0021-9975/$ - see front matter Ó 2021 Elsevier Ltd. All rights reserved.
https://doi.org/10.1016/j.jcpa.2021.09.005
60 M Slaviero et al
cats (Foster and Martin, 2011). Consequently, data
on the involvement of viral agents in feline pneu-
monia may be underreported.
Studies on the frequency of pneumonia and de-
scriptions of pathological features of pneumonia in
cats are scarce (Bart et al, 2000; Macdonald et al,
2003). Furthermore, there are no descriptive or illus-
trated studies of fatal feline pneumonia that associate
the gross and histological morphological patterns
with microbiological information and immunohisto-
chemical investigation of viral agents in cats.
Thus, the objectives of this study were to describe
the pathological features of fatal pneumonia in cats
and to investigate the infectious agents involved, in
addition to co-infections by FIV and FeLV.
Materials and Methods
Cases
A retrospective study of fatal cat pneumonia diagno-
ses was carried out by analysing necropsy reports filed
at the Department of Veterinary Pathology, Univer-
sidade Federal do Rio Grande do Sul, Porto Alegre,
Brazil, between January 2010 and June 2020. The
database was searched for cases based on combina-
tions of keywords including ‘feline’, ‘cats’, ‘pneu-
monia’ and ‘pleuropneumonia’. Only cases in which
pneumonia was directly related to the cause of death
were included in the study. Cases diagnosed with
pneumonia due to systemic causes, such as feline in-
fectious peritonitis and septicaemia, or cases of pleur-
itis without the involvement of the lung parenchyma
or with mild involvement were excluded.
The evaluated animals were grouped into the
following age categories based on the report of Vogt
et al (2010): ‘kitten’, ‘junior’, ‘prime’, ‘mature’, ‘se-
nior’ and ‘geriatric’. Predisposing factors for pneu-
monia and causes of immunosuppression were
analysed from the information provided by the refer-
ring clinical veterinarians or from necropsy results.
Review of Gross and Histopathological Findings
The gross and histopathological findings of all cases
were reviewed as described by Bianchi et al (2020). As
reported by Lopez and Martinson (2017), pneumonia
was classified into the following morphological patterns
according to the predominant gross lesions and histo-
logical features: bronchopneumonia; interstitial, bron-
chointerstitial and granulomatous pneumonia; and
pleuropneumonia. When the inflammatory infiltrate
comprised mainly neutrophils and macrophages,
pneumonia was classified as pyogranulomatous pneu-
monia and when there was intense airway necrosis asso-
ciated with a foreign body, it was classified as
‘aspiration pneumonia’.
Investigation of Infectious Agents
Information on previous bacteriological cultures was
analysed from necropsy records. In addition, from
April 2019 to June 2020, fresh lung fragments were
collected during post-mortem examination of pneu-
monic cats for bacteriological culture (Bianchi et al,
2020).
Lung tissue from all cases was subjected to immu-
nohistochemistry (IHC) for FeHV 1 and FCV using
the antibodies and protocols listed in Table 1. IHC
for FIV and FeLV was also carried out on bone
marrow or lymph node sections. IHC was also per-
formed to exclude feline coronavirus (FCoV) involve-
ment in the selected cases. IHC for Escherichia coli was
performed in cases in which the histopathological le-
sions were compatible with bacterial infection, but
either no growth was obtained in culture or culture
was not performed. Positive controls for IHC
comprised tissues previously confirmed as positive
for the respective antigens. As a negative control,
the primary antibody was replaced by an irrelevant
primary antibody (Ramos-Vara and Miller, 2014).
In cases that were immunonegative for E. coli or those
in which immunolabelling was mild and multifocal,
Gram Brown‒Hopps staining was performed. In
cases where intralesional yeast fungal microorganisms
were observed during the histopathological examina-
tion, the periodic acideSchiff reaction and Alcian
blue staining (PAS-AB) was performed.
Results
From January 2010 to June 2020, 1,749 post-mortem
examinations were carried out on cats. Pneumonia
was identified as the cause of death in 78 (4.5%)
cats. Fourteen of these cats were kittens (17.9%), 19
juniors (24.4%), 13 prime (16.7%), 14 mature
(17.9%), eight senior (10.3%) and five geriatric
(6.4%). In five cases (6.4%), age information was
not available. Most of the cats were mixed-breed
(70; 90.0%), four (5.1%) were Himalayan, two
(2.5%) Persian, one (1.2%) Siamese and one
(1.2%) Domestic Shorthair. Forty-nine (62.8%)
cats were male and 29 (37.2%) were female.
The main lung lesion found was bronchopneu-
monia (27/78; 34.6%), followed by interstitial (15/
78; 19.3%), bronchointerstitial (13/78; 16.7%), gran-
ulomatous (8/78; 10.2%), aspiration (8/78; 10.2%)
 Table 1
Antibodies and immunohistochemical protocols used in cases of feline pneumonia

Antigen Antibody/clone Dilution Antigen retrieval Amplification signal Chromogen Positive control

Escherichia coli Polyclonal (Virostat, 1:200 5 min, microwave oven, MACH 4 Universal Romulin AEC (Biocare Large intestine (swine
Westbrook, Maine, citrate buffer, pH 6.0 HRP-Polymer Medical) colibacillosis)
USA) (Biocare Medical,
Pacheco, California,
USA)
Mouse anti-feline Monoclonal (FCV1-43) 1:50 20 min, 37
C protease- MACH 4 Universal Romulin AEC Pellet cells (cat)
calicivirus (Custom Monoclonals XIV HRP-Polymer
International,
Sacramento,
California, USA)
Mouse anti-felid Monoclonal (FHV7-5) 1:100 20 min, 37
C protease- MACH 4 Universal Romulin AEC Skin and lung (cat)
herpesvirus 1 (Custom Monoclonals XIV HRP-Polymer

Fatal Pneumonia in Domestic Cats

International)
Mouse anti-feline Monoclonal (C11D8) 1:500 40 min, 96
C, digital MACH 4 Universal Romulin AEC Pellet cells (cat)
leukaemia virus, gp 70 (Bio-Rad, Hercules, pressure cooker, Tris HRP-Polymer
California, USA) EDTA buffer, pH 9.0
Mouse anti-feline Monoclonal (PAK32C1) 1:100 40 min, 96
C, digital MACH 4 Universal Romulin AEC Lymph node (cat)
immunodeficiency (Bio-Rad) pressure cooker, HRP-Polymer
virus, p24 gag citrate buffer, pH 6.0
Mouse anti-coronavirus Monoclonal (FIPV3-70) 1:100 40 min, 96
C, digital MACH 4 Universal Romulin AEC Lymph node (cat)
(Santa Cruz pressure cooker, HRP-Polymer
Biotechnology, Dallas, citrate buffer, pH 6.0
Texas, USA)

AEC, 3-amino-9-ethylcarbazole.

61
62 M Slaviero et al

Table 2
Morphological pattern of lesions and infectious agents identified in cases of fatal feline pneumonia

Morphological pattern Aetiology Total cases Only FIV Only FeLV FIV and FeLV No. co-infections with both retroviruses

Bronchopneumonia Bacterial* 27 6 7 7 20
Interstitial FCV 15 3 4 3 10
Bronchointerstitial FeHV 1 10 1 3 4 8
FeHV 1 and FCV 3 1 2 0 3
Granulomatous Aelurostrongylus abstrusus 5 1 1 1 3
Cryptococcus spp 3 0 2 1 3
Aspiration e 8 2 1 1 4
Pyogranulomatous Filamentous bacteria† 3 0 1 0 1
Aspergillus section Nigri 2 0 0 0 0
Pleuropneumonia Pasteurella multocida 2 1 0 1 2

Total 78 15 21 18 54
100% 19.2% 26.9% 23.1% 69.2%

FIV, feline immunodeficiency virus; FeLV, feline leukaemia virus; FCV, feline calicivirus; FeHV 1, felid herpesvirus 1.
*
Escherichia coli, Pasteurella multocida, Streptococcus canis, Staphylococcus spp, Acinetobacter spp and other unidentified bacteria.
†
Bacteria with filamentous morphology (histopathology); no growth in culture.

and pyogranulomatous (5/78; 6.4%) pneumonia, and
pleuropneumonia (2/78; 2.6%) (Table 2).
Bacterial pneumonia was identified in 41.0% of
cases (32/78), followed by viral pneumonia (28/78
[36.0%]: 15/28 FCV; 10/28 FeHV 1 and 3/28 com-
bined FCV and FeHV 1) with nine cases of secondary
bacterial infection (32.1%). Other causes were aspi-
ration (8/78; 10.2%), fungal (5/78; 6.4%) and para-
sitic pneumonia (5/78; 6.4%). Positive
immunolabelling of FIV or FeLV antigens was found
in 54 cases (69.2%) (26.9% FeLV, 23.1% both FIV
and FeLV and 19.2% FIV). Potential predisposing
factors for pneumonia or causes of immunosuppres-
sion were identified in 71.4% of the kittens, 84.2%
of the junior cats, 69.2% of the prime cats, 85.7% of
the mature cats and 100% of the senior and geriatric
cats (Table 3).
Bacterial culture was performed on 24 cats, of
which 13 had bacterial growth. Pure isolates corre-
sponded to Pasteurella multocida (6), Streptococcus canis
(3), Staphylococcus spp (1) and Acinetobacter spp (1).
One case had abundant mixed growth of E. coli and
Staphylococcus spp and another had abundant mixed
growth of E. coli and S. canis. In cases with no bacterial

Table 3
Potential causes of immunosuppression and predisposing factors in cats with fatal pneumonia by life stage

Kitten (14/78) Junior (19/78) Prime (13/78) Mature (14/78) Senior (8/78) Geriatric (5/78) NK (5/78)

Infectious pneumonia 10 18 13 13 6 5 5
Only FIV positive 3 5 0 1 0 0 3
Only FeLV positive 1 8 6 1 2 0 1
FIV and FeLV 2 2 3 8 1 2 1
positive
FeLV positive and 0 0 0 0 1 0 0
CKD
CKD 0 0 0 1 0 2 0
Diabetes mellitus 0 0 0 0 1 1 0
Aspiration pneumonia 4 1 0 1 2 0 0
Neurological disease 2 0 0 0 0 0 0
Hospitalization 0 0 0 1 1 0 0
Forced feeding 1 1 0 0 0 0 0
Oesophageal stricture 1 0 0 0 0 0 0
Decubitus vomiting 0 0 0 0 1 0 0

Total 10/14 16/19 9/13 12/14 8/8 5/5 5/5

71.4% 84.2% 69.2% 85.7% 100% 100% 100%

NK, not known; FIV, feline immunodeficiency virus; FeLV, feline leukaemia virus; CKD, chronic kidney disease.
 Fatal Pneumonia in Domestic Cats 63

growth (11/24), eight cats had received broad-
spectrum antimicrobial treatment before death. E.
coli antigen was detected by IHC in lung tissues of
26 cats, including 16 marked and diffuse immunolab-
elling of bacterial colonies.
In three cases, immunolabelling was mild and
multifocal, and co-infection with gram-positive cocci
colonies was identified with Brown‒Hopps staining.
Thus, of the 21 E. coli infections, 15 (71.4%) corre-
sponded to bacterial bronchopneumonia, three
(14.3%) to secondary infections in cases of FeHV 1
viral pneumonia and three (14.3%) to secondary in-
fections in cases of FCV viral pneumonia. Fourteen
(66.6%) also had co-infection with FIV or FeLV
(seven FeLV, five FIV and two with both FIV and
FeLV).
Bacterial Pneumonia: Bronchopneumonia and
Pyogranulomatous Pattern
Bronchopneumonia was the main morphological
pattern seen in 27 cases of bacterial pneumonia
(Table 4) and involved cats in all age groups
(Supplementary Table 1). Grossly, affected lungs
had multifocal firm, predominantly cranioventral
areas, which sometimes extended irregularly to other
lobes (Fig. 1A and B). Microscopically, the character-
istic finding was an abundant, predominantly neutro-
philic, inflammatory infiltrate at the
bronchioloalveolar junction (Fig. 1C), which
extended to adjacent bronchi and alveoli and was
often associated with few to high numbers of bacterial
aggregates.
The second pattern identified in bacterial infec-
tions was pyogranulomatous pneumonia, which
affected three mixed-breed, one junior and two
prime male cats. Grossly, affected lungs did not
collapse and were diffusely red, and approximately
70e80% of the parenchyma was obliterated by
soft, multifocal yellowishewhite nodules (Fig. 1D).
Microscopically, these nodules corresponded to a
marked inflammatory infiltrate of neutrophils and
macrophages, located mainly in the alveolar spaces.

Fig. 1. Bacterial pneumonia, lungs, cats. (A) E. coli bronchopneumonia: uncollapsed lung with reddish area of cranioventral consolidation.
Bar, 2 cm. (B) P. multocida bronchopneumonia. Multifocal whiteereddish consolidated areas extend to caudal lobe. Bar, 2 cm. (C)
E. coli bronchopneumonia: intense neutrophilic infiltrate at bronchioloalveolar junction with thrombosis (arrow) and marked
congestion. HE. Bar, 200 mm. Inset: large number of coccobacilli immunolabelled for E. coli antigen. IHC. Bar, 50 mm. (D) Pyog-
ranulomatous pneumonia: yellowish multifocal nodules in all lobes. Bar, 2 cm. Inset: dense bacterial myriad surrounded by eosin-
ophilic material and pyogranulomatous inflammatory infiltrate. HE. Bar, 50 mm.
64 M Slaviero et al

Table 4
Histological lesions in lungs of cats with a post-mortem diagnosis of infectious pneumonia

Histological findings Bacterial Viral Fungal Parasitic

BR PG PL IN BI GR PG GR

Total no. cases 27 3 2 15 13 3 2 5

Airway epithelial necrosis 11 0 0 0 13 0 2 0

Pyknotic pneumocytes 0 0 0 15 13 0 0 0
Extensive parenchymal necrosis 25 0 2 0 0 0 0 0
Neutrophilic* inflammatory infiltrate 27 0 2 14 13 0 0 1†
Pyogranulomatous* inflammatory 0 3 0 0 0 0 2 1
infiltrate
Lymphohistiocytic* inflammatory infiltrate 0 0 0 1 0 3 0 3
Fibrin septa or alveolar spaces 27 0 2 14 13 0 2 0
Thrombosis 14 0 0 7 7 0 0 0
Pneumocyte type II hyperplasia 7 3 3 8 5 3 1 2
Syncytial cells 3 0 0 2 3 1 0 1
Alveolar fibrosis 1 3 0 2 0 1 1 0
Arterial smooth musculature hyperplasia 2 3 0 4 2 1 0 5
Myofibroblast hyperplasia 1 3 0 3 2 1 0 5

BR, bronchopneumonia; PG, pyogranulomatous pneumonia; PL, pleuropneumonia; IN, interstitial pneumonia; BI, bronchointerstitial pneu-
monia; GR, granulomatous pneumonia.
*
Predominant cell type in inflammatory infiltrate.
†
Associated with eosinophils.

There were mild, basophilic, filamentous bacterial
aggregates within the inflammatory infiltrates, some-
times surrounded by radiating club-shaped hypereo-
sinophilic material (SplendoreeHoeppli
phenomenon) (Fig. 1D). However, the aetiology
could not be confirmed due to absence of growth
in the bacterial culture medium.
Viral Pneumonia: Interstitial and Bronchointerstitial Pattern
Interstitial pneumonia was observed in 15 cases, all of
which were FCV positive by IHC (Supplementary
Table 2). Both young and adult cats were affected,
with half the cats belonging to the kitten and junior
life stages. Grossly, the lungs were diffusely pale, un-
collapsed and elastic, sometimes with an impression
of the ribs on the pleura. White, multifocal punctate
areas, distributed randomly in the pulmonary lobes,
were also observed (3/15). In cases with secondary
bacterial infection (5/15), there were firm white or
red, mainly cranioventral but also caudodorsal areas
of pulmonary consolidation (Fig. 2A). Histological
analysis revealed pneumocyte necrosis associated
with intense fibrin exudation and marked infiltration
of alveolar macrophages and neutrophils into alveolar
spaces (Fig. 2B). In cases with secondary bacterial
infection (5/15), the morphological pattern was
mixed with characteristics of bronchopneumonia
(Fig. 2C). In three cases with bacterial co-infection,
marked E. coli immunolabelling was seen (Fig. 2C).
IHC for FCV revealed mild to marked multifocal
viral antigen in the cytoplasm of alveolar macro-
phages and pneumocytes (Fig. 2D).
Viral pneumonia was associated with bronchoin-
terstitial pneumonia in 13 cases (9/13 kitten or ju-
nior cats), all of which had FeHV 1 infection
(Supplementary Table 3). Grossly, affected lungs
were uncollapsed, elastic with rib impressions on
the pleura, and pale, sometimes with multifocal to
coalescent whitish areas. Multifocal areas of cranio-
ventral consolidation were seen in cases of secondary
bacterial infections (4/13) (Figs. 3A and B). Micro-
scopically, in all 13 cases, fibrinonecrotic pneumonia
was observed with necrosis of bronchial, bronchiolar
and septal epithelial cells. Eosinophilic intranuclear
inclusion bodies were identified in epithelial cells in
four cases (Fig. 3C). Four cats had concomitant sec-
ondary bacterial infections (Fig. 3C). Multifocal im-
munolabelling of FeHV 1 antigen was seen in the
necrotic epithelium of bronchi and bronchioles, peri-
bronchial glands, pneumocytes and macrophages
(Fig. 3D).
Fungal Pneumonia: Granulomatous and Pyogranulomatous
Pattern
Fungal infections were identified in five cats, three of
which had granulomatous pneumonia caused by
Cryptococcus spp infection. All three of these animals
were males: one junior cat and two mature cats.
Grossly, the lungs occasionally exhibited multifocal
to coalescent, white, soft nodules randomly
 Fatal Pneumonia in Domestic Cats 65

distributed across all pulmonary lobes (Fig. 4A). His-
tological analysis revealed pneumonia associated with
a few yeast-like fungal structures surrounded by an
unstained or slightly basophilic PAS-AB-positive
halo (Fig. 4B), morphologically compatible with
Cryptococcus spp in all cases. Infection with Aspergillus
section Nigri, associated with infiltrative pyogranu-
lomatous pneumonia, was observed in two cats previ-
ously diagnosed with diabetes mellitus (Leite-Filho
et al, 2016).
Parasitic Pneumonia: Granulomatous Pattern
Parasitic pneumonia was found in five cases and cor-
responded to Aelurostrongylus abstrusus infection in both
junior (2/5) and prime (3/5) cats. Four of these cats
were female and one was male. Grossly, the pneu-
monia was characterized by multifocal to coalescent
multiple nodular to linear yellowewhitish structures
on the pulmonary surface that extended to the paren-
chyma (Fig. 4C). Microscopically, these areas
comprised clusters of numerous embryonic parasite
eggs (30e40 mm) and larval structures
(150e170 mm), which joined to form large nodules
(Fig. 4D).
Aspiration Pneumonia
Aspiration pneumonia was observed in eight cases,
mainly in kittens (4/8). Grossly, there were multi-
focal, firm, white to red consolidated areas in the right
or left cranial lobes. However, in five cases, these areas
were present in all the pulmonary lobes. Microscopi-
cally, bronchi and bronchioles were occluded by a
large amount of golden or amphophilic granular ma-
terial or homogeneous eosinophilic amorphous mate-
rial. The respiratory epithelium was diffusely
necrotic. In five cases, this content was associated
with mixed bacterial aggregates, degenerated neutro-
phils and fibrin.
Pleuropneumonia
In two cats, there was marked inflammation of the
lung parenchyma and pleura, and for this reason
they were classified separately. The affected cats

Fig. 2. Interstitial pneumonia, lungs, feline calicivirus (FCV), cats. (A) Uncollapsed lung with rib impressions (arrowhead) and reddish
area of cranioventral consolidation in a cat with FCV and secondary E. coli infection. Bar, 1.25 cm. (B) Alveolar spaces filled with
inflammatory neutrophil and macrophage infiltrate. Moderate multifocal deposition of fibrin in alveolar septa (arrowheads). HE.
Bar, 100 mm. (C) FCV associated with bacterial infection: many bacteria in alveolar spaces associated with severe fibrin deposition.
HE. Bar, 100 mm. Inset: intense immunolabelling of E. coli. IHC. Bar, 50 mm. (D) Multifocal immunolabelling of FCV in cytoplasm
of macrophages and/or desquamated pneumocytes. IHC. Bar, 50 mm.
66 M Slaviero et al

were male, mixed-breed: one junior and one prime
cat. Grossly, there was marked pyothorax and the
lungs showed marked and diffuse fibrin deposition
on the pleura. Histological analysis showed extensive
necrosis of the pulmonary parenchyma, extending to
the parietal and visceral pleura, associated with
marked deposition of fibrin, inflammatory infiltrate
of degenerated neutrophils and myriad bacterial
basophilic coccobacilli. Pasteurella multocida was iso-
lated from lung tissue of both cats.
Discussion
The diagnosis and characterization of fatal pneu-
monia in these cats were based on the pathological,
immunohistochemical and microbiological findings.
Pneumonia accounted for 4.5% of the deaths in this
cohort of cats. Similarly, previous retrospective
studies of the cause of death in cats reported fre-
quencies of pneumonia of between 1% and 6.5%
(Egenvall et al, 2009; Togni et al, 2018). Breed predis-
position has not been proven in diseases of the caudal
respiratory tract (Macdonald et al, 2003; Foster et al,
2004). However, it has been reported that male cats
tend to have a 2.4 times greater chance of developing
pneumonia than females (Foster et al, 2004), which is
probably related to the latter’s greater environmental
exposure due to territorial and copulation behaviour
(Biezus et al, 2019).
In contrast to previous studies in which young an-
imals were found to be most affected by infectious
pneumonia (Bart et al, 2000; Chvala-Mannsberger
et al, 2009; Monne Rodriguez et al, 2014), all life stages
were similarly affected in the present study. Thus, it is
important that the possibility of infectious pneumonia
should be considered in the differential diagnosis of
disease cats of all ages and that it should be treated
as a severe illness that can progress and cause death.
While young animals are naturally more at risk to
the development of pneumonia due to their lower
levels of immunity, primary pneumonia in adult
cats is considered uncommon. In these cases, it is
important to investigate predisposing factors (Bart
et al, 2000; Dear, 2020), which include those that
lead to systemic immunosuppression, such as feline
retrovirus infections, endocrine or metabolic diseases,
chemotherapy or immunosuppressive therapy (Cohn
and Reinero, 2007; Foster and Martin, 2011). In the

Fig. 3. Bronchopneumonia, lungs, felid herpesvirus 1 (FeHV 1). (A) Lung slightly collapsed, reddish and with rib impressions on pleural
surface. Bar, 2 cm. (B) FeHV 1 with bacterial co-infection: whitish multifocal areas mainly in the cranial pulmonary lobe associated
with areas of consolidation that extend to caudal lobe. Bar, 2 cm. (C) Necrotic bronchial epithelium associated with marked bac-
terial infiltration. Eosinophilic intranuclear inclusion bodies in epithelial cells (arrow). HE. Bar, 50 mm. HE. Inset: intense immu-
nolabelling of E. coli antigen in bronchus. IHC. Bar, 50 mm. (D) Intense immunolabelling of FeHV 1 in bronchial epithelial cells and
peribronchial glands. IHC. Bar, 100 mm.
 Fatal Pneumonia in Domestic Cats 67

present study, more than 80% of the mature cats and
all of the senior and geriatric cats had some predispos-
ing factor. In addition to FIV and FeLV, uraemia
due to chronic kidney disease (CKD) and diabetes
mellitus were important factors identified at these
ages, especially in cases of bacterial pneumonia.
These results demonstrate the importance of investi-
gating the involvement of FIV/FeLV and other meta-
bolic diseases in cats with lung disease. The corollary
is that the possibility of severe pneumonia must be
considered in cats known to be FIV/FeLV positive
or with CKD and, in these cases, an early diagnosis
is essential for a better outcome.
The correlation between the development of respi-
ratory infections and secondary bacterial infections in
FIV- and FeLV-positive cats has been reported with
20e30% of cats infected with FeLV and 14.3% of cats
with FIV having pneumonia (Reinacher, 1989;
Knotek et al, 1999). In the present study, >60% of
the cats were co-infected with these retroviruses. Sys-
temic immunosuppression in both FIV and FeLV in-
fections contributes to death from opportunistic
infections (Ogilvie et al, 1988; Cohn and Reinero,
2007). Furthermore, FIV- and FeLV-positive cats
tend to develop more severe clinical disease with a
higher risk of death (Tenorio et al, 1991; Chvala-
Mannsberger et al, 2009; Dear, 2020). FIV and
FeLV seroprevalence has been reported to be 3.6%
and 3.1%, respectively, in North America (Burling
et al, 2017), with corresponding prevalences of 3.2%
and 3.6% in Germany (Gleich et al, 2009) and 6%
and 5% in the UK (Hosie et al, 2009). However, in
Brazil, the reported frequencies vary from 7.6% to
10.1% for FIV and from 28.4% to 31.0% for FeLV
(Costa et al, 2017; Biezus et al, 2019), which is similar
to the findings of the present study.
Bacterial infections were the main cause of pneu-
monia, as reported in another retrospective study
(Macdonald et al, 2003), and were mainly associated
with bronchopneumonia. Grossly, the characteristic

Fig. 4. Granulomatous pneumonia, lungs, cats. (A) Cryptococcus spp pneumonia: uncollapsed lung with multifocal to coalescent areas, whit-
ish, and slightly elevated. Bar, 2 cm. (B) Thickening of alveolar septa by inflammatory infiltrate surrounding an unstained yeast-like
structure with capsule (arrow). HE. Bar, 50 mm. Inset: PAS-positive yeast-like fungal structure with AB-positive capsule. PAS-AB.
Bar, 50 mm. (C) A. abstrusus pneumonia: uncollapsed, reddish lung with linear to nodular, yellowishewhite multifocal areas. Bar,
2 cm. (D) Many morulae (black arrow), eggs (white arrow) and larvae (arrowhead) of A. abstrusus obliterate alveoli and replace
parenchyma, associated with moderate inflammatory infiltrate of lymphocytes, plasma cells and macrophages. HE. Bar, 50 mm.
68 M Slaviero et al
lesion of bacterial bronchopneumonia in animals is
cranioventral consolidation, although in dogs and
cats it is common to find an irregular distribution of
lesions throughout the lung (Caswell and Williams,
2016), as was observed in some cases in the present
study.
All genera of bacteria identified in the present study
have been isolated from the cranial respiratory tract,
oral cavity or tracheobronchial region of healthy cats
(Padrid et al, 1991; Dye et al, 1996; Freshwater, 2008).
Thus, simultaneous viral infections, immunosuppres-
sive conditions or stress-related factors facilitate bac-
terial proliferation in the caudal airways. This is
associated with reduced defence mechanisms, which
result in deficient bacterial elimination, leading to
the development of pneumonia (Lee-Fowler and
Reinero, 2012).
E. coli pneumonia is poorly described in cats and is
mainly related to mortality in kittens due to intersti-
tial pneumonia secondary to septicaemia (Bart et al,
2000; Sura et al, 2007). In contrast, although the pre-
sent study did not include septicaemia, E. coli was
often identified from cases of bronchopneumonia. E.
coli invades the caudal respiratory tract mainly
through aspiration of colonized material from the
nasal cavity and oropharynx and immunosuppression
can facilitate the proliferation of this organism (Lee-
Fowler and Reinero, 2012). However, the relatively
high frequency of E. coli detection may be related to
the use of IHC as a diagnostic method.
Although Bordetella bronchiseptica is a primary path-
ogen in the respiratory system of cats (Foster and
Martin, 2011), there are variations in its reported fre-
quency among previous retrospective studies of pneu-
monia in cats (Bart et al, 2000; Macdonald et al, 2003;
Foster et al, 2004), and no cases were found in the pre-
sent study. Different risk factors for natural infections
by B. bronchiseptica in cats have been identified in
epidemiological studies (Binns et al, 1999), which
may explain the variation in the different populations
studied.
Bacterial pyogranulomatous pneumonia was asso-
ciated with filamentous bacterial aggregates in the
present study. Grossly, a diffuse and nodular pattern
was observed; therefore, it is important to include
neoplasms and fungal and parasitic infections in the
differential diagnosis (Sykes et al, 2010; Sykes, 2012;
Pereira et al, 2017). Microscopically, the inflamma-
tory neutrophil and macrophage infiltrate associated
with fibrosis and filamentous bacterial aggregates sur-
rounded by the SplendoreeHoeppli phenomenon
suggests infection by Actinomyces spp. However,
chronic infections by Nocardia spp may have a similar
presentation (Sykes, 2012). Although uncommon in
cats, these bacteria are reported in cases of feline pyo-
thorax, pleuritis and primary pneumonia (Barrs and
Beatty, 2009; Sykes, 2012; Caswell and Williams,
2016). However, a definitive diagnosis in these cases
is often challenging, as Actinomyces is an anaerobic
fast-growing bacterium and the growth of Nocardia
may be inhibited by prior treatment with antimicro-
bials (Sykes, 2012).
Both FCV and FeHV 1 are known to cause infection
mainly in the cranial respiratory tract but can occa-
sionally lead to the development of pneumonia
(Chvala-Mannsberger et al, 2009; Monne Rodriguez
et al, 2017, 2018). Viral pneumonia is reported to be
the main cause of death in kittens from shelters or over-
populated areas (Radford et al, 2009; Monne
Rodriguez et al, 2014, 2018). In the present study, viral
pneumonia was mainly associated with FCV. In
contrast, none of the previous retrospective studies re-
ported FCV as a cause of pneumonia in cats (Bart et al,
2000; Macdonald et al, 2003; Foster et al, 2004). How-
ever, it should be considered that no specific diagnostic
technique for detecting FCV has been used previously.
The diagnosis of viral pneumonia by histopathology
alone can be challenging, especially in the context of
secondary bacterial infections, as the lesions can be
confused. In cases of FeHV 1, although the visualiza-
tion of intraepithelial inclusion bodies can aid diag-
nosis, they occur only in the initial phase of the
infection, and the intense necrosis commonly observed
in epithelial cells can hinder their identification
(Monne Rodriguez et al, 2017). Thus, ancillary tests
for viral detection are essential to establish an accurate
diagnosis of viral pneumonia. IHC is particularly use-
ful in infectious disease diagnosis when formalin-fixed,
paraffin-embedded tissues are available because the
viral antigens can be localized to the characteristic le-
sions (Maxie and Miller, 2016). The results of the pre-
sent study indicate that both FCV and FeHV 1 can be
involved in pneumonia in cats of different ages and
may be underdiagnosed in the clinic.
Grossly, infections by FeHV 1 and FCV had several
similar gross post-mortem features, although a single
common characteristic was not identified. In addition,
due to secondary bacterial infections, cranioventral
consolidation can be observed in both infections.
The histological lung lesions in cats infected with
calicivirus in this study were similar to those in other
cats (Radford et al, 2009; Monne Rodriguez et al,
2014). The frequency of fibrinosuppurative pneu-
monia suggests that cats die more commonly with
acute disease. Although neutrophils are not always
present (Monne Rodriguez et al, 2014), they were
commonly found in the present study, even in cases
without apparent secondary infection. Severe fibrino-
necrotic bronchointerstitial pneumonia was observed
in cases of FeHV 1 infection, as found by Chvala-
 Fatal Pneumonia in Domestic Cats
Mannsberger et al (2009). In these cases, neutrophils
were also commonly observed. Both neutrophils and
macrophages can be found at an early stage in inflam-
matory conditions of the respiratory tract (Cohn and
Reinero, 2007).
Fungal and parasitic pneumonia were observed less
frequently than viral and bacterial infections, as in
previous reports (Macdonald et al, 2003; Foster et al,
2004). Granulomatous pneumonia was the main
pattern identified in both cases. Lung infection by
Cryptococcus spp is considered uncommon in cats
(Sykes, 2012) and colonization of the respiratory tract
is generally asymptomatic (Pennisi et al, 2013), with
mild histological lesions and no gross lesions (Sykes,
2012). Cryptococcus spp have a thick polysaccharide
capsule, which inhibits phagocytic function and sup-
presses host cell defences, consequently decreasing the
inflammatory response (Caswell and Williams, 2016).
In contrast, in the present study, a moderate intersti-
tial to alveolar inflammatory infiltrate was noted,
often with granulomatous nodular lesions, which
could be related to retrovirus co-infection. It has
been suggested that FIV/FeLV-positive cats have a
more unfavourable prognosis and a greater predispo-
sition to cryptococcosis (Gerds-Grogan and Dayrell-
Hart, 1997; Jacobs et al, 1997). Although generally
asymptomatic and self-limiting (Traversa et al,
2008; Pereira et al, 2017), severe infection with A. ab-
strusus can lead to severe pneumonia and an increased
risk of death. The predominantly granulomatous
pattern demonstrates that the cats died in the chronic
stage of infection, as eosinophil and neutrophil infil-
trates are associated with the early stages of infection
(Headley, 2005).
As this was a retrospective study, it has limitations.
First, the involvement of Mycoplasma spp cannot be
evaluated. Studies have reported Mycoplasma spp as
the main cause of pneumonia in cats (Foster et al,
2004) and the third main cause (Bart et al, 2000).
However, the molecular techniques necessary for its
identification from formalin-fixed, paraffin-
embedded tissue were not available. Second, informa-
tion regarding vaccination status, environmental con-
ditions or contact with other cats was not available.
Acknowledgments
We thank all members of the Department of Veteri-
nary Pathology at the Universidade Federal do Rio
Grande do Sul and all clinical veterinarians who
contributed to the study.
Funding
Financial support was provided by Conselho Nacio-
nal de Desenvolvimento Cientı́fico e Tecnologico, Co-
69
ordenaç~ao de Aperfeiçoamento de Pessoal de Nı́vel
Superior e Finance code 001, and Pro-Reitoria de
Pesquisa, Universidade Federal do Rio Grande do
Sul.
Conflict of Interest Statement
The authors declared no conflicts of interest in rela-
tion to the research, authorship or publication of
this article.
Supplementary data
Supplementary data to this article can be found on-
line at https://doi.org/10.1016/j.jcpa.2021.09.005.
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½ Received,
Accepted, September 25th, 2021 
May 28th, 2021