An evaluation of the clinical, cytological, infectious and

histopathological features of feline acne

Blackwell Publishing Ltd

E. Jazic*, K. S. Coyner*, D. G. Loeffler and

T. P. Lewis*
*Dermatology Clinic for Animals, Gilbert, Arizona, USA
DVM Pathology, Phoenix, Arizona, USA
Correspondence: Ed Jazic, 86 West Juniper Avenue, Gilbert, AZ, USA
Tel.: (480)633 2277.
E-mail: ejazic1278@sbcglobal.net

Abstract
Clinical, cytological, microbial and histopathological
features of feline acne were investigated in 22 cats
referred or volunteered to a veterinary dermatology
practice in the south-west region of the USA. For
comparison, same parameters were evaluated in five
unaffected pet cats. Additionally, all cats were evaluated
by immunohistochemistry (IHC) for the presence of
feline calicivirus (FCV) and feline herpes virus (FHV-1)
in acne lesions. The age of onset of acne in affected
cats ranged from 6 months to 14 years with a median
of 4 years. The most common dermatologic lesions
were comedones (73%), alopecia (68%), crusts (55%),
papules (45%) and erythema (41%). Pruritus was
reported in 35% of the affected cats. Cytological
evidence of Malassezia pachydermatitis was present
on 4/22 (18%) of affected cats. Microsporum canis was
isolated from a single affected cat. Bacteria were
isolated from 10 of the 22 (45%) affected cats; coagulasepositive staphylococci and alpha-haemolytic streptococci were most common. Histopathological features
included lymphoplasmacytic periductal inflammation
(86%), sebaceous gland duct dilatation (73%), follicular
keratosis with plugging and dilatation (59%),
epitrichial gland occlusion and dilatation (32%),
folliculitis (27%), pyogranulomatous sebaceous adenitis
(23%) and furunculosis (23%). In one affected cat from
a household with five cats, simultaneously having
feline acne, FCV antigen was detected in the biopsy of
the chin by IHC. Chin tissue samples from all other
affected cats, as well as the five healthy cats, were
negative by IHC for FCV and FHV-1 antigens.
Received 13 January 2005; accepted 16 January 2006

Introduction
Feline acne is a well-recognized skin disease in the cat13
that is believed to be an idiopathic disorder of follicular
keratinization.24 The pathogenesis of this condition is
unknown but a variety of causes such as changes in the
hair growth cycle, poor grooming habits, stress, underlying seborrheic predisposition, production of abnormal
134

sebum, immunosuppression and the affect of concurrent

chronic viral infections have been proposed.3,5 None of
these factors have been demonstrated to be causal. In
humans, acne is a multifactorial disease of the pilosebaceous unit1 and factors such as alterations in the pattern
of follicular keratinization, excessive sebum production,
and hormonal imbalances are thought to play a role.1
Feline acne is a relatively common disorder for the
general veterinary practitioner; however, there has been
very little investigation into this disease.6 The goal of this
prospective study was to identify the clinical, cytological,
microbial and histopathological features of feline acne, as
well as to investigate, via immunohistochemistry (IHC),
the presence or absence of feline calicivirus (FCV) and
feline herpes virus (FHV-1) in chronic refractory cases.

Materials and methods

Animals
From the south-west region of the USA, 22 cats with feline acne15
were evaluated in a 14-month period. Seventeen of the affected
cats were privately owned, five affected cats were from the Hermitage No-Kill Shelter in Tucson, Arizona. Additionally, five healthy pet
cats with no skin disease and owned by veterinary staff were concurrently evaluated as healthy control subjects. Feline acne lesions were
defined as comedones with crusts, erythema, and/or alopecia of the
chin 1,5 Primary investigator evaluated each cat for the presence or
absence of the following lesions along the chin or lower lip region:
comedones, crusts, erythema, alopecia, papules, swelling, pustules,
nodules/fistulas, and scarring. For inclusion in this study, clinical signs
of feline acne had to be present and persistent for more than 3 weeks.
All forms of therapy were discontinued for a minimum of 3 weeks
prior to evaluation.
Owners or shelter personnel completed a questionnaire providing
the name, age, sex and breed of the cat, where the cat was obtained,
vaccination history, environment of the cat (indoors, outdoors, combination), previous medical history with specific query regarding
previous upper respiratory disease, clinical signs of feline acne,
number of other pets in the household, and if other cats in the household also had feline acne. Each owner signed a form that described
the procedures to be performed and provided consent for the cat to
be included in the study.

Animal procedures
All 27 cats received a complete physical examination and the following diagnostic tests. First each cats chin was cultured for dermatophytes: material for culture was obtained by the Mackenzie
toothbrush technique7 and then inoculated on both Dermatophyte
test medium (DTM) and Sabourauds Agar utilizing Dermduet culture
plates (Bacti-Laboratory, Mountain View, CA, USA). These cultures
were kept at room temperature and monitored for fungal growth
daily for 21 days. Next, surface impression cytology of the chin area
was collected and assessed for the presence of Malassezia. This step
was followed by deep skin scrape to assess for feline demodicosis.

Histopathology and bacterial cultures

To obtain skin biopsies of the chin, the cats were sedated with
a combination of ketamine HCl 36 mg kg1 (Vetaket Injectable,

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Feline Acne

100 mg mL1) (Lloyd Laboratories, Shenandoah, IA, USA), acepromazine

0.20.3 mg kg1 (Acepromazine Maleate Injectable, 10 mg mL1)
(VEDCO, St. Joseph, MO, USA), and atropine 0.020.05 mg kg1
(Atropine Sulphate Injectable, 0.54 mg mL1) (VEDCO) administered
intravenously. The hair from the chin and associated lip region was
clipped and an area aseptically prepared to obtain samples using a
4-mm punch biopsy for aerobic and anaerobic bacterial culture. The
tissue specimen was then placed in a sterile glass tube with 1 mL
of sterile water until processing for bacterial culture. Skin biopsy
samples for histopathology were obtained with a 6-mm punch from a
separate area of the chin from the biopsy for culture and preserved
in 10% formalin. Biopsy sites were routinely closed with 3-0 nylon
suture.
At the laboratory, the 4-mm biopsy specimen was macerated for
culture. Two trypticase soy agar plates with 5% sheep red blood cells
were inoculated. One plate was incubated at 37 C in 10% carbon
dioxide, the other anaerobically. Additional cultures were grown on
chocolate agar incubated at 37 C in 10% carbon dioxide and MacConkey agar incubated at 37 C. For fastidious microorganisms, subcultures from the chocolate agar were grown in thioglycolate broth
incubated at 37 C in 10% carbon dioxide. The 6-mm samples were
processed routinely for histologic evaluation and embedded in paraffin wax. Four sections were stained routinely with haematoxylin and
eosin (H&E) and evaluated by a board-certified pathologist. The
pathologist was aware of the clinical classification of each biopsy
specimen (affected cat vs. control). The biopsy specimens from each
affected and control cat were evaluated for changes involving the
epidermis, hair follicles, adnexal structures, dermis and panniculus.
An additional section was utilized to investigate for the presence
or absence of FCV and FHV-1 antigens via IHC.

Immunohistochemistry feline herpes virus-1 and

feline calicivirus
The procedure utilized was the avidinbiotin complex immunoperoxidase detection of FHV-1 and FCV in formalin-fixed paraffin-embedded
tissues. Each paraffin block was subjected through the process of
deparaffinization and rehydration. Each slide was submerged in the
following solution order for two minutes at a time: xylene no.1, xylene
no. 2, Absolute alcohol, 95% ethanol, 70% ethanol and water. The
sections were not allowed to dry out at any time during the pretreatment staining. Endogenous peroxidases were inactivated by
immersing the slides in a solution of 4 mL of 50% H2O2 and 100 mL
of methanol for 12 min at room temperature. The slides were then
washed three times in a phosphate buffered solution (PBS). The
slides were then immersed in a solution of Protease XIV (Sigma no.
P5147) (50 mg 100 mL1 PBS) (Sigma, St. Louis, MO, USA) and were
incubated for 20 min at 37 C. The slides were then washed three
times in PBS. Nonspecific antibody binding sites were blocked by covering the tissue sections with three to four drops of a solution of 4%
normal horse serum in PBS. The samples were then incubated for
10 min at room temperature in a covered humidified chamber.
Specific primary FHV-1 antibody or FCV antibody and negative control
antibody were diluted in the blocking solution and two to four drops
were added to each section. The samples were then incubated in
a covered humidified chamber, for 1 h at 37 C. The samples were
then washed three times for 30 min in PBS. Avidinbiotin peroxidase
solution (VECTASTAIN Elite Cat no. PK6100) (Dimension Laboratories,
Mississauga, Ontario, Canada) was then applied to the slides. This
solution was made 30 min prior to applying it to the slides. The slides
were then incubated for 45 min at 37 C, and then washed three
times in PBS. A 2 mg mL1 solution of 3, 3-diaminobenzidine-4 HCl
(DAB) was prepared by adding 100 L of frozen DAB to 10 mL of
PBS. Immediately prior to use, 4 L of 50% H2O2 was added to the
DAB. Two to four drops of the DAB were added to each slide and
incubated for exactly 5 min. The excess DAB was tipped off and the
slides were washed numerous times with distilled water or PBS.
Slides were then counterstained with haematoxylin (1:7 dilution of
Gills no. 3), dehydrated through the alcohols mentioned earlier, and a
coverslip was placed over each slide. For FHV-1, a positive reaction
was indicated by the presence of brown cytoplasmic and intranuclear
staining. For FCV, a positive reaction was indicated by the presence

of brown cytoplasmic staining. The positive controls for both viruses

tested positive via IHC and each virus was isolated through polymerase chain reaction (PCR).

Results
Animals (Table 1)
The age of onset for 14/22 affected cats was known and
ranged from 6 months to 14 years with a median of
4 years. Sixteen were castrated males (73%) and six were
spayed females (27%). The majority of cats (17, 77%)
were domestic shorthaired cats (DSH). The other five cats
were a domestic longhaired (DLH), Bengal, Maine Coon,
Manx and an Abyssinian. The healthy pet cats that served
as unaffected controls were all DSH, two castrated males
and three spayed females, ranging in age from 1 to 9 years
with a median of 4 years. Pruritus was reported in 6/17
(35%) of the client-owned affected cats. Seven of the
affected cats had clinical signs that correlated with active
upper respiratory disease (variable sneezing, ocular and
nasal discharge, conjunctivitis, voice change).
The length of time feline acne lesions had been present
at the time of study evaluation was known for 14 cats and
ranged from one month to 5 years with a median of one
year. Duration of disease could not be determined for the
five cats from the Hermitage No-Kill Shelter and not
known for three of the client-owned cats.
Although all affected cats had lesions that were consistent with those described in the literature,1,5 there was
much variation. The most common lesions were comedones (73%), alopecia (68%), crusts (55%), papules (45%)
and erythema (41%). Less frequently observed lesions
were swelling (18%), pustules (9%), nodules/fistulas (9%)
and scarring (4.5%) (Fig. 1). Pruritus was confined strictly
to the chin region in five of the affected cats. No other
dermatological lesions were noted in 21 of the affected
cats. A single cat, with chin comedones, erythema and
crusts, had multiple regions (face, limbs, inguinal, abdomen)
that were pruritic and exhibited erythema with barbered
hair, and eventually was diagnosed with atopic dermatitis.
Animal procedures (Table 1)
No Demodex organisms were identified with microscopic
evaluation (10) of material from the skin scrapings of
the chin region of the 22 affected cats and the five healthy
cats. However, impression cytology revealed 24
Malassezia/100 oil immersion in four of the 22 (18%)
affected cats but none of the healthy unaffected cats.
Microsporum canis was cultured from a single affected
cat that was from the animal shelter.
Histopathology and bacteriology (Table 1)
Biopsy specimens from the chin region of 22 affected and
five unaffected cats were reviewed. One specimen was
submitted per case. Epidermis was mildly acanthotic
in nine (41%) of the 22 affected cats. Mild epidermal spongiosis was noted in five (23%). Mild focal parakeratosis
was present in one cat, focal serocellular crusting in one
other. A deep dermal infiltrate was present in biopsy specimens from two cats. In one cat, this was pyogranulomatous nature. The second cat had large aggregates of
neutrophils, macrophages and lymphoplasmacytic cells.

2006 The Authors. Journal compilation 2006 European Society of Veterinary Dermatology.

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E Jazic et al.

Table 1. Summary of Historical, Clinical and Diagnostic findings

Feline

Age
(years)

Age of
Sex onset

Concurrent
Duration of respiratory
Bacteria
disease
signs
Pruritus cultured

Malassezia Dermatophyte
Cytology
culture

Feline
FHV-1 calicivirus
IHC
IHC

Microsporum canis

1
2
3

6
5
4

FS NA
FS
3
MN 4

NA
2 years
1 month

4
5
6

7
5
3

MN NA
MN NA
MN NA

NA
NA
NA

NA
NA

7
8

5
8

FS
FS

NA
NA

NA
NA

9
10

5
5

MN NA
MN 2

NA
3 years

NA
+

11
12

6
5

MN
MN

1
4

5 years
1 year

13
14
15

6
10
15

MN 5
FS
8
MN 14

1 year
2 years
1 year

+
+

16
17
18

3
6
11

MN
FS
MN

3
6
6

1 month
1 month
5 years

1
MN 1
4
MN 4
7 months MN NA
5
MN 5

1 month
1 year
NA
0.5

+
+
+

19
20
21
22

NA
NA

Alpha-haemolytic
Streptococcus,
Coagulase-positive
Staphylococcus
Escherichia coli

Alpha-haemolytic
Streptococcus

Alpha-haemolytic
Streptococcus

Coagulase-positive
Staphylococcus

Coagulase-positive
Staphylococcus

Coagulase-positive
Staphylococcus

Bacillus cereus
Coagulase-positive
Staphylococcus

Micrococcus sp.

FS, female spayed; MN, male neutered; NA, not available.

Figure 1. Chin of an affected cat. Note the erythema, papules,

crusts, comedones and exudate

Mild to moderate lymphoplasmacytic periductal inflammation was identified in 19 (86%) of the 22 affected cats.
Sixteen (73%) had sebaceous gland duct dilatation that
varied from mild to severe (Fig. 2). Moderate periductal
fibrosis was present in the biopsy specimens from one
cat. Pyogranulomatous sebaceous adenitis was present
in five (23%). Seven (32%) had mild to severe epitrichial
gland occlusion and dilatation. Peri-epitrichial gland
lymphoplasmacytic infiltrates were observed in four (18%).

136

Figure 2. Sebaceous gland duct dilatation with mild lymphoplasmacytic periductal inflammation. H&E, 400.

2006 The Authors. Journal compilation 2006 European Society of Veterinary Dermatology.

Feline Acne

Follicular changes were present in 13 (59%) cats: follicular keratosis, occlusion or plugging, and dilatation that
varied from mild to severe (Fig. 3). Folliculitis was present
in six (27%). This was suppurative luminal folliculitis in two
cats, and lymphoplasmacytic mural folliculitis in four.
Follicular hyperplasia was present in four (18%). Furunculosis
was also noted in five (23%). Finally, four (18%) cats had mild
to moderate perifolliculitis. Cats that had histopathological
evidence of folliculitis and furunculosis all had bacterial
growth from the biopsy tissue cultures.
Histopathological evaluation of biopsy specimens from
four (80%) of the five healthy unaffected cats were interpreted to have very mild lymphoplasmacytic inflammation.
Interestingly, four (80%) of the five control cats had very
mild lymphoplasmacytic periductal inflammation present.
Aerobic and anaerobic bacterial cultures demonstrated
had extensive growth in 10 (45%) of the 22 affected cats.
A coagulase-positive Staphylococcus organism was isolated in four affected cats, alpha-haemolytic streptococci in
two affected cats, and Escherichia coli, Bacillus cereus,
and Micrococcus spp. were each isolated in three separate affected cats. Both alpha-haemolytic Streptococcus
and coagulase-positive Staphylococcus were isolated
from one cat. Pseudomonas aeruginosa was isolated from
one of the unaffected healthy cats.
Immunohistochemistry feline herpes virus-1 and
feline calicivirus
There was no immunohistochemical evidence of FHV-1
infection in the tissue samples of the affected cats. There
was positive immunohistochemical staining for FCV in the
tissue sample from one affected cat. Immunohistochemical

Figure 3. Comedones, H&E, 100.

staining for these viruses was negative in all five unaffected

control cats.
Case report
The single affected cat that was positive for FCV antigen
came from a household of five cats. All cats in this household had varying degrees of pruritic chin dermatitis. All five
cats stayed completely indoors and had recently relocated
from Florida to Arizona. The lesions developed 2 months
after the move. Plastic bowls were changed to stainless
steel with no improvement. The owner had tried numerous topical products consisting of benzoyl peroxide,
mupirocin and antibiotic/steroid combinations, in combination with systemic antibiotics without improvement. The
problem had started with a single cat and then gradually
appeared in the other cats. The owner did not observe
signs of upper respiratory disease prior to or after chin
lesion development in any of the cats, with the exception
of a periodic voice change in one cat. Yearly respiratory
vaccines had been administered after chin lesions
developed in two of the cats (4 months prior to the
biopsy). However, two other affected cats did not receive
any vaccinations that year. Therefore, it seems less likely
that vaccination status played a role in these cases. Three
cats from this household were examined. Chin lesions
varied from only comedones to variable crusting, and a single
cat had severe furunculosis. Skin scrapings and dermatophyte cultures were negative on all three cats. Cytology of
the most severely affected cat revealed no Malassezia
organisms, but did demonstrate pyogranulomatous
inflammation with rare rod-shaped bacteria. A biopsy was
obtained from the most severely affected cat. A bacterial
tissue culture was negative. Histopathological changes
included mild acanthosis and mild epitrichial gland dilatation.
The deep dermis contained several large aggregates of
mixed neutrophils, macrophages, and lymphoplasmacytic
cells (Fig. 4). The superficial and mid-dermis had mild
to moderate perivascular to interstitial infiltrate of lymphoplasmacytic cells. These inflammatory foci extended to
the deeper margins of the biopsy. The hair follicles were
predominantly in anagen, without keratin plugging or
inflammation. There was a very mild lymphoplasmacytic
periductular infiltrate present. Otherwise, the sebaceous
glands were within normal limits. The deep dermis had
several large mixed aggregates of neutrophils, macrophages, and lymphoplasmacytic cells. Calicivirus was found
immunohistochemically in this region of inflammation in
the deep dermis. These histopathological changes were
not consistent with the findings regarding the more virulent form of FCV. It is important to note that Caliciviridae
exhibit a remarkable genetic diversity. These more virulent
strains are genetically distinct, which could explain the
differences with respect to the pathogenesis, clinical
presentation and histological changes. It would have been
interesting to have been able to have biopsied the four
other cats to investigate for the presence of FCV. It is
possible that a cat in the household has been a carrier
for FCV. In terms of therapy, two of the affected cats
(including the calicivirus-positive cat) improved with the
use of low dose oral Interferon (30 IU PO daily) and a
topical zinc/lysine gel (MAXIGUARDZn7, Addison
Biological Laboratory Inc., Fayette, MO) The other affected

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E Jazic et al.

Figure 4. Area of neutrophils, macrophages and lymphoplasmacytic

cells in the deep dermis of the FCV-positive cat. H&E, 100.

cats in the household with milder lesions did not respond

to this form of therapy.

Discussion
In this study, clinical, cytological, microbial and histopathological features of feline acne were investigated in 22 cats.
In our study, a strong sex predilection for castrated males
(73%) over spayed females (27%) was reported. This is in
contrast to previous reports.1,2,6 The cause for this difference is not readily explained. Androgens were an unlikely
contributing factor to these cats, as all the study animals
were neutered. The predominance of domestic shorthaired cats is most probably a reflection of the prevalence
of this breed in the area where the samples were collected. The age at examination of the affected cats varied
considerably, ranging from 6 months to 14 years (with a
median of 4 years), further supporting the observation
that, in contrast to human acne, feline acne is not confined
to adolescence.1
Of the clinical signs noted in the 22 affected cats, the
high percentage of comedones (73%) and crusts (55%)
is in agreement with previous reports.1,3,5 Other common
lesions included alopecia (68%), papules (45%), and
erythema (41%). Pruritus was experienced by 35% (6/17)
of the affected cats. In the cats with pruritus isolated
to the chin region, all had evidence of bacteria pyoderma
(5/5, 100%), and one of these five cats also had evidence
of Malassezia (1/5, 20%). A single cat with generalized
pruritus was diagnosed with atopic dermatitis. Bacterial
pyoderma,1 Malassezia pachydermatitis1,5,6,9 infection,
and demodicosis1 may cause or be related to the clinical
signs of feline acne. Demodicosis was not found in any of
the skin scrapings from the affected cats.

138

More advanced cases of feline acne may be complicated

with secondary bacterial infections. Three types of bacteria
have been previously reported to be involved in feline
acne: Pasteurella multocida, beta-haemolytic streptococci,
and coagulase-positive Staphylococcus.1 In this study, 10
of (45%) of the 22 affected cats had bacteria isolated via
aerobic and/or anaerobic culture. An alpha-haemolytic
streptococcus or coagulase-positive staphylococcus was
isolated from six cats, while both bacteria were isolated
from one other cat. The remaining organisms isolated
were Micrococcus spp., E. coli and B. cereus. The resident
flora of the skin of cats includes Micrococcus spp.,
coagulase negative staphylococci, alpha-haemolytic
streptococci, and Acinobacter spp.10 Coagulase-positive
staphylococci, including both Staphylococcus aureus and
Staphylococcus intermedius, are also commonly isolated
from normal feline skin and are considered should be
considered resident microflora.1113 These resident organisms can act as secondary invaders in cats with feline
acne. The relatively rare colonies isolated of E. coli and
B. cereus from two individual cats likely represent transient
flora. A single clinically normal cat had a heavy growth of
P. aeruginosa. This organism could represent a transient
or a contaminant present during the biopsy procedure.
E. coli, Bacillus spp., and P. aeruginosa are considered
transient organisms in normal feline skin.1
In this study, the most prominent features of feline acne
were lymphoplasmacytic periductal inflammation and
sebaceous gland duct dilatation, which were seen,
respectively, in 86% and 72% of the affected cases. Interestingly, four of the five clinically normal cats also had mild
lymphoplasmacytic periductal inflammation. It is possible
that this periductal inflammation could represent early
histopathological changes associated with feline acne. In
agreement with previous reports,6 nearly 60% of the
affected cats demonstrated follicular keratosis, plugging
and dilatation with varying severity. Current literature
describes feline acne as an idiopathic disorder of follicular
keratinization.24 In more advanced cases, perifolliculitis,
folliculitis and furunculosis with an associated pyogranulomatous dermatitis and sebaceous adenitis may be
seen.1,3,5,6 In this study, less than one-third of the affected
cats had focal regions of pyogranulomatous sebaceous
adenitis and mild to severe epitrichial gland occlusion and
dilatation. Folliculitis, furunculosis and perifolliculitis were
noted, respectively, in 27%, 23% and 18% of affected
cats. Eosinophilic granuloma has been reported as a cause
of feline acne.13,5 There was no histopathological evidence
of eosinophilic granuloma development in any of the
affected cats. Epidermal changes were mild and occurred
sparsely amongst the affected cats. Lesions included mild
acanthosis and spongiosis, focal parakeratosis and
serocellular crusts.
Outbreaks of feline acne in multiple cat households
have been reported and an infectious aetiology has been
suspected but never confirmed.3 Three households and
the shelter represented in this report consisted of two or
more cats with feline acne. Dermatophytosis has been
reported to play a role in the development of feline acne
lesions.1,5,8 Microsporum canis was isolated from a single
cat that was from the shelter. There was no evidence
histologically of dermatophyte infection in this cat. This cat

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Feline Acne

was likely a subclinical carrier of M. canis and played no

role in the development of this cats acne.
Seven of the affected cats demonstrated clinical signs
consistent with upper respiratory disease (variable sneezing, ocular and nasal discharge, conjunctivitis). The major
recognized causes of feline upper respiratory tract disease
are FHV-1 and FCV.14 FHV-1 is a double-stranded DNA
virus and accounts for 50% to 80% of upper respiratory
infections in cats worldwide.14,15 FHV-1 has been recognized as a cause of ulcerative facial and nasal dermatitis,16
in which histological lesions were vesicular, ulcerative,
crusted, necrotizing and inflammatory, often containing
numerous eosinophils. Variable adnexal necrosis occurred
with extrusion of hair shafts. Occasional collagen degeneration was observed. A variable number of inclusion bodies
were present at the surface and adnexal epithelium and
are usually located near areas of adnexal epithelium. No
evidence of FHV-1 was found histopathologically or immunohistochemically in any of the cats enrolled in this study.
Based on the results of this study, FHV-1 should not be
considered a differential diagnosis in feline acne.
Feline calicivirus is a nonenveloped, single-stranded
RNA virus.15 FCV infection has been associated with
upper respiratory infections, ulcerative glossitis, chronic
lymphoplasmacytic or proliferative stomatitis, pneumonia,
footpad lesions, and lameness.15,17 In the past few years,
several outbreaks of haemorrhagic calicivirus disease
have been reported.18 This condition is characterized
by cutaneous oedema (most commonly distal limbs),
alopecia, crusting and ulceration (most prominent on
nose, lips, pinnae, periocularly, and on the distal limbs).
The syndrome has a mortality rate that approaches 50%,
and is characterized variably by fever, upper respiratory
tract signs, anorexia, occasionally icterus, vomiting and
diarrhea. In these more virulent cases, the most consistent histopathological change was epithelial necrosis and
ulceration. The initial lesion in haired skin was segmental
epithelial necrosis of the stratum basale and stratum
spinosum. The follicular epithelium also demonstrated
evidence of necrosis. In early lesions involving the paw
pads, necrosis and neutrophilic inflammation were most
severe at the junction between haired and nonhaired skin.
The more chronic lesions demonstrated full thickness
epithelial necrosis, with ballooning degeneration in superficial layers and loss of distinct epithelialsubepithelial
margin. In this study, a single affected cat was positive for
FCV antigen on IHC. Other affected and clinically normal
cats were negative for FCV antigens.
The negative viral IHC results in the majority of these
cats suggest that FHV-1 and FCV do not play an important
role in cats with chronic acne. However, it must be
recognized that the viral antigens may be present in only
a single section of the biopsy specimen and could potentially
be missed by IHC and thus yield false negative results.
Future studies into the role of viruses in the pathogenesis
of feline acne should submit multiple tissue sections per
biopsy in order to attempt to minimize this possibility.
Studies utilizing PCR techniques may be more definitive to
identify FCV and FHV-1 antigens as aetiologic factors in
chronic feline acne.
In conclusion, this study confirms the most common
histological features of feline acne in a larger group of cats

that has previously been reported. These include lymphoplasmacytic periductal inflammation, sebaceous gland
duct dilatation, and follicular keratosis with plugging and
dilatation. These histopathological features are suggestive
that many cases of feline acne are caused by a follicular
keratinization disorder. Almost 50% of the affected cats in
this study were determined to have concurrent bacterial
infections. The most common organisms isolated were a
coagulase-positive Staphylococcus and alpha-haemolytic
Streptococcus. Malassezia was found in 22% of the
affected cats. These findings suggest that secondary
infection is an important component of feline acne and the
identification of these bacterial and fungal organisms may
improve treatment outcome. There was no evidence of
FHV-1 playing a role in feline acne; however, further investigation into the role of FCV may be a direction for further
research into situations where comingled cats concurrently or sequentially develop feline acne.

Acknowledgements
The authors would like to thank the Dermatology Clinic for
Animals for sponsoring this study. Many thanks go to Phyl
Koch for her efforts in collecting our feline subjects and to
Dr. Ted Clark for his assistance in editing the histopathological photographs. Finally, thanks to the personnel of the
Hermitage No-Kill Cat Shelter in Tucson, Arizona for their
contribution of five our affected cats.

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and Kirks Small Animal Dermatology, 6th edn. Philadelphia: W.B.
Saunders, 2001: 10423.
2. Bond R. Canine and feline acne. In: Raw ME, Parkinson TJ, eds.
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Rsum Les donnes cliniques, cytologiques, microbiologiques et histopathologiques de lacn fline ont
t tudies chez ving deux chats rfrs ou prsents une clinique de dermatologie vtrinaire dans le
sud ouest des USA. Pour comparaison, les mmes paramtres ont t valus chez cinq chats non malades.
En outre, tous les chats ont t valus par immunohistochimie (HC) pour la prsence de calicivirus (FCV)
et dherpsvirus flin (FHV-1) dans les lsions dacn. Lge lapparition des signes cliniques variait de 6 mois
14 ans avec une mdiane de 4 ans. Les lsions les plus frquentes taient des comdons (73%), une alopcie
(68%), des crotes (55%), des papules (45%) et de lrythme (41%). Un prurit tait dcrit chez 35% des chats.
Des Malassezia pachydermatitis taient visualises chez 4/22 (18%) des chats atteints. Microsporum canis
a t isol dans un cas. Des bactries ont t isoles chez 10/22 (45%) des chats atteints. Les bactries
les plus communes taient des Staphylococci coagulase positive et des Streptococci alpha-hemolytiques.
Les modifications histopathologiques incluaient une inflammation lymphoplasmocytaire priductale
(86%), une dilatation des canaux des glandes sbaces (73%), une kratose folliculaire avec une dilatation
(59%), une occlusion et une dilatation des glandes pitrichiales (32%), une folliculite (27%), une adnite
sbace pyogranulomateuse (23%), et une furonculose (23%). Chez un chat appartenant une famille vivant
avec 5 chats prsentant galement une acn, des antignes de FCV ont t isols des lsions du menton
biopsies. Tous les autres prlvements examins par HC taient ngatifs pour le FCV ou le FHV-1.
Resumen Las caractersticas clnicas, citolgicas, microbiolgicas e histopatolgicas del acn felino se
investigaron en veinticuatro gatos referidos o trados de forma voluntaria a una clnica de dermatologa
veterinaria en la regin sudoeste de los Estados Unidos. En comparacin, los mismos parmetros se
evaluaron en cinco gatos no afectados. Adems, todos los gatos se evaluaron mediante inmunohistoqumica
(IHC) frente a calicivirus felino (FCV) y herpesvirus felino (FHV-1) en las lesiones de acn. La edad de aparicin
de acn en los gatos afectados vari entre 6 meses y 14 aos, con una media de cuatro aos. Las lesiones
dermatolgicas mas frecuentes fueron comedones (73%), alopecia (68%), costras (55%), ppulas (45%) y
eritema (41%). Se describi prurito en un 35% de los gatos afectados. Asmismo, observamos evidencia
citolgica de Malassezia pachydermatis en 4/22 (18%) de los animales afectados. Se aisl Microsporum
canis en slo uno de los gatos afectados. Tambin se aislaron bacterias en 10/22 (45%) de los gatos afectados;
siendo las ms comunes Staphylococci coagulasa + y Streptococci alpha-hemolticos.
Las caractersticas histopatolgicas incluyeron inflamacin linfoplasmactica periductal (86%), dilatacin
de glndulas sebceas (73%), keratosis folicular con taponamiento y dilatacin (59%), oclusin y dilatacin
de glndulas epitriquiales (32%), foliculitis (27%), adenitis sebcea piogranulomatosa (23%) y furunculosis
(23%). En uno de los gatos afectados en una casa con cinco gatos simultneamente afectados, se detect
antgeno de FCV en la biopsia de la barbilla mediante inmunohistoqumica. Biopsias de la misma regin de
todos los gatos afectados, as como de los cinco gatos sanos, fueron negativas para los antgenos de FCV
y FHV-1 mediante inmunohistoqumica.
Zusammenfassung Klinische, zytologische, mikrobielle und histopathologische Charakteristika von
Katzenakne wurden bei zweiundzwanzig Katzen untersucht, die an eine Veterinrdermatologiepraxis im
Sdwesten der Vereinigten Staaten berwiesen oder dieser zur Verfgung gestellt wurden. Zum Vergleich
wurden dieselben Parameter bei fnf nicht erkrankten Hauskatzen evaluiert. Zustzlich wurden alle Katzen
mittels Immunhistochemie (IHC) auf das Vorkommen von felinem Calicivirus (FCV) und felinem Herpesvirus
(FHV-1) in den Aknelsionen untersucht. Das Alter zum Zeitpunkt des ersten Auftretens der Akne bewegte
sich bei den erkrankten Katzen zwischen 6 Monaten und 14 Jahren mit einem Medianwert von 4 Jahren.
Die hufigsten Hautvernderungen waren Komedonen (73%), Alopezie (68%), Krusten (55%), Papeln (45%)
und Erythem (41%). Juckreiz wurde bei 35% der erkrankten Katzen beschrieben. Malassezia pachydermatis
wurde bei 4/22 (18%) der erkrankten Katzen zytologisch nachgewiesen. Microsporum canis wurde von
einer einzigen erkrankten Katze isoliert. Bakterien wurden bei 10/22 (45%) der erkrankten Katzen isoliert;
koagulase-positive aus lymphoplasmazytrer periduktaler Entzndung (86%), Dilatation des Staphylokokken
und alpha-hmolytische Streptokokken waren am hufigsten.
Histopathologische Merkmale bestanden Talgdrsengangs (73%), follikulre Keratose mit Plugging
und Dilatation (59%), Verschlu der apokrinen Schweidrsen und Dilatation (32%), Follikulitis (27%),
pyogranulomatse Sebadenitis (23%) und Furunkulose (23%). Bei einer erkrankten Katze aus einem Haushalt
mit 5 Katzen, die alle gleichzeitig Katzenakne hatten, wurde FCV Antigen in der Biopsie des Kinns mittels
IHC nachgewiesen. Gewebeproben vom Kinn von allen anderen erkrankten sowie von den fnf gesunden
Katzen waren mittels IHC negativ fr FCV und FHV-1 Antigene.

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2006 The Authors. Journal compilation 2006 European Society of Veterinary Dermatology.