Unusual presentation of pseudomonas infection

Abstract

We describe three cases of an uncommon presentation of pseudomonas infection consisting of extensive oropharyngeal ulceration and facial cellulitis with pronounced swelling of the face and associated septicaemia.

Full text

TABLE
tI-Existing
workload
and
notional
half
days
required
if
undertaken
by
consultants
No
of
Notional
half
days
Nature
sessions
Currently
done
by
if
done
by
consultant
Operating
theatre
lists
plus
pre/postoperative
assessment
38-5
Consultants
64-0
Operating
theatre
lists
plus
pre/postoperative
assessment
8-0
Junior
doctors
12-2
Operating
theatre
lists
10-0
Associate
specialist/clinical
assistant
No
change
Intensive
care
sessions
3
0
Consultant
Obstetric
sessions
2-0
Consultant
Intensive
care/obstetric
cover
Registrar/clinical
assistant
5-7
Teaching
and
administration
0.0
6-5
First
consultant
on
call
at
night
Registrar
28-0
Second
consultant
on
call
at
night
Consultant
8-0
Day
time
duty
doctor
Registrar
11-4
Total
141-5
doubling
of
the
consultant
staff
to
replace
three
registrars
and
1F6
whole
time
equivalent
clinical
assistants
was
compared
with
the
staffing
at
Milton
Keynes
Hospital.
There,
10
consultants,
one
registrar,
and
four
senior
house
officers
deal
with
a
workload
86%
of
that
in
this
hospital
(using
the
workload
indicator
adopted
for
the
calculations
made
by
North
West
Thames
region).
In
addition,
to
provide
internal
cover
for
annual
leave
and
study
leave
a
further
27-0
notional
half
days
would
be
required.
Thus
a
total
of
15-3
consultants
would
be
required,
an
additional
8-8
whole
time
equivalents.
The
total
cost
of
these
extra
consultant
staff
would
be
£296
000,
although
this
would
be
offset
by
savings
in
the
costs
of
registrars
(£66
000)
and
locums
(£89
000
in
1987),
leaving
the
total
cost
of
achieving
a
balance
at
£108
000.
This
figure
assumes,
perhaps
unreasonably,
that
the
16
consultants
would
be
prepared
to
share
the
present
one
secretary
in
anaesthetics.
Discussion
In
Achieving
a
Balance
it
was
proposed
that
the
numbers
of
consultants
should
increase
by
2%
per
year.
In
this
study
we
calculated
that
to
maintain
the
existing
workload
an
expansion
of
9%
per
year
would
be
required.
When
we
compared
this
hospital
with
Milton
Keynes
Hospital
our
findings
were
not
as
far
fetched
as
they
at
first
seemed.
Our
estimates
of
consultant
staffing
are
30%
greater
than
those
pertaining
in
Milton
Keynes,
while
our
workload
is
20%
greater.
For
the
health
authority
the
cost
of
achieving
a
balance
would
be
prohibitive.
If
all
specialties
in
all
districts
implemented
such
an
increase
in
consultant
staff
not
only
would
the
costs
be
phenomenal
but
there
would
not
be
sufficient
numbers
of
trained
doctors
to
fill
the
vacancies.
The
balance
would
again
be
lost.
We
thank
Dr
M
J
Cowen,
consultant
anaesthetist,
Milton
Keynes
Hospital,
and
the
consultant
anaesthetic
staff
of
Bedford
General
Hospital.
1
Department
of
Health
and
Social
Security.
Hospital
medical
staffing-achieving
a
balance-a
plan
for
action.
London:
HMSO,
1987.
2
Department
of
Health
and
Social
Security.
Performance
indicators
for
the
NHS.
London:
DHSS,
1988.
3
Association
of
Anaesthetists
of
Great
Britain
and
Ireland.
Workload
for
consultants.
London:
Association
of
Anaesthetists,
1983.
4
Association
of
Anaesthetists
of
Great
Britain
and
Ireland.
Workload
for
consultant
anaesthetists:
implications
of
reductions
in
junior
staff
and
the
consultant-only
hospital.
London:
Association
of
Anaesthetists,
1984.
(Accepted
19July
1988)
Lesson
of
the
Week
Unusual
presentation
of
pseudomonas
infection
Michael
J
Weinbren,
Gary
Forgeson,
Gilla
Helenglass,
Beryl
Jameson,
Ray
Powles
Colonisation
in
the
patient
with
neutropenia
often
heralds
impending
invasive
pseudomonas
infection'
which
is
associated
with
a
high
mortality.23
We
describe
three
cases
of
an
uncommon
presentation
of
pseudomonas
infection
consisting
of
extensive
oropharyngeal
ulceration
and
facial
cellulitis
with
pronounced
swelling
of
the
face
and
associated
septi-
caemia.
Case
reports
Case
I-A
24
year
old
woman
developed
a
low
grade
fever
and
mild
oedema
of
the
face
after
a
relapse
of
acute
myeloid
leukaemia.
Examination
showed
that
the
mucous
membranes
of
the
mouth
were
normal;
bacteriological
cultures
of
the
mouth
and
oropharynx
failed
to
grow
any
pathogens;
and
the
peripheral
white
blood
cell
count
was
7
x
1O9I/
with
90%
myeloblasts.
She
was
treated
with
gentamicin,
metronidazole,
cefuroxime,
and
erythromycin.
As
the
peripheral
myeloblast
count
was
rising
she
was
given
tumour
necrosis
factor,
an
experimental
biological
response
modifier.4
Gum
lesions
developed
which
were
thought
to
be
leukaemic
infiltrates.
She
had
a
fever
during
which
Pseudomonas
aeruginosa
was
isolated
from
repeated
blood
cultures
and
a
mouth
swab.
The
antibiotics
were
continued
and
her
fever
settled
within
48
hours.
She
received
a
further
course
of
tumour
necrosis
factor,
and
24
hours
later
had
severe
pain
in
the
mouth
and
oropharynx
and
rapidly
progressive
oedema
of
the
lower
face
and
neck.
Haemorrhagic
necrosis
was
seen
in
the
oral
cavity,
which
was
thought
to
be
drug
induced
angio-oedema
and
she
was
treated
with
systemic
corticosteroids
and
the
same
antibiotics.
Her
condition
deteriorated,
and
she
died
within
12
hours.
Necropsy
showed
tissue
invasion
with
Gram
negative
bacilli
compatible
with
pseudomonas
(see
figure).
Case
2-A
47
year
old
man
who
had
a
relapse
of
acute
myeloid
leukaemia
and
was
undergoing
re-
induction
chemotherapy
developed
severe
bilateral
oedema
of
the
lower
face
and
neck
over
12
hours.
He
was
neutropenic,
with
a
white
blood
count
of
0-1
x
10O/1.
He
had
had
a
temperature
of
380C
to
400C
for
the
preceding
six
days
and
been
treated
with
combinations
of
gentamicin,
piperacillin,
flucloxa-
cillin,
metronidazole,
amphotericin
B,
and
cefuroxime
sequentially
with
no
resolution
of
the
fever.
A
strain
of
Pseudomonas
aeruginosa
resistant
to
piperacillin
had
been
isolated
from
routine
mouth
swabs
seven
days
before
this.
There
were
extensive
areas
of
infected,
necrotic
tissue
in
the
oral
cavity
affecting
the
hard
palate
and
buccal
mucosa.
Pseudomonas
aeruginosa
sensitive
to
gentamicin,
amikacin,
and
ciprofloxacin
but
resistant
to
piperacillin
was
isolated
from
blood
cultures
and
repeat
mouth
swabs.
Treatment
was
Departments
of
Medicine
and
Microbiology,
Royal
Marsden
Hospital
and
Institute
of
Cancer
Research,
Sutton,
Surrey
Michael
J
Weinbren,
MB,
senior
registrar,
microboology
Gary
Forgeson,
FRACP,
senior
registrar
in
medical
oncology
Gilla
Helenglass,
MRCP,
honorary
senior
registrar,
leukaemia
unit
Beryl
Jameson,
FRCPATH,
consultant
microbiologist
Ray
Powles,
FRCP,
consultant
physician
in
charge,
leukaemia
unit
Correspondence
to:
Dr
Michael
J
Weinbren,
Department
of
Microbiology,
Queen
Mary's
Hospital,
Roehampton,
London
SW15
5PN.
1034
BMJ
VOLUME
297
22
OCTOBER
1988

When
routine
cultures
of
swabs
of
the
mouth
show
Pseudomonas
aeruginosa
this
should
be
treated
locally
to
reduce
the
degree
of
colonisation
in
an
attempt
to
prevent
systemic
infection
changed
to
ciprofloxacin,
metronidazole,
and
benzyl
penicillin
with
intermittent
doses
of
amikacin
and
amphotericin
B
as
determined
by
his
renal
function.
He
also
received
infusions
of
single
donor
white
cells,
but
he
remained
critically
ill
for
seven
days,
with
progressive
oedema
of
the
face,
hypotension,
and
oliguric
renal
failure.
His
fever
and
the
facial
oedema
finally
abated,
and
the
white
cell
count
rose.
He
was
discharged
in
remission
25
days
after
the
onset
of
facial
cellulitis.
Case
3-A
35
year
old
man
was
admitted
with
neutropenia
(white
blood
count
0
x
109/1)
after
reinduction
chemotherapy
for
relapse
of
acute
lympho-
blastic
leukaemia.
His
temperature
was
39°C
and
he
had
had
swelling
on
the
left
side
of
the
face
for
six
hours.
He
had
had
a
minor
injury
to
the
buccal
mucosa
24
hours
earlier.
Pseudomonas
aeruginosa
was
isolated
from
blood
cultures
and
mouth
swabs
taken
on
admis-
sion.
He
was
treated
with
gentamicin,
ciprofloxacin,
flucloxacillin,
and
metronidazole
and
with
infusions
of
single
donor
white
cells.
His
fever
settled
within
a
day
but
the
facial
oedema
increased
over
the
next
two
days
and
he
developed
extensive
necrotic
areas
of
the
buccal
mucosa
and
hard
palate.
Five
days
later
he
had
entered
remission,
his
white
blood
count
was
2
5
x
lO9/l.
The
oral
lesions
healed
completely.
Discussion
Infection
with
Pseudomonas
aeruginosa
begins
with
colonisation,
followed
by
a
break
in
host
defences
with
local
invasion,
and
culminates
in
dissemination
and
systemic
disease.
Swabs
taken
routinely
showed
that
in
two
of
our
patients
infection
was
preceded
by
oral
colonisation.
Ulceration
of
the
oral
mucosa
would
have
provided
a
largely
unopposed
initial
break
in
host
defences
to
tissue
invasion
during
the
period
of
neutro-
penia.
A
common
complication
of
cytotoxic
drug
treatment
is
mucositis,
which
sometimes
progresses
to
frank
oral
ulceration.
But
the
first
patient
had
in
addition
extensive
gum
lesions
that
were
thought
to
be
leukaemic
in
origin,
and
in
the
third
patient
injury
to
the
buccal
mucosa
resulted
in
cellulitis
developing
within
24
hours.
Attempts
at
preventing
colonisation,
which
may
result
in
systemic
infection,
are
aimed
at
either
avoid-
ing
the
organism
or
suppressing
its
growth.
For
this
oral
intestinal
decontamination
is
used,5
combined
Gram
stained
section
of
pharynx
showing
extensive
perivascular
infiltration
(arrows)
with
Gram
negative
bacilli,
compatible
with
pseudomonas'
I
with
sterile
food
and
good
oral
hygiene.
Though
all
three
patients
were
instructed
in
oral
hygiene,
colonisation
occurred
because
of
poor
compliance,
persistence
of
organisms
at
inaccessible
sites,
such
as
the
posterior
pharynx,
or
the
ineffectiveness
of
many
antiseptics
against
pseudomonas.
For
the
two
patients
who
responded
to
treatment
we
had
chosen
a
combination
of
ciprofloxacin
with
an
aminoglycoside
for
its
antipseudomonal
activity.
Ciprofloxacin
has
the
theoretical
advantage
of
excellent
tissue
penetration
when
given
either
by
mouth
or
parenterally.6
We
had
not
seen
this
unusual
presentation
of
pseudomonas
infection
before
and
cannot
explain
the
occurrence
of
all
three
cases
within
one
year.
Over
the
year
there
had
been
no
change
in
patient
population
or
treatment
regimens,
and
the
results
of
serology
and
phage
typing
show
the
three
strains
of
pseudomonas
to
be
distinct.
It
may
be
argued
that
the
first
two
patients
(cases
1
and
2)
showed
unusual
late
manifestations
of
inadequately
treated
pseudomonas
infection.
A
combination
of
an
aminoglycoside
and
another
anti-
pseudomonal
agent
is
generally
regarded
as
the
best
treatment.
For
the
patient
in
case
1,
despite
pseudo-
monas
being
isolated
from
both
routine
and
blood
cultures,
only
one
of
these
agents
was
being
used
in
treatment.
Likewise,
in
the
second
patient
the
isolation
earlier
of
a
pseudomonas
resistant
to
pipericillin
from
a
routine
culture,
together
with
evidence
of
systemic
infection
shown
by
the
high
fever,
should
have
prompted
the
earlier
treatment
with
a
second
effective
antipseudomonal
drug.
Finding
Pseudomonas
aeruginosa
in
a
routine
culture
requires
careful
attention
as
it
often
predates
invasive
infection
in
a
patient
with
neutropenia.
We
now
treat
colonisation
with
colistin
gargles
and
adapt
systemic
antibiotic
treatment,
wheii
it
is
required,
to
provide
intensive
antipseudomonas
drug
cover.
We
thank
the
PHLS
Gram-Negative
Reference
Laboratory
at
Colindale
for
typing
the
strains
of
pseudomonas
and
the
photographic
department
at
our
hospital
for
their
help.
We
also
thank
the
Leukaemia
Research
Fund
and
the
Bud
Flanagan
Research
Fund
for
support
of
this
study.
1
Schimpff
SC,
Moody
M,
Young
VM.
Relationship
of
colonisation
with
Pseudomonas
aeruginosa
to
development
of
pseudomonas
bacteremia
in
cancer
patients.
In:
Hobby
GL,
ed.
Antimicrobial
agents
and
chemotherapy
1970.
Washington
DC:
American
Society
of
Microbiology,
1971:240.
2
Hersh
EM,
Bodey
GP,
Nibs
BA.
Cause
of
death
in
acute
leukemia.
JAMA
1%5;193:
105-9.
3Baltch
A,
Griffin
PE.
Pseudomonas
aeruginosa
bacteremia:
a
clinical
study
of
75
patients.
Am3JMed
Sci
1977;274:119-29.
4
Selby
P,
Hobbs
S,
Viner
C,
Jackson
E.
Tumour
necrosis
factor
in
man:
clinical
and
biological
observations.
BrJ
Cancer
(in
press).
5
Schimpff
SC,
Young
VM.
Epidemiology
and
prevention
of
infection
in
the
compromised
host.
In:
Rubin
HR,
Young
SL,
eds.
Clinical
approach
to
infection
in
the
compromised
host.
New
York:
Plenum,
1981;5-33.
6
Wise
R,
Donovan
IA.
Tissue
penetration
and
metabolism
of
ciprofloxacin.
In:
Neu
HC,
Percival
A,
Lode
H,
eds.
Ciprofloxacin:
a
major
advance
in
quinolone
chemotherapy.
AmJ
Med
1987;82(4A):
103-7.
(Accepted
16
August
1988)
ANY
QUESTIONS
Is
hormonal
disturbance
a
possible
cause
of
postnatal
depression
and
if
so
is
hormonal
treatment
recommended?
There
is
no
convincing
evidence
of
a
hormonal
basis
for
postnatal
depression,
but
many.
believe
that
hormonal
factors
play
an
important
part.
At
present
there
is
no
scientific
basis
for
hormonal
treatment
of
such
depressions
and
abundant
evidence
of
the
importance
of
environmental
factors.
-SYDNEY
BRANDON,
professor
of
psychiatry,
Leicester
Brandon
S.
Depression
after
childbirth.
BrMedJ
1982;284:6134.
Stein
G.
Maternity
blues.
In:
Brockington
I,
Kumar
R,
eds.
Motherhood
and
mental
illness.
London:
Academic
Press,
1982:119-54.
BMJ
VOLUME
297
22
OCTOBER
1988
1035