Wound botulism associated with subcutaneous drug use
BMJ 2002; 325 doi: https://doi.org/10.1136/bmj.325.7371.1020 (Published 02 November 2002) Cite this as: BMJ 2002;325:1020
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Wound botulism associated with subcutaneous drug use.
Mr A Sloan. Dr M Coupe. Dr J Gough
Royal Gwent Hospital, Newport, South Wales
The recent 'lesson of the week’ (1) proved invaluable in the
diagnosis and management of a patient admitted to hospital in Newport,
South Wales.
A 48-year-old female attended the A&E department with a 3-day
history of dysphagia, dysarthria, blurring of vision, and weakness in her
neck and upper limbs. She admitted to subcutaneous injections of heroin
(skin-popping). On examination she had bilateral ptosis, slight weakness
in the upper limbs, crepatations at the right lung base, and an abscess on
her left thigh. Blood investigations revealed a raised WCC. She was
admitted and treated for a probable chest infection.
Within 12 hours the patient had developed worsening type II
respiratory failure, and had 2 asystolic cardiac arrests from which she
was resuscitated. The patient was transferred to ITU where she required
ventilation and inotropic support.
The differential diagnosis at this stage was intracranial infection,
myasthenia gravis, Guillain - Barre syndrome or wound botulism. After
incision and drainage of the thigh abscess, we gave botulism antitoxin.
CT head, lumbar puncture, and a Tensilon test were all normal. Two
weeks after admission, Clostridium Botulism toxin, type A, was identified
from pus aspirated from the abscess of her left thigh. The patient
required ventilatory support for 6 weeks, and although still an inpatient
we expect her to make a full recovery.
Due to the heightened awareness of wound botulism, we were able to
provide treatment quickly and effectively for this patient. Werner et al
(2) recommended that once the diagnosis is considered, there should be
immediate administration of antitoxin, before laboratory confirmation, to
prevent disease progression and death. The majority of patients where
Type A botulism toxin is isolated require ventilatory support.(3)
Patients treated with antitoxin on day 1 of their symptoms have a shorter
recovery period than those who have delayed treatment.(4) The extended
delay in isolating clostridium botulism toxin in this case, highlights the
importance of prompt antitoxin administration based upon high clinical
suspicion alone.
We believe this to be the first case in Wales, although the incidence
in the United Kingdom appears to be increasing. As stated in the article,
in the 1990s there was a dramatic increase in the number of wound botulism
cases in California.(5) Are we going to see a similar picture unfold in
Great Britain? If so, we must increase our awareness of this still
relatively rare clinical condition.
Word Count - 392
References:
1.. Merrison A F A, Chidley K E, Dunnett J, Sieradzan K A. Wound
Botulism associated with sucutaneous drug use.
BMJ 2002;325:1020-1021
2. Werner SB, Passaro D, Mcgee J, Schechter R, Vugia DJ. Wound
botulism in California, 1951-1998: recent epidemic in heroin injectors.
Clinical Infectious Diseases 200; 31:1018-1024
3. Woodruff BA,Griffin PM, McCroskey LM, et al. Clinical and
laboratory comparison of botulism toxin types A, B, and E in the United
States 1975-1978. Journal of Infectious Diseases 1992;166:1281-6
4. Tacket CO, Shandera WX, Mann JM, Hargrett NT, Blake PA. Equine
antitoxin use and other other factors that predict outcome in food borne
botulism. American Journal of Medicine. 1967;76:794-8
5.Passaro DJ, Werner SB, Mcgee J, MacKenzie WR, Vugia DJ. Wound
Botulism Associated with Black Tar Heroin Among Injecting Drug Users.
JAMA, 1998:279:859-863
Editorial note
The patient whose case is described has given her signed informed consent to publication.
Competing interests:
None declared
Competing interests: No competing interests
Reports of wound botulism (WB) in injecting drug users (IDUs) are a
relatively new phenomenon with no clinically diagnosed cases in the UK up
to the end of 1999.Thirteen WB in UK been reported to the PHLS Food Safety
Microbiology Laboratory (FSML) since the beginning of 2002 (communication
from PHLS).California in US has experienced an increase in WB since
1988,associated with injecting black tar heroin (BTH),a dark tarry form of
the drug(1).
Merrison,et al's case report on WB promted us to consider this
diagnosis in a 32-year old male IDU.In November 2002 this man presented
with a complaint of shortness of breath.He was on a methadone regimen but
has been injecting BTH sub-cutaneously over the past 12-months,as all his
veins had sclerosed.He had no obvious skin lesion apart from multiple
scars.
24-hours later he developed a proximal muscle weakness (MRC 4/5).On
day 3,his muscle weakness became severe (MRC 0/5).He was dysarthric,and
dysphagic with drooling.He had a tachycardia but was normotensive.Late he
needed ventilation in the ITU due o development of respiratory failure
(RF).Chest X-ray had shown bilateral basal consolidation which was thought
to be aspirational.Antibiotics were began.
On day 7,he developed bilateral complete ptosis with unequal pupil
sluggishly reacting to light and had bilateral facial palsy.He was able to
obey commands.He also developed a labile hypertension needing clonidine
infusion and oral amlodipine.Based on the Merrison,et al's report WB was
thought to be a strong possibility in this case.Trivalent botulinum
antitoxin was administered,along with intravenous immunoglobulin.Miller-
Fisher variant Guillain-Barre and Myaesthenia Gravis were also
considered.Acetyl choline recptor antibody test was negative.Neuro-
physiological testings were consistent with neuro-muscular junction
transmission defect of the pre-synaptic type,suggestive of
botulism.Botulinum type-A toxin was eventually identified in his
serum.Within 48-hours he showed some improvements (MRC 1/5),ptosis became
partial and the pupil became equal and reacted to light.Tracheostomy was
performed on day 8.We anticipate a prolonged hospital stay for this man.
This case further illustrates that WB should be considered in IDUs
who present with cranial nerve palsies and descending paralysis(2,3).In
one series(4) 75% of the WB cases in IDUs developed RF.57% required
ventilation if the antitoxin was given within 12-hours,compared to 85% of
cases who received the antitoxin after 12-hours.Early tracheostomy (<_10 days="days" after="after" initial="initial" intubation="intubation" was="was" associated="associated" with="with" a="a" shorter="shorter" duration="duration" of="of" ventilation4.he="ventilation4.he" had="had" episodes="episodes" hypertension="hypertension" thought="thought" to="to" be="be" due="due" autonomic="autonomic" dysfunction="dysfunction" as="as" has="has" been="been" noted="noted" before5.="before5." p="p"/> References:
1.Passaro DJ,Werner SB,McGee J,MacKenzie WR,Vugia DJ. Wound botulism
associated with black tar heroin among injecting drug users. JAMA
1998;279:859-63.
2.Merrison AFA,Chidley KE,Dunnett J,Sieradzan KA. wound botulism
associated with subcutaneous drug use. BMJ 2002;325:1020-21.
3.Burningham MD,Walter FG,Mechem C,Haber J,Ekins BR. Wound botulism. Ann
Emerg Med 1994;24:1184-87.
4.Sandrock CE,Murin S. Clinical predictors of respiratory failure and long
-term outcome in black tar heroin-associated wound botulism. Chest
2001;120:562-66.
5.McGarrity L. Wound botulism in injecting drug users. Anaesthesia
2002;57:301-02.
Competing interests:
None declared
Editorial note
The patient whose case is described has given his signed informed consent to publication of his case.
Competing interests: No competing interests
Merrison et al (1) reported a difficult diagnostic case of
wound botulism, which led to a helpful diagnostic table
for distinguishing clinical features from Guillian-Barre
syndrome, Miller-Fisher variant and myasthenia gravis
being formulated. To increase the body of knowledge
for aetiology, recognition and the treatment of wound
botulism with subcutaneous drug use, a case in a 20
year heroin user is reported. This case illustrates that
the history of substance misuse can cloud the picture
even more than the clinical presentation, and that early
treatment can be vital.
With a 20 year history of street heroin use, this man
had poor intravenous access and therefore injected
blindly to his buttocks. After developing an abscess on
one side he injected to the other for three weeks, then
returned to the initial injection site believing that it had
healed. During this time the anaerobic conditions were
prefect for bacterial growth and toxin production. By
injecting though this abscess into the gluteal muscle
he developed a C. botulinum systemic infection, which
became clinically apparent after one day. He attended
his local A&E department after three days with malaise,
dizziness, facial weakness, slurred speech and
difficulty swallowing. After triage he was judged to have
a chest infection with the implication that he was under
the influence of substances and he was asked to leave
the department. The next day he was reviewed at a
community drug clinic with a presentation of muscle
weakness, ataxia, ptosis, sluggish papillary
responses, dysphagia and dysarthria (normal
transcribed language). He also had opiate withdrawal
symptoms of piloerection, muscle pain, sweating
without pyrexia and tachycardia. Within a few hours of
representation to A&E he had respiratory failure and
was transferred to ITU. The differential diagnosis of
Guillian-Barre syndrome and botulism was treated with
botulinum antitoxin (before the toxin was isolated) and
with wound management.
Botulinum antitoxin was prescribed effectively due to
untangling the clinical presentations, and this man was
out of hospital and back to normal within four weeks.
This is in comparison to the treatment reported by
Merrison et al (1), which did not include antitoxin
treatment and resulted in neurological morbidity seven
months after treatment. The problems of management
in both cases are associated with co-morbid opiate
withdrawal signs and symptoms, non-obvious
cutaneous evidence of a wound infection, but the most
important in the above reported case, was the stigma
of an injecting substance misuse history.
Competing interests: None
Editorial note
The patient in this case has given his signed informed signed consent to publication.
Reference
1. Merrison AFA, Chidley KE, Dunnett K, Sieradzan KA.
Wound botulism associated with subcutaneous drug
use. BMJ 2002; 325: 1020-1021
Competing interests:
None declared
Competing interests: No competing interests
Absence of obvious wound site should not rule out suspicion about a diagnosis of wound botulism
Editor-Merrison et al recently reported a case of wound botulism in
an injecting heroin user.1 We emphasise the important message contained
in their ‘Lesson of the Week’ by reporting two further cases.
Firstly, Merrison et al recommend undertaking a search for wound
sites. Whilst this is helpful if an obvious or infected lesion is found,
one of our reported cases did not have an apparent wound. Others have
also stressed the need to be aware that a wound may not be obviously
infected or even evident.2,3,4 The absence of a wound should not exclude
suspicion about a diagnosis of wound botulism. Even in injecting drug
users who use heroin sub-cutaneously (skin-popping), relatively innocuous,
previously healed wound sites may harbour toxin released from Clostridium
botulinum bacteria.
In our first case a 30 year old female injecting drug user presented
to an accident and emergency unit in Manchester in late 2001 complaining
of a 24 hour history of progressive blurred vision, slurred speech,
swallowing difficulties and limb weakness. The second case concerned a 33
year old male injecting drug user who presented to an accident and
emergency unit in Liverpool in early 2002 with a similar history,
worsening over 3 days. Following admission both patients’ neurological
status and respiratory function deteriorated over a day or so and both
required urgent intubation and ventilation.
The first patient received botulinum antitoxin on the second day
after admission and by day 34 had ventilatory support withdrawn. She was
discharged without any residual disability after 8 weeks.
Despite the presence of multiple small areas of newly healed tissue
the second patient had no obvious clinically infected or open wounds. Due
to delay in diagnosis he did not receive botulinum antitoxin. He was
ventilated for 73 days. After extensive physical rehabilitation he made a
good recovery and was fit for discharge after 6 months. He had a residual
mild weakness of shoulder abduction and complained of some blurred near
vision.
An important practical second point is that routine laboratory
testing of any specimens to detect C. botulinum is not helpful.
Specialist advice should be sought urgently from an infectious disease
physician and ultimately all blood samples or wound specimens will be sent
to the Public Health Laboratory Service (PHLS). The PHLS keep details of
centres around the country that hold antitoxin. Out of hours the
Communicable Disease Surveillance Centre duty doctor may be contacted.
Detailed advice is available on the PHLS website.5
1 Merrison AFA, Chidley KE, Dunnett J, Sieradzan KA. Wound botulism
associated with subcutaneous drug use. BMJ 2002; 325: 1020-1021. (2
November.)
2 Maselli RA, Ellis W, Mandler RN et al. Cluster of wound botulism in
California: clinical, electrophysiologic and pathologic study. Muscle
& Nerve 1997; 20: 1284-1295
3 Mulleague L, Bonner SM, Samuel A et al. Wound botulism in drug
addicts in the United Kingdom. Anaesthesia 2001; 56: 120-123
4 McDonald KL, Rutherford GW, Friedman SM et al. Botulism and
botulism-like illness in chronic drug abusers. Ann Intern Med 1985; 102:
616-618
5 Public Health Laboratory Service
www.phls.org.uk/topics_az/injectingdrugusers/menu.htm
Competing interests:
None declared
Editorial note
The patients whose cases are described have given their signed informed consent to publication.
Competing interests: No competing interests