Working with Persons Who Inject Drugs: Be Aware of Wound Botulism

On January 4, 2019, the Centers for Disease Control and Prevention (CDC) published Wound Botulism Outbreak Among People Who use Black Tar Heroin – San Diego County, California, 2017- 2018.¹ From September 2017 to April 2018, 9 cases of wound botulism were reported in San Diego County, California. All patients reported injecting heroin, and 7 used black tar heroin; 6 reported injecting subcutaneously.¹ Botulism is rare, treatable, but potentially fatal; 1 person died in the San Diego outbreak.^1,2 There is concern about the potential increased use of black tar heroin during the current opioid crisis and subsequent increases in wound botulism cases. Providers of wound care should be aware of wound botulism and refer patients for emergency care when suspicious.

Black tar heroin is so named due to the dark, sticky appearance of the heroin that results from the way it is produced, generally on the volcanic hillside of Jalisco, Mexico. By 1990, black tar heroin led the heroin market west of the Mississippi River.^2,3 In the early 2000s, use spread to the eastern United States.³ During transport, black tar heroin is cut with brown organic materials (eg, shoe polish, wood pulp, coffee grounds, dirt) that increase its weight for sale and increase contamination risk from botulism.³ White heroin also can become contaminated with botulism; this usually occurs from dust during transport from Afghanistan and Pakistan as well as during preparation for injecting.³

Clostridium botulinum is an anaerobic gram-positive bacterium commonly present in soil worldwide. The immunologically different types of toxin of C botulinum are noted by the letters A through G; 4 are noted in human disease (A, B, E, F), and the most common types in wounds are serotype A (subtype A predominates) and B.^3,4 The spores survive in extreme environments. C botulinum produces a highly potent neurotoxin. In humans, it enters the blood stream and paralyzes muscles by irreversibly blocking the release of acetylcholine at peripheral neuromuscular junctions.^4,5

The most common forms of C botulinum are food, infant, and wound.^4,5 Food botulism is caused by ingesting food containing the toxin (eg, improperly canned foods). The infant form usually is caused by the ingestion of spores such as those found in honey.⁵

Wound botulism is very rare.^4,5 It was first described in 1951 in a case study of a patient with traumatic wounds contaminated with soil.³ The first reported case of wound botulism from injection drug use was in 1982 in a cluster of 6 cases in New York City.^2,3 Now injection drug use accounts for most of the cases of wound botulism; ~75% occur in California. Risk for wound botulism in persons who inject drugs is primarily associated with skin popping or injecting into extravenous subcutaneous tissue or muscle, typically in the areas of the deltoid, gluteus, and quadriceps.³ Skin popping bypasses exposure to the bloodborne immunologic response. Combining heroin with a vasoconstrictor like cocaine or methamphetamine (“speedballing”) further decreases blood flow to the site and exacerbates ischemia.³

Persons with wound botulism from heroin tend to be 20 to 60+ years old. Although more men than women inject heroin, women account for 30% to 50% of the persons with wound botulism.^5,6 Most cases occur in the US.

There is no test to expediently diagnose wound botulism; serum, feces, and vomit can be cultured to determine C botulinum.⁴ Real-time polymerase chain reaction or mouse assay can detect the toxin, but results often are not rapid.⁴ Definitive diagnosis involves identifying the neurotoxin in serum or wound aspirate.⁵ The neurotoxin is not identified in all serum; an electromyogram can be helpful while waiting for serum toxin results. Misdiagnoses may occur because manifestations (ptosis, weakness, dysarthria) may mimic intoxication, which is a concern for persons with alcoholism. Many laboratory tests can be normal (complete blood cell count, chemistry, urinalysis, cerebrospinal fluid, liver function tests) unless an infection is present.⁵

The diagnosis often is made after thoroughly reviewing the person’s history and clinical manifestations. Because wound botulism generally is associated with skin popping and abscesses in those areas, skin should be thoroughly examined for injection sites and abscesses.² The hallmark clinical features include cranial nerve palsies with descending paralysis.⁵ The most common symptoms are dysphagia/trouble swallowing, proximal muscle weakness of the upper and lower extremities, neck flexor muscle weakness, ophthalmoplegia, bilateral ptosis, dysarthria, double vision, blurred vision, and dry mouth.^2,3,5 Sensations and mentation are not affected.⁵

Differential diagnoses include a variant of Guillain-Barre syndrome, autoimmune neuromuscular diseases (myasthenia gravis, Lambert-Eaton syndrome), organophosphate poisoning, paralytic shellfish poisoning, brain stem stroke, tick paralysis, hyperkalemic periodic paralysis, or poliomyelitis.^3,5 Diagnoses can be confirmed by computerized tomography or magnetic resonance imaging of the head. Wound botulism may occur more than one time.

Yuan et al⁶ examined surveillance data in California from 1993 to 2006 that identified 17 persons who injected drugs with recurrent wound botulism. All injected heroin: 88% used black tar heroin and 76% reported subcutaneous injection.

Prompt treatment with botulism antitoxin helps decrease hospitalization and mortality; it is most effective if given within 24 hours of the onset of symptoms.⁵ In the US, the antitoxin is obtained from the state health department and the CDC.³ The CDC authorizes release of the antitoxin from designated storage facilities. In 2010, the US Food and Drug Administration approved the first heptavalent equine botulism antitoxin that neutralizes toxin subtypes A–G.³ This was used in the San Diego county outbreak.¹ There also is reported use of the trivalent equine antitoxin.² The dose is administered intravenously at a rate based on age and tolerance; the person should be monitored for allergic reaction. The antitoxin acts on free neurotoxin that has not been taken up into the motor neuron; it does not reverse the action of toxin that has already disabled acetylcholine release at a neuromuscular junction.⁵
Wound care. Wounds need to be debrided surgically to stop disease progression. The toxin continues to be produced within an anaerobic area of the heroin injection site. Wound care after debridement will depend on the size and attributes of the created wound. Antibiotic therapies can be effective against C botulinum, but helpfulness or necessity has not been established.⁵ Aminoglycosides and clindamycin are avoided because they can increase presynaptic neuromuscular blockade.⁵ According to Gonzales y Tucker and Frazee,³ supportive (eg, respiratory) care is used if necessary; mechanical ventilation should be considered for a vital capacity <30% predicted or maximal inspiratory force <30 cm of H₂O. Once respiratory failure develops, ventilatory support may be required for 2 months or longer because presynaptic nerve terminals slowly regenerate. Parenteral or enteral fluids and nutrition may be needed if swallowing was affected. Abavare and Abavare⁵ note extensive rehabilitation is used for prolonged convalescence to regain functioning; the survival rate from botulism is 85% to 90%.

A systematic literature review⁷ of clinical features of foodborne and wound botulism identified that of 402 patients, 346 cases (86%) were foodborne. The median time from illness to hospitalization was 2 days. Because so few patients had wound botulism, the authors generally did not differentiate type of botulism. Persons with wound botulism rarely experienced nausea and vomiting compared to those with food botulism. Weakness or paralysis of at least one cranial nerve on admission was present in 375 patients (93%).

Because of the severity of wound botulism, prevention is critical. The only true prevention is to stop injecting drugs; there is no immunity to wound botulism and the condition may recur. No vaccine is licensed for current use,⁸ and in 2011, the CDC stopped providing the pentavalent botulinum toxoid vaccine for workers at risk for occupational exposure. Health departments can deliver messages within the drug use community, refer persons to medication-assisted treatment, and do timely surveillance and notify people who inject drugs when wound botulism clusters are detected.¹ Practitioners and public health officials should recognize the clinical features of wound botulism and the potential for rapid progression when infection occurs. Persons who inject drugs and fail to respond to naloxone need to have their bodies searched for wounds and treated for wound botulism based on clinical manifestations. The risk for wound botulism remains even using safe injection practices to inject black tar heroin.