Pleural Effusion in a Patient with Injection Heroin Use: An Unusual Presentation with an Unusual Pathogen

Sir,

According to a recently conducted nation-wide survey, in India, about 8.5 lakh people use injection drugs. Punjab, with nearly 88,000 people who inject drugs (PWID), has the second-largest drug-using population. ¹ Injection drug use (IDU) can cause a wide array of infective and non-infective pulmonary complications: pneumonia, cardiogenic edema, acute lung injury, pulmonary hemorrhage, and aspiration pneumonia.^{2, 3} We report a rare pulmonary complication of injection drug use: septic emboli caused by an unusual agent, Burkholderia cepacia, which resulted in pleural effusion.

Case Report

A 22-year-old unmarried, unemployed male, resident of urban Chandigarh, was admitted in the surgical emergency in mid-December 2019 with complaints of acute onset of chest pain (which worsened during inspiration), breathlessness, and intermittent pain in the right lower abdomen for the last one week and fever for two days. History revealed regular use of heroin for the last five years and use was predominantly via injections for the last two years; if unable to procure heroin, he would chase Smack once or twice a month. He would share injection equipment and use tap water as a re-constituent. The place of injection would largely be empty and dirty parking lots and public toilets. Urine drug screen revealed the presence of morphine and cannabis. Initial assessment revealed a pulse rate of 94/min, blood pressure 120/76 mmHg, and an axillary temperature of 101° F. The chest auscultation was unremarkable. His past medical record revealed hepatitis C seropositivity.

Initial blood investigations revealed the following: hemoglobin 12 g/dl, total leucocyte count 7300/mm³ (differential count: neutrophil 67%, lymphocyte 32%, monocyte 7%, and eosinophil 4%), platelet 2,73,000/mm³, bilirubin (total: 0.7 mg/dl; conjugated: 0.2 mg/dl), and total protein 7.1 gm/dl. He was seronegative for both hepatitis B and human immunodeficiency virus (HIV1&2). Electrocardiogram was unremarkable. A chest radiogram revealed right-sided pleural effusion. Ultrasonogram (USG) whole abdomen, done as a part of acute abdomen work-up on the same day, showed mild splenomegaly, right-sided loculated pleural effusion (2.8 cm wide, with thick septations), and appendicolith.

He was diagnosed with pleural effusion and acute appendicitis. He was treated with empirical antibiotic therapy (ciprofloxacin and metronidazole) and intravenous fluids. After one day, 10 F pigtail catheter was placed in the right pleural space under USG guidance. Pleural fluid investigations revealed the following: sugar 17 mg/dl, protein 5.7 mg/dl, adenosine deaminase 53 IU/L, and cell count 680/cmm (polymorphonuclear cells: 60%, lymphocytes: 40%). The report was indicative of exudative effusion, possibly of infective origin. Real-time polymerase chain reaction for tuberculosis was negative. Culture and sensitivity report of the pleural fluid showed Burkholderia cepacia with intermediate sensitivity to cefoperazone-sulbactam and resistance to ceftazidime, ciprofloxacin, levofloxacin, and meropenem. But the antibiotic regime was not changed as the patient showed clinical improvement.

After five days, the pigtail catheter was removed, and the patient was discharged on ciprofloxacin and metronidazole (to be continued for another five days). There was a temporary resolution of fever and breathlessness. History obtained in the emergency ward revealed past treatment in a private de-addiction service with buprenorphine assisted therapy, to which he was poorly adherent. He was admitted subsequently to the addiction psychiatry ward for buprenorphine reinduction. Then the chest pain reappeared. A chest radiogram was repeated, which revealed minimal right-sided pleural effusion. After consultation with pulmonary medicine, the patient was kept under observations, with a fortnightly repeat of chest radiogram. The pain was controlled by buprenorphine. However, the level of effusion remained unchanged, and an intermittent mild right-sided chest pain, radiating to back, continued. But he did not experience breathlessness or fever. After 25 days, he was discharged on 14 mg buprenorphine and was referred to pulmonary medicine OPD. On serial monitoring with chest radiogram, the effusion gradually reduced and finally resolved in another month.

Discussion

PWID are around three times more susceptible to bacterial empyema. These complications might happen due to contaminated substance (including the fillers), paraphernalia or reconstitutes (often unsterile tap water), unsafe injection-practice, unhygienic place of injecting, and higher cutaneous bacterial colonization in PWID. ⁴ The most common identified agents for bacterial empyema are streptococcus and staphylococcus. ⁵ To the best of our knowledge, this is the first report of Burkholderia cepacia-related pleural effusion in a patient with IDU.

Burkholderia cepacia complex (BCC) is a lactose nonfermenting gram-negative bacillus with low virulence. BCC organisms are commonly found in plant roots, rhizosphere, soil, and tap water. It is an important pathogen in hospital-acquired infections and opportunistic infections in immunocompromised patients (e.g., cystic fibrosis and chronic granulomatous disease). ⁶ Immunosuppression is common among chronic opioid users. ⁷ In this case, the source of infection might be contaminated heroin, paraphernalia (environmental contamination or sharing of paraphernalia from infected users), tap water, and/or unhygienic injecting place. Burkholderia cepacia endocarditis is reported among PWID. ⁸ Despite low virulence, the extreme antimicrobial resistance makes the agent difficult to treat.

PWID should be actively monitored for unusual opportunistic infections. Moreover, this report highlights the importance of disseminating “safe injection practices” as a harm reduction measure.