91 Infectious complications in the injection and non-injection drug user
Drug abuse is a widespread public health problem because many of its medical complications are infectious due to the transmission of bloodborne, environmental, and respiratory infectious agents. Availability of highly active antiretroviral therapy (HAART) in human immunodeficiency virus (HIV)-infected substance abusers has reduced the severity and frequency of opportunistic infections seen in the intravenous drug users (IVDUs) and other drug users (DUs). That said DUs/IDUs remain the groups least likely to access care and to maintain adherence for optimal benefit. Recent studies find social and access factors related to criminalization are major barriers to care including HAART for these individuals. Increasing treatment options and societal acceptance of harm reduction efforts have been demonstrated to improve outcomes in countries that have undertaken them.
Endocarditis, a life-threatening infection of the heart valves and/or endocardium, is associated with septic parenteral injections. Right-sided valvular infections are very frequent in IDUs because of septic inoculations. Intravenous injection with low-pressure venous return increases the susceptibility of right-sided valvular and other structures to infection. Concurrent pulmonary hypertension from drug adulterants, such as talc, may also predispose to right-sided disease.
Despite the high prevalence of endocarditis, the offending pathogens are not specific to injectors. Staphylococcus aureus, often methicillin-resistant S. aureus (MRSA), is the most commonly identified organism, but other pathogens are seen. These include Pseudomonas, Serratia, enterococci, Streptococcus groups A and B, and Streptococcus viridans. Increasingly, fungal pathogens are seen with and without immunodeficiency.
Clinical diagnosis of endocarditis in the drug abuser can be difficult. The hallmark symptom is fever. Other constitutional symptoms such as chills, sweats, and arthralgia are less specific, but they are commonly observed in opiate withdrawal. The physical signs associated with left-sided endocarditis are seldom present. Coexistent HIV-1 immunodeficiency appears to predispose to more severe systemic infections.
Because clinical diagnosis alone presents challenges, echocardiographic findings have developed into the primary method to diagnose and treat endocarditis. Blood cultures and other routine tests should be used to identify the offending pathogen and antimicrobial sensitivities.
Transthoracic (TTE) and transesophageal echocardiography (TEE) are used to evaluate suspected endocarditis (e.g., high clinical suspicion but negative blood cultures). Detection of valvular vegetations, valve disease with hemodynamic compromise, associated shunts or abscesses, or patients with persistent fever, continued bacteremia, or clinical deterioration may mandate serial testing.
Therapy should be multidisciplinary as patients may be unwilling to comply with adequate treatment regimens especially if long-term hospital stays and serial testing are required. Combination short course IV followed by oral therapy may be considered. Left-sided disease, large vegetations, or presence of cardiovascular compromise mandates more intensive therapy. Medication selection is an evolving science and isolation of pathogen and drug sensitivities are critical in this respect. Mortality with right-sided disease is low; the presence of left-sided valvular and/or chordae tendineae involvement, fungal pathogens, congestive heart failure, other cardiovascular compromise, vegetation size > 20 mm, and HIV with immune compromise all greatly increase risk. Inflammatory myocarditis can be seen independently and with endocarditis; it is multifactorial in substance abusers with cocaine or HIV-1 infection, and inflammatory responses from adulterants in drugs are common causes.
Complications due to intravenous drug use include pneumonia, aspiration pneumonitis, lung abscess, and septic pulmonary emboli. Talc contamination of the injected drugs enters the bloodstream and lodges in the pulmonary capillary bed, causing foreign-body granulomatosis that results in pulmonary fibrosis and acute inflammatory pneumonitis. Septic pulmonary emboli may result in clinically evident ventilatory and perfusion mismatch on scintigraphic imaging.
Chronic inhalation of drugs and their adulterants will accelerate alveolar destruction and result in early-onset chronic obstructive pulmonary disease (COPD) and emphysema. Chronic immunosuppression from HIV increases likelihood of pneumonitis, and community and immune-compromised respiratory disorders. Chronic opiate and cocaine addiction is often associated with COPD, from smoking the drug. Smoking (nicotine/marijuana) may result in decreased vital capacity and a decrease in diffusion capacity and small airway disease. IDUs also have a 10-fold increased risk of community-acquired pneumonia compared to the general population, due to failure to vaccinate, the destructive action of marijuana/tobacco abuse, and increased susceptibility to viral and bacterial exposures.
Bone and joint infections
Septic arthritis and osteomyelitis from disseminated cutaneous infection as well as direct injection at or near the affected area has been described in the IDU. Gram-positive organisms and Pseudomonas aeruginosa are the most commonly implicated organisms. Osteomyelitis most commonly affects the fibrocartilaginous joints such as the vertebral, sternoarticular, and sacroiliac joints. In addition to bacterial infections, fungal infections are increasingly described in both immunocompetent and immunodeficient hosts, i.e., diabetics, end-stage renal disease, HIV, and neoplastic disease. Treatment protocols do not differ from other immunosuppressed hosts; bone or joint cultures are necessary for accurate diagnosis. Compliance with long-term therapies poses additional problems with adherence in the DUs/IDUs.
Skin and soft-tissue infections
Septic parenteral injections frequently lead to skin and soft-tissue infections. Infectious and chemical thrombophlebitis, abscesses, and cellulitis are common venous insults. Life-threatening cutaneous infections include fasciitis, myonecrosis, and gangrene. Tissue crepitance, extensive cellulitis, evidence of systemic toxicity, severe pain, and sepsis suggest serious and life-threatening infections. Plain radiographs may be helpful though MRI would be optimal to determine the extent of soft tissue, bone, and marrow involvement.
Injected drugs and their adulterants are often damaging to veins. Progressive sclerosis of the veins is common. With loss of peripheral access, deeper and more dangerous sites, i.e., femoral, axillary, jugular, penile, and mammary veins may be used. More serious infections, thrombosis, and gangrene may result from injections at these sites.
Once easy intravenous access is not available, many substance abusers will administer drugs subcutaneously. Staphylococci and streptococci are frequent pathogens. However, with immunosuppression, other bacterial pathogens are encountered. Escherichia coli, Klebsiella, Bacteroides, Clostridia, and mixed flora consisting of both aerobic and anaerobic organisms as well as fungal organisms such as Candida may be encountered.
Small localized infections can usually be treated locally with or without systemic antibiotics. Severe infections should be managed with surgical debridement and inpatient antibiotic therapy.
The epidemiology of hepatitis A has changed dramatically in the past decade, with drug abuse being recognized as a significant risk for its transmission. Hepatitis A is associated with fecal–oral transmission. Contaminated marijuana has been reported as a transmission agent for hepatitis A.
Hepatitis B, C, and D (HBV, HCV, and HDV, respectively) are associated with parenteral transmission. The incidence of HBV and HCV in IDU populations is very high worldwide, with a significant proportion infected with both HBV and HCV.
Chronic HBV infection is associated with persistent hepatitis B surface antigen (HBsAg) and hepatitis Be antigen (HBeAg), although hepatic inflammation varies widely. HBeAg is associated with increased infectivity, more severe disease, and eventual cirrhosis. The HBV virion is not cytotoxic but mediates a host cytotoxic T-cell response that causes hepatocellular inflammation and necrosis. Coinfection with HIV-1 with its associated cellular immune deficiency reduces the severity of the host cytopathic response. Progressive HIV-1-associated cellular immunodeficiency manifests with reduced hepatic inflammation and lower serum transaminase concentrations. Other serologic measures of HBV infection in HIV-1 are not diminished.