A 53-year-old right-hand-dominant man with a history of fibromyalgia and chronic prostatitis but otherwise in good health sustained superficial abrasions to his right fourth finger from an electric sander while doing woodwork. The patient described the initial wounds as “raw, red, tender” and “with some bumpy edges,” similar to the lesions of psoriasis he had seen previously in a friend. Although the wounds were mild, the patient noted unusually slow healing, with resolution occurring approximately 6 weeks after the initial trauma. He did not experience fevers, chills, malaise, or other symptoms that would arouse concern during this time, and he did not seek medical care.
The patient had no further symptoms until 10 weeks after his initial injury, a month after his wounds healed. At that time, he noted swelling, erythema, and tenderness in the right fourth finger, accompanied by generalized myalgias but no fevers. These symptoms slowly worsened during the next month, with gradual proximal spreading of the erythema and edema over the patient's palm, wrist, and adjacent fingers, which finally prompted the patient to seek medical attention.
On initial evaluation, the patient denied any history of infectious exposures or further trauma. The patient's right hand was notable for dusky erythema with edema surrounding the right fourth proximal interphalangeal (PIP) joint but showed no clinically significant induration, fluctuation, or disruption of the overlying skin. A thorough examination of the hand showed considerable tenderness over the flexor tendon sheath with mild crepitus; finger range of motion was preserved with no frank triggering or locking. Laboratory results were as follows (reference ranges shown parenthetically): neutrophil count, 8.2 × 109/L (1.7-7.0 × 109/L); normal differential erythrocyte sedimentation rate, 1 mm/h (0-22 mm/h); C-reactive protein level, 1.29 mg/L (<0.8 mg/L); antinuclear antibody titer, less than 0.9 U (≤1.0 U); rheumatoid factor, 8 IU/mL (0-39 IU/mL); and uric acid, 4.9 mg/dL (4.3-8.0 mg/dL). Given the recent history of trauma to the affected joint, a plain radiograph was obtained, which showed an old volar plate avulsion fracture of the right fourth middle phalanx.
- 1.On the basis of the patient's history and physical and laboratory findings, which one of the following is the most likely diagnosis?
- a.Posttraumatic arthritis
- b.Rheumatoid arthritis
- c.Tenosynovitis
- d.Septic joint infection
- e.Gouty arthritis
- a.
Posttraumatic arthritis typically arises years after a precipitant traumatic injury has caused mechanical instability of the joint and degeneration of the articular surface. The history provided by the patient is not consistent with this mechanism or time frame of injury. Although rheumatoid arthritis can affect the PIP joint, this diagnosis is less likely because the characteristic bilateral and symmetrical joint swelling were absent, multiple joints were not involved, changes to the hand (eg, erosions or bony decalcifications) were not evident on radiographs, and nonspecific markers of inflammation or rheumatoid factor were not elevated.
Tenosynovitis can arise from repetitive use injury or from infection in or trauma to the soft-tissue connective tissues. The tenderness over the tendon sheath in our patient makes this diagnosis the most likely. The satisfactory range of motion in the joint, the lack of warmth on examination, and the absence of elevated inflammatory markers make joint sepsis less likely. Acute gout is typically characterized by monoarticular severe pain, redness, swelling, and disability, classically in a great toe. However, gout can also occur in the finger, wrist, or knee with edema extending beyond the joint, sometimes causing diagnostic confusion. The lack of substantial pain in the affected joint and the normal levels of serum uric acid make gout less likely as the diagnosis.
Magnetic resonance imaging of the right hand confirmed mild tenosynovitis of the right fourth digit superficial flexor tendon extending 7 mm proximal and distal to the joint with surrounding soft-tissue edema. The patient was diagnosed as having synovitis of the right fourth finger associated with the PIP joint and flexor tendon sheath. Given the patient's ongoing discomfort and inflammation in the absence of evidence of active infection, an injection of 10 mg of triamcinolone acetonide was administered into the tendon sheath.
Our patient subsequently experienced 3 days of substantial pain relief and a reduction in swelling. However, during the next 2 weeks, he noted a return of progressive swelling and redness as well as worsening redness and tenderness at the site of the injection. At 2-week follow-up, the patient had redness streaking proximally up his arm, blistering at the injection site, fixed limitation to range of movement at the PIP joint, and a temperature of 38.2°C. A second laboratory evaluation on site yielded the following results: white blood cell count, 10.4 × 109/L (3.5-10.5 × 109/L); a differential of 86% neutrophils (41.6%-71.1%); erythrocyte sedimentation rate, 6 mm/h (0-22 mm/h); and Creactive protein concentration, 18.65 mg/L.
- 2.Which one of the following is the most appropriate next step in the management of this patient?
- a.Two weeks of empiric outpatient antibiotic therapy for cellulitis
- b.Admission to the hospital for administration of parenteral antibiotics for cellulitis
- c.Joint aspiration and cultures, followed by outpatient treatment with antibiotics while awaiting culture results
- d.Admission to the hospital for intravenous administration of broad-spectrum antibiotics and urgent orthopedic surgical consultation for biopsy and cultures
- e.Close follow-up without further intervention, because the findings likely represent a pseudoseptic reaction to the injection
- a.
Our patient presented with fever, an elevated white blood cell count, and streaking erythema, all symptoms that could suggest an acute bacterial or fungal infection. If he had such an infection, outpatient management with oral antibiotics would be inadequate, and empiric therapy should be used in conjunction with cultures to identify a causative organism. A diagnosis of cellulitis alone is not likely because of involvement of the deeper tissue structures and fixed immobility at the joint on physical examination. Even with the addition of cultures and aspiration, the patient's rapidly progressive course would make outpatient management an inadequate option.
At this point, the differentiation between tenosynovitis (especially septic tenosynovitis) and septic arthritis is essential to determining appropriate treatment, including surgical options. The patient's current examination findings demonstrate classic Knavel signs of flexor tenosynovitis: flexed posture of the affected digit, tenderness along the tendon sheath to palpation, fusiform swelling, and pain with passive movement. The finding that points to flexor tenosynovitis in this patient is the anterior localization of flexor tendon surface involvement; pain and swelling centered at the PIP joint on the dorsal aspect of the digit would have instead aroused suspicion for septic arthritis. On the basis of this information, the most appropriate course of action would be admission to the hospital for administration of broad-spectrum antibiotics until therapy could be tailored to an identified causative organism. An orthopedic surgeon should be urgently consulted to evaluate the extent of infectious involvement, to obtain biopsy specimens, and to perform surgical debridement, if necessary. Pseudoseptic reactions, ie, acute flares that can occur with hyaluronate injections and typically last hours vs weeks, are not associated with symptomatic progression or systemic symptoms such as fever.
Our patient was admitted to the hospital for emergency treatment, at which time he underwent incision and drainage with open carpal tunnel release and tenosynovectomy of the right wrist, hand, and ring and long fingers. Nonmal-odorous gross purulence was noted with copious amounts of thick, yellowish, adherent boggy synovium and dark yellow, gelatinous tenosynovial tissue with a “fish-flesh” consistency.
- 3.Which one of the following is the most likely explanation for this patient's operative findings?
- a.Iatrogenic infection of the joint space due to corticosteroid injection
- b.Flare of a subclinical bacterial infection after corticosteroid injection
- c.Autoimmune destruction of synovial tissue in response to injection particulate triggers
- d.Hematogenously seeded infection
- e.Tuberculous tenosynovitis
- a.
The risk of iatrogenic infection as a result of joint injection is extremely rare (about 1 in 10,000 procedures). Although acute worsening in symptoms after an injection is of concern because of the possibility of introducing bacteria into the joint space and causing septic arthritis, the intraoperative findings in our patient of marked tissue destruction of the tenosynovial tissues make a diagnosis of recent iatrogenic infection unlikely. The flare of a subclinical infection would be the most likely diagnosis, given the progression of symptoms for 48 hours or longer after injection with glucocorticoids, which could cause suppression of local immune-mediated processes acting to control an infection.
Autoimmune tissue degradation is not characterized by gross purulence, and the presence of streaking erythema is suggestive of an infectious process. Hematogenous seeding is thought to be responsible for most cases of joint sepsis but not for infections of deep-tissue spaces, such as that found in this patient with septic tenosynovitis. Tuberculous tenosynovitis, an extremely rare extrapulmonary manifestation of tuberculosis, could conceivably cause such tissue changes; however, it would be improbable in a patient without other suspect clinical symptoms or a high risk for tuberculosis (ie, elderly or immunocompromised patients, an immigrant from an endemic area, or a member of a prison population).
Multiple cultures of surgical specimens were obtained. Results of Gram stains were negative, but those of acid-fast stains were positive. An infectious disease consultation was obtained after empiric therapy was initiated; bacterial and fungal cultures are pending.
- 4.On the basis of the current findings in this patient, which one of the following antibiotics would provide the most appropriate empiric coverage?
- a.Imipenem-cilastatin sodium, amikacin sulfate, clarithromycin, ethambutol hydrochloride (HCl), and rifampin
- b.Vancomycin HCl and clindamycin
- c.Rifampin and ethambutol HCl
- d.Imipenem-cilastatin sodium and gentamycin sulfate
- e.Imipenem-cilastatin sodium, gentamycin sulfate, and fluconazole
- a.
The first step in treatment would be to ensure coverage for acid-fast bacilli (the presence of which was established by initial Gram stains), as well as broad-spectrum coverage for possible superinfection with gram-positive skin flora such as methicillin-resistant Staphylococcus aureus, gram-negative organisms such as Pseudomonas species, and anaerobes. Only the combination of imipenem-cilastatin, amikacin sulfate, clarithromycin, ethambutol HCl, and rifampin would meet all these criteria. Vancomycin HCl and clindamycin would not provide antibacterial coverage for mycobacterial infections. A combination of rifampin and ethambutol HCl would treat mycobacterial infections, as well as some gram-negative infections (such as Neisseria meningitidis). However, rifampin is more commonly used for synergy and not as a sole agent in broadening coverage of gram-positive infections, and rifampin and ethambutol HCl would not be the preferred combination for broad-spectrum coverage. Imipenem-cilastatin sodium and gentamycin sulfate would provide broad coverage against gram-positive, gram-negative, and anaerobic organisms; however, this combination would not provide appropriate empiric coverage for acid-fast bacilli. Addition of fluconazole would confer antifungal but not antimycobacterial activity.
While awaiting test results for microbiologic identification and susceptibilities, we treated the patient empirically with imipenem-cilastatin, amikacin sulfate, clarithromycin, ethambutol HCl, and rifampin. Serologic findings were negative for human immunodeficiency virus and coccidioidomycosis, and findings of tuberculin skin tests were likewise negative. A plain radiograph of the chest revealed only a small, incidental, calcified granuloma in the left lower lobe. No bacterial, fungal, or viral growth was noted on surgical tissue cultures.
The patient underwent 2 further operative irrigation and debridement procedures with partial wound closure. The acid-fast bacilli were subsequently identified. After being given the diagnosis, the patient recalled having submerged his hand in the family's fish tank to adjust heater settings shortly after his initial sander injury.
- 5.Given this additional history, which one of the following is the most likely causative organism?
- a.Vibrio vulnificus
- b.Mycobacterium tuberculosis
- c.Mycobacterium avium complex
- d.Aeromonas species
- e.Mycobacterium marinum
- a.
Although V vulnificus is one of the most common causes of waterborne infection, it is not an acid-fast bacillus but rather a gram-negative bacterium. It is acquired from wound exposure to contaminated waters or shellfish, which have the ability to concentrate the bacteria. Although M tuberculosis is capable of causing tenosynovitis such as that observed in our patient, neither it nor M avium complex causes waterborne infections, and both are therefore unlikely culprits. Aeromonas species inhabit the foregut of leeches and can be acquired through leech attachment and disruption of skin (as a result of swimming in leech-inhabited waters) or via medical therapy with leeches for relief of venous congestion at surgical sites; neither scenario was relevant to our patient's case. Only M marinum is both an acid-fast and waterborne bacillus; it is commonly acquired from exposure to the contents of a fish tank and thus is the most likely causative organism of our patient's infection.
The acid-fast bacilli were confirmed to be M marinum via DNA probe identification. After a 12-day hospitalization, our patient was discharged home with his finger immobilized in a preformed orthoplast hand splint; he received trimethoprim-sulfamethoxazole and clarithromycin pharmacotherapy, as well as extensive outpatient occupational therapy for compromised right hand function, decreased range of movement, and scar tissue management. After 6 months of antibiotic treatment and occupational therapy, the patient was noted to have no evidence of infection and a nearly complete return to full function in his right hand.
DISCUSSION
M marinum infection (otherwise known as fish tank granuloma) is a rare cause of chronic granulomatous flexor tenosynovitis that leads to substantial morbidity in the hand.
1
Treatment can be delayed by months or even years because of a lack of consideration of this diagnosis.In general, M marinum infection is 1 of the 5 most common bacterial soft-tissue infections that arise as a complication of skin and soft-tissue injuries that are exposed to aquatic environments or marine animals. The other 4 common waterborne infectious bacterial species are Aeromonas species, Edwardsiella tarda, Erysipelothrix rhusiopathiae, and V vulnificus.
Patients typically present with an M marinum infection after a traumatic injury, such as a puncture wound caused by fishhooks or fish spines or lacerations caused by boat motor propeller blades. M marinum is found in bodies of both salt and fresh water, including fish tanks.
In immunocompetent hosts, an M marinum infection typically has an indolent course, with initial papules on elbows and knees, followed by progression to shallow ulcerations and scar formation. Involvement of regional lymph nodes or invasion of deeper structures is not uncommon. In 1 case series of 31 patients with M marinum cutaneous disease, 27 patients (87%) had upper extremity involvement, and 25 patients (81%) had lymphatic or local spread at initial examination or during the observation period.
2
Testing of wounds should include Gram stains and staining for acid-fast bacilli, as well as cultures of soft-tissue drainage specimens or biopsy specimens. Optimally, culture sets should be incubated on 2 different culture media at 2 different temperatures: (1) the standard agar plate with incubation at 37°C for typical pathogens and (2) the Lowenstein-Jensen medium with incubation at 28°C to 30°C (with observation for up to 6 weeks) when an atypical mycobacterium is suspected.
3
Blood cultures should be added to the testing when systemic toxicity is suspected or in patients with underlying cirrhosis or cancer. In immunocompromised hosts, M marinum has been described as causing bacteremia, septic arthritis, osteomyelitis, and other systemic complications.
4
Broad-spectrum antibiotics should be administered against the more common S aureus and β-hemolytic streptococci skin pathogens, as well as polymicrobial flora typical of infections caused by waterborne bacteria.
4
Isolates of M marinum have shown susceptibilities to clarithromycin, sulfonamides, tetracyclines, rifampin, and ethambutol HCl.
3
Ciprofloxacin is not recommended because of the prevalence of resistant strains and the potential for mutational resistance with immunotherapy. Although no comparative trials of treatment regimens for skin and soft-tissue infections due to M marinum have been conducted, current American Thoracic Society guidelines recommend treatment with 2 active agents for 1 to 2 months after resolution of symptoms, with a typical course of treatment lasting 3 to 4 months.3
Rifampin could be added in cases of osteomyelitis or other deep-structure infection. Susceptibility testing is generally reserved for cases of treatment failure.In addition to antibiotic therapy, surgical debridement could be required for patients with necrotizing or deepspace infections, as well as for patients with a disease that has failed to respond to standard therapy.
Physicians' awareness of the possibility of infection by an atypical mycobacterium, as well as by other waterborne infectious pathogens, could promote timely diagnosis, appropriate laboratory orders and surgical specimens, correct and adequate therapy, and a substantial reduction in morbidity resulting from this type of infection.
REFERENCES
- Mycobacterium marinum as a cause of chronic granulomatous tenosynovitis in the hand.J Infect. 2007 Jun; 54 (Epub 2007 Jan 4.): 584-588
- Mycobacterium marinum skin infections: report of 31 cases and review of the literature.Arch Intern Med. 1994; 154: 1359-1364
- ATS Myocobacterial Diseases Subcommittee. An official ATS/IDSA statement: diagnosis, treatment, and prevention of nontuberculous mycobacterial diseases.Am J Respir Crit Care Med. 2007; 175: 367-416
- Mycobacterium marinum infection causing septic arthritis and osteomyelitis.Br J Rheumatol. 1997; 36: 1207-1209
Article info
Footnotes
This article was presented in part at Academic Excellence Day, Banner Good Samaritan Regional Medical Center, Phoenix, AZ, May 2, 2007.
Identification
Copyright
© 2008 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc. All rights reserved.
