Uche, Chukwudum MD*; Silibovsky, Randi MD*; Jungkind, Donald PhD†; Measley, Robert MD*
*Division of Infectious Diseases and †Clinical Microbiology and Laboratory, Thomas Jefferson University Hospital, Philadelphia, PA.
Address correspondence and reprint requests to Chukwudum Uche, MD, Division of Infectious Diseases, Thomas Jefferson University Hospital, 125 S 9th St, Suite 403, Philadelphia, PA 19107. E-mail: email@example.com.
A 60-year-old woman was admitted to Thomas Jefferson University Hospital, Philadelphia, PA, on July 12, 2006, with complaints of fever and generalized weakness for 2 days. She denied loss of consciousness, alteration in mental status, neck stiffness, and photophobia. She had a history of grade 1 subarachnoid hemorrhage in August 2003, requiring an anterior communicating artery clipping and a ventriculoperitoneal shunt (VPS). In October 2003, she had a VPS revision for shunt malfunction and wound dehiscence. Other medical and surgical history included hypertension, bunion surgery, and an allergy to sulfa drugs. She was on levetiracetam and irbesartan.
On physical examination, she appeared acutely ill. Her temperature was 100.5°F, and her pulse was 98 beats per minute, respiratory rate was 18 breaths per minute, and blood pressure was 154/99 mm Hg. She was alert and fully oriented with a normal neurological examination. Her VPS was pumping and refilling normally. Her neck was supple. Examinations of the face, eyes, ears, nose, throat, cardiorespiratory system, abdomen, and skin were unremarkable.
Laboratory data included a white blood cell count of 10,400 cells/μL with neutrophils 78%, lymphocytes 13%, and normal basic metabolic profile. Computed tomographic scan of the abdomen showed anterior mid-intra-abdominal phlegmon and right anterior abdominal subcutaneous fluid at the distal end of the VPS. A VPS tap was performed and clear, colorless cerebrospinal fluid (CSF) was obtained. Cerebrospinal fluid opening pressure was 5 cm H2O, and analysis revealed 4 red blood cells per microliter; 29 white blood cells per microliter with neutrophils 60%, lymphocytes 32%, and monocytes/macrophages 6%; glucose 75 mg/dL (serum glucose 119 mg/dL); and protein 21 mg/dL. Cerebrospinal fluid Gram stain showed many gram-positive bacilli. Intravenous (IV) vancomycin was started, and the VPS was externalized.
Repeat CSF examination on July 13 showed gram-positive bacilli on Gram stain and 2 days later showed gram-positive bacilli and gram-variable rods. The patient continued to have fevers. On July 16, acid-fast bacilli (AFB) was noted on CSF culture consistent with rapidly growing atypical mycobacteria. Subsequently, multiple CSF cultures grew AFB. Intravenous imipenem, amikacin, and clarithromycin were initiated. The VPS was removed on July 18, and the patient's fever resolved. Culture of the explanted VPS also grew AFB. She was discharged on the 3-drug antimycobacterial regimen.
On August 11, the referral laboratory identified the mycobacteria as Mycobacterium goodii by 16S rDNA sequencing. It was sensitive to imipenem, ciprofloxacin, amoxicillin clavulanate (Augmentin), cefoxitin, amikacin, tobramycin, kanamycin, doxycycline, gatifloxacin, moxifloxacin, trimethoprim/sulfamethoxazole, and linezolid. The isolate was resistant to azithromycin and clarithromycin. The antibiotic therapy was switched to IV imipenem and oral moxifloxacin.
On outpatient follow-up 11 days later, she was doing well and reported no symptoms. She had completed 5 weeks of imipenem and was continued on oral moxifloxacin monotherapy with an anticipated total length of treatment of 4 to 6 months. The neurosurgical team decided not to replace the VPS at that time. She was seen 2 months later and remained asymptomatic, with plans to take oral moxifloxacin for 1 more month. Three months after she had completed therapy, she was asymptomatic.
To the best of our knowledge, this is the first reported case of M. goodii VPS infection. Mycobacterial infections should be considered in similar situations when the Gram stain shows gram-positive or gram-variable rods.
Brown et al1 in 1999 demonstrated 3 taxonomic groups in the Mycobacterium smegmatis group: Mycobacterium smegmatis sensu stricto (group 1), M. goodii (group 2), Mycobacterium wolinskyi (group 3) by genetic studies including high-pressure liquid chromatography, 16S ribosomal DNA sequencing, and tobramycin susceptibility testing which shows tobramycin susceptibility, intermediate resistance, and resistance, respectively. Mycobacterium smegmatis group is distinguished from the other rapidly growing mycobacteria (Mycobacterium fortuitum and Mycobacterium chelonae abscessus group) by the general lack of susceptibility to the newer macrolides (eg, clarithromycin).2 Mycobacterium smegmatis group was considered a saprophyte of no clinical significance until recently. It is widely distributed geographically and is found in all parts of the United States. It has also been reported from Canada, Europe, and Australia.2
Mycobacterium goodii is a gram-positive, AFB and alcohol-fast bacillus that produces visible growth in 2 to 4 days. It initially produces nonpigmented smooth to mucoid off-white to cream-colored colonies on Middlebrook and trypticase soy agar. Most strains show a delayed (10-14 days) production of yellow to orange pigment. The colonies are negative for arylsulfatase and positive for nitrate reductase. 16S ribosomal DNA sequencing is useful for species confirmation. Isolates are susceptible to amikacin, ethambutol, and sulfamethoxazole; intermediately susceptible to ciprofloxacin, doxycycline, and tobramycin; variably susceptible to cefoxitin and clarithromycin; and resistant to isoniazid and rifampin.1,2
Brown et al1 studied 28 isolates of M. goodii collected over 19 years. Clinical information for these patients showed 12 cases of community-acquired wound and bone infections, 6 cases of nosocomial infections (2 of which were pacemaker site infection, 1 case of osteomyelitis after cardiac bypass surgery, and 1 case of infection after breast reduction surgery), 6 cases of respiratory infections (3 of which were in patients with lipoid pneumonia), and 4 other cases (1 of which had M. goodii in the CSF, but lacked further clinical information).
Several other case reports and series have reiterated the diverse range of infection by M. goodii. Mycobacterium goodii has been reported to cause blood stream infection and pacemaker lead infection3 and postcataract endophthalmitis.4 A case report series on nontuberculous mycobacteria in Zambia reported a case of a 66-year-old man with alveolar infiltrates and pleural effusion. Mycobacterium goodii was obtained from the culture of the pleural effusion.5 It has also been noted to cause olecranon bursitis in a 60-year-old man with a history of osteoarthritis, type 2 diabetes mellitus, and benign monoclonal gammopathy.6 Mycobacterium goodii abdominal wall abscess was also described in a patient who underwent inguinal hernia repair with a synthetic mesh,7 and an outbreak of M. goodii wound infection was identified in 3 patients who received surgical implants at a Colorado hospital. No source was identified.8
It is not clear if immunosuppression plays a role in M. goodii infection. Review of the literature suggests that traumatic or surgical wounds, IV catheters, and lipoid pneumonia may be risk factors. The length of antibiotic therapy is also unclear, but as for most rapidly growing mycobacteria, 4 months is adequate for mild disease and 6 months for serious disease.
Parenteral antibiotics should be used for the first 2 to 6 weeks. Surgical debridement and an attempt to remove foreign bodies are also important for therapeutic success.2
Among the other rapidly growing mycobacteria, only M. fortuitum has been reported to cause VPS9,10 and ventriculoatrial shunt infections.11 These are treated with prolonged antibiotic courses and device removal, which is very similar to our management in this case report.
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: case report. Neurosurgery
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