Rhodococcus
Chetan Jinadatha MD, MPH
Introduction
• Rarely produces infection in humans
• First reported case in 1967
• Increased incidence as an oppurtunistic infection
• Originally was names a Corynebacterium equi
• Was orginally isolated from foals with pneumonia
Microbiology
Rhodococcus Scientific classification
Kingdom: BacteriaPhylum: ActinobacteriaOrder: ActinomycetalesSuborder: CorynebacterineaeFamily: NocardiaceaeGenus: Rhodococcus
Microbiology
• Aerobic and grows on non selective media at 37°C
• Non sporulating• Non motile• Gram positive can be acid fast• Rod-to-coccus growth cycle variation• Presence of tuberculostearic acid and cell wall
mycolic acids• Large, smooth, irregular, highly mucoid colonies
develop by 48 hours
Microbiology
• Initially colorless• After 4-7 days they may develop salmon pink
colored colonies• Solid media: cocci• Liquid media: long rods• May be acid fast• LJ media may promote it
Microbiology
• Gelatinase-negative• Catalase positive• Urease positive• Oxidase negative • Equi factors interact with the products of other
organisms, including the beta toxin of Staphylococcus aureus, to produce hemolysis (CAMP test)
• Commercial panels: API Rapid CORYNE®, bioMérieux Vitek Inc., Hazelwood, MO
Pathogenesis
• Granulomatous reaction: macrophages filled with granular cytoplasm that is periodic acid Schiff (PAS) stain-positive and may contain large numbers of gram-positive coccobacillary forms
• Malacoplakia: chronic granulomatous inflammation characterized by aggregates of PAS positive histiocytes containing lamellated iron and calcium inclusions named Michaelis-Gutmann bodies.
Clinical Manifestations
• Adults and children can be affected
• Mostly affects immunocompromised population especially HIV
• Can cause pulmonary, blood, CNS, skin and soft tissue, bone and joints, vitreous fluid, indwelling devices, and ENT.
Pulmonary Infections
• Most common form of human disease
• Accompanying extrapulmonary infection ~ 18 percent
• Extrapulmonary sites without evidence of pulmonary involvement ~ 24 percent
• Usually a chronic infection
• Can occur in immunocompetant host
Pulmonary Infections
• High fever, cough with/without phlegm, fatigue, chest pain, +/- hemoptysis.
• Cavitation ~ 50%
• Pleural effusion ~20%
• Recurrent pneumothorax can occur
• Multiple pulmonary nodules can occur
Extra-pulmonary Infection
• Most common sites: Brain and subcutaneous tissue
• Wound infections — Septic arthritis, cellulitis, meningitis; endophthalmitis following corneal lacerations.
• Peritoneal catheter-related infections
• Fever and isolated bacteremia: in patients with central venous catheters, neutropenia, or recent chemotherapy associated with underlying malignancies
• Cervical or mesenteric lymphadenitis, peritonitis, and pelvic and/or paraspinous masses
Diagnosis
• High index of suspicion
• Gram positive coccobacillus or acid fast organism from an immunocompromised patient with cavitary lung disease should raise suspicion for R. equi infection
Radiology
Immunocompromised (Non HIV/AIDS)
• commonly causes consolidation
• May evolve to a thick-walled cavity
• Slightly lower rate of bacteremia
HIV/AIDS• Frequently produces
a cavitary lesion in HIV
• Higher rate of accompanying bacteremia
Treatment
• Frequently resistant to a number of agents • In vitro susceptibilities methods of this pathogen
to antibiotics are not standardized • Combination antimicrobial therapy should be
used in immunocompromised hosts. • Usually susceptible to erythromycin and
extended spectrum macrolides, rifampin, fluoroquinolones, aminoglycosides, glycopeptides, amp-sulbatum and imipenem
Treatment
• 2/3rd are susceptible to clindamycin, chloramphenicol, tetracyclines, and trimethoprim-sulfamethoxazole
• Most human isolates are resistant in vitro to penicillins and cephalosporins
• Beta-lactams probably should be avoided, even if initial susceptibility testing is favorable, since resistance has been shown to develop during therapy
• The emergence of resistance during treatment has also been demonstrated with doxycycline, rifampin, and TMP-SMX
Treatment
• In vitro susceptibility findings should guide selection (excluding penicillins and cephalosporins); in vitro studies of synergy/antagonism of combinations can be considered.
• In immunocompetent persons, single agent therapy may be sufficient, probably best provided with an extended-spectrum macrolide or fluoroquinolone.
• In immunocompromised persons, two or more agents should be initiated, at least one of which should have excellent penetration into macrophages.
CNS Treatment
• Vanc penetrates CNS variably, so we may need to measure vanc levels in CSF
• Rifabutin instead of Rifampin in HIV patients on PI’s
• Multiple agents with good CNS penetrations should be used
Therapy Duration
• Initial therapy in immunocompromised persons: at least two months secondary to frequent relapses following shorter courses
• Longer initial therapy with persistence of radiographic or clinical evidence of infection
• Initially IV, PO can be used in cases where the initial response was good (still 2 or more months)
• surgical resection of infected tissue combined with antimicrobial therapy has improved survival
• secondary prophylaxis for persistently immunosuppressed patients
References
• www.sciencedaily.com/images/2008/02/080226115618-large.jpg
• http://labmed.bwh.harvard.edu/microbiology/teaching/cases/bacteriology/rhodococcus/Rhodococcus.CAMP.jpg
• http://path.upmc.edu/cases/case146/images/micro19.jpg• http://wever.files.wordpress.com/2008/02/rha1.jpg• http://www.scielo.br/img/revistas/jbpneu/v32n5/e06f3.jpg• http://www.scielo.br/img/revistas/clin/v62n6/20f2.jpg• http://www.aids-images.ch/slides/1085,700,600,0,0.jpg• www.uptodate.com• www.wikipedia.com