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: Bacteria
Phylum: Actinobacteria
Order: Actinomycetales
Suborder: Corynebacterineae
Family: Nocardiaceae
Genus: 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 MichaelisGutmann 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 thickwalled 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 extendedspectrum 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/2008/02/080226115618large.jpg
• http://labmed.bwh.harvard.edu/microbiology/teaching/ca
ses/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