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