Vol. 21, No. 3
THE JOHNS HOPKINS MICROBIOLOGY NEWSLETTER
Tuesday, January 29, 2002
B. The Johns Hopkins Hospital, Department of Pathology, Information
provided by M. Ali Ansari-Lari, MD, Ph. D.
Case description:
The patient is a 4 year old white male with a past medical history significant for fulminant liver failure status post orthotopic liver transplant (3/2000), complicated by subsequent development of aplastic anemia (4/2000), status post left upper lobe resection of the lung for aspergillosis (5/2000), and currently on chronic immunosuppression. The patient was recently discharged on 11/17/01 after treatment with ceftriaxone for an upper respiratory tract infection and a positive blood culture for Rhodococcus equi. He was sent home on amoxicillin/clavulanate. He was readmitted on 11/27/01 for a one-day history of fever of 38.3 C, vomiting and headache. Laboratory data was significant for total white blood cell count of 4,630, hemoglobin of 10.2, and a platelet count of 77,000. His chest X-ray was within normal limits. Prior to initiation of ceftriaxone, one of his blood cultures returned positive for Rhodococcus equi. The infection was felt to be a low-grade bacteremia without any sign of disseminated disease. His central line was removed, his ceftriaxone was discontinued and he was discharged to home on a 5-day course of azithromycin and rifampin.
Rhodococcus equi
Organism:
Rhodococcus equi, previously known as Corynebacterium equi
and Mycobacterium rhodochrous, belongs to the suprageneric taxon
nocardioform actinomycetes. It is a strictly aerobic, facultative intracellular
gram-positive coccobacillus that primarily causes zoonotic infections,
but uncommonly can infect humans.
Epidemiology:
Rhodococcus species are widely distributed in soil and have
been found in bovine, porcine, and equine fecal flora. R. equi can
cause pulmonary infections in foals and other domestic animals (e.g. cattle,
pigs, horses). Human infection is believed to primarily occur via a respiratory
route as a result of contact with infected animals, animal carriers, or
soil. Acquisition through the oral route and by traumatic inoculation or
superinfection of wounds have been documented. It grows best at temperatures
between 18-29 C, in a dry environment. The population at risk includes
immunocompromised patients, especially those with AIDS, transplant recipients,
and patients with lymphoma, leukemia, diabetes mellitus, alcoholism, and
chronic renal failure. Rare cases of R equi infections in immunocompetent
hosts have been reported. The reported mortality rates from R. equi
infection among immunocompetent, non-HIV- immunocompromised, and HIV-infected
patients were 11%, 20-25% and 50-55%, respectively. The significant mortality
rate among immunocompetent patients may be due to misidentification or
inappropriate initial antibiotic therapy.
Clinical features:
The primary site of infection is pulmonary. Usually, patients have
a slowly progressive granulomatous pneumonia, resulting in development
of cavitary lesions that may be mistaken for tuberculosis. The course of
infection in patients with AIDS can be more severe with invasive pneumonia
and dissemination to the brain, liver, spleen and other organs The presenting
symptoms depend on the site of infection. The symptoms of pulmonary infection
develop insidiously and include cough, dyspnea, hemoptysis, pleuritic chest
pain, and fever. Radiologic findings include cavitary lesions in lung (50-70%)
and pleural effusion (18-34%). Other sites of infection may cause abscesses
of the central nervous system, pelvis and subcutaneous tissue, lymphadenitis,
endophthalmitis, arthritis, osteomyelitis, and meningitis.
Diagnosis:
Culture is performed from biopsy or aspirate obtained form the site
of infection. Positive blood cultures for R equi range from 30%
in immunocompetent patients and 80-100% in HIV-infected patients. The organism
has been isolated from sputum and bronchioalveolar lavage specimens. On
blood agar, the organism forms mucoid and coalescing colonies that develop
salmon-pink to red-orange pigmentation after 2-3 days of incubation, and
grows as rod-shaped cells, which fragments into coccoid cells. Like Nocardia,
it may be partially acid fast using the modified Kinyoun stain. Other tests
such as synergistic hemolysis by cross streaking on sheep blood agar with
any number of bacteria (e.g. S. aureus) may be helpful in identification.
In our laboratory, identification is made using cellular fatty acid analysis.
R. equi yields a very characteristic fatty acid profile. Histological
examination of the infected tissues may reveal numerous neutrophils with
intracellular pleomorphic bacteria, microabscesses, and malakoplakia.
Treatment:
R. equi is commonly susceptible to erythromycin, rifampin, ciprofloxacin, vancomycin, aminoglycosides, imipenem, and meropenem, variably susceptible to clindamycin, ceftriaxone, TMP-SMX, tetracycline, and chloramphenicol, and usually resistant to penicillin G, oxacillin, ampicillin, carbenicillin, and cefazolin. The duration and route of administration of antibiotic(s) varies and depends on the severity and the site of infection.
Immune response:
Cell mediated immunity appears to have a primary role in host defense against R. equi. CD4+ Th1 cells expressing gamma interferon are important in clearance of R. equi from the lungs of mice. Furthermore, using a murine model, the killing of R equi appears to depend on generation of peroxynitrite by gamma-interferon activated macrophages. Humoral immunity may also have a role in protection against R. equi.
References:
1. Linder, R. Rhodococcus equi and Arcanobacterium haemolyticum: two "coryneform" bacteria increasingly recognized as agents of human infection. Emerg Infect Dis. 1997; 3:145-153.
2. Darrah, PA et al. Cooperation between reactive oxygen and nitrogen intermediates in killing of Rhodococcus equi by activated macrophages. Infect Immun. 2000; 68: 3587-3593
3. Kedlaya et al. Rhodococcus equi infections in immunocompetent hosts: case report and review. Clin Infect Dis. 2001; 32: e39-e46.
4. Koneman et al. Color Atlas and Textbook of Diagnostic
Microbiology, 5th Edition, Lippincott-Raven, Philadelphia,
1997.
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