Disseminated Rhodococcus equi infection in HIV infection despite highly active antiretroviral therapy

Abstract

Background: Rhodococcus equi (R.equi) is an acid fast, GRAM + coccobacillus, which is widespread in the soil and causes pulmonary and extrapulmonary infections in immunocompromised people. In the context of HIV infection, R.equi infection (rhodococcosis) is regarded as an opportunistic disease, and its outcome is influenced by highly active antiretroviral therapy (HAART).

Case presentation: We report two cases of HIV-related rhodococcosis that disseminated despite suppressive HAART and anti-rhodococcal treatment; in both cases there was no immunological recovery, with CD4+ cells count below 200/μL. In the first case, pulmonary rhodococcosis presented 6 months after initiation of HAART, and was followed by an extracerebral intracranial and a cerebral rhodococcal abscess 1 and 8 months, respectively, after onset of pulmonary infection. The second case was characterized by a protracted course with spread of infection to various organs, including subcutaneous tissue, skin, colon and other intra-abdominal tissues, and central nervous system; the spread started 4 years after clinical resolution of a first pulmonary manifestation and progressed over a period of 2 years.

Conclusions: Our report highlights the importance of an effective immune recovery, despite fully suppressive HAART, along with anti-rhodococcal therapy, in order to clear rhodococcal infection.

Figure 1

Central nervous system (CNS) immune reconstitution white matter lesions and R. equi brain abscesses by Magnetic Resonance Imaging (MRI) (case report 1). a-c. Brain lesions at the onset of focal neurological symptoms. a. Axial FLAIR brain sequence showing non specific asymmetric bilateral hyperintensity in the subcortical region, expression of immune recconstitution inflammatory reaction. b. Axial FLAIR sequence showing abscessual lesion, surrounded by oedema, in the right temporal region. c. Gadolinium (Gd)-T1 sequence shows the presence of nodular enhancement of the right temporal lesion. d-f. Evolution of brain lesions 1 month after onset of symptoms. d. Axial FLAIR sequence shows the persistence of the non specific white matter hyperintensity; e. Axial FLAIR sequence shows an increase of lesion size and oedema of the right temporal lesion; f. Gd-T1 sequence shows the evolution of contrast enhancement, now presenting as ring enhancement, typical of an abscessual lesion.

Figure 2

R. equi lesions in disseminated infection (case report 2). a Chest radiograph (May 2005) shows a non specific subpleural opacity in the right upper lobe without evidence of pleural effusion. b Contrast enhanced multidetector computed tomography (MDCT)(May 2005). A scan at the level of the main bronchi demonstrates a subpleural focal consolidation in the right upper lobe. There is no evidence of lymphoadenopathy or pleural effusion. c, d Contrast enhanced magnetic resonance imaging (MRI) of the right thigh (August 2009). The axial T2 sequence (c) and the axial T1 contrast enhanced sequence with fat suppression (ccGRE T1FS) (d) show an oval shaped enhancing mass in the vastus medialis muscle with central area of necrosis and oedema of the surrounding tissue and muscle. e Positron emission tomography (PET) and computed tomography (CT) images (August 2009) show focal increased fluodeoxyglucose (FDG) uptake in the upper lobe of the right lung and in the spleen, which is larger than normal, a large area of increased uptake in the right lower abdomen consistent with colon localization, and an irregular area of increased FDG uptake in the soft tissue of the right proximal thigh. f MDCT of the abdomen (March 2010). A scan through the lower abdomen shows a large obstructing mass in the right colon with stranding of the pericolonic fat and several enlarged lymph nodes. g Cutaneous nodular rhodococcal lesions (March 2010). h Brain axial T2 weighted sequence (August 2010) shows multiple (right temporal, left mesial occipital, left temporoinsular) expansive oedematous lesions. All the lesions show central hypointensity and peripheral hyperintensity. Oedema is also present in right occipital and anterior temporal lobes. i Brain axial T1 weighted sequence after Gd injection (August 2010) shows enhancement of the two nodular lesions in right temporal region and in left occipitomesial lobe. Smooth cortical enhancement is also seen in the left occipital lobe.