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Case report |
Departments of 1 Radiology and 2 Pulmonology and Critical Care, Department of Medicine, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa
Correspondence: Dr Fathima Vawda, Principal Radiologist/Lecturer, Department of Radiology, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, Durban, Private Bag 7, Congella, Durban 4013, South Africa. E-mail: vawdaf{at}webmail.co.za; vawdaf1{at}ukzn.ac.za
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A septic screen, which included microscopy and culture of endotracheal aspirates, blood and urine samples, was negative for bacteria, acid-fast bacilli and fungal organisms.
Chest radiograph (Figure 1
) demonstrated a large right paratracheal mass lesion. CT-guided biopsy of the right paratracheal mass was performed. The CT (Figure 2a) revealed a right paratracheal and retrotracheal mass causing marked attenuation of the tracheal lumen. An associated consolidative infiltrate was noted.
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Cerebrospinal fluid analysis yielded a negative cryptococcal antigen and culture result. A human immunodeficiency virus enzyme-linked immunosorbent assay (ELISA) screen was negative.
Treatment was initiated with intravenous fluconazole 400 mg twice daily for a period of 3 weeks followed by 400 mg of oral fluconazole daily for 10 weeks. The patient required ventilation for a period of 26 days. The hypoxaemia secondary to airway compromise was exacerbated by ventilator-associated complications, namely a right-sided pneumothorax and Proteus mirabilis pneumonia. The latter infection was treated with intravenous amoxicillin/clavulanic acid 1.2 g three times daily for 6 days.
On a follow-up CT examination of the chest (Figure 2b
), performed 3 weeks after the initiation of antifungal therapy, there was a reduction in the degree of lymphadenopathy and re-establishment of airway patency.
Ultrasound examination at 32 weeks' gestation revealed no fetal abnormalities. The patient at this stage demonstrated significant symptomatic improvement and was discharged. The patient failed to return for follow-up examination following discharge to her local obstetric unit.
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Discussion |
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The prevalence of cryptococcosis among patients with cell-mediated immune defects is well recognized, occurring particularly in the context of human immunodeficiency virus-related [3] and transplant-related immunosuppression [4]. Other purported immunosuppressive causes include malignancies and corticosteroid treatment [4]. The occurrence of cryptococcosis among patients who are immunocompetent is also widely accepted. However isolated pulmonary cryptococcosis in an immunocompetent pregnant or parturient patient remains a rare entity with few documented cases in the literature [5, 6]. In this subset of patients, cryptococcal meningitis or disseminated cryptococcosis is more commonly reported [5].
The pregnant host undergoes several physiological immune system adjustments, designed primarily to prevent rejection of the antigenically different fetus. Reduction in lymphocyte proliferative response [7, 8], natural killer cell activity and helper T-cell pool occurs [9]. The altered hormonal parameters of pregnancy make further contributions to the depressed cell-mediated immune response [10]. Maximum changes occur in the third trimester of pregnancy with normalization at 3–5 months postpartum [7, 9]. A consequence of this physiological reduction in maternal cell-mediated immunity is enhanced susceptibility of the gravida to pathogens, which require a cell-mediated immune response, including fungal organisms [11, 12]. Cryptococcosis may thus have a more rapidly progressive course in a pregnant host [11]. Pre-existing maternal disease, anaemia, use of illicit drugs, alcohol and tobacco represent further identifiable predisposing factors for pneumonia in a pregnant patient [13].
The primary pulmonary–lymph node complex comprises a primary pulmonary focus with lymphogenous involvement of hilar lymph nodes. Very early reports [14] questioned the existence of the primary pulmonary–lymph node complex in cryptococcosis. It is now a recognized entity which has been described in pathological studies [15, 16] that reviewed lymph node material from autopsy or post-thoracotomy cases. The primary lymph node complex in cryptococcosis is rare in comparison with its occurrence in childhood tuberculosis and histoplasmosis. The cryptococcal complex in the immunocompetent host comprises small, circumscribed pulmonary and lymph node granulomas, which probably accounts for its uncommon radiographic visualization. In the immunocompromised host, diffuse cryptococcal pneumonia with massive lymphogenous spread results in large diffuse lesions of lymph nodes [15].
The radiographic pattern of pulmonary cryptococcal disease, and in particular radiographic evidence of cryptococcal lymphadenopathy, correlates to a large degree with the underlying immune status of the host. Although some overlap exists, cryptococcal lymphadenopathy has been shown in several studies [17, 18] to correlate more closely with an immunocompromised status.
Lymphadenopathy and pulmonary interstitial infiltrates are the dominant radiographic manifestations in human immunodeficiency virus-infected hosts. Large nodules, masses or consolidative infiltrates are uncommonly seen, being more prevalent in immunocompetent hosts and among hosts immunocompromised by conditions other than human immunodeficiency virus infection [17].
Immunocompetent hosts more often have a morphological pattern of solitary or multiple nodular opacities [18, 19] attributable to intact cell-mediated localization of the cryptococcal infection. There is a lower incidence of lymphadenopathy in immunocompetent hosts [19, 20]. In a study [18] that compared the radiological appearance of thoracic cryptococcosis in relation to the immunological competence of the host, lymphadenopathy was not observed in the immunocompetent subset of patients.
The human immunodeficiency virus-negative immunocompromised host more often demonstrates extensive disease, with a wider spectrum of radiographic abnormalities including nodules, masses, cavitary lesions, consolidative infiltrates, pleural effusions and lymphadenopathy [18].
Massive lymphadenopathy, which is more usually associated with other granulomatous diseases, especially histoplasmosis, has very occasionally been described in pulmonary cryptococcosis involving immunocompetent non-pregnant patients [21, 22]. Feigin [21] in his radiological–pathological study of the granulomatous form of pulmonary cryptococcosis detected lymph node enlargement radiographically in eight cases and suspected it in a further two. In two of the eight cases lymphadenopathy was documented as marked, both cases occurring in immunocompetent non-pregnant patients. The third case of massive lymphadenopathy in this series [21] occurred in a proboscis monkey. Sinha and co-authors [22] described a mediastinal cryptococcoma, with infiltration of the tracheobronchial tree, in an immunocompetent non-pregnant patient. Although Gordonson et al [23] described massive lymphadenopathy in 3 of 26 patients with pulmonary cryptococcosis the findings of this study were not distinguished according to the immune status of patients, limiting comparison.
Literature addressing the morphological patterns of pulmonary cryptococcosis and, in particular, the prevalence of lymphadenopathy in immunocompetent pregnant or parturient hosts is limited. In a case series of four immunocompetent pregnant or parturient patients with isolated pulmonary cryptococcosis, Ely et al [5] reported a single case of radiographically evident lymphadenopathy but without massive involvement. LaGatta et al [6] reported a human immunodeficiency virus-negative case of isolated pulmonary cryptococcosis diagnosed at 3 weeks postpartum, with radiographic appearances of multiple pulmonary nodules, consolidative infiltrates and perihilar fullness.
To our knowledge, the present case provides the first report of massive mediastinal lymphadenopathy in an immunocompetent pregnant patient with isolated pulmonary cryptococcosis. Given the rarity of isolated pulmonary cryptococcosis occurring in immunocompetent pregnant or parturient hosts, the current case report serves to expand on the morphologic patterns of disease possible in this unique subset of affected patients.
Received for publication June 25, 2006. Revision received November 13, 2006. Accepted for publication November 15, 2006.
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