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PubMed1992

Activity of azithromycin against Mycobacterium avium infection in beige mice.

The comparative activities of azithromycin and clarithromycin and the activities of azithromycin alone and in combination with other antimycobacterial agents were evaluated in the beige mouse model of disseminated Mycobacterium avium complex infection. Azithromycin was similar in activity to clarithromycin. Azithromycin plus clofazimine plus ethambutol reduced the number of splenic organisms more than azithromycin alone, while the combination was less active than azithromycin alone for bacteria in lungs. Rifabutin had activity similar to that of azithromycin for organisms in spleens and lungs. Rifabutin plus azithromycin was more active than either agent alone for organisms in spleens, but the combination's activity was not significantly different from that of rifabutin for organisms in lungs. The activity of azithromycin against several M. avium complex isolates was evaluated. The reduction of viable cell counts in spleens ranged from 1.7 to 0.8 log units. For the three isolates studied, there was little correlation between the in vitro MIC and the in vivo activity.

Animals↗
PubMed1991

Immunomodulation of mouse macrophage killing of Mycobacterium avium in vitro.

When C57BL/6 mice were infected intravenously with Mycobacterium avium, bacterial growth continued within the spleen until more than 10(8) CFU/g of tissue were attained. This contrasted with Mycobacterium bovis BCG infections where growth declined after 2 weeks. In vivo M. avium-infected splenic macrophages were harvested from chronically infected mice and cultured in vitro for 4 days at 37 degrees C. The number of viable mycobacteria within the resulting macrophage monolayers decreased when cultured in the presence of autologous sensitized T cells and an exogenous source of interleukin-2 (recombinant interleukin-2; 50 U/ml) compared with untreated controls (P less than 0.05). Incubation of the infected macrophages with autologous T cells and soluble M. avium antigens also significantly reduced the number of viable organisms. These results indicate that the mycobactericidal activity of M. avium-infected macrophages can be enhanced in a way that may have important therapeutic implications for patients infected with this opportunistic pathogen.

Animals↗
PubMed1998

Disseminated aspergillus fumigatus infection: case report.

A case of disseminated aspergillus fumigatus infection is reported in a 43 year old Ugandan female with no known immune system disorder(not neutropenic and HIV-1 sero negative). She presented with multiple cutaneous ulcers, recurrent empyema thoracis, a past history of intra-abdominal abscess and bowel infarction. Empirical treatment for tuberculosis was previously given without improvement. A diagnosis of aspergillus fumigatus based on a combination of tissue wet potassium hydroxide preparation, fungal culture and tissue histologic typing was made. Despite antifungal therapy with intravenous amphotericin B infusion in 5% dextrose, after a normal baseline renal function test, the patient died in the second week of admission. Autopsy showed disseminated aspergillosis involving the pleural space, pericardium, spleen, and meningitis in addition to the cutaneous sites. Disseminated aspergillus fumigatus infection in a non-immunocompromised is rare antemortem diagnosis. This case highlights the difficulty in making a diagnosis in the face of many endemic conditions with similar presentation.

Adult↗
PubMed2004

Chronic pneumonia despite adaptive immune response to Mycobacterium bovis BCG in MyD88-deficient mice.

To assess the role of Toll-like receptor (TLR) signalling in host response to mycobacterial infection, mice deficient in the TLR adaptor molecule myeloid differentiation factor 88 (MyD88) were infected with the vaccine strain Mycobacterium bovis (BCG), and the immune response and bacterial burden were investigated. Macrophages and dendritic cells from MyD88-deficient mice stimulated in vitro with BCG mycobacterial antigens produced very low levels of proinflammatory cytokines, while the expression of costimulatory molecules such as CD40 and CD86 was preserved. Upon systemic infection with BCG (2 x 10(6) CFU i.v.) MyD88-deficient mice developed confluent chronic pneumonia with two log higher CFU than wild-type mice. Interestingly, the infection was controlled in liver and spleen and there was efficient systemic T-cell priming with high IFNgamma production by CD4+ splenic T cells in MyD88-deficient mice. Lung infiltrating cells showed IFNgamma production by pulmonary CD4+ T cells upon specific restimulation, and a reduced capacity to produce nitric oxide and IL-10. In summary, despite the dramatic reduction of the innate immune response, MyD88-deficient mice were able to mount an efficient T-cell response to mycobacterial antigens, which was however insufficient to control infection in the lung, resulting in chronic pneumonia in MyD88-deficient mice.

Adaptor Proteins, Signal Transducing↗
PubMed1998

A long-lasting interferon-gamma response is induced to a single inoculation of antigen-pulsed dendritic cells.

Vaccines against infectious organisms must produce not only long-lasting immunity but also the appropriate immune response to clear the infection. Obligate intracellular parasites, such as mycobacteria, require a predominantly cell-mediated immune response rather than antibody. Presentation of antigen by dendritic cells (DC) has been associated with the development of strong cell-mediated responses generating the production of interferon-gamma (IFN-gamma). This cytokine has an essential role in the elimination of mycobacteria. Therefore, we investigated both the duration and the nature of the immune response after priming with DC pulsed with mycobacterial antigen and compared this with priming using a conventional adjuvant. We used two strains of mice: C57BL/6, which inherently produces a T-helper 1 (Th1)-type response to mycobacterial antigen, and BALB/c, which does not. DC-enriched cell suspensions, purified DC or cultured bone marrow cells resembling DC (BMAPC) were prepared, pulsed overnight with PPD and injected intravenously (i.v.) into naive mice. Six and 12 weeks later, splenic T lymphocytes from these mice were challenged in vitro with antigen and their proliferative response and cytokine production was determined. Significant antigen-specific proliferation was observed in all assays on rechallenge with antigen in vitro 6 and 12 weeks after the initial priming with DC. IFN-gamma was detected in both strains but was only antigen specific in the C57BL/6 strain. Purified protein derivative (PPD)-pulsed BMAPC generated similar responses 6 weeks after priming. Thus, long-term T-lymphocyte responses and the production of IFN-gamma can be generated using a single inoculation of PPD-pulsed DC.

Animals↗
PubMed1995

Inflammatory response following intranasal infection with Mycobacterium avium complex: role of T-cell subsets and gamma interferon.

The role of CD4+ and CD8+ T cells in the response to intranasal infection with a Mycobacterium avium complex isolate (MAC) was investigated. Depletion of CD4+ T cells by injected antibody exacerbated infection in the lung, spleen, and liver. There were decreased numbers of inflammatory cells in the lungs of CD4-depleted mice and a significant decrease in lung cytotoxic activity. The neutrophil response was unaffected, and in CD4-depleted mice, unlike intact infected mice, these cells were found with large numbers of associated MAC. Purified CD4+ splenic T cells produced gamma interferon (IFN-gamma) in vitro in response to MAC antigen. IFN-gamma production by cultured spleen, lung, or mediastinal lymph node cells was markedly reduced in CD4-depleted mice. In contrast, CD8+ T cells did not produce IFN-gamma in vitro, and depletion of CD8+ T cells from infected mice had no effect on bacterial growth or lung cell activation. Depletion of IFN-gamma by injected monoclonal antibody had effects similar to those of CD4 depletion, namely, exacerbation of infection and decreased lung cell cytotoxicity. We conclude that CD4+ T cells are the main T cells involved in the lung response to MAC infection and that this response is at least partially dependent on the production of IFN-gamma.

Animals↗
PubMed1992

[Immunosuppressive macrophages induced in Mycobacterium avium complex infection induced in mice].

Profiles of generation and characteristic of splenic macrophages (M phi s), which suppress the ConA mitogenic response of splenic T cells, induced in mice during the course of Mycobacterium avium complex infections were investigated. In MAC-infected mice, reduction of ConA mitogenesis of spleen cells (SPCs) was seen after week 2 and the reduced state thereafter durated as long as at least for 8 weeks. Splenic M phi s with a potent suppressive activity against SPC mitogenesis were transiently induced around 2 weeks after infection. Splenic M phi s of BALB/c (MAC-susceptible) mice had similar but somewhat weaker suppressor activity, as compared to those of CBA/JN (MAC-resistant) mice. The suppressor activity of BALB/c M phi s durated much longer than did CBA/JN M phi s. MAC-induced splenic M phi s were markedly elevated in chemiluminescence and this coincided with increase in immunosuppressive activity. These M phi s inhibited the generation of IL-2-reactive T cell populations in response to ConA-signals, without showing any inhibitory effect against IL-2 producing ability of target T cells. Because immunosuppressive M phi s having the same characteristics were also induced in BALB/c athymic nude mice, thereby indicating that mature T cells are not prerequisite for induction of the present suppressor M phi s in MAC-infected host mice. Prostaglandins (PGs), nitric oxide radical (NO.) and free long chain fatty acids are thought to play certain role in the expression of suppressor action of MAC-induced M phi s, because of the following reasons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Effect of methanol extraction residue tubercle bacillus fraction treatment in vivo and in vitro on the release and activity of suppressor factor inhibiting the efferent phase of contact sensitivity in mice.

BALB/c mice subjected to injection of dinitrobenzenesulfonate (DNBSO3) and skin painting with dinitrofluorobenzene (DNFB) produce splenic T-suppressor (Ts) cells that, when transferred to DNFB-sensitized recipients, suppress the efferent (eff) phase of contact sensitivity (CS). Splenocyte populations containing such Ts-eff cells release a specific soluble suppressor factor (SSF) in vitro that similarly suppresses CS in sensitized recipient mice. Treatment with the methanol extraction residue (MER) tubercle bacillus fraction, a known immunomodulating agent, of animals exposed to DNBSO3 and DNFB ("DNBSO3-DNFB" donors) prevented release of SSF by their spleen cells at in vitro incubation. Incubation of DNBSO3-DNFB donor splenocytes with MER in vitro also abolished SSF release, and treatment with MER of test animals prior to DNFB sensitization prevented the suppressive action of subsequently administered SSF. The observations are discussed with regard to the potentiating capacities of MER on cellular immunity and states of resistance.

Adjuvants, Immunologic↗
PubMed2002

Autologous mixed lymphocyte responses in experimentally-induced arthritis of the Lewis rat.

Lewis rats develop immune-mediated arthritis following injection with a variety of agents including bovine type II collagen (bCII), mycobacteria, muramyl dipeptide and CP20961. Since susceptibility to experimentally-induced arthritis has been linked to the genes encoding the major histocompatibility complex, it is hypothesized that antigen presentation to autoreactive T-cells is a critical event in the pathogenesis of disease. T-cells, isolated from Lewis rats immunized with bCII or mycobacteria, were co-cultured with splenic or thymic antigen presenting cells (APC) and proliferative responses to antigen were assessed by 3H-thymidine incorporation. T-cell proliferation was observed upon culture with APC without requiring the addition of antigen. T-cells from rats injected with non-immunogenic adjuvants also demonstrated an increased autologous MLR compared to T-cells from non-injected animals. In contrast, T-cells from animals immunized with non-arthritogenic antigens, including ovalbumin or tetanus toxoid, proliferated only when co-cultured with specific antigen-pulsed APC. These results suggest that immunization with arthritogens activates a population of self-reactive T-cells, which respond in an autologous MLR. We propose that these autoreactive T-cells recognize endogenously-derived self peptides rather than peptides derived from a joint autoantigen.

Adjuvants, Immunologic↗
PubMed2001

Infection of mice with Mycobacterium avium primes CD8+ lymphocytes for apoptosis upon exposure to macrophages.

Mycobacterial infection is associated with granuloma formation in which the presence of apoptosis has been recognized. The role of CD4+ T and CD8+ T cells in host protection against mycobacterial infections has been demonstrated. Previous studies, however, have shown that CD8+ T cells have a limited role in host defense against Mycobacterium avium infection, and we hypothesize that M. avium infection could lead to T cell apoptosis. To investigate this hypothesis, C57BL/6 mice were infected with M. avium strain 101, and the rate of apoptosis of splenic lymphocytes cultured ex vivo with peritoneal macrophages was determined and compared with that of controls. When exposed to infected macrophages ex vivo, splenic lymphocytes from M. avium-infected mice underwent apoptosis, as determined by the TUNEL assay. This increased T cell apoptosis above the control level was observed after 3 weeks but not after only 1 week of infection in mice. No splenic T cell apoptosis was observed when lymphocytes from Mycobacterium smegmatis-infected mice were cultured in the presence of M. smegmatis-infected peritoneal macrophages. Likewise, macrophages infected in vitro with heat-killed M. avium did not trigger T cell apoptosis. Culture of macrophages in different chamber from lymphocytes, separated by a transwell membrane, was not associated with increase of apoptosis compared with uninfected control, suggesting a requirement for direct cell-cell interactions to trigger lymphocyte apoptosis. Using a double staining TUNEL followed by anti-mouse CD4 or anti-mouse CD8 monoclonal antibodies, it was observed that only CD8+ T cells but not CD4+ T cells underwent apoptosis at 3 weeks of infection. In conclusion, M. avium infection in C57/BL6 mice for 3 weeks renders CD8+ T cells prone to apoptosis when exposed ex vivo to macrophages infected with M. avium.

Animals↗
PubMed2002

Established T(H1) granulomatous responses induced by active Mycobacterium avium infection switch to T(H2) following challenge with Schistosoma mansoni.

Mycobacterium avium established a systemic infection with granulomatous inflammation in mice. Mice chronically infected with M. avium and subsequently co-infected with Schistosoma mansoni developed additional, but morphologically distinct, hepatic granulomas. Schistosome eggs were not deposited in the spleen, and splenic granulomas in co-infected mice contained mycobacteria. In complete contrast to the T(H1) cytokine pattern observed with granuloma lymphocytes from M. avium-infected mice, granuloma lymphocytes from co-infected mice stimulated with PPD elaborated IL-4, but not IFN-gamma. Furthermore, mycobacterial granulomas in concurrently infected mice contained large numbers of eosinophils, a feature never seen in granulomas of M. avium-infected mice. Serum IgG1 and IgE levels in concurrently infected mice were significantly higher, but IgG2a levels significantly lower, than those in M. avium-infected mice, further evidence that the T(H1) component induced by M. avium is modulated subsequent to co-infection with S. mansoni. The dominance of the T(H2) response observed in this model could have clinical implications in areas where parasites and mycobacteria co-exist.

Animals↗
PubMed1993

Suppressive activity of splenic macrophages induced by transparent and opaque colonial variants of Mycobacterium avium complex against lymphoproliferative response.

Splenic macrophages (M phi s) induced by the two colonial variants of Mycobacterium avium complex, SmT variant (smooth, transparent, flat) and SmD variant (smooth, opaque, domeshaped), were studied for their suppressive activity against mitogenic response of splenic T cells to concanavalin A (ConA). The SmT variant is much more virulent than the SmD variant and causes more severe infection in host mice. Moreover, suppressed state of ConA mitogenic response of host spleen cells persisted much longer in SmT-infected mice than in SmD-infected ones. However, the suppressive activity of SmT-induced M phi s, induced around 2 weeks after infection, against lymphoproliferative response was significantly weaker than SmD-induced M phi s. In contrast, the former M phi s showed somewhat higher active oxygen-producing ability than the latter, as based on the chemiluminescence. These findings indicate that the immunosuppressive M phi s transiently induced in the early phase of M. intracellulare infection hardly affect the host resistance to the organisms and, thus, play relatively minor role in the progression of the infection.

Animals↗
PubMed1994

Nitrite production by macrophages derived from BCG-resistant and -susceptible congenic mouse strains in response to IFN-gamma and infection with BCG.

Reactive nitrogen intermediates (RNI) have been implicated in the interferon-gamma (IFN-gamma)-induced anti-microbial action of macrophages against a wide variety of pathogens. We have been studying the production of NO2- by macrophage lines derived from the bone marrow of either B10.A (Bcgs) strain mice (B10S cell lines), or their congenic BCG-resistant partners of the B10A.Bcgr (Bcgr) strain (B10R cell lines). We have discovered that there is a significant difference in the production of NO2- of B10S compared with B10R macrophages in response to IFN-gamma. By 48 hr following treatment with 10 U/ml IFN-gamma, B10R macrophages had produced an approximately threefold higher level of NO2- than B10S macrophages. Similar results were obtained when experiments were performed with total splenic cells harvested from the spleens of B10.A.Bcgr and B10.A strain mice. The bacteriostatic activity, as assessed by the [3H]uracil incorporation by Mycobacterium bovis BCG, was higher in B10R macrophages compared to B10S macrophages. The bacteriostatic activity of B10R and B10S macrophages correlated with the amount of nitric oxide produced by the macrophages. The anti-mycobacterial activity was inhibited by NgMMLA, a specific inhibitor of nitrite and nitrate synthesis from L-arginine. Addition of L-arginine to IFN-gamma-stimulated macrophages in the presence of NgMMLA restored nitrite production and bacteriostatic activity of macrophages. Northern blot analysis of macrophage nitric oxide synthase (iNOS) revealed that the difference in NO2- production by IFN-gamma-treated B10S and B10R lines was reflective of the difference in iNOS mRNA expression.

Animals↗
PubMed1998

IL-12 promotes drug-induced clearance of Mycobacterium avium infection in mice.

The intracellular pathogen Mycobacterium avium is a major cause of opportunistic infection in AIDS patients and is difficult to manage using conventional chemotherapeutic approaches. In the current study, we describe a strategy for the treatment of M. avium in T cell-deficient hosts based on the simultaneous administration of antibiotics and the immunomodulatory cytokine IL-12. In contrast to SCID mice, which were partially resistant, animals lacking a functional IL-12 p40 gene were found to be highly susceptible to M. avium infection, suggesting that the cytokine can control bacterial growth even in immunodeficient mice. Indeed, rIL-12 that was injected into infected SCID mice in high doses caused small but significant reductions in splenic pathogen loads. Moreover, a lower dose of IL-12, when combined with the antimycobacterial drugs clarithromycin or rifabutin, induced a decrease in bacterial numbers that was significantly greater than that resulting from the administration of the cytokine or drug alone. A similar synergistic effect of IL-12 and antibiotics was seen when immunocompetent mice were treated with the same regimen. The activity of IL-12 in these experiments was shown to be dependent upon the induction of endogenous IFN-gamma. Nevertheless, IFN-gamma itself, even when given at a higher dose than IL-12, failed to significantly enhance antibiotic clearance of bacteria. Together these findings suggest that IL-12 may be a particularly potent adjunct for chemotherapy of M. avium infection in immunocompromised individuals and may result in more effective control of the pathogen without the need for increased drug dosage.

Adjuvants, Immunologic↗
PubMed1995

Primed avian gamma delta T cells respond to mycobacterial antigens, but show no preference for the 65-kDa heat shock protein.

We have studied the reactivity of chicken T cells to mycobacterial antigens. Neither peripheral blood nor splenic lymphocytes isolated from unprimed chickens proliferated in response to mycobacterial antigens (mycobacterial sonicate, purified protein derivative, or recombinant 65-kDa heat-shock protein HSP65). After immunization with complete Freund's adjuvant (CFA) a strong response appeared, and a transient increase of peripheral blood gamma delta T cells was observed. Analysis of spleen cells isolated from CFA-primed chickens showed that both alpha beta and gamma delta T cells were activated by the mycobacterial antigens, apparently at equal levels. Both subsets also responded to HSP65, but no preference of gamma delta T cells to respond to it or any of the other mycobacterial antigens was observed. These results indicate that although HSP65 is an important mycobacterial antigen, it is not dominant in the chicken gamma delta T cell repertoire. Moreover, the results show a clear distinction between the naive and primed repertoire of gamma delta T cells.

Animals↗
PubMed1992

Inflammatory bowel disease in children--clinical, endoscopic, radiologic and histopathologic investigation.

This paper reviews our five years' clinical experience (1987 to 1991) of 22 patients with inflammatory bowel disease (IBD). There were 12 patients with Crohn's disease and 10 patients with ulcerative colitis. The mean age at diagnosis was 8.7 years (2 to 14 years). Clinical impressions before referral were chronic diarrhea in 11, irritable bowel syndrome in 5, colon polyp in 4, lymphoma in 3, intestinal tuberculosis in 2, amoebic colitis in 2, ulcerative colitis in 2 children and other diseases. The mean interval from the onset of symptoms to the diagnosis of IBD was 18 months. Diagnosis of Crohn's disease was delayed for more than 13 months in 8 (67%), whereas that of ulcerative colitis was delayed for more than 13 months in 4 (40%). Diarrhea (50%), abdominal pain (36%) and rectal bleeding (36%) were the three most frequent presenting complaints of IBD. Moderately severe abdominal pain was a more common chief complaint in Crohn's disease (58%) than in ulcerative colitis (10%). Hematochezia (90% vs 17%) and moderately severe diarrhea (90% vs 75%) were more common gastrointestinal manifestations in ulcerative colitis than in Crohn's disease. The associated extraintestinal manifestations were oral ulcer in 7, arthralgia in 11 and arthritis in 4, skin lesions in 2, eye lesions in 2 and growth failure in 9 patients. Of 12 children with Crohn's disease, granuloma was found in 5, aphthous ulcerations in 8, cobble stone appearance in 8, skip area or asymmetric lesions in 6, transmural involvement in 7, and perianal fistula in 3. Among 10 children with ulcerative Colitis, there were crypt abscess in 8, granularity or friability in 10 and rectosigmoid ulcerations with purulent exudate in 8 children. The main sites of involvement in children with Crohn's disease were both the small and large bowels in 7 (58%), small bowel only in 2 (16%), and colon only in 3 (25%). Terminal ileum involvement was seen in 75% of Crohn's disease cases. The main sites of involvement in children with ulcerative colitis were total colon in 4 (40%), up to the splenic flexure in 2 (20%), rectosigmoid in 3 (30%) and rectum only in one (10%). Medical treatment including sulfasalazine, and systemic or topical steroid was administered initially in most patients. Seven of 12 patients with Crohn's disease and 2 of 10 patients with ulcerative colitis were operated on.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed2000

Interferon gamma eliminates responding CD4 T cells during mycobacterial infection by inducing apoptosis of activated CD4 T cells.

In Mycobacterium bovis Bacille Calmette-Guérin (BCG)-infected wild-type mice, there was a large expansion of an activated (CD44(hi)) splenic CD4 T cell population followed by a rapid contraction of this population to normal numbers. Contraction of the activated CD4 T cell population in wild-type mice was associated with increased apoptosis of activated CD4 T cells. In BCG-infected interferon (IFN)-gamma knockout (KO) mice, the activated CD4 T cell population did not undergo apoptosis. These mice accumulated large numbers of CD4(+)CD44(hi) T cells that were responsive to mycobacterial antigens. Addition of IFN-gamma to cultured splenocytes from BCG-infected IFN-gamma KO mice induced apoptosis of activated CD4 T cells. IFN-gamma-mediated apoptosis was abolished by depleting adherent cells or Mac-1(+) spleen cells or by inhibiting nitric oxide synthase. Thus, IFN-gamma is essential to a regulatory mechanism that eliminates activated CD4 T cells and maintains CD4 T cell homeostasis during an immune response.

Animals↗
PubMed1997

Hepatosplenic fungal disease: diagnostic accuracy and spectrum of appearances on MR imaging.

OBJECTIVE: We describe our 6-year experience in the prospective examination of patients with suspected hepatosplenic fungal disease to show the diagnostic accuracy of MR imaging and the spectrum of appearances on MR images. SUBJECTS AND METHODS: All patients who underwent MR examination for suspected hepatosplenic fungal disease from January 1990 to January 1997 in three university institutions were included in the study. Patients presented with persistent fever or no response to antibacterial antibiotics. Patients were grouped as acute, subacute treated, and chronic treated, according to the duration of their symptoms. Patients with 2 weeks or fewer of possible infection were acute presentation, patients on antifungal therapy longer than 2 weeks but shorter than 3 months were subacute treated presentation, and patients on antifungal therapy for 3 months or longer or who had completed antifungal therapy and had a history of hepatosplenic fungal disease were chronic treated presentation. MR studies were prospectively interpreted for the presence of hepatosplenic fungal lesions. The appearances of fungal lesions in patients in each category were determined. The sensitivity, specificity, positive predictive value, negative predictive value, and accuracy for detecting lesions in patients with acute presentation were also determined. RESULTS: Sixty-nine patients were included in the study. MR imaging revealed signs consistent with hepatosplenic fungal lesions in 22 (32%) of 69 patients and no demonstration of hepatosplenic lesions in 47 (68%) of 69 patients. In the 60 patients with acute presentation, MR imaging in 13 patients revealed hepatosplenic lesions that were interpreted as fungal disease. True-positive lesions were present in 11 of these 13 patients. These lesions measured less than 1 cm in diameter and were best shown as well-defined high-signal-intensity foci on T2-weighted images. The remaining two of the 13 patients had false-positive lesions; one was shown to have tuberculosis, and the other had graft-versus-host disease. For acute presentation, MR sensitivity was 100%, specificity was 96%, positive predictive value was 85%, negative predictive value was 100%, and accuracy was 97%. In the five patients with subacute presentation, lesions were present that measured less than 1 cm in diameter and were best shown as mildly hyperintense on T1-weighted images. A perilesional ring nearly void of signal intensity was seen on unenhanced and gadolinium-enhanced T1-weighted images in all five patients. The four patients with chronic healed lesions all had lesions that were 1-3 cm in diameter with irregular, angular polygonal margins. These lesions, which were best shown on images obtained immediately after gadolinium administration, appeared as regions of diminished enhancement with no perilesional changes. CONCLUSION: MR imaging has high diagnostic accuracy for the diagnosis of acute hepatosplenic fungal disease. Patients with acute, subacute treated, and chronic healed presentations may have lesions that can be distinguished by their MR appearances.

Acute Disease↗