, 2009; Cutrufello et al., 2010). PCR has been demonstrated as an extremely useful technique for an early diagnosis of intraocular TB since it can be performed with very small sample sizes obtained from eyes and the clinical improvement with ATT has been observed in most of the patients with positive PCR (Cheng et al.,

2004; Gupta et al., 2007). A nested PCR targeting MPB-64 protein gene was earlier demonstrated in formalin-fixed paraffin-embedded tissue of epiretinal membrane (Madhavan et al., 2000). This assay could detect 0.25 fg of DNA, and the quantity is sensitive RXDX-106 mouse enough to detect a single bacillus in epiretinal membrane from Eales’disease, however, lesser sensitivity was observed with the same nested PCR assay in vitreous samples (Madhavan et al., 2002; Table 1). Recently, the utility of real-time PCR based on IS6110 or MPT-64 protein gene target has been explored in the diagnosis of ocular TB with promising results (Sharma et al., 2011c; Wroblewski et al., 2011). In addition,

M. tuberculosis could be detected in corneas from donors using PCR assay, and such findings may be used to re-evaluate criteria for suitability of donors with active TB, and further studies should be carried out to investigate whether recipients with PCR-positive corneas would eventually lead Smad inhibitor to disease transmission (Catedral et al., 2010). Pericardial TB is the most common cause of pericarditis in African and Asian countries (Cherian, 2004). It arises secondary to contiguous spread from mediastinal nodes, lungs or during miliary dissemination (Golden & Vikram, 2005). The elevated levels of ADA and IFN-γ have been documented in pericardial TB (Burgess et al., 2002), but these assays have limitations as detailed earlier in pleural

TB. The utility of conventional PCR as well as nested PCR has been described for the diagnosis of acute pleuropericardial TB and chronic constrictive pericarditis (Tzoanopoulos et al., 2001; Zamirian et al., 2007). The clinical find more diagnosis of thyroid TB is rarely investigated unless there is multinodular goitre, abscess or chronic sinus in the gland (Bulbuloglu et al., 2006). The diagnosis of primary thyroid TB is mostly dependent on chest X-ray and ultrasonography; however, these methods usually fail (Ghosh et al., 2007). Multiplex PCR targeting IS6110, 65 kDa and dnaJ genes has been established to confirm thyroid TB (Ghosh et al., 2007). TB mastitis or breast TB is a rare presentation of EPTB even in endemic countries. The most common clinical presentation of breast TB is usually a solitary, ill-defined, unilateral hard lump situated in the central or upper outer quadrant of the breasts (Baharoon, 2008). Mycobacterium tuberculosis bacilli can reach breasts through lymphatic, haematogenous or contiguous seeding (Sharma & Mohan, 2004).

To gain insights into the impact of Cav1 on Akt-STAT5 signaling, we transfected murine alveolar epithelial MLE-12 cells with either WT cav1 or a dominant negative

(DN) cav1 expressing plasmid as described previously [[18]]. MLE-12 cells are widely used as a model for murine lung epithelial function [[11]]. Twenty-four hours after transfection, cells were infected with K. pneumonia for 1 h at 10:1 MOI and lysed in order to evaluate CFUs. As expected, decreased bacterial clearance was observed in cav1 knockdown cells as compared with WT or vector control cells (Fig. 6A). Similarly, blocking STAT5 with a chemical inhibitor WP1066 decreased bacterial clearance, although to a lesser extent than PI3K Inhibitor Library ic50 did cav1 DN transfection (Fig. 6A). Consistent with the in vivo data, the levels of ROS were also elevated in cav1 knockdown cells compared with control cells following K. pneumonia infection (Fig. 6B, p = 0.01) as quantified by the H2DCF assay and similarly increased ROS was also measured with the NBT method (Supporting Information Fig. 3). Furthermore, we determined cell survival after transfection with the cav1 DN plasmid. As assessed by the MTT cell proliferation assay, we saw significantly decreased

survival of cav1 DN transfected cells when compared with WT cells following K. pneumonia infection (Supporting Information Fig. 4). These results indicate Sclareol that more cell death occurred in the cav1 knockdown cells than in WT cells challenged by K. pneumonia. Importantly, mutation of Cav1 resulted in a similar increase in phospho-STAT5 selleck screening library while no apparent increase in total STAT5 protein was observed at 1 h (note that the tissue was obtained 24 h postinfection). Although Cav1 mutation resulted

in significantly decreased β-catenin protein expression following 1 h infection, the WT plasmid transfected cells showed a much greater increase. These results are largely consistent with the data from cav1 KO mice, indicating that Cav1 deficiency altered the expression of STAT5 and Akt. This change may contribute to the dysregulated cytokine profile, resulting in extremely high levels of IL-6 and IL-12a (Fig. 6C). To confirm the role of STAT5, a STAT5 inhibitor (WP1066) was used to pretreat the cav1 DN cells. WP1066 has been demonstrated to inhibit the phosphorylation of STAT5, thereby blocking STAT5 signaling [[19]]. Perturbation of STAT5 by WP1066 significantly reduced phospho-STAT5 and downregulated IL-6 and IL-12a expression (Fig. 6D), but did not impact the expression of β-catenin, Akt, and STAT5 protein. These data support the notion that STAT5 plays a crucial regulatory role in the activation of cytokine secretion under Cav1 deficiency. In addition, Cav1 may directly influence the function of β-catenin as Cav1 DN transfection dramatically reduced its expression levels.

2b). The dltA gene codes for one of the proteins

responsible for the d-alanylation of teichoic acids,28 and tagO codes for an enzyme responsible for the transfer of N-acetylglucosamine phosphate to the lipid carrier,28 an essential step in the synthesis of WTA. SA0614 and SA0615 code for proteins that compose a two-component system of S. aureus, which induces the expression of the dltABCD operon.29,30 On the basis of the results obtained with mutant strains deficient in these genes as well as with the ltaS mutant lacking LTA, we hypothesized that d-alanylated WTA is required for the TLR2-mediated phosphorylation of JNK in macrophages. To more directly determine the role of WTA, we prepared a fraction of S. aureus cell wall free from peptidoglycan and examined its action. This fraction was considered to be enriched in WTA based on the

content of phosphorus Nivolumab ic50 and the staining pattern in PAGE (left and middle panels in Fig. 2c): note that no appreciable signals were obtained in either assay with a fraction prepared from the tagO mutant lacking an enzyme essential for WTA synthesis, and that a difference in the migration of WTA prepared from the dltA mutant was probably attributable to a lack of d-alanine. In fact, WTA of the dltA mutant strain seemed to be devoid of d-alanine whereas that of the parental and lgt mutant strains retained selleck products it (right panel in Fig. 2c). This preparation of WTA has been shown to directly induce innate immune responses in an insect system (K. Kurokawa and B. L. Lee, unpublished data). When macrophages were incubated with these WTA preparations, the phosphorylation of JNK was not induced irrespective of the presence of bound d-alanine

Celecoxib in WTA (Fig. 2d), indicating that WTA does not serve as a ligand for TLR2. We next tested whether WTA influences the action of the TLR2 ligand. To this end, macrophages were incubated with Pam3Cys, a synthetic TLR2 ligand, in the presence and absence of WTA. However, the level of phosphorylated JNK was not altered by the addition of WTA (Fig. 2d). These results suggested that d-alanylated WTA does not directly act on TLR2 or TLR2 ligand but modulates the cell wall milieu for lipoproteins so that they effectively serve as a ligand for TLR2 to induce the phosphorylation of JNK. We next determined the level of superoxide production in S. aureus-incubated macrophages, which we previously showed to be inhibited by phosphorylated and thus activated JNK.10 The level of superoxide released from macrophages into the culture media was significantly higher on incubation with a mutant strain lacking the expression of dltA, tagO or lgt than with the parental strain (left panel in Fig. 3a).

The abluminal membrane and most attached caveolae were devoid of terbium labeling. SRT1720 purchase Dual axis tilting

generated tomograms with better resolution than those acquired from single axis tilting. Reconstructed tomograms revealed discreet, unattached vesicles both labeled with terbium (Figure 3 and Video S1a) and unlabeled (Figure 4 and Video S2). Thresholding and surface rendering of a labeled free vesicle clarified its relationship with other vesicular structures and surface membranes (Video S1b). Translation of a single orthoslice through the model verified the accuracy of the model representing terbium deposition and the vesicle interior (Video S1c). A similar tomographic series through an unlabeled vesicle showed it appearing and disappearing without any connection with

other vesicular compartments (Figure 4, Video S2) In another tilt series, a large membranous compartment was revealed to be connected to Selleck Metabolism inhibitor both luminal and abluminal membranes (Figure 5). Only the luminal membrane of the compartment exhibited bound terbium indicating the absence of glycocalyx on the abluminal portion of the compartment (Video S3). This structure represents a large thoroughfare through the capillary wall not commonly seen in continuous capillaries. In several regions, vesicles labeled with terbium were attached to the abluminal membrane by a stoma (mouth) (Figure 6, Video S4) and presented the possibility of a transendothelial Oxalosuccinic acid channel. In one instance, a single tomographic

slice indicated a transendothelial channel open to both luminal and abluminal surfaces (Figure 6A). A tomographic series acquired at one of these locations showed a labeled abluminal vesicle that appeared connected to the lumen of the capillary (Figure 7). Creating a model of this vesicular compartment interior by thresholding the terbium revealed a channel-like structure through the capillary wall (Video S5a). An animated journey through the channel was generated with Amira beginning at the abluminal stoma (mouth) of a caveola, a rotation of the camera perspective in mid-channel and backing out through the luminal side (Video S5b) The anatomical correlates of transport pathways across continuous capillary walls have long been a subject of vigorous debate [4,11,18,20,21,23]. Pappenheimer et al. [15] postulated the existence of a single system of small pores (3–5 nm radius) to account for microvascular permeability. Grotte [6] introduced the concept of an additional smaller population of large pores (15–25 nm radius) to account for the transport of larger solutes. These estimates were based on the transendothelial transport dynamics of a range of different-sized solutes. Recent estimates of the ratio of large pores to small pores in skeletal muscle capillaries are about 1/5000 [12].

The present results also confirm the previous studies describing co-aggregate formation of wild type and CTF TDP-43.[32, 38] Similar results Navitoclax supplier were also obtained when we infected the cells with adenoviruses encoding mutant TDP-43 instead of wild type TDP-43; we failed to observe any differences in effects between wild type and mutant TDP-43 expressing

adenoviruses to induce aggregate formation. The toxic effect of the mutation in TDP-43 gene remains elusive, as several reports also failed to demonstrate enhancing effects by the mutation to form aggregates in cultured cells.[8, 35-37] As for aggregate formation by FUS transgenes in transfected cells in vitro, it has been described that FUS point mutations showed a varying degree of cytoplasmic accumulation, ranging from mild (R521C, R521G), intermediate (R522G) to

severe (P525L) mislocalization.[40, Ruxolitinib mouse 41] The degree of cytoplasmic mislocalization was inversely correlated to the age of disease onset.[40, 41] In line with these observations, we demonstrated that adenovirus-induced FUS with R521C or R521G mutation was localized both in the nucleus and cytoplasm with granular appearance, and FUS with R522G or P525L mutation was localized predominantly in the cytoplasm forming larger aggregates. Furthermore, like TDP-43 adenoviruses, aggregate formation was enhanced when the cells were infected with the mutated FUS adenoviruses in the presence of MG-132 or 3MA, or in combination with PSMC1, ATG5 or VPS24 shRNA adenovirus infection (Table 1). The relationship between cytoplasmic aggregates of TDP-43

and FUS proteins and stress granules has been extensively studied.[40-44] Although whether Coproporphyrinogen III oxidase cytoplasmic aggregates demonstrated in the present study also related to stress granules awaits further investigation, it is noteworthy that inhibition of the proteasome activity by MG-132 induces the formation of stress granules in HeLa cells,[45] suggesting that the present treatments of MG-132 or PSMC1 shRNA adenovirus also induced stress granules and subsequent aggregate formation in neuronal and glial cells. In the present study, we demonstrated retrograde transport of facial nerve-injected adenoviruses encoding TDP-43, FUS and shRNAs for protein degradation pathways to the rat facial motoneurons and expression of the virus-induced foreign genes in these motoneurons. In a similar manner to the present in vitro experiments as described above, facial motoneurons showed cytoplasmic aggregate formation when infected with adenoviruses encoding wild type and CTF TDP-43 and shRNAs for proteasome, autophagy, or endosome, or mutated FUS with these shRNAs, indicating that impairment of protein degradation pathways also greatly accelerates formation of TDP-43 and FUS-positive aggregates in adult rat facial motoneurons in vivo.

This could also suggest that specific tissues use their intrinsic physiological properties as a starting point to establish

control over an ongoing local immune responses aiming ultimately, to restore the balance of tissue function. Within the immune system there are many cells with regulatory function, aiming to keep the immune response under a balanced activity.[83] Mesenchymal stromal cells have been described as present in many tissues and current literature shows Fluorouracil cell line that they can establish connection and modulate the activity of many cells of the immune system. In line with the initial idea that MSC have an active role in promoting the innate tissue surveillance and also have an important part in the control of exacerbated tissue immune responses; we could say that the immunosupressive effect of C59 wnt ic50 MSC is focused on restoring tissue homeostasis or, that it is aimed

at restoring ‘tissue innate tolerance’ and this, as has previously been suggested, could be a property shared by all stromal cells.[72, 84] Considering the immnuomodulating properties of MSCs discussed above; we would like to suggest that, among other cells that constitute the tissue’s basic architecture MSC have the role of setting the background and actively participate in bringing together cells involved in the local tissue immune response aiming to maintain tissue homeostasis. The authors declare no conflict of interest. “
“Seeking biomarkers reflecting disease development in cystic echinococcosis (CE), we used a proteomic approach linked

to immunological Non-specific serine/threonine protein kinase characterisation for the identification of respective antigens. Two-dimensional gel electrophoresis (2-DE) of sheep hydatid fluid, followed by immunoblot analysis (IB) with sera from patients with distinct phases of disease, enabled us to identify by mass spectrometry heat shock protein 20 (HSP20) as a potential marker of active CE. Using IB, antibodies specific to the 34 kDa band of HSP20 were detected in sera from 61/95 (64%) patients with CE, but not in sera from healthy subjects. IB revealed anti-HSP20 antibodies in a higher percentage of sera from patients with active disease than in sera from patients with inactive disease (81 vs. 24%; P = 10−4). These primary results were confirmed in a long-term follow-up study after pharmacological and surgical treatment. Herewith anti-HSP20 antibody levels significantly decreased over the course of treatment in sera from patients with cured disease, relative to sera from patients with progressive disease (P = 0·017). Thus, during CE, a comprehensive strategy of proteomic identification combined with immunological validation represents a promising approach for the identification of biomarkers useful for the prognostic assessment of treatment of CE patients.

i., and 22·1 times higher on day 31 p.i. Perhaps unexpectedly, Group 5 hamsters (primary + secondary infections) made a slower start, with eosinophil numbers just 9·4 times higher 10 days p.c., but caught up rapidly and by day 17 p.c. eosinophil counts were 27·7 times higher than those STA-9090 clinical trial in naïve animals on day 10 (day 73 of the experiment), before falling by days 24 and 31 p.c. This curve was best described by the quadratic equation y = −437·9 +87·1x−1·95×2 (where y = eosinophils/mm2 and x = days after challenge); R2 = 41·3%, F2,15 = 5·3, P = 0·019). In naïve hamsters, Paneth cell numbers average 1–3 cells per crypt (18), and here the values in naive animals were well within

the normal range (Figure 6). As found earlier, (18) the mean numbers in animals experiencing a primary infection were lower

(Figure 6, days 73 and 94 p.i. in Group 2, primary continuous infection). When hamsters were given the second infection alone (Group 4), Paneth cell numbers were in the naive control range on day 10 p.i., but already lower by day 31 p.i. Removal of the adult worm population in Group 3 (primary abbreviated infection), caused an exaggerated response (Figure 6), with mean numbers more than doubling on days 73 and 94 p.i. (actually 38 and 59 days PLX3397 nmr after removal of adult worms, see Table 1). Immunized-challenged hamsters (Group 5, primary + secondary infections) appeared to maintain these higher levels of Paneth cell counts, without any detectable change in cell density/crypt in the period 10, 17, 24 and 31 days p.c. (regression of Paneth cells/mm2 of mucosal tissue on days after challenge, confined to Group 5; Rp = 0·037, n = 20, P = N.S.). The results reported in this paper show clearly that despite tolerating long-lasting chronic infections with the hookworm, A. ceylanicum, hamsters undergo profound changes in the mucosal environment that are typical of Th2-driven immune responses generated by helminths in the mammalian gut. Notwithstanding the intense changes occurring in the mucosa, selleck screening library some adult worms appeared to be remarkably resilient and survived for lengthy periods of time in the grossly abnormal

environment of the inflamed intestine in both primary and challenge infections. In this study, hamsters given a primary infection with 50L3 still had adult worms 73 and 94 days later. Despite the length of time from infection to examination, the infected animals had remarkably high mast cell, goblet cell and eosinophil counts, and markedly reduced villi and hypertrophied crypts. These data extend those reported in our earlier paper in which animals were subjected to heavier infections and studied only until day 42 p.i. and support also the idea that the persistence of the inflammatory changes is attributable to the surviving adult worms. Nevertheless, none of the animals in the current study showed overt clinical signs of infection, indicating that hamsters can sustain and tolerate a long drawn out mucosal inflammatory response, lasting for weeks.

In contrast, CSF IL-6 levels were slightly elevated in patients with NBD and significantly elevated in patients with AM and MS compared with healthy controls. Patients with NBD were subdivided into two groups according to their clinical course (eight patients with a slowly progressive course presenting with psychosis and dementia and 10 patients with an acute course including aseptic meningitis, brainstem involvement and myelopathy). BAFF levels

were significantly increased in those with a slowly progressive course compared with those with an acute course. CSF BAFF levels did not correlate with serum BAFF levels, CSF cell counts or CSF IL-6 levels in patients with NBD. These data suggested that BAFF was produced within the central nervous system and may be associated with the development of NBD, particularly with a progressive course. “
“Patients carrying activating killer

cell immunoglobulin-like Galunisertib receptor (KIR) genes are significantly protected from CMV-associated complications after solid selleckchem organ or hematopoietic stem cell transplantation. Whether previous infection with CMV affects NK-cell function in healthy donors is unknown. We studied the KIR repertoire and alterations of KIR expression after in vitro exposure to CMV in 54 healthy donors. The expression of neither activating nor inhibitory KIRs was different at baseline between 23 seropositive and 31 seronegative donors. However, after co-culture of NK cells with CMV-infected fibroblast cells, expression of the inhibitory N-acetylglucosamine-1-phosphate transferase receptors KIR2DL1 and KIR2DL3 and the activating receptor KIR3DS1 significantly increased in CMV-seropositive donors. In CMV-seronegative donors, changes were subtle and restricted to the subset of NK cells expressing NK-cell group antigen 2C (NKG2C). Expansion of inhibitory KIRs occurred exclusively in donors carrying the cognate HLA class I ligands, whereas the presence of the putative ligand HLA-Bw4 was not necessary for the expansion of KIR3DS1-expressing NK cells. Our data show that previous infection with CMV does not alter the resting NK-cell

receptor repertoire, but appears to modify how NK cells respond to re-exposure to CMV in vitro. NK cells are an important component of the immune system in the control of viral infection [1]. Unlike B and T cells, NK cells do not display rearranged receptors but instead are regulated by the integration of signaling from germline encoded activating and inhibitory receptors. One important and incompletely characterized family of receptors are the killer cell immunoglobulin-like receptors (KIRs) [2]. KIRs are almost exclusively expressed on NK cells and encoded by 15 different gene loci, nine inhibitory iKIRs, and six activating aKIRs. The KIR genes cluster in chromosome 19, forming haplotypes composed of 7–11 individual KIR genes. The most common haplotype in Caucasians contains mostly iKIRs accompanied by a single or no aKIR gene and is called “A” haplotype [3].

Furthermore, the association between SIRT1 and cortactin, an actin-binding protein, was investigated by immunostaining, WB, or immunopreciptation in vivo and in vitro. Results: Seven days after glomerular disease induction, u-alb/cre, BUN and the ratio of glomerular injury in SIRT1pod−/− mice were

significantly higher than those in wild-type mice. Consistently, significant decrease in podocyte-specific molecules was demonstrated in SIRT1pod−/− mice. Electron microscopy revealed the exacerbation of foot process effacement and actin cytoskeleton derangement buy Enzalutamide in SIRT1pod−/− mice. Similarly, actin cytoskeleton derangement in H2O2 (as a mimic of anti-GBM antibody)-treated LY294002 ic50 cultured podocytes became prominent when the cells were pretreated with SIRT1 inhibitors, while it was ameliorated by a SIRT1 activator. Furthermore, we assessed the link between SIRT1 and cortactin, which acts to polymerize and maintain actin cytoskeleton. While the cytoplasmic cortactin was colocalized with actin fiber, it was dissociated in association with cytoskeleton derangement. Importantly,

the increased actin cytoskeleton derangement by SIRT1 inhibition was correlated with an increase in the level of acetylated cortactin, which was detectable only in nucleus and co-precipitated with SIRT1. These results showed that SIRT1 deacetylated Tolmetin cortactin in the nucleus and that the deacetylated

cortactin was transported to the cytoplasm for maintenance of actin cytoskeleton. Conclusion: SIRT1 regulates the functional state of cortactin by deacetylation, and thereby maintains actin cytoskeleton integrity, indicating that SIRT1 is a critical factor for podocyte homeostasis, especially structure of slit diaphragm. TANAKA ERIKO1,2, ASANUMA KATSUHIKO1,3, TAKAGI MASATOSHI2, KOYANAGI AKEMI4, MIZUTANI SHUKI2, YAGITA HIDEO5, TOMINO YASUHIKO1 1Division of Nephrology, Department of Internal Medicine, Juntendo University Faculty of Medicine; 2Department of Pediatrics and Developmental Biology, Graduate School of Medicine, Tokyo Medical and Dental University; 3Medical Innovation Center, Laboratory for Kidney Research(TMK project), Kyoto University Graduate School of Medicine; 4Division of Cell Biology, Biomedical Reseach Center, Juntendo University Graduate School of Medicine; 5Department of Immunology, Juntendo University School of Medicine Background: Notch signaling pathway is an evolutionarily conserved intracellular signaling pathway that regulates cell fate. Activation of Notch1 and Notch2 has been recently implicated in human glomerular diseases and Notch1 reactivation is reported to correlates with glomerulosclerosis. However, the role of Notch2 reactivation remains unclear.

C. albicans dimorphism (YH) was highly sensitive to geranium oil constituents tested (IC50 approximately 0.008% v/v). Geraniol, geranyl acetate and citronellol brought

down MICs of FLC by 16-, 32- and 64-fold respectively in a FLC-resistant strain. Citronellol and geraniol arrested cells in G1 phase while geranyl acetate in G2-M phase of cell cycle at MIC50. In vitro cytotoxicity study revealed that geraniol, geranyl acetate and citronellol were non-toxic to www.selleckchem.com/products/PD-0332991.html HeLa cells at MICs of the C. albicans growth. Our results indicate that two of the three geranium oil constituents tested exhibit excellent anti-Candida activity and significant synergistic activity with fluconazole. “
“Lobomycosis, a disease caused by the uncultivable dimorphic onygenale fungi Lacazia loboi, remains to date as an enigmatic illness, both due to the impossibility of its aetiological agent to be cultured and check details grown in vitro, as well as because of its unresponsiveness to specific antifungal treatments. It was first described in the 1930s by Brazilian dermatologist Jorge Lobo and is known to cause cutaneous and subcutaneous localised and widespread infections in humans and dolphins. Soil and vegetation are believed to be the chief habitat of the fungus, however, increasing reports in marine mammals has shifted the attention to the aquatic environment. Infection in humans has also been associated with proximity to water, raising the hypothesis

that L. loboi

may be a hydrophilic microorganism that penetrates the skin by trauma. Although its occurrence was once thought to be restricted to New World tropical countries, its recent description in African patients has wrecked this belief. Antifungals noted to be effective in the empirical management of other cutaneous/subcutaneous mycoses have proven unsuccessful and unfortunately, no satisfactory therapeutic approach for this cutaneous infection currently exists. “
“Invasive aspergillosis (IA) presents a diagnostic and therapeutic dilemma for the physicians who take care of the patients with severe underlying diseases and immunosuppression. This study aimed to evaluate the usefulness of serum galactomannan (GM) measurements Farnesyltransferase in the routine practice and surveillance of IA along with possible caveats in diagnosis and treatment. Adult patients with high-risk haematological malignancies admitted to the Internal Medicine wards during the 2-year study period were followed up by daily visits for vital signs, existing or newly developing signs and symptoms, clinical and laboratory findings. Blood samples were analysed for GM levels by the ELISA method at the end of the study period. Data of 58 hospitalisation episodes in 45 patients were analysed. Proven IA was diagnosed in one patient, probable IA was diagnosed in four patients. The sensitivity was 60% and the specificity was 21% when the index cut-off for positivity was accepted as 0.5.