Electron microscopy also showed that in the case of the wild-type S. Enteritidis uptake, the Salmonella-containing vacuoles (SCV) developed towards the spacious ones while in the case of all the rfa mutants, the vacuole closely fitted the S. Enteritidis cell inside and signs of bacterial cell disintegration could be observed inside the vacuole (Fig. 2). In this study, we have characterized the interactions between attenuated S. Enteritidis mutants and porcine WBC in vitro. Such knowledge might be useful for the prediction of the properties of attenuated click here S. enterica mutants used as vaccines against salmonellosis itself or as vectors for targeting particular cell types including cancer cells. Three different

types of association profiles have been found among the tested attenuated mutants. First, the phoP and aroA mutants did not differ from the wild-type S. Enteritidis in any of the assays. Second, the check details fliC and ΔSPI1-5 mutants, exhibited only minor differences when compared with the wild-type strain – likely due to the defect in chemotaxis in the fliC mutant (Khoramian-Falsafi et al., 1990; Jones et al., 1992) and the defect in cell invasion in the ΔSPI1-5 mutant (Kaniga et al., 1995). The last group comprising of rfaC,

rfaG and rfaL mutants was characterized by a highly increased association with the host immune cells. The differences from the interaction with the wild-type strain could also be seen in the development of SCV, which, unlike the spacious one seen after the wild-type strain infection (Alpuche-Aranda et al., 1994; Boyen et al., 2006), fitted closely to the surface of the rfaC mutant (Fig. 2). Our results show that type III secretion systems encoded by SPI-1, SPI-2 or flagellar operons have only a minor influence on the initial interactions of S. Enteritidis with porcine leukocytes. Instead, this interaction was dependent on the oligosaccharides Celecoxib exposed at the surface of S. Enteritidis. Interestingly, even within the rfa mutants, there were certain differences. In the absence of serum, the rfaL mutant expressing

lipopolysaccharide without the O-antigen exhibited an increased affinity for T-lymphocytes while the rfaC and rfaG mutants expressing lipopolysaccharide without the outer and the inner oligosaccharide core, respectively, associated more than the rfaL mutant with B-lymphocytes. All of these results might be used in rational vaccine design. However, if critically evaluated, live Salmonella vaccines for animal use are administered orally and therefore will be exposed to blood leukocytes only very rarely. On the other hand, attenuated S. enterica strains that were tested for tumor therapy in mice and humans were administered intravenously (Toso et al., 2002; Zhao et al., 2005; Leschner et al., 2009; Vendrell et al., 2011), i.e. they were immediately subjected to interactions with the blood leukocytes and via the circulation also to other cell types.

All patients were required to have a suppressed viral load, defined as a viral load ≤500 copies/mL, at baseline. Patients were excluded if there was no viral load meas-urement in the 6 months after BVD-523 supplier baseline. Virological failure was

defined as a viral load >500 copies/mL measured at least 4 months after baseline. Patient follow-up was measured from baseline to date of virological failure or date of last viral load measurement. Poisson regression analysis was used to identify viral load response prior to baseline associated with virological failure after starting new ARVs. Potential explanatory variables included age, gender, year of starting cART, ARV exposure status at cART initiation (ARV-naïve or ARV-experienced), risk group, ethnicity, region of Europe, baseline

CD4 cell count, CD4 nadir, peak viral load, previous AIDS diagnosis, time on cART, current HIF-1�� pathway treatment regimen, number of previous treatment regimens, time spent on cART prior to baseline, number of ARVs to which the patient was previously exposed and the reason reported for starting the new ARV. In addition to the traditional explanatory variables investigated above, variables that summarized the history of viral suppression after cART initiation prior to baseline were investigated. The variables used to summarize the history of viral suppression after cART initiation were as follows. 1 Months to initial suppression (HIV RNA ≤500 copies/mL) after starting cART. Viral suppression was

defined as a measurement of HIV RNA ≤500 copies/mL. Viral rebound was defined as a viral load >500 copies/mL measured after a period of suppression prior to the regimen change. For variable 5, any period of time when the patient was off cART and the first 4 months after starting a new cART regimen were excluded. Thus, only periods during which the patient was on cART and should have been virally suppressed were included. Any variable that was significant at the 10% level in the univariate model was then included in a multivariate model. The sensitivity analysis considered confirmed virological failure after baseline (i.e. two consecutive viral load measurements above 500 copies/mL) and, in the subgroup of patients who had viral load measured using an assay with a lower limit Axenfeld syndrome of detection of 50 copies/mL, virological failure after baseline defined as a viral load above 50 copies/mL. Analyses were also repeated taking account of HIV drug resistance at baseline in the subset of patients with resistance data, using genotypic sensitivity scores (GSS) calculated using the rega algorithm, version 7.1 [29]. A total of 1827 patients (67%) were included in the analysis. Table 1 describes the characteristics of the patients included in the analysis. Eight hundred and seventy-eight patients (48%) were treatment naïve at cART initiation.

, 1998; Smith et al., 2002; Aertsen et al., 2004; Liveris et al., 2004) that, when bound to RecA, induces its co-proteinase activity, which enhances autocatalysis of the LexA repressor and activates the SOS response. This results in a choreographed transcription

of multiple genes (UvrA, UvrB, UvrC, UvrD, DNA polymerase I, DNA ligase), which repair intrachain DNA damage by nucleotide excision (Black et Tanespimycin al., 1998; Aertsen et al., 2004; Fry et al., 2005; Maul & Sutton, 2005). Not all bacteria have an SOS response or induction of uvrA transcription in response to DNA damage. In Pseudomonas aeruginosa (Rivera et al., 1997) and Neisseria spp. (Black et al., 1998; Davidsen et al., 2007), DNA damage does not trigger an SOS response and does not induce uvrA, suggesting that E. coli and B. subtilis paradigms regarding the regulation of uvrA are not universal. Because many host defenses involve production of DNA-damaging reactive oxygen species (ROS) and reactive nitrogen species (RNS), the ability of pathogenic bacteria to repair damaged DNA is important to their survival in hosts. In Mycobacterium tuberculosis, uvrA mutants show decreased ability to survive within macrophages (Graham & Clark-Curtiss, 1999) and uvrB mutants are attenuated in mice (Darwin & Nathan, 2005). Similarly, in Helicobacter

pylori and Yersinia sp., defects in uvrA are accompanied Lorlatinib ic50 by attenuation in mice (Bijlsma et al., 2000; Garbom et al., 2004). These experimental results strongly suggest that lack of DNA repair

mediated by the uvrA gene product attenuates bacterial pathogens because they cannot overcome the DNA-damaging systems of the host (Janssen et al., 2003). The genome of Borrelia burgdorferi, the cause of Lyme disease, contains a minimal set of genes devoted to DNA repair and appears to lack an SOS response despite the presence of orthologues Fenbendazole of uvrA, uvrB, uvrD, DNA polymerase I and DNA ligase (Fraser et al., 1997). It also lacks an orthologue for the repressor of the SOS response, lexA, and none of the genes potentially involved in DNA repair display consensus LexA binding boxes similar to those found in E. coli (Fraser et al., 1997). recA also does not appear to be involved in repair of UV-induced DNA damage in B. burgdorferi (Liveris et al., 2004; Putteet-Driver et al., 2004). Borrelia burgdorferi is exposed to antibacterial levels of ROS and RNS in infected ticks (Pereira et al., 2001) and mammals (Benach et al., 1984; Cinco et al., 1997; Hellwage et al., 2001) intracellularly, following phagocytosis, and extracellularly, by diffusion from intracellular sources or by production at the phagocyte plasma membrane (Putteet-Driver et al., 2004). Borrelia burgdorferi can also be exposed to solar UVB radiation in the erythema migrans skin lesion (Born & Born, 1987).

Aim.  To investigate the effects of the addition of early caries lesions (ECL) into WHO threshold caries detection methods on the prevalence of caries in primary teeth and the epidemiological profile of the studied population. Design.  In total, 351 3- to 4-year-old preschoolers participated in this cross-sectional study. Clinical exams were Sorafenib cell line conducted by one calibrated examiner using WHO and WHO + ECL criteria. During the exams, a mirror, a ball-ended probe, gauze, and an artificial light were used. The data were analysed by Wilcoxon and Mc-Nemar’s tests (α = 0.05). Results.  Good intra-examiner Kappa

values at tooth/surface levels were obtained for WHO and WHO + ECL criteria (0.93/0.87 and 0.75/0.78, respectively). The dmfs scores were significantly higher (P < 0.05) when WHO + ECL criteria were used. ECLs were the predominant

caries lesions in the majority of teeth. Conclusions.  The results strongly suggest that Ulixertinib ic50 the WHO + ECL diagnosis method could be used to identify ECL in young children under field conditions, increasing the prevalence and classification of caries activity and providing valuable information for the early establishment of preventive measures. “
“To identify potential risk indicators of dental erosion (DE) among 12- to 14-year-old Jordanian school children. A random cross-sectional sample was selected from Amman, Irbid, and Al-Karak governorates. A weighted multistage random sampling system was used to yield 3812, 12- to 14-year-old school children from 81 schools. The study utilized a self-reported questionnaire of factors reported in the literature and thought to be associated with DE. Full mouth recording using

the tooth wear index modified by Millward et al. (1994) was performed by a single calibrated examiner. Logistic regression analysis defined the risk indicators that were simultaneously associated with DE with geographical location, medical condition including frequent mouth dryness, and having frequent bouts of vomiting or using a cortisol inhaler, dietary habits including consumption of carbonated beverages, lemon, sour candies, and sports drinks, keeping soft drinks Florfenicol in the mouth for a long time, brushing teeth following soft beverages or drinking lemon juice at bed time. Dental erosion is a multifactorial condition in which mouth dryness, vomiting, cortisol inhaler use, keeping soft drinks in the mouth, drinking beverages at bed time, consumption of lemon, sour candies, and having confectionary as snacks are risk indicators, and area of residence are all potential factors. Dental erosion (DE) is the irreversible loss of dental hard tissue due to a chemical process of acid dissolution not involving bacterial plaque and not directly associated with mechanical or traumatic factors or with dental caries[1].

Overall, the mean scores on all of the subscales and the total score in the HIV-positive group were significantly higher than those in the control group (t=6.45–16.09; P<0.001). The total score for the HIV-positive group was >160, which suggests psychological distress. www.selleckchem.com/PARP.html In particular, the mean

scores on the obsessive–compulsive, depression, anxiety and anger/hostility subscales for the HIV-positive group were higher than the threshold score (2.0) (Table 2). Both male and female HIV-positive participants had significantly higher scores and mean subscale scores than their control counterparts (P<0.05). There was no significant difference in SCL-90 scores between the male and female control groups (P>0.05). In the HIV-positive group, female subjects had significantly higher mean depression and anxiety subscale scores than male subjects (P<0.05), and these were the highest among the mean scores of all subscales for both male and female subjects (Table 3). The percentage of HIV-positive participants with mean subscale scores >2.0 was higher for female than for male HIV-positive participants (P<0.05 for obsessive–compulsive disorder, interpersonal sensitivity, depression, anxiety, phobic anxiety and psychoticism; P>0.05 for hostility, paranoid

ideation and somatization) (Fig. 1). The average number of subscales with mean scores Olaparib in vitro >2.0 was 4.1 for female HIV-positive individuals and 3.7 for male HIV-positive individuals. The four most frequent types of psychological distress were depression

(66.7% for male HIV-positive individuals and 84.6% for female HIV-positive individuals), anxiety (58.6% for male HIV-positive individuals and 63.5% for female HIV-positive individuals), obsessive–compulsiveness (53.1% for male HIV-positive individuals and 55.8% for female HIV-positive individuals) and anger/hostility (52.5% for male HIV-positive individuals and 51.9% for female HIV-positive individuals). The most common psychosocial experiences of HIV-positive participants regarding HIV infection were fear (36.9%) and helplessness (31.8%). Overall, 90.2% of participants were reluctant to tell others about their HIV infection for fear of their family members being discriminated against (42.5%) or being excluded (26.9%) or abandoned (23.3%). However, the HIV-positive status of the people studied Quinapyramine in this paper was known in their communities. The main stresses in their daily lives were discrimination from their acquaintances (colleagues, friends and neighbours; 38.8%) and potential job loss and reduced quality of life (36.9%), while the financial burden of the disease was not a main stress of daily life for these HIV-positive individuals (only 10.3% reported financial burdens). After discovering their HIV-positive status, most members of their communities, including neighbours, colleagues, doctors and family members, showed negative attitudes towards the HIV-positive participant. More than 80% of people showed alienation, coldness, aversion or fear.

, 2003). Our discussion therefore mainly focuses on the induced genes in our dataset. A complete list of all genes differentially expressed by BC treatment can be found in Table S2. To validate the microarray data, QRT-PCR assays were performed with the same cDNA preparations used in array selleck chemicals llc hybridizations. Overall, nine genes of interest were selected. A strong positive correlation (Pearson’s correlation coefficient R=0.97) between the microarray and QRT-PCR data

was observed (Fig. 3), indicating that the microarray data obtained from the present work were reliable. In the present study, most of the key elements involved in replication initiation, such as DnaA, subunits of DNA polymerase III, DnaG and DnaC, were induced by BC. Of these proteins, DnaA (encoded by dnaA) binds to the origin of replication, oriC, resulting in the initiation of chromosome replication. Evidence suggests that transcription from the promoters of gid operon and mioC are involved in the initiation control of the replication

of the whole E. coli chromosome when oriC is under suboptimal conditions (Ogawa & Okazaki, 1991; Bates et al., 1997). As a result, the induction find more of gidAB, mioC and dnaA in our study strongly suggests that berberine may influence dnaA and oriC function. It has been established that berberine binds strongly to DNA predominantly by intercalation with a preference for the AT sequence (Pilch et al., 1997). Generally, replication origins contain AT-rich sequences. Sf301 has an E. coli-like origin with an AT-content of 59% (Sugimoto et al., 1979), which is much higher than the average value (49%) of Sf301 whole genome. Therefore, it is likely that BC may

be able to inhibit the initiation of replication through interaction with the origin region of Sf301. MreB has been shown to be necessary for the segregation of origin-proximal chromosome. During a state associated with inhibition of cell division, the expression of mreB was generally upregulated (Chiu et al., 2008). We found that mreB was induced Resveratrol by BC, which was further confirmed by QRT-PCR. It has been reported that excessive copies of the mreB gene led to filamentous cells, a reflection of cell division inhibition (Wachi & Matsuhashi, 1989). In the present study, microscopic examination of Sf301 treated with 160 μg mL−1 of BC for 30 min revealed an increase in the percentage of elongated cells (Fig. S1). These results indicate that chromosome segregation may be inhibited. It has been shown that inactivation of DnaA dramatically inhibited segregation of the oriC region in E. coli (Kruse et al., 2006). Therefore, it is likely that the drug may inhibit cell segregation through its influence on dnaA and oriC function. Additionally, a set of DNA repair genes –hepA, recJ, xseA, recQ, nfo, lig, SF2540, nei and dead– were also induced by BC, indicating that the drug may cause certain DNA damages.

The significant role of the polysaccharide structure on swarming has been revealed in previous studies (Toguchi et al., 2000; Inoue et al., 2007).

To support this CP-868596 clinical trial point, swarming cells of C. freundii were observed to be more hydrophilic compared with vegetative cells (0.961 for swarming cells; 0.814 for vegetative cells, P<0.05; Fig. S2) in this work. In swarming colonies, C. freundii cells moved actively. However, the cells at the periphery of colonies were less active due to the decreased moisture capacity in areas where the cells moved out and back occasionally, or were pushed by the actively moving cells in the central region. As a result, the edge of colonies expanded outward continuously. Citrobacter freundii did not display alternating cycles of swarming and consolidation during the development of swarming colonies as in P. mirabilis.

Once differentiation occurred at the inoculation site, swarming cells spread continuously, until they occupied the entire agar surface. Even when inoculated onto a large plate with a diameter over 20 cm, alternating cycles of swarming and consolidation were not observed. Transposon mutagenesis involving the use of Mini-Tn5 on a suicide plasmid pUT was carried out to further Erlotinib understand the genetic determinants of swarming motility in C. freundii. A total of 85 swarming-defective mutants were screened from approximately 6000 transconjugants; of the 85 mutants, 53 were defective in both swimming and swarming. The remaining 32 mutants were defective in swarming but not swimming. The mutants with normal swimming pattern were subjected to further sequence analysis to determine the insertionally mutated gene. Given that swarming is dependent on functional flagella, as demonstrated in previous studies, of the 53 swimming-defective mutants, only five randomly selected mutants were further subjected to sequence analysis. As a whole, sequences produced valid results with only four exceptions

(CF407, CF415, CF701, and CF711). In most cases, the most similar genes obtained through the homology searches usually belonged to Citrobacter koseri ATCC BAA-895, a species of Citrobacter with complete genome sequence information. The results of the homology searches are listed in Tables 1 and 2 and are also described Interleukin-2 receptor in the following two sections on genes that have been previously characterized in other species and those first identified in this study. As many as 16 swarming-related genes identified in our study have already been characterized previously in other species. The underlying causes for the defective swarming motility of the mutants are listed in Table 1. However, some of them are worthy of further discussion. As expected, flhD, motA, and motB mutants were identified among the five mutants found to be defective in both swarming and swimming motilities.

The diagnostic conserved GH18 sequence motif DXXDXDXE, which contains important catalytic residues (Synstad et al., 2004), including buy Barasertib the glutamic acid (E) acting as catalytic acid which is present in

all three proteins (Fig. 1). The strong similarity between EfEndo18A and EndoH was also shown at the structural level, using modeller v9.4 (Eswar et al., 2006) to construct a model of EfEndo18A using EndoH as template (data not shown). Production of EfEndo18A in E. coli and subsequent purification were straightforward. The procedure described in ‘Materials and methods’ typically yielded 30–40 mg of highly pure protein per litre of culture. The functionality of EfEndo18A was tested using RNaseB, human

IgG, fetuin, ovalbumin, mucin and serum proteins as substrates. CAL-101 in vitro Possible deglycosylation of these substrates was analyzed by looking at band shifts in SDS-PAGE gels and by analyzing released carbohydrates using MALDI-TOF MS. RNaseB is a well known substrate for this type of study; it has one N-linked glycosylation site containing glycans of the high-mannose type (Fu et al., 1994). Ovalbumin is N-glycosylated at one site that may carry both high-mannose and hybrid-type glycans (Nisbet et al., 1981; An et al., 2003). Human IgG, fetuin and serum proteins contain N-linked glycans of the complex type as well as O-linked glycans (Spiro, 2002; Chu et al., 2009), whereas mucin mainly contains O-linked glycans (Bansil & Turner, 2006). Figure 2 shows clear band shifts for RNaseB and ovalbumin, one shift for the former and two shifts for the latter, indicating hydrolysis of N-linked glycans of ifenprodil the high mannose and possibly also the hybrid type (see below). The absence of band-shifts after EfEndo18A-treatment of fetuin, human IgG, mucin and serum proteins indicates that EfEndo18A is unable to hydrolyze O-linked glycans and N-linked glycans

of the complex type. It is well known that enterococci cannot release O-linked glycans from mucin (Hoskins et al., 1985; Corfield et al., 1992). To verify that the observed band shifts are the result of hydrolysis of glycans, the supernatants were analyzed using MALDI-TOF MS. The spectra for RNase B (Fig. 3a and b) showed four signals with masses corresponding to 1 GlcNAc plus five to eight mannoses. This corresponds to four of the known glycoforms of the glycans of RNaseB, in which between two and five mannose residues can be coupled to the core GlcNAc2Man3 pentasaccharide (Fu et al., 1994). The MALDI-TOF MS spectrum of released oligosaccharides from ovalbumin (Fig. 3c and d) showed three clear signals corresponding to GlcNAcMan5, GlcNAcMan6 and GlcNAcMan5HexNAc2 (Fig. 3c and d). This is in accordance with the notion that both high-mannose and hybrid type glycans are linked to the N-glycosylation site of ovalbumin (An et al., 2003).

, 1990; Itin et al., 1998). This species can contaminate antiseptic creams and (skin) lotions, sodium bicarbonate solutions used as a neutralizing agent for a sodium hydroxide sterilizer for artificial lenses, selleck chemicals llc and colonize materials such as catheters and plastic implants (Pettit et al., 1980; Orth et al., 1996; Itin et al., 1998). A 3-year surveillance study showed that Purpureocillium lilacinum was frequently found in water distribution system of a bone marrow transplantation unit. Purpureocillium lilacinum positive sites included water from water tanks and showers, sinks, showers (including drains), toilets and air. This species can thrive on wet and moist surfaces

of water distribution

systems and form a biofilm, together with other species such as Aspergillus, Fusarium and Acremonium (Anaissie et al., 2003). Although biofilm formation by filamentous fungi has been poorly studied, it is postulated that adhesion, colonization and matrix formation are key criteria in the biofilm formation process (Martinez & Fries, 2010). The capacity of Purpureocillium lilacinum to adhere to the waxy host cuticle of nematodes and its ability to colonize surfaces under harsh conditions with low nutrient concentrations (fungal biofilters, plastics) and low oxygen levels (Mountfort IWR-1 solubility dmso & Rhodes, 1991; Vigueras et al., 2008) suggested that this species is able to form a biofilm. Concordant with our results, Okada et al. (1995) showed that Purpureocillium

lilacinum is a dimorphic species and is able to form an Acremonium-state in and/or on agar media. This Acremonium-state phenotypically resembles Fusarium solani, a fungal pathogen causing severe corneal disease and the causal agent of an outbreak of lens-associated keratitis. Remarkably, the most frequent manifestation of Purpureocillium lilacinum is also keratitis (Pastor & Guarro, 2006), suggesting that both species might have similar properties besides their phenotypic similarity. In this respect, it needs to be noted that Imamura et al. (2008) showed that F. solani has the ability to form biofilms on lenses; however, this appears to be strain rather than species dependent. Paecilomyces Endonuclease can cause hyalohyphomycosis, and two species, Purpureocillium lilacinum (=P. lilacinus) and P. variotii, are the most frequently encountered (Walsh et al., 2004; Houbraken et al., 2010). The phylogenies described here and elsewhere explain why some treatments will work for one species and fail for the others. Major differences in antifungal susceptibility profiles were found between P. variotii and Purpureocillium lilacinum in vitro. Amphotericin B showed good activity against P. variotii and related species in vitro, as was the case for flucytosine (Aguilar et al., 1998; Castelli et al., 2008; Houbraken et al., 2010).

difficile infection should be treated with metronidazole with consideration of vancomycin for fulminant disease, relapsing disease or non-responsive infection (category IV recommendation), following the recommendations for treatment in HIV-seronegative

populations outlined in Department of Health guidelines [50]. Therapy Hydroxychloroquine cost is indicated for C. difficile infection regardless of the CD4 cell count. Acute bacterial diarrhoea in HIV-seropositive individuals with CD4 counts >200 cells/μL usually does not require treatment, but should be treated when the CD4 count is <200 cells/μL (category IV recommendation). 4.4.1.4 Impact of HAART. Trimethoprim-sulphamethoxazole (TMP-SMX, co-trimoxazole) reduced the incidence of infectious diarrhoea

in the pre-HAART era [51]. Retrospective studies suggest that introduction of antiretroviral therapy, including zidovudine monotherapy, has been more effective than targeted antimicrobial prophylaxis in preventing recurrence learn more of nontyphoidal salmonella [52], and that duration of antimicrobial prophylaxis, with agents such as fluoroquinolones need not exceed 30 days in patients established on HAART [53]. The incidence of bacterial diarrhoea declined steadily after the introduction of HAART [28], therefore HAART is the mainstay of preventing bacterial diarrhoea (category III recommendation). 4.4.2.1 Background and epidemiology. Cytomegalovirus (CMV) is a member of the herpes family of viruses, usually acquired during

childhood. CMV infection remains dormant unless an individual becomes immunosuppressed, when reactivation of latent infection may occur [54,55]. In the pre-HAART era, retinitis was the most common presentation of CMV [56], followed by gastrointestinal disease (see C1GALT1 Table 4.2 for a list potential clinical manifestations of CMV in the GI tract). Most of the data about incidence of CMV were obtained from populations with retinitis. The majority of affected individuals had CD4 counts <100 cells/μL, with 80% of episodes occurring in those with CD4 counts <50 cells/μL. Since the advent of HAART, CMV infection may occasionally occur as part of immune reconstitution syndromes, but the overall incidence of CMV in individuals living with HIV has dramatically reduced [57]. 4.4.2.2 Presentation. CMV may affect all sections of the gut. Table 4.2 illustrates clinical presentation according to area affected. 4.4.2.3 Diagnosis. CMV viraemia, detected by polymerase chain reaction (PCR), may be positive in the absence of end-organ disease and several studies have shown this to be of negligible diagnostic use [58,59]. As indicated in Table 4.2, endoscopy may reveal classical CMV ulceration of the gut mucosa and biopsy with histopathological review may identify characteristic intranuclear and intracytoplasmic ‘owl’s eye’ inclusions [60]. The absence of ulceration makes a diagnosis of CMV colitis very unlikely [61].