But the fact that this protein is present in the solid fraction of the culture and in the protein mixture after solubilization indicates that Cry1Ac′3 is an insoluble protein, or that it is accumulated into small inclusion bodies undetectable by contrast phase microscopy. Second instar

larvae of E. kuehniella were exposed to different doses of Cry1Ac, find more Cry1Ac′1 and Cry1Ac′3 δ-endotoxins. Whereas Cry1Ac showed an LC50 of 1300 μg g−1 of semolina after 10 days, Cry1Ac′1 and Cry1Ac′3 showed no mortality, indicating that the two mutations Y229P and F603S affected the toxicity of the proteins. In vitro processing of the two mutant δ-endotoxins Cry1Ac′1 and Cry1Ac′3 was carried out to study their stability. After 2 h incubation of crystals and inclusions in 50 mM Na2CO3 with trypsin at a concentration of 1/100 (trypsin/δ-endotoxins, Etoposide price w/w), Cry1Ac was totally converted to a doublet of 65 and 60 kDa. However, Cry1Ac′1 was converted to a weak band of 65 kDa and Cry1Ac′3 was totally degraded (Fig. 4). Therefore, the protein Cry1Ac′1 was able to persist in the processing but the truncated protein Cry1Ac′3

was affected by proteases. This could explain the abolishment of the toxicity of Cry1Ac′3, as the activation is a key step in the mechanism of toxicity of Cry proteins. To explore the effect of Y229P and F603S substitutions at a molecular level, a three-dimensional model of Cry1Ac was constructed on the basis of the crystal structure of 1CIY of B. thuringiensis kurstaki strain HD-1 (Grochulski et al., 1995). The analysis

of the generated model showed that Cry1Ac is made up of three distinct domains. The N-terminal domain, known as domain I, is a helical bundle of seven alpha helices in which the central helix 5, which is relatively hydrophobic, is surrounded by the helices. Domain II consists of three antiparallel β-sheets joined in a Greek key topology, Amrubicin arranged in a β-prism. Domain III is formed by two antiparallel β-sheets with a jelly roll topology. Figure 5 illustrates the overall structure of Cry1Ac and the positions of Y229 and F603. Residue Y229 is located near the bottom of the α7 helix; it is a partially surface-exposed residue with no intramolecular interaction. Y229P mutation shortens the α7 helix by seven residues and generates a huge loop of 12 amino acids (Fig. 5b and c). The resultant mutant is inactive and the crystals produced are very small, suggesting that these alterations have affected, in some way, the stability of this mutant. In fact, the Y229P mutation affects the structure and the stability of the loop connecting helices α6 and α7 of domain I. This part of the toxin is maintained exclusively by tightly packed hydrophobic residues centered on Y229 and connecting the α6 and α7 helices. The hydrophobic network is the consequence of the interaction between residues W226, Y229, F232 and R233 of the α7 helix and residues L215, V218 and W219 of α6.

The patients were well enough to give informed consent and to take oral medications, and therefore the findings may not be generalizable to those who are severely unwell or requiring intensive care. Previous observational data suggest a survival benefit for HIV-positive patients who are started on ART while in the intensive care unit [3, 4], but the data are insufficient to make

a recommendation in this group [3, 4]. There was no increase in the incidence of immune reconstitution disorders (IRD) or adverse events generally with early ART initiation in ACTG 5164 [1,5]. However, those with intracranial Navitoclax solubility dmso opportunistic infections (such as cryptococcal meningitis [6]) may be more prone to severe IRDs with early ART initiation and increased observation of these patients may be warranted (although it is still recommended to initiate ART about 2 weeks after the commencement of opportunistic infection therapy assuming the patient is stable). Those presenting with TB and malignancies are discussed in Section 8. We recommend patients presenting with PHI and meeting any one of the following criteria start ART: Neurological involvement (1D). Any AIDS-defining illness (1A). Confirmed CD4 cell count <350 cells/μL (1C). Proportion of patients presenting with PHI and neurological involvement, or an AIDS-defining illness or confirmed CD4 cell count <350 cells/μL started on ART. The

scientific rationale for treating with ART in PHI is as follows. Preservation of specific anti-HIV CD4 T lymphocytes that would otherwise Meloxicam be destroyed GSK-3 inhibition by uncontrolled viral replication, the presence of which is associated with survival in untreated individuals [1]. Reduction in morbidity associated with high viraemia and profound CD4 cell depletion during acute infection [2-4]. Reduction in the enhanced risk of onward transmission of HIV associated with PHI [5-10]. Treatment of patients with PHI who present with AIDS-defining illnesses, neurological disease or a CD4

cell count of <350 cells/μL is consistent with the recommendations for patients with chronic infection. The rationale for treating patients with neurological disease is that ART may lead to regression of otherwise irreversible neurological disease (although there is no high-quality evidence for this effect of treatment in primary infection). Data from the CASCADE collaboration [11] showed that patients with primary infection, who had at least one CD4 cell count of <350 cells/μL in the first 6 months of infection, had a significantly greater mortality than those whose CD4 cell counts remained above this threshold, which supports early treatment in patients with lower CD4 cell counts. Multiple observational studies have shown encouraging but inconclusive results following short-course ART initiated in PHI for individuals in whom ART would not otherwise be indicated [12, 13].

The patients were well enough to give informed consent and to take oral medications, and therefore the findings may not be generalizable to those who are severely unwell or requiring intensive care. Previous observational data suggest a survival benefit for HIV-positive patients who are started on ART while in the intensive care unit [3, 4], but the data are insufficient to make

a recommendation in this group [3, 4]. There was no increase in the incidence of immune reconstitution disorders (IRD) or adverse events generally with early ART initiation in ACTG 5164 [1,5]. However, those with intracranial selleck chemical opportunistic infections (such as cryptococcal meningitis [6]) may be more prone to severe IRDs with early ART initiation and increased observation of these patients may be warranted (although it is still recommended to initiate ART about 2 weeks after the commencement of opportunistic infection therapy assuming the patient is stable). Those presenting with TB and malignancies are discussed in Section 8. We recommend patients presenting with PHI and meeting any one of the following criteria start ART: Neurological involvement (1D). Any AIDS-defining illness (1A). Confirmed CD4 cell count <350 cells/μL (1C). Proportion of patients presenting with PHI and neurological involvement, or an AIDS-defining illness or confirmed CD4 cell count <350 cells/μL started on ART. The

scientific rationale for treating with ART in PHI is as follows. Preservation of specific anti-HIV CD4 T lymphocytes that would otherwise Ribonucleotide reductase be destroyed Obeticholic Acid by uncontrolled viral replication, the presence of which is associated with survival in untreated individuals [1]. Reduction in morbidity associated with high viraemia and profound CD4 cell depletion during acute infection [2-4]. Reduction in the enhanced risk of onward transmission of HIV associated with PHI [5-10]. Treatment of patients with PHI who present with AIDS-defining illnesses, neurological disease or a CD4

cell count of <350 cells/μL is consistent with the recommendations for patients with chronic infection. The rationale for treating patients with neurological disease is that ART may lead to regression of otherwise irreversible neurological disease (although there is no high-quality evidence for this effect of treatment in primary infection). Data from the CASCADE collaboration [11] showed that patients with primary infection, who had at least one CD4 cell count of <350 cells/μL in the first 6 months of infection, had a significantly greater mortality than those whose CD4 cell counts remained above this threshold, which supports early treatment in patients with lower CD4 cell counts. Multiple observational studies have shown encouraging but inconclusive results following short-course ART initiated in PHI for individuals in whom ART would not otherwise be indicated [12, 13].

The patients were well enough to give informed consent and to take oral medications, and therefore the findings may not be generalizable to those who are severely unwell or requiring intensive care. Previous observational data suggest a survival benefit for HIV-positive patients who are started on ART while in the intensive care unit [3, 4], but the data are insufficient to make

a recommendation in this group [3, 4]. There was no increase in the incidence of immune reconstitution disorders (IRD) or adverse events generally with early ART initiation in ACTG 5164 [1,5]. However, those with intracranial http://www.selleckchem.com/products/LDE225(NVP-LDE225).html opportunistic infections (such as cryptococcal meningitis [6]) may be more prone to severe IRDs with early ART initiation and increased observation of these patients may be warranted (although it is still recommended to initiate ART about 2 weeks after the commencement of opportunistic infection therapy assuming the patient is stable). Those presenting with TB and malignancies are discussed in Section 8. We recommend patients presenting with PHI and meeting any one of the following criteria start ART: Neurological involvement (1D). Any AIDS-defining illness (1A). Confirmed CD4 cell count <350 cells/μL (1C). Proportion of patients presenting with PHI and neurological involvement, or an AIDS-defining illness or confirmed CD4 cell count <350 cells/μL started on ART. The

scientific rationale for treating with ART in PHI is as follows. Preservation of specific anti-HIV CD4 T lymphocytes that would otherwise Miconazole be destroyed Tofacitinib purchase by uncontrolled viral replication, the presence of which is associated with survival in untreated individuals [1]. Reduction in morbidity associated with high viraemia and profound CD4 cell depletion during acute infection [2-4]. Reduction in the enhanced risk of onward transmission of HIV associated with PHI [5-10]. Treatment of patients with PHI who present with AIDS-defining illnesses, neurological disease or a CD4

cell count of <350 cells/μL is consistent with the recommendations for patients with chronic infection. The rationale for treating patients with neurological disease is that ART may lead to regression of otherwise irreversible neurological disease (although there is no high-quality evidence for this effect of treatment in primary infection). Data from the CASCADE collaboration [11] showed that patients with primary infection, who had at least one CD4 cell count of <350 cells/μL in the first 6 months of infection, had a significantly greater mortality than those whose CD4 cell counts remained above this threshold, which supports early treatment in patients with lower CD4 cell counts. Multiple observational studies have shown encouraging but inconclusive results following short-course ART initiated in PHI for individuals in whom ART would not otherwise be indicated [12, 13].

The experiments were prepared in

triplicate and repeated three times. Bacterial cultures were centrifuged at 3000 g for 5 min at 4 °C to pellet the cells. The supernatants were removed and the bacterial cells were washed with sterile water three times. Then the cells were resuspended in PDB dilutions (PDB 1 : 50) to yield different working concentrations (0.33, 1, 1.67, 2.33, 3.0 and 3.67 × 107 CFU mL−1, using dilution plating on nutrient agar). These solutions were used to bioassay for trap formation. The negative controls were PDB dilutions (PDB 1 : 50). The experiments were prepared in triplicate and repeated three times. Bacteria learn more cells were obtained as described above and resuspended in PDB dilutions (1 : 50) containing 20% v/v bacterial cell-free

culture filtrate to yield different working concentrations (0.33, 1, 1.67, 2.33, 3.0 and 3.67 × 107 CFU mL−1). These solutions were used to bioassay for trap formation. The negative controls were 20% NB (v/v) prepared by PDB dilutions (PDB 1 : 50). The experiments were prepared in triplicate selleck inhibitor and repeated three times. Bacterial cells were resuspended to yield working concentrations of 1.67 × 107 CFU mL−1 in PDB dilutions (1 : 50) containing 5%, 10%, 20%, 30% or 40% v/v bacterial cell-free culture filtrates. These solutions were used to assay trap formation. Four control plates were included in each test run. Two control plates were PDB dilutions (PDB 1 : 50) containing 5% NB (v/v) without or with bacterial cells (final concentration, 1.67 × 107 CFU mL−1). And the other two were PDB dilutions (PDB 1 : 50) containing 40% NB (v/v) without or with bacterial cells (final concentration, 1.67 × 107 CFU mL−1). The experiments were prepared in triplicate and repeated three times. Arthrobotrys oligospora conidia were cocultivated with bacterial cells (final concentration, 1.67 × 107 CFU mL−1) containing or not containing 20%

bacterial cell-free culture filtrates in PDB dilution (PDB old 1 : 50). Arthrobotrys oligospora conidia were cocultivated (PDB 1 : 50) with bacterial cells (final concentration, 1.67 × 107 CFU mL−1) in sterile water. Negative controls were PDB dilution (PDB 1 : 50) containing 20% NB (v/v) or sterile water. Fungal pellets absorbed by variable volume pipette were placed into another Petri plate and washed with 10 mL sterile water three times, mounted on a stub and coated with gold. The specimens were examined using a FEI Quanta 200 scanning electron microscope from FEI Company (Hillsboro) in the high-vacuum mode at 20 kV. Each treatment was performed in duplicate and the experiment was repeated three times. Bacterial cells were resuspended to a working concentration of 1.67 × 107 CFU mL−1 prepared by sterile water or a nutrient solution consisting of PDB, a series of dilutions of PDB (1 : 5, 1 : 10, 1 : 20, 1 : 30, 1 : 50, 1 : 100, 1 : 200) containing 20% v/v bacterial cell-free culture filtrates. These solutions were used to assay trap formation.

8% Indian and 6.2% others), the spectrum of diseases seen Selleck BLZ945 was as follows [disease – definite n (%), probable n (%)]: Arthritis: rheumatoid arthritis – 958 (22.9%), 68 (1.6%); osteoarthritis – 452 (10.8%), 39 (0.9%); crystal arthritis – 417 (10.0%), 18 (0.4%); spondyloarthritis – 227 (5.4%), 61 (1.5%); psoriatic arthritis – 158 (3.8%), 9 (0.2%); other inflammatory arthritis – 153 (3.7%), 94 (2.2%); Connective tissues diseases: systemic lupus erythematosus – 412 (9.9%), 26 (0.6%); vasculitis – 105 (2.5%), 22 (0.5%); Sjögren’s

syndrome – 81 (1.9%), 32 (0.8%); overlap syndromes – 73 (1.8%); scleroderma – 50 (1.2%), 4 (0.1%); undifferentiated connective tissue diseases – 45 (1.1%), 106 (2.5%); myositis – 41 (1.0%), 12 (0.3%); antiphospholipid syndrome – 22 (0.5%), 7 (0.2%); polymyalgia rheumatica – 16 (0.4%); Others: soft tissue rheumatism – 155 (3.7%); osteoporosis – 61 (1.5%); other non-rheumatologic conditions – 189 (4.5%); other rheumatologic conditions – 67 (1.6%). Rheumatoid arthritis, osteoarthritis and crystal arthritis were the three most common rheumatological diseases seen in a tertiary referral centre serving a Epigenetic inhibitor multi-ethnic urban Asian population in Singapore. “
“There is strong rationale for improving

care for people with chronic conditions, including osteoarthritis (OA). Successful implementation of healthcare reform requires new concepts and directions that are strongly supported by policy, new models of care (service redesign) and changes in day-to-day practice (healthcare provider and patient practice). In this paper we discuss the extent to which policy about management Parvulin of OA of the hip and knee has been translated into new service models in Australia. A structured search of government and other key health websites in Australia was performed to identify policy, funding initiatives and new services models for managing OA of the hip and knee. This search

was supported by a literature review. Musculoskeletal conditions were designated a National Health Priority in Australia in 2002. Under the Better Arthritis and Osteoporosis Care initiative, Australia has developed a national policy for OA care and national evidence-based clinical practice guidelines for management of OA of the hip and knee. Only two well-described examples of new chronic disease management service models, the Osteoarthritis Clinical Pathway (OACP) model and the Osteoarthritis Hip and Knee Service (OAHKS) were identified. Primarily focused within acute care public hospital settings, these have been shown to be feasible and acceptable but have limited data on clinical impact and cost-effectiveness. While policy is extant, implementation has not been systematic and comprehensive. Clinicians have evidence-based recommendations for OA management but are poorly supported by service models to deliver these effectively and efficiently.

16 Meanwhile this method has been adapted to suit smaller volumes (2 mL) of serum instead of 20 mL of plasma, without losing sensitivity. To perform a real-time PCR with sufficient specificity, a 121-bp tandem repeat sequence, identified by Hamburger in 1991, that consitutes about 12% of the S mansoni genome and is highly specific for all human schistosomes, was chosen as the real-time PCR target gene.17 Together with the patients’ test samples, a quantification standard plasmid (positive control), containing the nucleotides 39 to 79 bp from the 121-bp tandem repeat

sequence, and an internal negative control were run, as described by Panning.18 Plasmids were purified and subsequently 5FU quantified by spectrophotometry.

Dilutions of the standard plasmid were used as a quantification reference in real-time PCR. The cycle threshold value (Ct value) corresponds with the number of Selleckchem Stem Cell Compound Library PCR cycles needed to attain the threshold level of log-based fluorescence. A test was considered positive when the threshold was attained within 45 PCR cycles (Ct value <45). A lower Ct value corresponds with a higher amount of template DNA copies in the serum sample. In this cluster series, the specificity of the PCR assay for human schistosomes has not been assessed. This was already done by Wichmann in his original assay setup where he used plasma from 30 blood donors and 35 patients examined for other conditions to SPTBN5 be tested by large-volume plasma extraction and CFPD real-time PCR.16 None yielded positive results. We therefore felt it

unnecessary to have this experiment rerun. All patients were treated with a single dose of praziquantel at 40 mg/kg. Patients were instructed to take a single dose of methylpredisolone (0.5 mg/kg) in case fever developed soon after praziquantel treatment, and to contact the attending physician at our outpatient department for further advice regarding the duration of this treatment. Patients were seen again 5 weeks thereafter for evaluation of cure and a second single dose of praziquantel to be given to all, consistent with the established clinical practice at the outpatient clinic. For data analysis, a nonparametric test (Mann– Whitney/Wilcoxon) was used to compare continuous variables (including Ct values), and the Fisher exact test to compare proportions. Consistent with the in-house ethical guidelines for noninterventional studies, patients’ consent (or their adult guardians’ consent) was formally obtained to perform an additional diagnostic test on a preserved serum sample already used for antibody testing. The outcome of PCR test results did not interfere with the diagnosis, standard treatment, and follow-up procedure of schistosomiasis at the outpatient clinic.

16 Meanwhile this method has been adapted to suit smaller volumes (2 mL) of serum instead of 20 mL of plasma, without losing sensitivity. To perform a real-time PCR with sufficient specificity, a 121-bp tandem repeat sequence, identified by Hamburger in 1991, that consitutes about 12% of the S mansoni genome and is highly specific for all human schistosomes, was chosen as the real-time PCR target gene.17 Together with the patients’ test samples, a quantification standard plasmid (positive control), containing the nucleotides 39 to 79 bp from the 121-bp tandem repeat

sequence, and an internal negative control were run, as described by Panning.18 Plasmids were purified and subsequently TGF-beta inhibitor clinical trial quantified by spectrophotometry.

Dilutions of the standard plasmid were used as a quantification reference in real-time PCR. The cycle threshold value (Ct value) corresponds with the number of AG14699 PCR cycles needed to attain the threshold level of log-based fluorescence. A test was considered positive when the threshold was attained within 45 PCR cycles (Ct value <45). A lower Ct value corresponds with a higher amount of template DNA copies in the serum sample. In this cluster series, the specificity of the PCR assay for human schistosomes has not been assessed. This was already done by Wichmann in his original assay setup where he used plasma from 30 blood donors and 35 patients examined for other conditions to LY294002 be tested by large-volume plasma extraction and CFPD real-time PCR.16 None yielded positive results. We therefore felt it

unnecessary to have this experiment rerun. All patients were treated with a single dose of praziquantel at 40 mg/kg. Patients were instructed to take a single dose of methylpredisolone (0.5 mg/kg) in case fever developed soon after praziquantel treatment, and to contact the attending physician at our outpatient department for further advice regarding the duration of this treatment. Patients were seen again 5 weeks thereafter for evaluation of cure and a second single dose of praziquantel to be given to all, consistent with the established clinical practice at the outpatient clinic. For data analysis, a nonparametric test (Mann– Whitney/Wilcoxon) was used to compare continuous variables (including Ct values), and the Fisher exact test to compare proportions. Consistent with the in-house ethical guidelines for noninterventional studies, patients’ consent (or their adult guardians’ consent) was formally obtained to perform an additional diagnostic test on a preserved serum sample already used for antibody testing. The outcome of PCR test results did not interfere with the diagnosis, standard treatment, and follow-up procedure of schistosomiasis at the outpatient clinic.

Since these resources are unlikely to be present in the countries most frequently visited by traveling students and residents, the responsibility must go to the home institution to both educate and provide support

to their traveling constituents. Yale-New Haven Hospital and Yale University School of Medicine have a long history of sending medical students and residents abroad to both affiliated institutions and independent rotations. Faculty members at Yale developed a program which includes predeparture orientation, access to support staff 7 days a week by telephone, and either a week or month’s supply of antiretroviral medications (zidovudine/lamivudine and nelfinavir), depending on the postal accessibility of the location. Orientation involves an overview of precautions, types of exposures that require Seliciclib datasheet medical treatment, and the importance of follow-up testing. If they have a blood or body fluid exposure, residents are instructed to call a phone number that is staffed 7 days a week to receive counseling, further education, and the rest of the 28-day regimen, which is sent to the field site via express mail.12 Partners in Health, a nonprofit organization affiliated with the Brigham and Women’s Hospital and Harvard Medical School, also has an established www.selleckchem.com/hydroxysteroid-dehydrogenase-hsd.html protocol. After an exposure, both the source patient and exposed health care worker

are offered voluntary counseling and testing. Risk is assessed based on suspicion of HIV in the source, where the exposure occurred (surgery, phlebotomy, etc.), and the degree of exposure to the victim (mucosal, percutaneous, etc.). If there is a high degree of risk, both prophylaxis and baseline assessments are initiated. If the source 3-oxoacyl-(acyl-carrier-protein) reductase patient is determined to be HIV positive, therapy

is continued for 28 days, and HIV counseling and testing are repeated at 12 weeks and 6 months.13 Boston Medical Center and the Boston University School of Medicine (BUSM), in collaboration with the Maluti Hospital in Lesotho, developed guidelines for family medicine residents, pediatric residents, and medical students doing rotations in Lesotho. In addition to pretravel education on safety issues related to nosocomial exposure and guidelines for PEP, traveling health care workers are provided with a 4-week supply of tenofovir/emtricitabine, or zidovudine/lamivudine, and lopinavir/ritonavir. Prior to departure, residents and students are given the option to undergo screening for hepatitis B, hepatitis C, HIV, and tuberculosis. In the event of an exposure, the trainee is advised to immediately clean the exposed area with soap and water or a disinfectant, if available, and then to notify a supervisor and a BUSM faculty designate. The exposure is categorized based on the mode of injury, the exposure severity, and the serostatus of the source. Students/residents are provided with a cell phone for their rotation to ensure access to a home-based mentor.

Figure 3 shows that there was a gradual decrease in the ThyA level during the stationary growth phase to 40% of that in the selleck chemicals late-exponential phase cells in LB medium (Fig. 3a and c). Conversely, ThyX was maintained at the same

level in both the late-exponential and stationary phase cells (Fig. 3b and c), indicating that the levels of ThyA and ThyX were regulated by different mechanisms and that ThyX could play a role in the stationary growth phase of C. glutamicum. The thyX gene is located on an operon with dapB and dapA, and these genes are transcribed as a single unit, dapB-thyX-dapA (Park et al., 2010). Two putative promoter regions of dapB were identified by primer extension analyses (Pátek et al., 1996), and one of the promoters or both (p1-dapB and/or p2-dapB) might be recognized by SigB. SigB was shown to be induced during the transition from the exponential to the stationary growth phase (Larisch et al., 2007; Pátek & Nešvera, 2011).

To examine whether the level of ThyX was regulated by SigB, a ΔsigB strain was constructed by allelic replacement using a sucrose counter-selectable suicide plasmid. Deletion of sigB was confirmed Akt inhibitor by PCR amplification of the sigB region, with primers binding upstream and downstream of sigB. A 1329-bp fragment containing intact sigB was seen in the wild-type strain, and a 324-bp fragment was seen in the mutant strain (Fig. 1b). The transcriptional activity of the dapB-thyX promoter region was quantified in the wild-type and ΔsigB strain KH4 after the

introduction of plasmid pMTXL1. The thyX promoter in the ΔsigB strain revealed about 25% of the activity shown in the parental wild-type strain (Fig. 4a). Thus, SigB was shown to be necessary for the induction of thyX. The levels of ThyA or ThyX in the wild-type, KH4, and KH5 strains of C. glutamicum were analyzed by immunoblotting using antiserum against ThyA or ThyX, respectively. Whereas the level of ThyA in the ΔsigB strain was comparable to that of the parental wild-type, the level of ThyX was diminished significantly in the deletion mutant (Fig. 4b). Complementation of the ΔsigB mutation was performed with a plasmid containing wild-type sigB, including its putative promoter region. Western blotting analysis revealed that expression P-type ATPase of functional sigB in the complemented strain restored the accumulation of ThyX to nearly wild-type levels (Fig. 4b). This result confirmed that SigB is necessary for maintenance of the level of ThyX during transition into the stationary growth phase. To investigate the role of the sigma factor SigB on sensitivity to a DHFR inhibitor, WR99210-HCl, wild-type, KH4, and KH5 strains grown to log-phase were inoculated into MCGC minimal medium containing isocitrate and glucose with 3 µM WR99210-HCl. Growth was monitored for 36 h, and the KH4 strain appeared to be sensitive to WR99210-HCl.