Xanthomonas campestris pv. musacearum (Xcm) causes a disease on banana (Musa spp.) and enset (Ensete spp.) known as banana xanthomonas wilt (BXW). Recent studies have shown that Xcm is a strain of X. vasicola (Aritua et al., 2008). However, the status of pathovars within the species remains unclear. Prior to its discovery in Uganda in October 2001, the disease had been limited to Ethiopia (first reported 1968). Since then the disease has spread to the Democratic Republic of Congo and Rwanda (observed in May 2004 and September 2005 respectively). BXW can cause high yield losses and is a high priority concern within the Great Lakes region. A comprehensive review of the pathogen and disease was recently published by Smith et al. (2008). Thus far, outbreaks in Tanzania, Kenya and Burundi have only been referred to in symposium proceedings and on various websites. These new records are thus officially reported here for the first time. In Tanzania, the disease was first reported in the Kagera region of north west Tanzania, bordering Lake Victoria, Uganda, Rwanda and Burundi, in September 2005 (Mgenzi et al., 2006). Spread has continued, but not to other major banana growing areas. In Kenya, the disease was first reported in September 2006 in the Teso District, of western Kenya, bordering Uganda (Anon, 2006). Spread has since been reported as slow. In Burundi the disease was first observed during October 2006 (Anon., 2006). The current status of BXW in Burundi is unclear with no recent substantiated reports. Bacterial cultures were isolated from diseased racemes from Tanzania and Burundi at CABI, UK and from Kenya at KARI (NARL). All cultures were identified to species level at FERA by fatty acid profiling (MIDI system) and DNA analysis using X. vasicola specific primers (Aritua et al., unpublished data) and partial sequencing of the gyrase B gene (Parkinson et al., 2007). Koch's postulates were fulfilled for all strains at FERA by stem inoculation of banana plants (height approximately 30 cm) with a bacterial suspension (200 μL with ∼107 cfu/mL) under controlled environmental conditions (minimum temperature 27ºC). Identification of Xcm isolates from Burundi and Kenya was further supported by Ohio State University and KARI, respectively, using X. vasicola specific primers (Lewis-Levy Miller, unpublished data) that have a different target site to those of Aritua et al. (unpublished data). Reference cultures are held by the UK National Collection of Plant Pathogenic Bacteria, Accession Nos. NCPPB 4392-5 (Tanzania), 4434 (Kenya) and 4433 (Burundi).

OBJECTIVE:To determine the clinical utility of fatty acid ethyl esters (FAEEs) in the blood as a short-term confirmatory marker for ethanol intake and a longer-term marker for ethanol intake after ethanol is no longer detectable.DESIGN:Single-center controlled clinical trial and a blinded comparison involving 48 blood samples that were positive, negative, or equivocal for blood ethanol.PARTICIPANTS:Seven healthy subjects (4 men and 3 women, aged 21 to 23 years) participated in the clinical trial. Blood samples from participants for the blinded comparison portion of the study were numbered from 1 to 48 and not identified by name.INTERVENTION:The 7 healthy subjects ingested a known amount of ethanol at a fixed rate. The concentration of FAEEs in the blood after ethanol intake was determined for a period of up to 24 hours. There was no intervention in the blinded comparison study.MAIN OUTCOME MEASURES:In the clinical trial, a pharmacokinetic analysis of FAEE concentration in the blood after ethanol intake was completed for 7 individuals whose blood ethanol level was elevated from 25 to 35 mmol/L. In the blinded comparison, the 48 blood samples that were positive, negative, or equivocal for blood ethanol were analyzed for FAEE concentration.RESULTS:In the clinical trial, the disappearance of FAEEs from the blood followed a decay curve that initially resembled the decay curve for blood ethanol. However, because of a very slow secondary elimination phase, the FAEEs were found to persist in the blood for at least 24 hours after ethanol intake was completed. In the blinded comparison, all 20 samples that were positive for ethanol were positive for FAEEs, 7 of 7 samples equivocal for ethanol were positive for FAEEs, and 21 of 21 negative samples for ethanol were negative for FAEEs.CONCLUSIONS:Serum concentration of FAEEs can serve as an excellent short-term confirmatory test for ethanol intake as well as a longer-term marker of ethanol ingestion. Measurement of FAEEs in the blood may be a more sensitive indicator of ethanol ingestion than the measurement of blood ethanol .

We have developed a two-step method to purify fatty acid ethyl esters (FAEE) using solid-phase extraction (SPE), with a recovery of 70±3% (mean±S.E.M.) as assessed using ethyl oleate as a recovery marker from a standard lipid mixture in hexane. The first step of the SPE procedure involves application of a lipid mixture to an aminopropyl-silica column with simultaneous elution of FAEE and cholesteryl esters from the column with hexane. Gas chromatographic analysis of FAEE without interference from cholesteryl esters may be performed using the eluate from the aminopropyl-silica column, thus eliminating the need for an octadecylsily (ODS) column in this case. The FAEE can then be separated from the cholesteryl esters, if necessary, by chromatography on an ODS column and elution with isopropanol-water (5:1, v/v). Both the aminopropyl-silica and ODS columns were found to be effective for up to four uses. To permit isolation of specific FAEE species following isolation of total FAEE by the two-step SPE method, we have also developed a purification scheme for individaal FAEE by high-performance liquid chromatography (HPLC). Thus, this simple method allows for reproducible isolation of total FAEE by SPE and isolation of individual FAEE species by HPLC.

Transient hilar and mediastinal lymphadenopathy accompanying right-sided bacterial endocarditis without concurrent roentgenographically-demonstrable pulmonary parenchymal abnormalities has not, to our knowledge, been previously reported. The roentgenographic finding of hilar or mediastinal lymphadenopathy should not be considered incompatible with the diagnosis of bacterial endocarditis in the appropriate clinical setting. Possible mechanisms for the development of lymphadenopathy secondary to bacterial endocarditis are discussed.