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PubMed1996

Microorganisms in honey.

Knowledge of the moisture and temperature conditions influencing growth of microorganisms in honey has long been used to control the spoilage of honey. However, the need for additional microbiological data on honey will increase as new technologies for, and uses of honey develop. Microorganisms in honey may influence quality or safety. Due to the natural properties of honey and control measures in the honey industry, honey is a product with minimal types and levels of microbes. Microbes of concern in post-harvest handling are those that are commonly found in honey (i.e., yeasts and spore-forming bacteria), those that indicate the sanitary or commercial quality of honey (i.e., coliforms and yeasts), and those that under certain conditions could cause human illness. Primary sources of microbial contamination are likely to include pollen, the digestive tracts of honey bees, dust, air, earth and nectar, sources which are very difficult to control. The same secondary (after-harvest) sources that influence any food product are also sources of contamination for honey. These include air, food handlers, cross-contamination, equipment and buildings. Secondary sources of contamination are controlled by good manufacturing practices. The microbes of concern in honey are primarily yeasts and spore-forming bacteria. Total plate counts from honey samples can vary from zero to tens of thousands per gram for no apparent reason. Most samples of honey contain detectable levels of yeasts. Although yeast counts in many honey samples are below 100 colony forming units per gram (cfu/g), yeasts can grow in honey to very high numbers. Standard industry practices control yeast growth. Bacterial spores, particularly those in the Bacillus genus, are regularly found in honey. The spores of C. botulinum are found in a fraction of the honey samples tested-normally at low levels. No vegetative forms of disease-causing bacterial species have been found in honey. Bacteria do not replicate in honey and as such high numbers of vegetative bacteria could indicate recent contamination from a secondary source. Certain vegetative microbes can survive in honey, at cool temperatures, for several years. However, honey has anti-microbial properties that discourage the growth or persistence of many microorganisms. Typically, honey can be expected to contain low numbers and a limited variety of microbes. A routine microbiological examination of honey might include several different assays. A standard plate count provides general information. Specialized tests, such as a count of yeasts and an assay for bacterial spore-formers, may also be useful. An indicator of sanitary quality as provided by coliform counts might be included. Additional tests, to explain unusually high counts or address a certain problem, may be needed. The use of honey in products that receive no or limited heat treatment may require additional tests. More information on the source and control of microbes in honey is needed to answer the concerns currently facing the industry.

Anti-Bacterial Agents↗
PubMed2004

Natural honey lowers plasma glucose, C-reactive protein, homocysteine, and blood lipids in healthy, diabetic, and hyperlipidemic subjects: comparison with dextrose and sucrose.

This study included the following experiments: (1) effects of dextrose solution (250 mL of water containing 75 g of dextrose) or honey solution (250 mL of water containing 75 g of natural honey) on plasma glucose level (PGL), plasma insulin, and plasma C-peptide (eight subjects); (2) effects of dextrose, honey, or artificial honey (250 mL of water containing 35 g of dextrose and 40 g of fructose) on cholesterol and triglycerides (TG) (nine subjects); (3) effects of honey solution, administered for 15 days, on PGL, blood lipids, C-reactive protein (CRP), and homocysteine (eight subjects); (4) effects of honey or artificial honey on cholesterol and TG in six patients with hypercholesterolemia and five patients with hypertriglyceridemia; (5) effects of honey for 15 days on blood lipid and CRP in five patients with elevated cholesterol and CRP; (6) effects of 70 g of dextrose or 90 g of honey on PGL in seven patients with type 2 diabetes mellitus; and (7) effects of 30 g of sucrose or 30 g of honey on PGL, plasma insulin, and plasma C-peptide in five diabetic patients. In healthy subjects, dextrose elevated PGL at 1 (53%) and 2 (3%) hours, and decreased PGL after 3 hours (20%). Honey elevated PGL after 1 hour (14%) and decreased it after 3 hours (10%). Elevation of insulin and C-peptide was significantly higher after dextrose than after honey. Dextrose slightly reduced cholesterol and low-density lipoprotein-cholesterol (LDL-C) after 1 hour and significantly after 2 hours, and increased TG after 1, 2, and 3 hours. Artificial honey slightly decreased cholesterol and LDL-C and elevated TG. Honey reduced cholesterol, LDL-C, and TG and slightly elevated high-density lipoprotein-cholesterol (HDL-C). Honey consumed for 15 days decreased cholesterol (7%), LDL-C (1%), TG (2%), CRP (7%), homocysteine (6%), and PGL (6%), and increased HDL-C (2%). In patients with hypertriglyceridemia, artificial honey increased TG, while honey decreased TG. In patients with hyperlipidemia, artificial honey increased LDL-C, while honey decreased LDL-C. Honey decreased cholesterol (8%), LDL-C (11%), and CRP (75%) after 15 days. In diabetic patients, honey compared with dextrose caused a significantly lower rise of PGL. Elevation of PGL was greater after honey than after sucrose at 30 minutes, and was lower after honey than it was after sucrose at 60, 120, and 180 minutes. Honey caused greater elevation of insulin than sucrose did after 30, 120, and 180 minutes. Honey reduces blood lipids, homocysteine, and CRP in normal and hyperlipidemic subjects. Honey compared with dextrose and sucrose caused lower elevation of PGL in diabetics.

Adult↗
PubMed2003

Intravenous and intrapulmonary administration of honey solution to healthy sheep: effects on blood sugar, renal and liver function tests, bone marrow function, lipid profile, and carbon tetrachloride-induced liver injury.

Safety of intravenous (i.v.) or intrapulmonary administration of different concentrations of honey and their effects on blood sugar, renal and liver function tests, bone marrow function, lipid profile, and carbon tetrachloride (CCl(4))-induced liver damage were studied. Healthy sheep of either sex, 6-8 months old, were assigned randomly into the following groups: sheep received i.v. infusion of 5% honey in normal saline at 10-day intervals for 50 days and were compared with sheep that received 5% dextrose; sheep received higher doses of honey (50 g of honey) by i.v. infusion daily for 10 days; sheep received four higher doses of honey (80 g each dose) for 2 weeks; sheep received subcutaneous injection of CCl(4) after four doses of i.v. infusion of 80 g of honey, and estimations of serum gamma-glutamyl transpeptidase (SGGT), serum glutamic oxaloacetic transaminase (SGOT), and serum glutamate pyruvate transaminase (SGPT) were performed daily for 10 days postinjection; sheep received i.v. infusion of 40 g of honey, and blood sugar estimation was performed for 3 h at 30-min intervals after infusion and compared with sheep that received 5% dextrose; sheep received rapid i.v. injection of 40% honey or 40% dextrose, and blood sugar was estimated before and after injection; sheep received various concentrations of honey in distilled water (0.5 mL/1.5 mL, 0.75 mL/1.75 mL and 1.2 mL/2.2 mL), and blood sugar estimation was performed before and after inhalation. Results showed that i.v. or intrapulmonary administration of honey did not cause any adverse effect. Intravenous delivery of honey by slow infusion caused improvement of renal and hepatic function, bone marrow function, and lipid profile. It reduced SGOT, SGPT, triglyceride, cholesterol, blood urea nitrogen, and blood sugar and elevated serum protein, serum albumin, hemoglobin, white blood cell, and neutrophil percentage. Similar results were obtained with the use of higher doses of honey. CCl(4) caused mild elevation of SGPT and SGGT and lowering of SGOT in sheep that received repeated i.v. administration of honey before administration of CCl(4), whereas in control sheep CCl(4) caused significant elevation of all the liver enzymes. Intravenous infusion of 40 g of honey caused elevation of blood sugar for 90 min postinfusion, whereas it decreased blood sugar at 2 and 3 h postinfusion as compared with fasting blood sugar. Dextrose caused significant elevation of blood sugar at all time intervals. Similar results were obtained with the use of 10% dextrose or 80 g of honey. Addition of honey to dextrose caused less hyperglycemia as compared with dextrose alone. Acute injection of 20 mL of 40% dextrose significantly elevated blood sugar for 3 h postinjection, whereas little elevation in blood sugar was obtained after injection of 40% honey; the difference between honey and dextrose was significant. Inhalation of honey caused significant lowering of blood sugar during and after inhalation as compared with fasting blood sugar and water inhalation. The effect was greater with a higher concentration of inhaled honey. It might be concluded that slow i.v. infusion or rapid i.v. injection of honey in different concentrations was safe and could lower blood sugar and improve renal, hepatic, and bone marrow functions and lipid profile. Intravenous honey had a hepatoprotective effect against CCl(4)-induced liver injury. Inhaled honey was safe and reduced blood sugar significantly.

Administration, Inhalation↗
PubMed2004

Quantitative high-performance liquid chromatography analyses of flavonoids in Australian Eucalyptus honeys.

Flavonoids of nine Australian monofloral Eucalyptus honeys have been analyzed and related to their botanical origins. The mean content of total flavonoids varied from 1.90 mg/100 g of honey for stringybark (E. globoidia) honey to 8.15 mg/100 g of honey for narrow-leaved ironbark (E. crebra) honey, suggesting that species-specific differences occur quantitatively among these Eucalyptus honeys. All of the honey samples analyzed in this study have a common flavonoid profile comprising tricetin (5,7,3',4',5'-pentahydroxyflavone), quercetin (3,5,7,3',4'-pentahydroxyflavone), and luteolin (5,7,3',4'-tetrahydroxyflavone), which, together with myricetin (3,5,7,3',4',5'-hexahydroxyflavone) and kaempferol (3,5,7,4'-tetrahydroxyflavone), were previously suggested as floral markers for European Eucalyptus honeys. Thus, flavonoid analysis could be used as an objective method for the authentication of the botanical origin of Eucalyptus honeys. Moreover, species-specific differences can also be found in the composition of honey flavonoid profiles. Among these honeys, bloodwood (E. intermedia) honey contains myricetin and tricetin as the main flavonoid compounds, whereas there is no myricetin detected in yapunyah (E. ochrophloia), narrow-leaved ironbark (E. crebra), and black box (E. largiflorens) honeys. Instead, these types of Eucalyptus honeys may contain tricetin, quercetin, and/or luteolin as their main flavonoid compounds. Compared to honeys from other geographical origins, the absence or minor presence of propolis-derived flavonoids such as pinobanksin, pinocembrin, and chrysin in Australian honeys is significant. In conclusion, these results demonstrate that a common flavonoid profile exists for all of the Eucalyptus honeys, regardless of their geographical origins; the individual species-specific floral types of Eucalyptus honey so common in Australia could be possibly differentiated by their flavonoid profile differences, either qualitatively or quantitatively or both.

Australia↗
PubMed2005

The antimicrobial potential of honey from United Arab Emirates on some microbial isolates.

BACKGROUND: The study investigated activity of honey towards pathogens when grown in media contained honey, or when honey was added to cultures after inoculation. MATERIAL/METHODS: 1--Staphylococcus aureus (S. aureus), Streptococcus pyogenes (S. pyogenes), E.coli and Candida albicans (C. albicans) were cultured into broth containing 10-100% (wt/v) honey concentrations. 2--Honey was added to broth inoculated with isolates after inoculation. 3--Optimum growth of isolates, therapeutic period of honey, and time after addition of honey that showed optimum effect was measured. RESULTS: The optimum growth of E. Coli and C. Albicans was 10 hrs and S. aureus was 12 hrs. Honey (30-70%) prevents growth of all isolates. Honey (80%) inhibited growth of small (1 microl) and large size of inoculum (10 microl) of E. Coli and S. Aureus when added to their cultures during 24 hrs after inoculation. Honey inhibited growth of C. Albicans when added during 2 to 6 hrs after inoculation. Honey delayed the appearance of microbial growth on the plates. Reculturing of specimens collected from media that showed no growth after addition of honey yielded recovery growth for E.coli and C. Albicans, and therapeutic period of honey for E.coli and S. Aureus was 2-24 hrs and for C. Albicans was 2-6 hrs. CONCLUSIONS: Honey prevents growth of the isolates and inhibits their growth when honey was added to growing culture. The therapeutic period of honey and recovery growth of inhibited isolates necessitates adjustment of honey doses according to type of isolate and grade of growth.

Anti-Infective Agents↗