Beta Carotene: is it a Good Source of Vitamin A??

For my Agricultural Biochemistry class we had to write a research paper that focused on Golden Rice ( A genetically modified organism (GMO)) as a good source of Vitamin A. A long story short this rice was developed to provide Vitamin A to poor countries that have citizens with vitamin A deficiencies. The rice is created by taking genes from other plants and bacteria that synthesize beta carotene. These genes are then added to the rice’s genome to create this rice that is Golden in color hence the name. Beta carotene is a precursor of Vitamin A. Your body must convert the Beta Carotene to Vitamin A by biochemical processes that require the utilization of fat. So my paper discusses some of the issues of Beta Carotene as a source of Vitamin A.  Enjoy!





The Bioavailability and Bioefficacy of
Beta-carotene as a Source of Vitamin A
by Nadia Ruffin
Biochemistry 818 Fall Semester


indexGolden rice is a genetically modified organism that has incorporated beta-carotene genes from bacteria and dafodils into rice. The combination of beta-carotene into a staple food like rice could be the cure to ending Vitamin A deficiency thus combating blindness and reproductive issues in third world countries . While the methodology has shown promising results there is still much research that needs to be done on a biochemical level in regarding to the efficiency of beta-carotene being used as a main source of vitamin A. In my paper I decided to look at the bioavailability of beta-carotene in food. Then I looked into the bioefficacy of converting beta-carotene into retinol and how different factors can affect the outcome. Finally I looked at how absorption of retinol can be effected by varying levels of oil in the diet.

Vitamin A is a fat soluble vitamin. The name vitamin A is given to a group of organic compounds known as retinoids: these includes retinol, retinal, retinoic acid, and provitamin A carotenoids. The main dietary forms of preformed vitamin A are carotenoids (most common Beta-carotene) in fruits and vegetables and long-chain Fatty Acid esters of retinol in foods of animal origin (Plack, 1965). It is interesting how beta-carotene rich foods are always recommended as a good source of vitamin A. In actuality carotenoids are a precursor for vitamin A and must be converted into retinol before the body can utilize it. Animal products like liver, dairy or eggs would be better sources of retinol because they are already bioavailable and do not require them to them be converted. It is at this point that utilizing carotenoids as a source of vitamin A may become a problem.

Bioavailability is defined as the fraction of an ingested nutrient from food that is available for absorption in the intestine and metabolic process and storage (Jackson, 1997). There are many factors that affect bioavailability of beta-carotene like source of food, how it is prepared etc. In a study conducted by Dr. Hedren and colleagues they performed an in-vitro digestion simulation to see how much beta-carotene is actually extracted from carrots. Their setup consisted of batches of raw carrots just cut, pulped carrots with cooking oil, pulped carrots without oil and pulped cooked carrots with cooking oil added. They added pepsin-HCl dropping the pH to 2.0 and then raised the pH to 7.5 and a pancreatin-bile extract mixture was added at the end. It has been shown that bile salts play a role in extracting carotenoids from food. What they found is that three percent of the total beta-carotene content was released from raw carrots in pieces. When homogenized (pulped) 21% of beta-carotene was released. Cooking the pulp increased the accessibility to 27%. Addition of cooking oil to the cooked pulp further increased the released amount to 39% (Hedren et al, 2002). It was interesting that the amount of beta-carotene released after cooking and adding oil increased. While cooking beta-carotene rich vegetables does release more beta carotene there can also be some loss. According to the USDA vegetables can lose roughly 5 percent of their total beta-carotene through baking or roasting. When compared these cooking methods to boiling, the total loss of beta-carotene can be between 10 to 15 percent. The longer you boil food the more you give it the opportunity for beta-carotene to leach into the water. Also simply mashing the vegetables can release more beta-carotene than in it raw unadulterated form.
So how is this relevant to golden rice? Well to prepare rice it must be cooked for extensive period of time to get it to the desired tenderness. There was a study by Guangwen Tang et al. on Golden Rice that made a claim that it did not lose it’s beta-carotene content even after cooking, based off their analysis, but they never explained how they analyzed it. Their study also yielded an estimated 80% conversion rate of beta-carotene to retinol. This feeding trial was performed on only five healthy US volunteers, showed the effective conversion of Golden Rice β-carotene, even though all individuals were of normal vitamin A status (Tang, 2009). This study and other golden rice studies do not test the conversion of beta-carotene to retinol in vitamin A deficient populations which brings up the next point converting beta-carotene to retinol.

The mechanism to cleave beta-carotene in half uses an enzyme called dioxygenase, the product is two molecules of retinal that is further reduced using reductase to retinol. While this sounds simple it’s not that cut and dry. Bioefficacy is the capability of an individual —governed by individual internal factors— to convert β-carotene (provitamin A) into retinal, retinol (vitamin A) and retinyl esters. It is expressed as the amount of β-carotene required to yield one retinol activity equivalent (1 RAE) (Yeun, 2002). To explain this further 1 mcg of available retinol is equivalent to the following amounts from animal or plant dietary sources: 1 mcg of retinol, 12 mcg of beta-carotene, and 24 mcg of alpha-carotene or beta-cryptoxanthin. There are many factors that affect the conversion of beta-carotene to retinol. Some examples of these are gender, availability of carotenoids vs retinoids and most recently scientists have found that genetics plays a role as well.

In two separate studies by different researchers each looked at how gender played a role in beta-carotene conversion. Hinkenbottom et al. studied the conversion of beta-carotene to retinol in men and found that conversion rates were variable and surprisingly low. Using a double tracer study 11 healthy men were given orally 30 micromol hexadeuterated (D6) retinyl acetate (all-trans-19,19,19,20,20,20-[2H6]retinyl acetate) and then were given 37 micromol D6 beta-carotene (19,19,19,19′,19′,19′-[2H6]beta-carotene) one week later. All doses were given during breakfast. Plasma samples from each of the participants were analyzed for levels of D6 retinol, D6 beta-carotene, and trideuterated (D3) retinol (derived from D6 beta-carotene) (Hinkenbottom et al, 2002). Using HPLC they were able to see the conversion of D6 beta-carotene to D3 retinol.. Only 6 of the 11 men had measurable levels. The mean absorption of D6 beta-carotene in these 6 subjects was 4.097 +/- 1.208%, and the mean conversion ratio was 0.0540 +/- 0.0128 mol retinol to 1 mol beta-carotene (Hinkenbottom et al, 2002). This same study was conducted two years earlier on women by Lin, a colleague of Hinkenbottom. The results for this study were very similar to the results of the men’s study. Women had low conversion and it was variable. Eleven women were selected and of them only 6 were able to convert D6 beta-carotene to D3 retinol. The mean absorption of D(6) beta-carotene in these 6 subjects was 6.1 +/- 0.02% and their conversion ratio was 1.47 +/- 0.49 mol D(3) retinol to 1 mol D(6) beta-carotene. The remaining 5 subjects were low responders with </=0.01% absorption and a mean conversion ratio of 0.014 +/- 0.004 mol D(3) retinol to 1 mol D(6) beta-carotene (Lin, 2000). In both studies there were measurable levels of D6 retinol. This retinol was not derived from beta-carotene and did not require the conversion to be absorbed. Looking at these results it shows that getting the recommended amount of vitamin A from beta-carotene may not be a good source. Why is the conversion so varied and low for so many people?

Genetics plays a role in determine who can efficiently convert beta-carotene and who cannot. A study conducted in the UK by Wing Leung and colleagues investigated the effects of the four identified SNP 5’ (rs6420424, rs8044334, rs11645428, and rs6564851) upstream from the BCMO1 gene on beta-carotene bioconversion or conversion efficiency. Recent studies have shown that BCMO1 gene can affect circulating carotenoid concentrations. Twenty-eight women volunteered to be part of this study. The women fasted for 12 hours and were given a 120 mg β-carotene (10% SWS from DSM Nutritional Products) together with a fat-rich meal the consisted of a muffin, fruit yoghurt and water (Leung et al., 2009). Blood samples were taken before the supplement and meal was given and again three hours after the meal. A total of 36% of women had retinol equivalent intakes above the recommended nutrient intake of 600 μg/d and 14% had intakes below the lower recommended nutrient intake of 250 μg/d. Fasting mean plasma concentrations for β-carotene and retinol were 0.36 μmol/L (95% CI = 0.29–0.45 μmol/L) and 1.52 μmol/L (95% CI = 1.36–1.69 μmol/L), respectively (Leung et al., 2009). SNP analysis was performed using PCR on plasma samples collected from the blood. The women were categorized by either being responders or poor responders on their ability to convert beta-carotene. Women who carried these three alleles: A allele (rs6420424), G allele (rs11645428), and G allele (rs6564851) of these intronic SNPs showed a reduction in conversion efficiency by up to 59% (Leung, 2009). They found that there is variation among races and very well could be variations amongst genders. How is this relevant to golden rice? Providing beta-carotene as the only source of vitamin A, to people from different backgrounds, may be beneficial for some and not to others on a nutritional basis. Other issues like an individual’s overall health and stored retinol levels in liver will affect how beta-carotene is utilized in the body. Once again this study used healthy individuals. It would be interesting to see how conversion is affected in the population of people the rice is intended for. It has been suggested that a person with a vitamin A deficiency will convert beta-carotene to retinol better than someone who is not deficient. This brings up the final issue of retinol absorption.

Once the beta-carotene has been released from the food, converted to retinol it must be absorbed. Remember vitamin A or retinol is fat soluble. There needs to be some type of unsaturated fat in the diet for the retinol to be absorbed into the intestines so it can be distributed throughout the body via the lymphatic system or stored in the liver. Fat-soluble micronutrients including vitamin A and carotenoids are assumed to follow the fate of lipids in the upper gastrointestinal tract (Borel, 2003). Before retinol can be absorbed it must be esterified. These retinyl esters are then incorporated into chylomicrons. Chylomicrons are created from lipids obtained from the diet and intestinal lipoproteins. These chylomicrons are then secreted into the lymph via enterocytes.

A study conducted by Melody Brown et al. examined how fat-free, low-fat and full-fat salad dressings affected the absorption of carotenoids by extracting chylomicrons. Seven individuals were used in the study (a mixture of both males and females). Each person was fed 3 salads with equal amounts of spinach, romaine lettuce, cherry tomatoes, and carrots with salad dressings containing 0, 6, or 28 g canola oil. The salads were not all fed at once but randomly over a 2 week period. After eat feeding blood samples were taken hourly from time 0-12hrs. Chylomicrons were isolated from the samples and using HPLC the carotenoid absorption was determined. What they found is that when no fat was added plasma carotenoid levels found in chylomicrons were low but as fat was increased the carotenoid levels increase significantly with full-fat salad having the most. This in significant because if golden rice is going to be the staple food then for the people to get the full benefit of the beta carotene they are going to have fat incorporated into the diet. On the golden rice website they claim the addition or subtraction of fat in the diet did not matter and that the conversion of beta-carotene and the absorption of retinol would still be significant. I would disagree due the findings from other studies showing that the presence of oil is necessary. Again all their trials were conducted on health individuals who did not have a vitamin A deficiency. The absorption of retinol derived from golden rice would need to be studied on the group of people the rice is intended for. Also there would need to be some way to incorporate oil into the diet whether it be animal or plant based.

After looking at the bioavailability of beta-carotene in plant based foods, the bioefficacy of converting beta-carotene into retinol and the absorption of retinol the findings suggests that beta-carotene alone may not be a valuable source for populations with a vitamin A deficiency problem. All the tests conducted were on healthy individuals or in-vitro and gave variable low results. While golden rice seems to have it’s benefits to me it would have been simpler for them to teach people how grow beta-carotene rich foods like sweet potatoes and spinach. It would be even more beneficial if there could be a way to raise livestock like cattle or egg laying chickens so that people have a bio-available source of retinol that does not require conversion.


1. Borel, P. Factors affecting intestinal absorption of highly lipophilic food microconstituents
2. (fat-soluble vitamins, carotenoids and phytosterols). Clin. Chem. Lab. Med. 2003, 41, 979–994.
3. Hedrén E1, Diaz V, Svanberg U. 2002. Estimation of carotenoid accessibility from carrots determined by an in vitro digestion method. Eur J Clin Nutr. May;56(5):425-3
4. Hickenbottom SJ, Follett JR, Lin Y, Dueker SR, Burri BJ, Neidlinger TR, Clifford AJ. Am J Clin Nutr. 2002 May;75(5):900-7.
5. Jackson MJ. (1997). The assessment of bioavailability of micronutrients: introduction. Eur. J. Clin. Nutr., 51: S1-S2. MEDLINE
6. Leung WC, Hessel S, Méplan C, Flint J, Oberhauser V, Tourniaire F, Hesketh JE, von Lintig J, Lietz G (2009) Two common single nucleotide polymorphisms in the gene encoding beta-carotene 15,15’-monoxygenase alter beta-carotene metabolism in female volunteers. FASEB J. 23(4):1041-1053. doi: 10.1096/fj.08-121962.
7. Lin Y, Dueker SR, Burri BJ, Neidlinger TR, Clifford AJ. Am J Clin Nutr. 2000 Jun;71(6):1545-54.
8. Plack, P.A., 1965. Occurrence, absorption and distribution of vitamin A. Proc Nutr Soc 24: 146–153.
9. Tang G, Qin J, Dolnikowski GG, Russell RM, Grusak MA. Golden Rice is an effective source of vitamin A. The American Journal of Clinical Nutrition 2009;89(6):1776-1783. doi:10.3945/ajcn.2008.27119.
10. Yeum, K. J. and Russell, R. M., 2002. Carotenoid bioavailability and bioconversion. Annual Review of Nutrition. 22: 483–504.
11. USDA Table of Nutrient Retention Factors. Release 6. Beltsville, Md.: U.S. Dept. of Agriculture, Agricultural Research Service, Beltsville Human Nutrition Research Center, Nutrient Data Laboratory, 2007.

Aedes Mosquitoes: Vectors of Chikungunya

Paper I wrote for my medical entomology course. Enjoy!


No animal on earth has touched so directly and profoundly the lives of so many human beings. For all of history and all over the globe she has been a nuisance, a pain, and an angel of death. Mosquitoes have killed great leaders, decimated armies, and decided the fates of nations. All this, and she is roughly the size and weight of a grape seed (Spielman & D’Antonio, 2001).

Mosquitoes inhabit every continent on the planet except Antarctica. Not only are mosquitoes a nuisance, due to them biting you, but they are vectors of diseases for both humans and animals like Malaria, West Nile, Dengue and Chikungunya fever. This paper will discuss the latter.

Chikungunya, an alphavirus, is a vector-borne disease transmitted by Aedes aegypti and Aedes albopictus. Chikungunya is not a new disease it has been around for years in Asia and Africa. Recently, chikungunya has been re-emerging in these areas. Also, the disease has been emerging in areas it has never been seen before like the United States, US territories, Caribbean, Central and South America. The concern of chikungunya spreading through the United States has recently become elevated due to the presence of either or both these mosquitoes in most of the states and the presence of infected individuals in our country either via traveling to endemic areas or through local transmission.

Aedes aegypti and Aedes albopictus.

Mosquitoes belong to the family Culicidae, which has approximately 3,500 species and counting. All mosquitoes belong to the insect order Diptera, or the True Flies. Like all True Flies, they have two wings. Where mosquitoes differ from other true flies is that their wings have scales. Female mosquitoes’ mouthparts form a long piercing-sucking proboscis while males have mouthparts not designed to pierce skin. A mosquito’s principal food is nectar or similar sugar source. Many species of mosquito’s females require a blood meal to produce eggs. Males differ from females by having feathery antennae. The feathery antennae of males are used to pick up the buzzing of female mosquitoes. The mosquito life cycle is the same as other flies in the dipteran order. Mosquitoes undergo complete metamorphosis having an egg, larva, pupae and adult. Depending on the species of mosquito the location of where and how eggs are laid may differ.

Aedes is a genus of mosquitoes originally found in tropical and subtropical zones, but arenow found on all continents excluding Antarctica. Although the genus Aedes has over 100+ species Aedes aegypti and Aedes albopictus are two that are of great concern to human health.

Aedes aegypti


Figure 1. Aedes aegypti female taking a blood meal.

edes aegypti, the yellow fever mosquito, originating in Africa, was most likely brought to the new world on ships used for European exploration and colonization (Nelson 1986). In the United States Ae. aegypti is found in 23 states, including the southeastern U.S., up the east coast to New York, and west to Indiana and Kentucky (Darsie and Ward 2005). Aedes aegypti are roughly 4-7 millimeters with females being larger than males. Both males and females have white scales on the dorsal surface of the thorax that form the shape of a violin or lyre. The abdomen is generally dark brown to black, but also may possess white scales (Carpenter and LaCasse 1955). The tip of the abdomen comes to a point, which is characteristic of all Aedes species (Cutwa-Francis and O’Meara 2007). Adults prefer environments that are close to humans. They are day biters and also bite indoors as well as outdoors.

Life cycle

Female Aedes aegypti are anautogenous. After the female has taken a blood meal she will lay between 100-200 eggs per batch. The number of eggs she lays is highly dependent upon how much blood she consumes. A female can lay roughly 5 batches in her lifetime. The adult life span can range from two weeks to a month depending on environmental conditions (Maricopa, 2006). Eggs are laid singly instead of in a mass. The female prefers to lay her eggs on damp surfaces in areas likely to temporarily flood, such as tree holes and man-made containers. The female does not lay all of her eggs at once but can spread out laying over hours in different locations. Newly laid eggs are white but quickly turn black after a few minutes. Their eggs are roughly 1mm in length. In warm climates, such as the tropics, eggs may develop in as little as two days, whereas in cooler temperate climates, development can take up to a week (Foster and Walker 2002). Aedes aegypti eggs can survive desiccation for months and hatch once submerged in water, making the control of Ae. aegypti difficult (Nelson, 1986). Once hatched larva spend most of their time at the water surface. They feed on algae and other microorganisms in the water. Larvae undergo four instars before they pupate. The pupa stage is mobile and responds by swimming away if disturbed. It takes approximately two days for the adult mosquito to emerge from the pupal case. Adult mosquitoes do not overwinter as eggs like other Aedes species do and adults are killed by temperatures that go below freezing. Since they prefer to live in human dwelling they can survive through the winter by living and breeding indoors.

Aedes albopictus


Figure 2. Aedes albopticus female taking a blood meal.

he Aedes albopictus, the Asian tiger mosquito, is native to the tropical and subtropical areas of Southeast Asia; however, in the past couple of decades this species has invaded many countries throughout the world through the transport of goods and increasing international travel (Scholte & Schaffner, 2007). The Asian tiger mosquito was first documented in the United States in Texas in 1985 (Sprenger and Wuithiranyagool 1986) but now can be found in 866 counties in 26 states (CDC 2001). Aedes albopictus are roughly 2.0 to 10.0 mm with females being larger than males. Adult Aedes albopictus are easily recognized by the bold black shiny scales and distinct silver white scales on the palpus and tarsi (Hawley 1988). The back of both males and females is black with a distinguishing white stripe down the center. The abdomen also narrows to a point.

Life cycle

The life cycle of the Asian tiger mosquito is really similar to that of the yellow fever mosquito. The major difference is Ae. albopticus overwinter as eggs. The eggs can withstand desiccation for up to a year but may require numerous submersions before they hatch. The larvae go through four instars before pupating. They also require approximately 2 days of maturing before emerging as adults.

Aedes aegypti and Aedes albopticus vectors of Chikungunya Virus

Chikungunya virus is an alphavirus, viruses which attack the brain and/or the central nervous system, which is spread by both Ae. aegypti and Ae. albopticus. In Africa, chikungunya is spread via a sylvatic cycle in which the virus largely resides in other primates in between human outbreaks by Ae. Aegypti (Enserink, 2007). In Asian countries where chikungunya virus is found it is predominantly spread by Ae. albopticus. It has symptoms similar to Dengue, another virus vectored by these two mosquitoes, but does not have the hemorrhagic stage. It causes excruciating pain at the joints that can last for weeks, months or years. Recovery can vary by age with elder and immunocompromised individuals requiring a longer time frame to clear the virus.

Within the last three decades or so there has been an increase in chikungunya around the world. Chikungunya outbreaks have been reported from India, Africa, and Southeast Asia. Infections may occur in areas that are not considered endemic, or where the virus does not normally occur. Travel and globalization increase the possibility of epidemic outbreaks in other regions around the globe, wherever the mosquitoes capable of transmitting chikungunya are found (Connelly et al., 2007).

Chikungunya an emerging infectious disease in the United States

Before this year chikungunya had not been previously listed as a reportable disease here in the United States. Doctors and laboratories could report cases to ArboNET, an organization that tracks vector-borne diseases in the North America and US territories. In 2014, ArboNET had a total of 4,513 chikungunya virus disease cases reported from U.S. territories and of these 4,467 were locally-transmitted cases reported from Puerto Rico and the U.S. Virgin Islands. The other 46 cases were travelers who had returned from endemic areas. In 2014, a total of 2,492 chikungunya were reported in the United States (Figure 3) and of these eleven cases found in the Florida Keys were to not have engaged in any international travel to endemic areas suggesting that there is now local transmission of the virus amongst the mosquitoes in t

Figure 3-Chikungunya virus disease cases reported by state – United States, 2014 (as of February 10, 2015)

his area.

Since both vectors are already established in the United States it is just a matter of time before the viruses starts to circulate nationwide. Increased international travelers infected with chikungunya increases the possibility of an outbreak. Earlier The CDC has suggested that it is highly probable to see a Chikungunya outbreak in the southeastern United States because of the suitable climate and huge numbers of vector mosquitoes.


There are no vaccines or medications that can prevent chikungunya. Once a person has the virus there is no cure. The only way to prevent the spread of this and other viruses is to reduce mosquito populations. This however is easier said than done.

It was stated earlier that Ae. albopticus can overwinter as eggs. Controlling populations of this mosquitoes in difficult because of this. Management of adult populations is more complicated than for other species due to insecticide tolerance to malathion, temephos and bediocarb (Morbidity and Mortality Weekly Report 1987). It has been observed that Aedes albopictuslarvae out-compete Ae. aegyptilarvae for food, and develop at a faster rate thus greatly reducing their numbers in certain areas (Barrera 1996). The only way to prevent these and other mosquitoes is to eliminate breeding area. This can greatly reduce population if sources of still water are eliminated. Some examples of eliminating breed sites are emptying containers, preventing pooling of water, cleaning gutters, cleaning pet dishes, properly disposing of tires etc. Also periodically performing mosquito surveillance and testing for disease will allow areas to determine what mosquitoes and disease are circulating in a particular area. Surveillance programs for Aedes aegypti were very effective in the 1990s. Due to budget cuts the programs were terminated and populations exploded.

Physicians must also be educated on the symptoms of chikungunya and the proper testing for the virus. Many physicians in the United States are clueless that this infection even exist which mean there may indeed be more cases going undiagnosed or misdiagnosed as something else.


In conclusion mosquitoes have been vectors of diseases for centuries. Although chikungunya is not a new disease, it is an emerging disease in the United States. Ae. aegypti and Ae. Albopticus are the two major vectors of this disease. Both species have been introduced to this country and have spread at an alarming rates due to the assistance of humans. Since both species are capable of spreading chikungunya it will be only a matter of time before this disease becomes endemic to the United States. Chikungunya has already been found to have local transmission in the Florida Keys. Knowing this information it has been suggested by the CDC that the conditions are right in the southern states to have an outbreak. A better surveillance program must be put into place immediately, or the United States is going to have a situation that is going to be hard to control.


Barrera R. 1996. Competition and resistance to starvation in larvae of container-inhabiting Aedes mosquitoes. Ecological Entomology. 21: 117-127.

Carpenter SJ, LaCasse WJ. 1955. Mosquitoes of North America (North of Mexico). University of California Press, Berkeley, CA. 360 pp.

Centers for Disease Control. (2001). Information on Aedes albopictus. Arboviral Encephalitides. (21 January 2004).

Centers for Disease Control. 1987. Current trends update: Aedes albopictus Infestation—United States. Morbidity and Mortality Weekly Report 36: 769-773.

C. Roxanne Connelly, Christopher N. Mores, Chelsea T. Smartt, and Walter J. Tabachnick, 2007, Chikungunya, University of Florida Extension.

Cutwa-Francis MM, O’Meara GF. (2007). An Identification Guide to the Common Mosquitoes of Florida. Florida Medical Entomology Laboratory. (13 May 2008).

Darsie, RF, Ward, RA. 2005. Identification and Geographical Distribution of the Mosquitoes of North America, North of Mexico. University of Florida Press, Gainesville, FL. 300 pp.

Enserink M (December 2007). “Infectious diseases. Chikungunya: no longer a third world disease”. Science318.

Foster WA, Walker ED. 2002. Mosquitoes (Culicidae). In Mullen, G., Durden, L. (Eds.) Medical and Veterinary Entomology (p 203-262). Academic press, Sand Diego, CA. 597 pp.

Hawley WA. 1988. The biology of Aedes albopictus. Journal of the American Mosquito Control Association. Supplement #1. p. 1-40.

Maricopa County Environmental Services. 2006. Lifecycle and information on Aedes aegypti mosquitoes. Maricopa County, AZ. (13 May 2008).

Nelson MJ. 1986. Aedes aegypti: Biology and Ecology. Pan American Health Organization. Washington, D.C.

Rey J. (2007). What is Dengue? EDIS. (13 May 2008).

Scholte, J.E., Schaffner, F. 2007. “Waiting for the tiger: establishment and spread of the Aedes albopictus mosquito in Europe”. In Takken, W.; Knols, B. G. J. Emerging pests and vector-borne diseases in Europe1. Wageningen Academic Publishers.

Spielman, A., D’Antonio, M., 2001, “Mosquito : A natural history of our most persistent and deadly foe”, 1st edition.

Sprenger D, Wuithiranyagool T. 1986. The discovery and distribution of Aedes albopictus in Harris County, Texas. Journal of the American Mosquito Control Association 2: 217-219.


University of Florida Extension Site




hornwormontomatoplantHornworms…are one of your tomato plant’s worse enemies. An entire plant can be quickly defoliated in a day if you have a large number of them on it.

So what exactly is a hornworm? Well, they are actually caterpillars and not worms at all. There are two kind of hornworms: Tomato and Tobacco. Both are from the same family of moths (Sphingidae). Many people are familiar with the name tomato hornworm but in actuality the one on their plants is most likely a tobacco hornworm.  There is an easy way to tell the difference between the two. Although both caterpillars are green in color and large in size there is a difference between the body markings and horn. Tobacco worms have straight diagonal lines on their body and a red horn at their rear end while tomato hornworms have lines that create a “V” shape and a black horn. Hornworms feed only on solanaceous plants, most often on tomato. However, larvae will also attack eggplant, tobacco, pepper, and potato. Tomato hornworms (Manduca quinquemaculata) are the caterpillars of the five-spotted hawkmoth (also known as the sphinx or hummingbird moth). The adults are nectar feeders and do not damage plants. Tomato hornworms can be found throughout most of the northern states.  The tobacco hornworms (Manduca sexta) are the caterpillars of the Carolina sphinx moth. The adults are also nectar feeders and do not damage plants. Tobacco hornworms can be found throughout most of the United States and Canada.

tomatohornworm tobaccohornworm

Controlling Hormworms Organically

frassHow do you know if there is a hornworm on your plant? There are many signs to look for. First look for plants that have been heavily defoliated (numerous leaves missing) or fruit that looks like a huge bite has been taken out of it. Next, look for caterpillar droppings or frass. These can usually be seen on leaves or on the ground.

So what do you once you find a hornworm on your plant? If you are not squeamish the easiest thing to do is remove the caterpillars. During your caterpillar removal if you come across any that have little white projections on it that look kind of like rice, leave that one alone. The little white objects are actually the cocoons of the parasitic braconid wasp. These wasps are natural enemies to hornworms. The female wasps lay her eggs inside the hornworm. Once they hatch the wasp larvae feed on the inside of the caterpillar destroying muscle tissue eventually paralyzing it. Once the larvae mature (in roughly a week) they leave the caterpillar through pores in its skin and form a tiny cocoon. The reason you do not want to remove this caterpillar is because you want more parasitic wasp around your garden. They will aid you in controlling the caterpillars.

Another natural enemy is the Polistes  paper wasps. These wasps actually feed on caterpillars. While they may not prevent damage they are good at controlling hornworm populations which results in less damage. Other predators like lacewings and ladybugs will feed on young hornworms and eggs.

btYou can also spray your plants with Bacillus thuringiensis (Bt). Bt a bacterium that produces a toxin that is toxic to caterpillars but not to humans or other animals. You must mix with water in a sprayer and apply to both sides of the leaves on your plants (follow instructions on label).  Bt must be applied every 7-10 days or more frequently if you have a lot of rain. The caterpillars will still feed but within 24-48 hours of application they should become sick and stop feeding. You usually see them on the ground around the plants they were on once they succumb to the toxin. Bt works better on young immature hornworms.

Written by Nadia Ruffin.  hornwormdamage    640px-Hornworm_2

Imported Cabbageworm

Imported Cabbageworms are not worms but are caterpillars of the White Cabbage Butterfly.

Figure 1. Imported Cabbageworm on collard green plant. Photograph taken by Nadia Ruffin.

So how many of you out there are growing greens, cabbage, broccoli etc.? Have you started to notice any holes in your leaves? Have you seen any white butterflies flying around your garden? If you answered yes to any of these questions you probably have Imported Cabbageworms.

Imported Cabbageworms are not worms but are caterpillars of the White Cabbage Butterfly.

Common names: Imported Cabbageworm, cabbageworm, white cabbageworm, Cabbage White Butterfly, Cabbage White or Cabbage Butterfly

Scientific name: Pieris rapae belongs to the order Lepidoptera and is in the family Pieridae. The green caterpillar feed on plants in the cabbage family (Brassica).



Identifying Characteristics:

Figure 2. Larva of imported cabbageworm, Pieris rapae (Linnaeus). Photograph by John L. Capinera, University of Florida.

Larvae: Bright green caterpillars usually camouflaged on the host plants they feed on. As the caterpillar grows it usually will develop a small yellow stripe down each of its sides.





Figure 3. Male and Female White Cabbage Butterflies.

Adults: Small white butterflies usually seen first in early spring. Males and females only differ slightly with males being white with one small dark spots on each wing while females are an offwhite color with two larger dark spots.





Host Plant Range:
The larvae feed on plants from the family Brassica which include cabbage, broccoli, cauliflower, collards, kale, mustard greens, Chinese cabbage, and Brussels sprouts. The larvae also feed occasionally on turnips, radish, mustard, and even lettuce.

Adults do not feed on vegetation. They strictly eat nectar from a variety of flowers.

Description of Damage:

Figure 4: Damage caused by 4th-5th instar larvae. See the caterpillar in the center of the collard leaf? Photograph by Nadia Ruffin.Description of Damage:

Cabbageworms cause defoliation (leaf loss). Damage is small at first when caterpillars first hatch and start feeding. As caterpillars grow larger they can really cause considerable damage to plants.







Life History:
In early spring male and female butterflies emerge from overwintering chrysalises. Adults have a wing span of about 4.5 to 6.5 cm. Female Cabbage White Butterflies are innately biased to search for common green hosts. The female will lay a single egg on the underside of a leaf. The egg measures 0.5 mm in width and 1.0 mm in length, and initially is pale white in color but eventually turns yellowish. The egg will hatch in roughly 3-5 days. The caterpillars live the majority of their larval stage on the underside of the leaf but they can be found on the top as well. Larvae undergo 5 instars. The larva requires about 15 days (range 11 to 33 days) to complete its development. The rate of development is highly dependent upon temperature with cooler temperatures slowing down development and warmer temperatures speeding it up.

Larvae may pupate on the host plant or migrate away. Pupal stage may last up to 11 days. The caterpillars can overwinter as pupae.The number of generations reported annually is two to three in Canada, three in the New England states, three to five in California, and six to eight in the southern United States.

P. rapae was accidentally introduced to the United States and Canada in the 1800s. Originating from Europe. They can be found almost worldwide.

Sampling Techniques:
Sampling should include 25 plants selected randomly throughout the field. Of course if your growing area is small checking all plants for caterpillars is ideal. First observe for holes in the leaves. Look for small larvae and eggs on the undersides of leaves. Look for larger worms feeding on the center of the plant. Other ways to detect their presence is to look for brown fecal pellets on the plant. Observing for white butterflies flying around the brassica plants is a good indication that there will be caterpillars present in the next 3-5 days. You can also search for eggs on the underside of plants but they maybe hard to find.


Figure 4. Bt purchased from local chain hardware store. Photograph by Nadia Ruffin.

Controlling Imported Cabbageworms can be accomplished by using a number of different methods.

Cultural methods would consist of planting insect resistant species of cruciferous plants. If you cannot plant those varieties using barriers to prevent butterflies from accessing the plants would be very effective. This can include using nets or insect shields.  Removing caterpillars from the plants is also beneficial.

There are many natural enemies of cabbageworms but the most effective control method is using Bacillus thuringiensis(Bt).

Bt is a bacteria that produces a toxin that is harmful to caterpillars but not usually to other living organisms. Bt can be found at garden and hardware stores. To be effective Bt must be applied every 7-10 days up until harvest. Following mixing instructions on the label.

A Bt application usually takes effective within 24-48 hours. The caterpillars will still feed until they become sick from consuming the toxin.




1. Capinera, J.L. 2013, Feature Creatures, Imported Cabbageworm,

2. Down Garden Services, Small white Cabbage Butterfly (2000),

3. Snell-Rood, E. C., G. Davidowitz, and D. R. Papaj. 2011. Reproductive tradeoffs of learning in a butterfly. Behavioral Ecology 22: 291-302. Snell-Rood, E. C., A.

4. UC Pest Management Guidelines (2010), Adult imported cabbageworm., Cole Crops
Imported Cabbageworm

Neglected Diseases In the United States

Ascaris_lumbricoidesThis is a pretty good read. I’m getting my masters in Entomology with a focus in medical entomology. This article discusses the many neglected diseases (go untreated or there is no research money for them) here in the United States. These disease are mostly caused by insects and other invertebrates and some of them are zoonotic. They seem to of course occur in poverty stricken areas particularly those with minorities. Usually when they talk about neglected diseases they only talk about third world countries but this however happens right here in many major cities and regions.

The picture to the left is of a roundworm (female) Ascaris lumbricoides. Many of these nematodes live in the digestive tract or other organs throughout the body. Many times they either go undiagnosed because no testing for them has been conducted or an individual does not seek medical attention when they are sick. Roundworms can be carried by animals that shed the eggs in their feces. If you are walking barefoot or you handle something contaminated with the eggs, you can quickly infect yourself.  A. lumbricoides is the largest intestinal roundworm and is the most common helminth infection of humans worldwide, a disease known as ascariasis. Infestation can cause morbidity by compromising nutritional status, affecting cognitive processes, inducing tissue reactions such as granuloma to larval stages, and by causing intestinal obstruction, which can be fatal. (Wikipedia, 2014).


Checkout the article here:



Hydroponics…What’s That?

So what exactly is hydroponics?

Basically hydroponics is the process of growing plants solely in water. So I bet you are looking at your compimagesuter and saying to yourself this chick is crazy right? You can’t grow plants without using dirt. Well you really can.

Have you ever wondered how the produce you buy at the grocery store is grown? True some of it is still grown on a farm in fields but many companies use hydroponics as their method of growth.

So why use Hydroponics vs. using dirt?

Well there are many reasons. First off you can grow plants indoors. This is great because you can grow plants year round. So in the winter you can still have produce even when there are feet of snow outside on the ground. Secondly, you are not bothered by pests and diseases they come along with having your plants grow outside. Third anyone can have a garden. If you live an apartment and don’t have a place to plant in ground you can still grow produce right in your home. There are other reasons like its better for the environment because companies are not cutting down forests to create new farmland. Its also better for you health because you know exactly what you eating because you grew it.

I will be adding videos of me setting up a hydroponic system and will soon be selling hydroponics kits. For now check out this prezi presentation that my classmates and I created for a class project this past spring semester. Click on the full screen for best viewing quality.

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