Temperature, Effect on devlopment and growth of Insect

(effect of temperature on development of insect )

The body temperature of insects, as in other ectothermic organisms, is linked to changes in the ambient temperature.
Temperature fluctuations are small in environments such as the tropical rainforest, caves, and some aquatic habitats. In most habitats, however, the seasonal and diurnal temperature oscillations are considerable. For example, insect body temperature can change abrupdy by 10°C or more when exposure to direct sunlight is followed by the shade of a cloud. The way of life with fluctuating body temperatures is called heterothermy; this is in contrast to the homeothermy of endothermic organisms, such as birds and mammals, which regulate their body temperature, partly by generating endogenous heat.

DEVELOPMENTAL PARAMETERS

Every organism is adapted to a set temperature range. A general preference for high temperatures is referred to as thermophily, and the inclination to low temperatures is psychrophily. Insects living in warm climates or parasitizing warm-blooded animals are thermophilic, whereas those dwelling in soil are usually psychrophilic. Temperature preferences may change during development; for example, aquatic insects inhabit cold mountain streams during their immature stages but fly in warm air as adults. Temperature fluctuations within the species-specific physiological range determine the rate of development and often exert other physiological effects.

Development and reproduction occur at physiological temperatures that are delimited by an upper and a lower developmental threshold (UDT and LDT, respectively). Within this range, there is an optimal temperature for rapid development. The dependence on temperature can be expressed as a metabolic rate or as a developmental rate. The metabolic rate (MR) reflects the velocity of the energy-supplying biochemical processes and can be measured as oxygen consumption, carbon dioxide production, or heat generation. Many enzymatic reactions and the total body metabolism increase exponentially over a broader temperature range than is the span of physiological temperatures. Metabolic increase is usually two- to threefold with temperature elevation by 10°C and can be expressed by MR = , where a and k are constants and T is temperature.

Metabolic rate determines the developmental rate (DR), which is a reciprocal value of the developmental time (DT), DR = 1/DT. Measuring developmental times, such as duration of larval development, length of the reproductive period, or expanse of the entire life cycle, requires maintenance of defined conditions (notably temperature and nutrition). This is difficult to do for long periods of time and this is why DT and DR values are usually established for individual developmental stages and then recalculated for the entire life cycle. Circadian rhythmicity of some processes, for example, the synchrony of hatching or adult emergence at a certain time of day, complicates DT assessments.

In contrast to the exponential rise of the metabolic rate, the increase in DR within the physiological temperature range is linear. When a series of temperature and corresponding DR values is plotted in a graph, a straight line so obtained crossed the x axis at the theoretical LDT point. Close to this point, the relationship between developmental rate and temperature ceases to be linear, and the straight line is bent into a sigmoidal curve. Actual LDT is therefore somewhat lower then predicted. At the upper temperature range, the DR slows down before it reaches a maximum at the optimal temperature. After the maximum, DR sharply drops and at UDT the development is discontinued.

Developmental time depends on the effective temperature, i.e., temperature value above LDT (actual temperature T minus LDT). The constant product of effective temperature and developmental time is called the sum of effective temperatures (SET) and represents the heat required for the completion of a particular developmental stage. SET is conveniently expressed as the number of degree days. For example, a SET value of 100 degree days means that development at 5°C above LDT lasts 20 days and at 10°C above LDT 10 days. When the insects develop at fluctuating temperatures, the average temperature above LDT and the length of time when the temperature surpasses LDT are considered for each day, and the number of degree days established in this way is summed. Developmental stage is completed when the summation reaches the SET value.

A temporal drop in temperature below LDT is associated with developmental block and is counted as 0. Usually, there is no “negative developmental rate” at temperatures below LDT, i.e., no delay of development is observed after transfer to an effective temperature. Natural temperature fluctuations, however, may have a signaling effect and influence the SET value in some species, and this possibility must be checked experimentally.

The LDT and SET values are species-specific population characteristics. The LDT values are similar for all developmental stages of a given species, even when they develop in diverse seasons and experience disparate temperature fluctuations. The stability of LDT is manifested as developmental thermal isometry, i.e., the percentage of time spent in a particular stage at any constant physiological temperature is a stable fraction of the entire developmental time. The LDT and SET values established in the laboratory enable prediction of the course of development in the field. Control of many insect pests in agriculture and forestry largely relies on such predictions. For example, on the basis of the LDT and SET data for the codling moth (Cydia pomonella) we can predict, on the basis of daily temperature measurements in an orchard, the time of the first egg deposition and time insecticide sprays accordingly.

Both LDT and, especially, SET may vary between geographical populations because of adjustments to local climatic conditions. Insects that have spread to temperate zones from the tropical regions often maintain a high LDT and can reproduce and develop only in the hot season, spending most of the year in a state of dormancy. The survival in cold is made possible by increased cold hardiness, a parameter that seems to be more plastic than LDT.
DEVELOPMENTAL ARRESTS

Most insects must overcome long periods of adverse conditions when food is wanting and temperature remains outside the physiological limits. Insects cease development and reproduction but, if the temperature does not reach lethal extremes, they remain capable of resuming these processes as soon as the conditions become favorable. The state of easily reversible, directly temperature-dependent developmental arrest is known as quiescence. It is typical of insects adapted to relatively short periods of unfavorable, nonlethal circumstances, and it is usually associated with temperature acclimation.

Insects that will be exposed to severely hostile conditions that can last for many months enter a programmed developmental arrest, diapause. Diapause occurs in anticipation of a season in which the insect could not survive in the active state. It is induced by environmental signals acting before the adverse conditions set it, sometimes on a much earlier developmental stage and exceptionally on the parental generation.

Seasonal changes in the environment are specific for each latitude, altitude, and habitat, but always correlate with changes in the photoperiod, i.e., the length of day versus the length of night. Photoperiodic changes therefore provide ideal signal for the advent of unsuitable conditions. However, temperature can shift the diapause-inducing photoperiod response over a broad range. For example, 50% of caterpillars of Acronycta rumicis are induced to enter pupal diapause at a daylength of 19 h at 15°C, but at 16 h at 25°C. Low temperature normally enhances the effect of short photoperiod and high temperature enhances the effect of long photoperiod. Daily fluctuations of temperature, the thermoperiod, can induce diapause in a few species kept in constant darkness. On the other hand, high temperature can abolish the diapause-inducing effect of a short photoperiod. For most insects, the diapause is facultative and there is a variation in the critical photoperiod/thermoperiod at which each individual enters diapause.

Once induced, diapause is not terminated immediately after the diapause-inducing conditions disappear. A certain time must elapse, during which neurohormonal regulations return to the pattern supporting development and reproduction. The mechanisms controlling diapause termination are not known. The length of time in diapause depends on its “depth” and on environmental conditions, especially temperature, to which the diapausing insects are exposed. In the overwintering insects, diapause is often shortest at temperatures around 5°C (Fig. 1) and the photoperiod is irrelevant. Due to exposure to low temperatures in late fall, the overwintering insects terminate diapause in early winter, and the resumption of their development or reproduction is then halted only by a direct effect of low temperature: diapause turns into quiescence.

ALTERNATIVE DEVELOPMENTAL PATHWAYS

In certain insects, temperatures within the physiological range affect the course of non-diapause development. For example,

larvae of the yellow mealworm, Tenebrio molitor, develop in 11-15 instars at 25°C and in 15-23 instars at 30°C. Less dramatic changes in the number of molts and the growth rate were noted in a number of insects. Abnormal temperatures can also dissociate the onset of metamorphosis from the body size at which it normally occurs. In the wax moth, Galleria mellonella, placing newly ecdysed larvae of the last or penultimate instar on melting ice induces an additional larval molt. To cause such anomalies, the temperature must alter the secretion of hormones that control specific developmental events.

Some insect species occur in more than one form and their alternation depends on temperature. For instance, development of young caterpillars of Colias eurytheme at 18°C leads to mainly yellow, and development at 27—32°C to orange, butterflies. The spring and summer forms of some other butterflies are well known examples of seasonal dimorphism in which one form is linked to diapause.

LETHALITY AT EXTREME TEMPERATURES

A general response of insects to temperatures just below their LDT or above their UDT is the cessation of development and reproduction while the insects remain active and feed. The larvae may slowly grow and the adults accumulate reserves and to some extent undergo gonadal maturation. These processes are terminated at more extreme temperatures when the insects begin to die.

During cooling, the metabolic rate and motility gradually decrease. At a certain temperature, the neural and muscular activities are impaired and the insect lapses into cold stupor. The metabolic rate of such immobile insects continues to decline with decreasing temperature. The stupor point is as high as 12°C in some tropical insects and the honey bees, around 5°C in many temperate species, near 0°C in most overwintering insects, and below the freezing point in species living in very cold areas.
The nature of chill injuries is little understood. Desiccation and nutrient depletion during the cold-induced starvation are certainly incompatible with long-term survival, but death usually occurs earlier and is probably the result of damaging effects at cellular level. The loss of cell membrane fluidity, imperfect protein functions (enzymatic activities, transport, signaling, etc.), and the resulting asynchrony of the life-supporting processes cause metabolic disorders. For example, the ion pumps in the cell membrane become inefficient and sodium concentration in cytoplasm increases, while the potassium ions flow out into the hemolymph.

The upper temperature extremes are also lethal. Gradual warming past UDT, which is for many species around 35°C but is never sharply delimited, increases the metabolic rate, loss of water, and motility. At a certain temperatures, usually around 40°C, the water loss, and thereby the evaporative body cooling, increases sharply. The spiracles are wide open and the melting of cuticular lipids permits evaporation through the body surface. After some time at such a high temperature, the losses of water and nutrients lead to exhaustion, manifested as a rapid decrease of motility and a drop of transpiration. If this state is brief, it can be reversed. The temperature at which it occurs is the upper lethal threshold. A gradual temperature increase to this threshold may cause heat stupor.

Survival at temperatures above the threshold is a function of temperature and length of exposure. Warming to the absolute upper lethal temperature, which is usually around 50—55°C, causes irreversible tissue damage, and even a short exposure is lethal.

ACCLIMATION AND TEMPERATURE TOLERANCE

The survival at extreme temperatures is improved after an acclimation. Shortening of the photoperiod in late autumn and early winter usually acts synergistically with descending temperature in triggering a seasonal cold acclimation. An exposure to low temperature alone is often insufficient for full cold acclimation and successful winter survival because some physiological adjustments (for instance down-regulation of the ice nucleators and enhancement of cryoprotectant biosynthesis) require a preceding switch to the diapause developmental mode and this is controlled by the photoperiod. In other insects, cold acclimation is associated with temperature-dependent quiescence and the photoperiod is irrelevant.

Cold acclimation is a complex adjustment involving profound changes at the organismic and tissue levels. Accumulation of low-molecular-weight cryoprotective polyols and, in some insects, also synthesis of antifreeze proteins are characteristic features of cold acclimation. Other physiological changes include changes in cuticular lipids, increased fluidity of phospholipids in the cell membranes, conformation changes of some proteins, possibly production of alternative enzymes with activity optima at lower temperatures, and synthesis of heat-shock proteins. Acclimation may also encompass changes in morphology (e.g., cold-acclimated lacewings turn from green to reddish brown) and behavior (e.g., formation of cocoons with higher resistance to desiccation and ice penetration, voiding the gut to get rid of ice nucleators, and seeking dry places to prevent ice inoculation from the surroundings).

The temperature at which insects freeze is relatively low even without cold acclimation. Insects contain only low amounts of nucleators needed for the ice crystal formation and are therefore capable of considerable supercooling. The nonacclimated individuals freeze at —10 to — 15°C, while those with accumulated cryoprotectants and antifreeze proteins can be supercooled to temperatures below —20°C. All cryoprotec-tive compounds disappear from the organism after a certain time. The length of this deacclimation process also depends on temperature, but details have not been examined.

Changes associated with heat acclimation are litde known. Synthesis of heat-shock proteins, which were discovered in Drosophila exposed to elevated temperature, is a very general response not only to heat but also to cold and various other types of stress. Several types of heat-shock proteins are known from organisms ranging from bacteria to plants. It is believed that they are chaperones enabling or protecting functional protein conformations. Temperature or another stressing factor acts as a signal inducing their synthesis at transcriptional level. Accumulation in the cells of “unfolded” proteins is believed to be the common intracellular message triggering this transcription.




Ref: Frantisek Sehnal, Oldfich Nedved, and Vladimir Kost’al
Institute of Entomology, Academy of Sciences, Czech Republic

Role of insect in biological weapons

Role of insect in biological weapons
THE ROLE OF INSECTS AS BIOLOGICAL WEAPONS
The following is based on the notes for a seminar presented by R.K.D. Peterson in 1990 at the University of Nebraska . The information is from several published primary and secondary sources listed at the end of this article.
WHAT IS A BIOLOGICAL WEAPON?
Before discussing the role of insects in biological warfare (BW), we need to define biological warfare and just what a biological warfare agent is. The definition is from the 1972 biological weapons convention. The definition for a BW agent is fairly straightforward:
"Microbial or other biological agents, or toxins whatever their origin or method of production, of types and in quantities that have no justification for prophylactic, protective or other peaceful purposes."
This definition includes all living BW agents, including insects, as well as toxins produced from these agents (e.g., the botulinum toxin).
INSTANCES AND ALLEGATIONS OF BW (PRE 1800)
The recorded allegations and instances of BW before 1800 do not involve insects. However, it is important to discuss some of these records to understand the full spectrum of BW.
600 B.C.
Solon, the legislator of the Athenians, contaminated the river Pleisthnes with the plant root of helleborous to give the defenders of Kirrha violent diarrhea, which led to their defeat.
ca. 200 B.C.
Carthaginian general Maharbal purposely retreated from his encampment and left behind a large stock of wine that he treated with mandagora, a toxic root which produces a narcotic effect. The enemy, upon drinking the tainted wine, fell into a deep sleep and the Cartheginians returned to slay their enemy.
190 B.C.
Hannibal won a naval victory over king Eumenes of Pergamon by firing earthen vessels full of snakes into king Eumenes ships.
There are many records throughout the ages of armies dumping dead humans and animals into wells, ponds, streams, and rivers to pollute the enemies’ water supplies.
Mid 1300s
Mongol tartars, sieging the port city of Feodosia (then Kaffa) on the Black Sea , finally broke the three-year siege by catapulting plague-infested cadavers over the walls of the city.
The city fell from plague in 1346 and it was suspected that escaping residents of the city introduces plague into Italy , initiating the pandemic (the Black Death) that decimated the European populace between 1348 and 1350. 1763
The next recorded instance of BW was in the new world. Smallpox was strongly suspected of being used against the Indians in the French and Indian War. Sir Jeffrey Amherst, commander in chief of the British forces in the American colonies had two blankets and a handkerchief from a British smallpox hospital sent to Indian chiefs. A smallpox epidemic soon erupted.

INSTANCES AND ALLEGATIONS OF BW (1800-PRESENT)

The American Civil War
The American Civil War marked the first instance of alleged use of an insect as a weapon of war. The Confederacy accused the Union of deliberately introducing the harlequin bug, Murgentia histrionica, into the South.
Tremendous crop damage resulted in the South because of this pest. This allegation was never proven and it now appears that the harlequin bug moved on its own into the South from Mexico . However, humans may have aided in the movement of this pest.
Disease relationships (microbial and insect vector) were elucidated in the early twentieth century. As soon as the mechanisms were known, military planners began to apply them as possible warfare agents.

World War I
None of the belligerent countries in WWI took official notice of BW. No country involved had a BW research facility and there was no BW on a large scale.
BW clearly was used in sabotage operations in the war to end all wars. In 1915, German agents inoculated horses and cattle that were leaving the U.S. for allied ports with glanders and anthrax. In 1917, the Germans again were accused of spreading glanders to 4,500 donkeys on the French front, and of spreading plague on the Russian front in 1915 and 1916.
As most people know, WWI was known more for the development of chemical weaponry, which was spawned by advances in the dye industry.

Between the Wars
17 June 1925. Geneva Protocol for the prohibition of the use in war of asphyxiating, poisonous or other gases, and of bacteriological methods of warfare. Even though biological weapons were not used on a large scale in WWI, the framers of the Geneva Protocol viewed BW as a serious emerging threat and incorporated a bacterial warfare component into the protocol. Most major countries in the world at that time ratified the treaty.
The United States , however, did not ratify the treaty because of the then current isolationist movement in this country. The U.S. finally ratified this treaty in 1975, 50 years after its inception. The failure of the U.S. to ratify the treaty led the Japanese to not ratify the treaty either and to believe that BW was promising and had a future in warfare.

World War II
The world still is heavily influenced by the events that took place from 1939-1945, and in some respects the war finally ended less than a month ago with German reunification.
World War II also was pivotal when we consider the development and use of BW. I need to look at each belligerent country's involvement because each country's involvement was unique, both axis and allied.

GERMANY
German involvement in BW was not nearly as advanced as Japan or the Allied Nations. It now appears that BW and BW research was not taken seriously by the German military hierarchy. Hitler, especially, viewed the emerging sciences as some sort of Jewish plot. He called the physics of Einstein, Jew physics, and felt similarly about the new biology, and the new psychology.
After the successful Russian counterattacks in Russia in 1943, Hitler agreed to establish an SS BW research station at Posen. As the Russians got closer to the research station, work accelerated at the station, but no real advances were made before the Russians occupied the station in March 1945.
At the Posen BW research station, the Germans performed work on the diseases plague, cholera, typhus, yellow fever, and performed experiments on the feasibility of using insects such as the Colorado potato beetle to attack Allied potato crops. The Germans were accused of dropping cardboard boxes filled with Colorado potato beetles over England from 1941-1943. The containers were never recovered but abnormalities associated with the presence of the beetles prompted Sir Maurice Hankey, head of Britain 's BW effort, to write a memo to Winston Churchill with his concerns.
Also, as British invasion fears grew after the successful evacuation from Dunkirk , rumors spread that the Germans had created an omnivorous strain of grasshopper which would soon starve the British into surrender. This was a myth. However, the fact that Nazi doctors used human subjects for experiments on insect-borne diseases is no myth. Concentration camp inmates were intentionally infested with typhus-infected lice by SS doctors at Natzweiler, Dauchau, and Buchenwald . Many of these doctors and scientists were sentenced to death by the Nuremberg Tribunal after the war.

GREAT BRITAIN AND THE COMMONWEALTH
England had a viable BW research program since 1934. After hearing that Germany was initiating a program in 1936, a BW advisory group was established which procured antisera for human and animal diseases, and stocked insecticides and fungicides as a contingency for anti-crop attacks.
In 1939, the BW advisory group assessed BW as less effective than the conventional forms of warfare, but they advised the government to begin a BW research effort.
In 1940, shortly after the fall of France , a BW research unit was established within the chemical warfare research establishment at Porton Down. An experiment conducted in 1941 involved the dissemination of anthrax spores from small aircraft bombs at Gruinard Island off the northwest coast of Scotland . All the other work at Porton Down has been heavily classified and still is unavailable. The only reason the Guinard island episode is known to the general public is because the island is still uninhabitable to this day because of the presence of anthrax spores.
The British effort was combined with the Canadian effort in 1942. Canada had several BW research stations throughout the country. Field testing was performed at a proving ground near Ralston , Alberta . Not much is known about what was studied there. Apparently Canada feared that North American livestock were very susceptible to Old World diseases so several were studied. As a result they studied rinderpest and a few other diseases. Also, botulinal toxins were studied and antidotes were developed.
After the U.S. Entered the war, Canada and Britain shared their BW research experience with the U.S.

JAPAN
The only verified instance of BW during the war was the use by Japan against the Chinese, from 1937-1945.
The Japanese BW program was headed by General Shiro Ishii, an army surgeon with a doctorate in bacteriology. Before Ishii began his BW efforts, he was famous for developing a portable water filtration system, capable of being transported by army regiments.
Ishii strongly believed that the western powers had advanced BW programs and were prepared to use them. Again, failure of the U.S. to sign the 1925 Geneva Protocol influenced his thoughts and actions.
BW research was considered too risky to study in Japan proper. Therefore, the Japanese puppet state of Manchukuo (formerly Manchuria ), under complete Japanese control since 1932, was chosen as an ideal location for the studies.
Mukden POW Camp
In 1936, detachment 731 was formed in the town of Harbin . The official name of the detachment was “Epidemic Prevention and Water Supply Unit of the Kwantung Army." In reality, the mission of unit 731 was to forge deadly new biological weapons for the Japanese army to be used against all possible enemies.
In 1938, the success of the research and development efforts at Harbin necessitated the move of unit 731 to Pingfan, a more secure area outside of Harbin . The Pingfan complex included an insectary among its 150 buildings, where 1000 staff members worked around the clock. In total, with out-stations and personnel in the water purification units, 10,000 people were involved.
Like the German scientists, human subjects were used to study these diseases. As early as 1932, people were taken from prison camps (mainly Chinese soldiers, intellectuals, and local workers). The study subjects were called Marutas, which means logs of wood. This is how they were treated. Unspeakable horrors awaited those that entered the Ro block. No subjects that entered ever left alive.
The subjects were tied to posts and were forced to be bitten by plague-infested fleas. The progression of the disease was then charted very scientifically until the subjects died. If the subject did not die, he or she was usually killed, and the body dissected. Many of the human subjects were vivisected at the Ro block. A room existed there where body parts were kept and catalogued.
Of course, human subjects were used on all the diseases studied at Pingfan. Gangrene was studied by exploding gangrene soaked shrapnel bombs in front of tied up Marutas. Also, frostbite was studied by gradually freezing subjects.
It is estimated that 3600 people were sacrificed by the Japanese scientists in the Ro block. This was addition to possibly more than 200 American and British POW's, who were studied at the Mukden POW Camp. More than 1500 Allied soldiers may have been used in BW experimentation. The Japanese were curious to see if Anglo-Saxons and Caucasians in general responded differently to the treatments than the Chinese subjects.
The Pingfan facility was able to produce 300 kilograms of viable plague germs every month, Yersinia pestis. The facility also produced cholera, typhoid, paratyphoid, dysentery, and anthrax.
Ishii believed quite strongly that plague was a promising weapon of war and the insect vector was needed for delivery to the enemy. Therefore, a four-story granary was built which housed rats used as the plague reservoir. At production height in 1945, 4500 flea breeding machines were set up to produce 100 million fleas every few days. It is estimated that 3 million rats may have been used.
Bombs made primarily of clay were developed for dissemination of plague-infested fleas. Also, saboteur initiation of plague via distribution of rats with plague was studied. Plans were designed for the Japanese balloon bomb to carry pathogens to America . The balloon bombs were used to attempt to ignite forest fires in the Pacific Northwest (albeit with unsatisfactory results).
The actual use of bioweapons distinguished Japan from the other belligerents. Several attacks were launched against China from 1939-45. Plague-infested fleas were disseminated directly out of aircraft or via specialized bombs. In 1944, an assault team was assembled to sprinkle plague-infested fleas around the Saipan airfield, which the Americans held. The ship carrying the assault team, however, was sunk by an American submarine and the mission was never completed.
By war's end, Unit 731 was preparing for a major war with Russia. The enormous breeding program was interrupted when Russia invaded Manchuria on August of 1945. The remaining human subjects were slaughtered by the fleeing Japanese guards and Pingfan was abandoned with most of the complex intentionally set on fire to destroy particularly damaging information. A plague epidemic in the Harbin and Pingfan area occurred almost immediately after the abandonment of Pingfan. It is strongly suspected that escaped rats were responsible.
After the U.S. occupation of Japan, Russia began to begin making protests that the U.S. government knowingly was protecting Japanese BW specialists, and failing to bring them to justice. At the same time, the Truman administration sent a team of bacteriologists to investigate the Japanese BW program during the war.
It now appears that General Douglas Macarthur, who was in charge of the occupation of Japan after the war, and his intelligence staff deliberately withheld contacts and information from the Washington scientists. These U.S. scientists found out, after they granted immunity from prosecution to the Japanese scientists in exchange for their bw knowledge, that the Japanese scientists experimented on human subjects, and specifically American POWs. Immunity would not have been granted had the scientists known this. It appears, however, that Macarthur's intelligence staff knew this, but was so desperate for the Japanese BW information, that they deliberately coached the Japanese interviewees. The fear of Russia as the next major adversary was strong in Macarthur's eyes.
The Soviet Union was so frustrated by this episode, that they had their own trial and sentenced many of the scientists they captured in Manchuria to various prison terms, from 1 to 30 years. Many of the top Japanese BW scientists, however, lived comfortably in Japan, and some went on to become respected scientists of international repute.
Ishii continued to consult with American authorities, especially during the height of the Cold War, and died in 1959 of throat cancer.

THE SOVIET UNION
Russian outrage at the Japanese BW research and use may have been hypocritical. There are numerous reports that the Soviets themselves conducted studies involving human experimental subjects in Mongolia before and during the war. In one account, political prisoners and prisoners of war were chained in tents with pens of diseased rats until the subjects were bitten by the fleas. Supposedly, in the summer of 1941, one of the prisoner/experimental subjects escaped and began an epidemic that was controlled only because the Soviets bombed entire Mongol communities. It may never be known as to what extent Russia was involved in BW before, during, or after the war.

THE UNITED STATES
The U.S. army medical corps maintained a passing interest in BW since the 1920's. However, it was not until 1941 that the U.S. BW research program got off the ground, mainly because BW was viewed as a national security threat as the U.S. was drawn closer to the war.
In 1937, Roosevelt declared that the U.S. would never resort to the use of chemical or biological weapons unless they were first used by the enemy. Roosevelt, however, had to agree to increased research in BW as America was being drawn into the war.
The U.S. may have been one of the last major belligerent nations to research BW, but by the war's end the U.S. was probably the most advanced. By war's end, in August 1945, the U.S. BW effort employed 4,000 civilian and military workers, and vied with the Manhattan project for talented scientists and staff.
In all, the U.S. spent $45-50 million for BW installations during the war. The installations included the main research station at Camp Detrick, Maryland, a field-test station on Horn Island in the Mississippi sound, and a huge field-testing facility at the dug way proving grounds in Utah. Also, an ordnance plant was constructed at Terre Haute, Indiana was converted into BW agent production center.
Little is known about the U.S. BW research during the war. Most of the information is still heavily classified and may never be published. A 500 page monograph exists which details the U.S. effort during the war, but it is unavailable for publication because of its classification.
From the flood of journal papers published, it is known that during the war the bacteria of anthrax, glanders, brucellosis, tularemia, meliodosis, and plague were studied.
The fungus of coccidioimycosis was studied, as well as several plant .pathogens, including rice blast, rice brown-spot disease, late blight of potato, and stem rust of cereals. Also, animal pathogents such as rinderpest virus, newcastle disease virus, and fowl plague virus were studied.
Of course, insects played a large role in the study of many of these diseases. Fleas, lice, the yellow fever mosquito, and the Colorado potato beetle were reared in large quantities.
The U.S. also worked on aerosol transmission of pathogens, and freeze-drying of BW agents.
Korea and the Cold War
The U.S. BW research and development continued after WWII. As the cold war heated up, so did the BW effort at Fort Detrick.
In 1952, China accused the U.S. of engaging in germ warfare against the people of North Korea. The Chinese began producing large amounts of evidence which suggested that the U.S. was spreading bacteria-laden insects and other objects over the Korean countryside.
Also plague appeared in areas where it had not been documented for over 500 years.
Chinese entomologists accused the U.S. of distributing disease-carrying anthomyid flies, springtails, and stoneflies with P-51 fighters. Also, accusations were leveled stating that America was contaminating areas with plague infested rats and fleas, and anthrax infested flies and spiders. In all, the U.S. was accused of dropping ants, beetles, crickets, fleas, flies, grasshoppers, lice, springtails, and stoneflies. The alleged associated diseases included anthrax, cholera, dysentery, fowl septicemia, paratyphoid, plague, scrub typhus, and typhoid.
The Chinese set up an international scientific commission for investigating the facts about bacterial warfare. The commission, consisting of scientists from all over the world, ruled that the United States probably did engage in limited biological warfare in Korea.
The U.S. maintains that the commission was nothing more than a communist front, however, and denied all the allegations. The U.S. proposed that the United Nations send a formal inquiry committee to China and Korea and investigate, but China and Korea refused.
Most of the allegations were based on eyewitness reports, photographs of strange paper cartons, anomalous appearances of the insects in question, and testimony by POW's.
It is strange why the Chinese would pick insects such as springtails and stoneflies and allege they were deliberately infected with disease and dropped on Korea. Clearly these insects would not be the best choices if the U.S. wanted to initiate BW.
U.S. and Canadian entomologists claimed that the accusations were ridiculous and argued that the anomalous appearances of insects and appearances of new species to an area could be explained through natural phenomena. The U.S. wrote off the whole incident as communist propaganda, but speculation to this day exists as to whether the U.S. may have been experimenting in the field during the Korean war.
Ten years later it was admitted by Dale Jenkins, the chief entomologist at Fort Detrick, that the U.S. at the time of the allegations was able to initiate BW if they saw fit and this BW would have involved insects as vectors of human diseases. Also, during the Korean War U.S. BW specialists were consulting heavily with former Japanese 731 scientists who were granted immunity from war crimes prosecution.
Despite the allegations and negative press from the Korean war episode, BW research by the U.S. and Britain progressed at an accelerated pace through the 50's and 60's. Britain's BW effort tripled after WWII extensive fundamental research was done, including field testing, and promising results were passed on to the U.S. Top BW leaders in Britain and the U.S. grouped bioweapons in with atomic weapons as "weapons of mass destruction." They felt that situations might exist in which BW agents would be preferable to atomic weapons.
In 1951, BW and chemical warfare were incorporated into official strategic planning by the armed forces of the U.S. Brig. General Rothchild, chemical officer of the Far East command, in 1953 wrote that BW could have played a vital role in the Korean War, by distributing anthrax or yellow fever pathogens into the cold air flows that travel from Siberia through the populated areas of China.
Clearly, BW received strong support among the brass in the U.S. and British armed forces. By the end of the 50's the Fort Detrick labs were set up to breed 130 million yellow fever mosquitoes a month, infect them with yellow fever, and deliver them to the enemy via cluster bombs or from the warheads in a Sergeant Missile. Also, the facilities could accommodate the breeding of 50 million fleas per week. By 1960, the labs were experimenting with malaria, dengue, cholera, anthrax, and dysentery, relapsing fever, tularemia.
The 1960's and Vietnam
After the Cuban Missile Crisis, BW research and testing accelerated even further. President John F. Kennedy wished to balance the defense forces of the U.S. and therefore decided that BW and chemical weapons should be stepped up even further.
In 1962, General Stubbs told congress that insect strains were being developed that were more cold hardy and were resistant to insecticides. All other information pertaining to BW involving insects during the 60's to the present have been classified and have not appeared in the congressional testimonies.
In the early 60's, insects as BW vectors fell out of favor with the scientists and planners. This was due in large part to the successful development of dry biological formulations of toxins and microbes.
With dry formulations of BW agents, the practicality and ease of disseminating diseases was greatly increased. It became easy for pneumonic plague, botulinum toxin, q-fever, and other diseases to be spread reliably and efficiently without the need for insects.
Insects, however, were studied which could vector plant diseases. During the Cuban missile crisis, the U.S. considered destroying the sugarcane crop in Cuba with Fiji disease, which is vectored by leafhoppers.

THE BIOLOGICAL WEAPONS CONVENTION
In 1969, President Nixon called for the unilateral destruction of biological weapons. Three years later, the U.S. signed the Biological Weapons Convention Treaty, which banned the development, production, stockpiling, transfer, and acquisition of BW. In 1975, the U.S. also signed the Geneva Protocol of 1925, which also banned the use of these weapons in war. The treaties, however, do not ban research on BW.

BIOLOGICAL WEAPONS TODAY
BW development after 1975 virtually is unknown. Because all major nations signed the BW convention making BW illegal, little information is available as to what is going on today.

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insects in medicine

INSECTS IN MEDICINE

Insects and the substances extracted from them have been used as medicinal resources by human cultures all over the world. Besides medicine, these organisms have also played mystical and magical roles in the treatment of several illnesses in a range of cultures. Science has already proven the existence of immunological, analgesic, antibacterial, diuretic, anesthetic, and antirheumatic properties in the bodies of insects. Several authors have surveyed the therapeutic potential of insects, either recording traditional medical practices or employing insects and their products at the laboratory and/or clinical level. Thus, insects seem to constitute an almost inexhaustible source for pharmacological research. Chemical studies are needed to discover which biologically active compounds are actually present within insect bodies. The therapeutic potential of insects represents a significant contribution to the debate on biodiversity conservation, as well as opening perspectives for the economic and cultural valorization of animals traditionally regarded as useless. Their use needs to be at a sustainable level to avoid overexploitation insects.

Insects and insect-derived products have been widely used in folk healing in many parts of the world since ancient times. Promising treatments have at least preliminarily been studied experimentally. Maggots and honey have been used to heal chronic and post-surgical wounds and have been shown to be comparable to conventional dressings in numerous settings. Honey has also been applied to treat burns. Honey has been combined with beeswax in the care of several dermatologic disorders, including psoriasis, atopic dermatitis, tinea, pityriasis versicolor, and diaper dermatitis. Royal jelly has been used to treat postmenopausal symptoms. Bee and ant venom have reduced the number of swollen joints in patients with rheumatoid arthritis. Propolis, a hive sealant made by bees, has been utilized to cure aphthous stomatitis. Cantharidin, a derivative of the bodies of blister beetles, has been applied to treat warts and molluscum contagiosum. Combining insects with conventional treatments may provide further benefit.
Introduction: Why Insects?
Insects and other arthropods provide ingredients that have been a staple of traditional medicine for centuries in parts of East Asia, Africa, and South America. While many of these ingredients have not been evaluated experimentally, an increasing number have been shown in preliminary trials to have beneficial properties. Although medical practitioners in more economically robust countries may prefer conventional treatments, it may be more a result of squeamishness rather than science. Furthermore, in parts of the world where conventional medical care is scarcer than arthropods used by folk healers, insects may represent a feasible substitute in some cases. In sub-Saharan Africa alone, the World Health Organization estimates that $20 billion will be needed to replace the shortage of 800,000 conventional health care workers by 2015. (1) Globally ubiquitous, arthropods potentially provide a cheap, plentiful supply of healing substances in an economically challenged world.
Maggots
The most well-studied medical application of arthropods is the use of maggots--the larvae of flies (most frequently that of Lucilia sericata, a blowfly) that feed on necrotic tissue .(2) Traditional healers from many parts of the world including Asia, South America, and Australia have used "larval therapy," (3) and records of physician use of maggots to heal wounds have existed since the Middle Ages. (3) Figure 1 depicts maggots on a wound.
Fly larvae aid in wound healing via a number of mechanisms: (1) larval secretions break the larger adhesion molecules, fibronectin and collagen, into smaller fragments that promote fibroblast aggregation and tissue repair; (4) (2) larvae eat necrotic tissue that would otherwise form a nidus for infection, liquefying such tissue and aiding its digestion; (4) (3) maggots release antibacterial substances, some of which are produced by Proteus mirabilis bacteria that live naturally in the larval intestine; and (4) ingested bacteria are destroyed within maggots. (3)
Maggots commercially grown under sterile conditions are used in wound healing. In one application technique, a hole is cut in a hydrocolloid dressing over a wound. (3) The maggots are lifted out of a container on a piece of nylon netting, which is folded together and taped onto the dressing over the hole after removal of the moisture in the maggot growth medium. A piece of gauze is placed over the nylon and taped in place. (3)
[FIGURE 1 OMITTED]
In one study, maggots were grown in vitro and placed in the wounds of 30 individuals after bacterial swabs of the wounds were taken. (5) The patients had arterial or venous stasis ulcers, diabetic or pressure ulcers, or chronic postoperative wounds. Secretions taken either from maggots grown on sterile plates or from wound sites sampled from 1-5 days after the introduction of larvae were studied for antibacterial properties. Larval secretions successfully suppressed Staphylococcus aureus growth in vitro. In vivo, 51 wounds (83.2%) healed, with reduced bacterial counts within the wounds.
Maggots were also used to treat chronic leg wounds in several patient series. In one case series involving 34 leg wounds of at least three months duration in subjects ages 32-84, 85 percent of the wounds healed. (6) Of the healed wounds, 93 percent resolved within 7-10 days. In a second series, 70 patients, ages 25-94 with wounds of at least six weeks duration, were given treatment with one-day-old larvae added at a concentration of 5-10 larvae/[cm.sup.2]. (2) Eighty-six percent of the subjects had a 66- to 100-percent reduction of wound size. During treatment, 35 percent of subjects perceived more pain, 25 percent less pain, and 46 percent no difference in pain. In a third case series, larval therapy was applied to 70 chronic wounds; 43 percent of the wounds were completely debrided, and 29 percent were partially debrided. (7) There are also case reports of the successful use of maggots for treating the wound of a terminally ill patient (8) and for non-healing venous ulcers. (9)
One study examined the factors that predict better outcomes of larval therapy in a series of 117 wounds. Greater wound depth, older patient age, and presence of septic arthritis portended a worse outcome. (10)
Larval therapy has also been evaluated in controlled trials. In a randomized trial, 267 subjects with venous or arterial ulcers at least 25-percent covered with necrotic material were assigned to receive maggots or a conventional hydrogel dressing. (11) Although there was no difference in rate or timing of healing between groups, the maggot-treated wounds were debrided significantly faster (2.31 days; p< 0.001). On the other hand, subjects treated with maggots had a significantly higher pain score (approximately 40 points higher on a 150-point analog scale; p< 0001). In another trial involving diabetic leg ulcers, non-healing wounds were treated with either maggots, a conventional hydrogel, or the conventional therapy followed by larval treatment. (12) Wounds treated with maggots had significantly less necrotic tissue after two weeks. Thus, there is limited evidence that larval therapy can provide wound healing for lower extremity ulcers comparable to conventional treatment. A systematic review concluded that, in appropriate patients, use may be safe and effective. (13) Maggots may be appropriate especially when conventional therapies cannot be used, or in parts of the world where larvae are more easily obtainable than conventional treatment.
Honey Treatment
Honey is another insect-derived substance that has been used in wound healing and for treatment of other disorders, such as infections and irritable bowel syndrome. Therapeutic effects of honey have been documented from ancient times and it is still used in African folk medicine. (14, 15) Honey composition varies widely throughout the world depending on the species of bee and plants the bees feed on, both of which influence the honey's antioxidant and antimicrobial properties. (16-18) Four phenolic compounds in honey--p-hydroxybenzoic acid, naringenin, pinocembrin, and chrysin--are antimicrobials and antioxidants. The carbohydrate in honey is also antimicrobial. (16, 17) Honey also has antimutagenic properties. (19)
Wound Healing
The best studied use of honey is for wound healing. Honey promotes wound healing through osmotic properties that serve to moisturize the wound bed and reduce the risk of maceration. It also works via anti-inflammatory processes that reduce exudate and inhibit fibrin that adheres eschar to the wound bed, impairing tissue repair. (20)
Honey has been used to heal wounds in numerous situations. Many studies have found dressings that contain honey comparable to conventional dressings. In a randomized, double-blind, placebo-controlled trial, 100 patients who had toenail surgery were assigned to receive either a honey-coated dressing or a conventional paraffin dressing. (21) There was no significant difference between groups in days taken to heal the wounds.
However, in a single-blind study (blind to the investigator who examined the wounds), honey proved inferior in healing time to a conventional iodine dressing in 57 patients who had total avulsion toenail surgery, but comparable in wound-healing time to standard treatment after partial avulsion surgery. (22)
n a case series, eight patients (ages 22-83) with leg wounds that had not healed in a month were given once- or twice-weekly applications of honey on a non-adhesive dressing. (23) After a month of treatment there was an average 54.8-percent reduction in wound size, from a baseline mean wound size of 5.62 to 2.25 [cm.sup.2]. (23)
Two open (unblinded) trials also found significant wound healing with honey.

first internal marks

antenna

The antenna

The antenna are a pair of jointed appendages articulated with the head in front of the eyes or between them. The antenna vary greatly in form; in some insects they are thread-like, consisting of a series of similar segments; in others certain segments are greatly modified. The thread-like form is the more generalized.

In descriptive works names have been given to particular parts of the antennae, as follows (Fig. 5 i):
The Scape.—The first or proximal segment pf an antenna is called the scape (a). The proximal end of this segment is often subglobose, appearing like a distinct segment; in such cases it is called the bulb (a1).

Pedicel—The pedicel is the second segment of an antenna (b). In it differs greatly in form from the other segments.

The Clavola.—The term clavola is applied to that part of the antenna distad of the pedicel (c) ; in other words, to all of the antenna except the 1st and second segments. In some insects certain parts of the clavola are specialised antenna and have received particular names. These are the ring-joints, the funicle, and the club.

Ring-joints.—In certain insects (e.g., Chalcididae) the proximal segment or segments of the clavola are much shorter than the proceeding segments; in such cases they have received the name of ring-joins (c1).

The Club.—In many insects the distal segments of the antennae are more or less enlarged.

in such cases they are termed the club (c2).

The Funicle.—The funicle (e’) is that part of the clavola between the dub and the ring joints; or, when the latter are not specialized, between the club and the pedicel.

The various forms of antennae are designated by special terms. The more common of these forms are represented in Fig. 52. They are as follows: -

1. Setaceous : or bristle-like, in which the segments are successively smaller and smaller,

the whole organ tapering to a -point.

2. Filiform : or thread-like, in which the segments are of nearly uniform thickness.

3.Moniliform: or necklace-form, in which ‘the segments are more or less globosa, suggesting a string of beads.

4. Serrate: or saw-like, in which the segments are triangular and project like the teeth of a saw.

5. Pectinate : or comb-like, in which the segments have long processes on one side, like the teeth of a comb).

6. Clavate :club-shaped, in which the segments become gradually broader, so that the whole organ assumes the form of a club.

7. Copitate : or with a head, in which the terminal segment or segments form a large knob.

8. Lamellate: in which the segments that compose the knob are extended on one side into broad plates.

9. Geniculate: When an antenna is bent abruptly at an angle like a bent knee (Fig. 5) it is

said to be geniculate.

10. Aristate: (in house fly) pouch-like with lateral bristle on last clubbed segment.

11. Plumose: (brush-like) in mosquito.

Simple eye

THE ORGANS OF PHOTORECEPTION
A. THE GENERAL FEATURES
The two types of eyes of insects.—insects possess two types of eyes, the ocelli or simple eyes and the compound or facetted eyes. Typically both types of eyes are present in the same insect, but either may be absent. Thus many adult insects lack ocelli, while the larva of insects with a complete metamorphosis lack compound eyes. When all are present there are two compound eyes and, typically two pairs of ocelli; but almost invariably the members of one pair of ocelli are united and form a single median ocellus The median ocellus is absent in many insects that possess the other two ocelli. The distinction between ocelli and compound eyes.—The most obvious distinction between ocelli and compound eyes is the fact that in an ocellus there is a single cornea while in a compound eye there are many. Each ommatidium of a compound eye has been considered as a separate eye because its nerve-endings constituting the retinula are isolated from the retinube of other ommatidia by surrounding accessory pigment cells; but a similar isolation of retinui exist in some ocelli. It has also been held that in compound eyes there is a layer of cells between the corneal hypodermis and the retinas. the crystalline-cone- cells, which is absent in ocelli; but in the ocelli of adult Ephemerida there is a layer of cells between the lens and the retina, which, at least, is in a position analogous to that of the crystallinecone-cells; the two may have had a different origin, but regarding this, we have, as yet, no conclusive data.

The absence of compound eyes in most of the Apterygota.—
Typically insects possess both ocelli and compound eyes; when either kind of eyes is wanting it is evidently due to a; loss of these organs and
not to a generalized condition. Although compound eyes are almost universally absent in the Apterygota-in the few cases where they are present in this group they are of a highly developed type and not rudimentary; the compound eyes of Machills, for example, are as perfect as those of winged insects.

The absence of compound eyes in 1arve.—
The absence. of compound eyes in larva is evidently a secondary adaptation to their particular mode of life, like the internal development of wings in the same forms. In the case of the compound eyes of larva, the development of the organs is retarded, taking place in the pupal stage instead of in an embryonic stage, as is the case with nymphs and naiads. While, the development of the compound eyes as a whole is retarded in larva, a few ommatidia may be developed and function as ocelli during larval life.

B. THE OCELLI: There are two classes of ocelli found in insects: first, the ocelli of adult insects and of nymphs and naiads, which may be termed the primary ocelli; and second, the ocelli of most larva possessing ocelli, which may be termed adaptive ocelli.

The primary ocelli.—The ocelli of adult insects and of nymphs and naiads having been originally developed as ocelli are termed the primary ocelli. Of these there are typically two pairs; but usually when they are present there are only three of them, and in many cases only a single pair. When there are three ocelli, the double nature of the median ocellus is shown by the fact that the root of the nerve is double, while that of each of the other two is single. In certain generalized insects, as some Plecoptera, (Fig. 150) all of the ocelli are situated in the front; but in most insects, the paired ocelli have either migrated into the suture between the front and the vertex (Fig. xi), or have proceeded farther and are situated in the vertex.