What was the first recorded use of Aerial Weapons in warfare?

What was the first recorded use of Aerial Weapons in warfare?


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Fighter planes were popularised by their extensive use in WWI. What Aerial weapons were used before that period (if any)? What is earliest recorded use of Aerial Attacking and what was the technology employed?


Supposedly, the first time aviation was used in a war was during the American Civil War (meaning 1861). Both parties used balloons for reconnaissance, mostly hydrogen-filled. The balloons obviously couldn't be used for any kind of attack - they made a very big target and a single bullet was sufficient to ignite the hydrogen. Edit: It seems that first use of balloons for reconnaissance was earlier, during the French Revolution in 1794 (thanks @Nikko). The Austrians attempted to use balloons for bombing in 1849 and some of their successors apparently did so even with success - read the linked article.

The first time aviation played an important role was during World War I however (airplanes by then). It took some time to recognize the potential here, airplanes were mostly used for reconnaissance again. Using bombs was relatively rare and very experimental - typically the pilot would take a bomb and throw it overboard. As you can imagine, the precision of such bombing wasn't exactly high.

Air combat was also rare in WWI, with the necessary technologies still developing. The very first problem was mounting a machine gun so that it could shoot without damaging the propeller. Synchronized machine guns only became the accepted solution during the war, at the beginning of the war a bunch of other solutions were attempted as well. One option were machine guns mounted on the wings of the aircraft, the pilot then had to pull strings to trigger them (something that wasn't quite easy while steering the aircraft at the same time).

There is a large Wikipedia article on the use of aviation in World War I where you can find more details.


The first use of aeroplanes (as opposed to lighter-than-air balloons or dirigibles) in warfare occurred during the Italian invasion of Ottoman Libya in 1911. Airplanes were used initially for reconnaissance and then later in an improvised attack, when an Italian pilot dropped explosives by hand on Ottoman troops.


Aerial warfare of First World War, 1914-1918

A French SPAD S.XVI two-seat biplane reconnaissance aircraft, flying over Compeign Sector, France ca. 1918. Note the zig-zag patterns of defensive trenches in the fields below.

At the beginning of the war, the usefulness of air machines was met with a certain amount of skepticism by senior officers on all sides. In fact, aeroplanes were mostly involved in observation missions during the first year of the conflict. However, rapid progress enhanced aeroplanes’ performance. In 1915, the Dutch aircraft manufacturer Anthony Fokker, who was working for the Germans, perfected a French invention allowing machine-gun fire through the propeller. This discovery had a revolutionary consequence: the creation of fighter aircraft. This type of plane gave an edge to the Germans during 1915.

German pilot Richard Scholl and his co-pilot Lieutenant Anderer, in flight gear beside their Hannover CL.II biplane in 1918.

Their air superiority was to last until April 1916, two months after the beginning of the battle of Verdun. Thereafter, Allied dominance was gained through the creation of French fighting squadrons and the expansion of the British Royal Flying Corps. The control of the sky was to change hands again in the first half of 1917 when the Germans reformed their squadrons and introduced modern fighters. During April 1917, nicknamed ‘bloody April’, the British suffered four times more casualties than the Germans. But things were on the move on the Allied side. Successful reorganisations in France and Britain brought back air control for good until the Armistice.

During 1915, another important step was taken when the Germans organised strategic bombing over Britain and France by Zeppelin airships. In 1917-18 ‘Gotha’ and ‘Giant’ bombers were also used. This new type of mission, targeting logistic and manufacturing centres, prefigured a strategy commonly adopted later in the century. Inevitably, bombardments of ports and factories were quickly adopted by all sides and led to civilian deaths.

British Handley-Page bombers on a mission, Western Front, during World War I. This photograph, which appears to have been taken from the cabin of a Handley-Page bomber, is attributed to Tom Aitken. It shows another Handley-Page bomber setting out on a bombing mission. The model 0/400 bomber, which was introduced in 1918, could carry 2,000 lbs (907 kilos) of bombs and could be fitted with four Lewis machine-guns.

Although the number of civilians killed by aerial machines remained small during the war, these air raids nonetheless caused widespread terror. Yet, planes were on occasions a welcome sight. Indeed, aircraft and balloons were used by the Allies from 1915 to 1918 to drop propaganda leaflets over occupied France, Belgium and Italy in order to combat German psychological warfare. Propaganda was also dropped on German soldiers in an attempt to demoralise them.

In 1915, aviation caught the attention of the press both in Germany and in the Allied countries. Fighting pilots credited with at least five victories became known as ‘aces’ and were admired as celebrities on Home Fronts until the end of the conflict. This phenomenon illustrates the ability of war culture to penetrate all aspects of society, but also underlines a paradox: heroes of the air became glamorous because they were clean and deemed noble while their infantry counterparts remained an anonymous mass, stuck in the mud of the trenches. This romanticized admiration by the public of flying aces was a cause of tension and jealousy between army and air force.

German soldiers attend to a stack of gas canisters attached to a manifold, inflating a captive balloon on the Western front.

By the war’s end, the impact of air missions on the ground war was in retrospect mainly tactical – strategic bombing, in particular, was still very rudimentary indeed. This was partly due to its restricted funding and use, as it was, after all, a new technology. On the other hand, the artillery, which had perhaps the greatest effect of any military arm in this war, was in very large part as devastating as it was due to the availability of aerial photography and aerial “spotting” by balloon and aircraft.

Tactical air support had a big impact on troop morale and proved helpful both to the Allies and the Germans during 1918 when coordinated with ground force actions. But such operations were too dependent on the weather to have a considerable effect. Meanwhile, fighting planes had a significant impact in facilitating other aerial activities. Aviation made huge technological leaps forward during the conflict. The war in the air also proved to be a field of experimentation where tactics and doctrines were imagined and tested.

A German Type Ae 800 observation balloon ascending.

A captured German Taube monoplane, on display in the courtyard of Les Invalides in Paris, in 1915. The Taube was a pre-World War I aircraft, only briefly used on the front lines, replaced later by newer designs.

A soldier poses with a Hythe Mk III Gun Camera during training activities at Ellington Field, Houston, Texas in April of 1918. The Mk III, built to match the size, handling, and weight of a Lewis Gun, was used to train aerial gunners, recording a photograph when the trigger was pulled, for later review, when an instructor could coach trainees on better aiming strategies.

Captain Ross-Smith (left) and Observer in front of a Modern Bristol Fighter, 1st Squadron A.F.C. Palestine, February 1918. This image was taken using the Paget process, an early experiment in color photography.

Lieutenant Kirk Booth of the U.S. Signal Corps being lifted skyward by the giant Perkins man-carrying kite at Camp Devens, Ayer, Massachusetts. While the United States never used these kites during the war, the German and French armies put some to use on the front lines.

Wreckage of a German Albatross D. III fighter biplane.

Unidentified pilot wearing a type of breathing apparatus. Image taken by O.I.C Photographic Detachment, Hazelhurst Field, Long Island, New York.

A Farman airplane with rockets attached to its struts.

A German balloon being shot down.

An aircraft in flames falls from the sky.

A German Pfalz Dr.I single-seat triplane fighter aircraft, ca. 1918.

Observation Balloons near Coblenz, Germany.

Observer in a German balloon gondola shoots off light signals with a pistol.

Night Flight at Le Bourget, France.

British reconnaissance plane flying over enemy lines, in France.

Bombing Montmedy, 42 km north of Verdun, while American troops advance in the Meuse-Argonne sector. Three bombs have been released by a U.S. bomber, one striking a supply station, the other two in mid-air, visible on their way down. Black puffs of smoke indicate anti-aircraft fire. To the right (west), a building with a Red Cross symbol can be seen.

German soldiers attend to an upended German aircraft.

A Sunday morning service in an aerodrome in France. The Chaplain conducting the service from an aeroplane.

An observer in the tail tip of the English airship R33 on March 6, 1919 in Selby, England.

Soldiers carry a set of German airplane wings.

Captain Maurice Happe, rear seat, commander of French squadron MF 29, seated in his Farman MF.11 Shorthorn bomber with a Captain Berthaut. The plane bears the insignia of the first unit, a Croix de Guerre, ca. 1915.

A German airplane over the Pyramids of Giza in Egypt.

Car of French Military Dirigible “Republique”.

A German pilot lies dead in his crashed airplane in France, in 1918.

A German Pfalz E.I prepares to land, April 1916.

A returning observation balloon. A small army of men, dwarfed by the balloon, are controlling its descent with a multitude of ropes. The basket attached to the balloon, with space for two people, can be seen sitting on the ground. Frequently a target for gunfire, those conducting observations in these balloons were required to wear parachutes for a swift descent if necessary.

Aerial reconnaissance photograph showing a landscape scarred by trench lines and artillery craters. Photograph by pilot Richard Scholl and his co-pilot Lieutenant Anderer near Guignicourt, northern France, August 8, 1918. One month later, Richard Scholl was reported missing.

German hydroplane, ca. 1918.

French Cavalry observe an Army airplane fly past.

Attaching a 100 kg bomb to a German airplane.

Soldiers silhouetted against the sky prepare to fire an anti-aircraft gun. On the right of the photograph a soldier is being handed a large shell for the gun. The Battle of Broodseinde (October 1917) was part of a larger offensive – the third Battle of Ypres – engineered by Sir Douglas Haig to capture the Passchendaele ridge.

An aircraft. crashed and burning in German territory, ca. 1917.

A Sopwith 1 1/2 Strutter biplane aircraft taking off from a platform built on top of HMAS Australia’s midships “Q” turret, in 1918.

An aerial photographer with a Graflex camera, ca. 1917-18.

14th Photo Section, 1st Army, “The Balloonatic Section”. Capt. A. W. Stevens (center, front row) and personnel. Ca. 1918. Air Service Photographic Section.

Aerial photo of a cratered battlefield. The dark diagonal lines are the shadows of the few remaining tree trunks.

A British Commander starting off on a raid, flying an Airco DH.2 biplane.

The bombarded barracks at Ypres, viewed from 500 ft.

No. 1 Squadron, a unit of the Australian Flying Corps, in Palestine in 1918.

Returning from a reconnaissance flight during World War I, a view of the clouds from above.

Air force units were reorganized on numerous occasions to meet the growing need of this new weapon. Crucially, aerial strategies developed during the First World War laid the foundations for a modern form of warfare in the sky. During the course of the War, German Aircraft Losses accounted to 27,637 by all causes, while the Entente Losses numbered over 88,613 lost (52,640 France & 35,973 Great Britain).

(Photo credit: Bundesarchiv / Bibliotheque nationale de France / National World War I Museum, Kansas City, Missouri, USA / Text: Bernard Wilkin).


The Preparatory Commission

In 1993, Signatory States in Paris knew that a considerable amount of groundwork needed to be done before an international organisation capable of implementing the Chemical Weapons Convention could be established. Fortunately, the Convention provided that its entry into force was to occur at least two years after being opened for signature and only after 180 days had elapsed from the deposit of the 65th instrument of ratification. This left open a period of time in which such preparations could be made. In what was called the Paris Resolution, the Signatory States decided to set up a Preparatory Commission (PrepCom) with a mandate to make the necessary preparations for the first Conference of the States Parties and to continue work on issues that remained unresolved by the Convention’s negotiators. The PrepCom held its first Plenary Session in The Hague in February 1993 and established a Provisional Technical Secretariat.

After witnessing the effects of such weapons in World War I, it appeared that few countries wanted to be the first to introduce even deadlier chemical weapons onto the World War II battlefields. However, preparations were made by many countries to retaliate in kind should chemical weapons be used in warfare. Chemical weapons were deployed on a large scale in almost all theatres in the First and Second World Wars, leaving behind a legacy of old and abandoned chemical weapons, which still presents a problem for many countries.

During the Cold War, the United States and the Soviet Union both maintained enormous stockpiles of chemical weapons, amounting to tens of thousands of tonnes. The amount of chemical weapons held by these two countries was enough to destroy much of the human and animal life on Earth.

Trigger Point

When Hungary deposited the 65th instrument of ratification, it triggered the 180-day countdown to entry into force of the Chemical Weapons Convention.

The date of entry into force of the Convention was not determined until 31 October 1996, when Hungary became the 65th state to ratify. As required, the Convention entered into force 180 days later, on 29 April 1997. During the previous four years, the PrepCom met 16 times, laying the foundation for the workings of the future Organisation.

The PrepCom was successful in resolving a number of tasks within its mandate, the results of which were reflected in its Final Report. Among its major achievements were solutions to several substantive verification issues as well as the setting up of the OPCW Laboratory and Equipment Store, the development of a general training scheme for inspectors and the recruitment of inspector trainees, arrangements relating to the new OPCW headquarters building, and the development of draft documents, such as the Headquarters Agreement, the Staff and Financial Regulations, the Health and Safety Policy and Regulations, the Policy on Confidentiality, and the Media and Public Affairs Policy. The PrepCom was also responsible for the transfer of its property, functions and recommendations to the OPCW.


Last Air Actions in Burma 1945

The long southward trek by General Messervy’s IV Corps met its first serious obstacle at Gangaw in the Kabaw Valley, which was held by well-entrenched Japanese infantry. Messervy’s problem was that he could not attack in full strength without giving away the presence of his corps, and being only able to use light spearhead forces he called on EAC to achieve the rapid removal of the obstruction. EAC had developed two plans to meet situations such as this, code-named ‘Earthquake Major’ and ‘Earthquake Minor’. For the former, Liberator heavy bombers would bomb the target followed up by fighter-bombers strafing as ground forces advanced. Fighters would then make low-level dummy attacks to keep the enemy’s heads down as Allied infantry closed in. Earthquake Minor followed the same principle with the exception that Mitchell medium bombers would be used for the initial assault. In the event, ‘Earthquake Minor’ was ordered for Gangaw and carried out by four Mitchell squadrons of the USAAF plus Thunderbolts and Hurricanes of the RAF, fighter cover being provided by RAF Spitfires. RAF air control officers, experienced from operations with the Chindits and located with forward infantry companies, then called down strikes by Hurricanes onto any positions still intact after Earthquake. Ninety minutes after the air assault ceased five of the six main enemy positions were in IV Corps hands for the loss of two infantry wounded. The subsequent ease with which the Japanese were cleared from the area was attributed to a significant lowering of morale caused by the bombing.

Transport pilots watching the advance of IV Corps from the air said that a line of red dust thrown up by Corps vehicles, including everything from Sherman tanks to bullock carts, could be seen for miles as the column passed through Gangaw. Fortunately JAAF air reconnaissance was negligible and any aircraft that might have made the attempt was kept at a respectable distance by fighter cover. As IV Corps advanced, transport aircraft operating from the newly secured airstrips at Akyab and elsewhere in the Arakan parachuted supplies into designated Corps drop zones in dry river beds or landed at freshly bulldozed landing strips.

As the leading elements of IV Corps approached the Irrawaddy, 221 Group was called upon to instigate a game of subterfuge to confuse the enemy. Operation Cloak was designed to simulate flare-ups at numerous points along the river and draw enemy forces away from the village of Pagan, the location of the actual crossing. In similar fashion to operations carried out during the run-up to the Normandy landings, dummy parachutists were dropped as well as devices known as ‘canned battle’ which, on hitting the ground, precisely imitated the sound of rifle-fire punctuated by the explosion of hand grenades. Similarly ‘Aquakit’, when dropped onto water, sent up Very lights. These operations were carried out for several days from 6 February onwards and had the desired effect, 7th Division making their way over the river to establish a bridgehead through which IV Corps could pass. Air support during the river crossing included the use of both explosive and liquid-fire napalm bombs, which had now arrived in theatre. Napalm has since acquired a thoroughly unpleasant reputation and its effects on those unfortunate enough to be so attacked are truly horrific. Nevertheless, rightly or wrongly, its use was sanctioned against Japanese troops in part as a response to their barbarous treatment of Allied prisoners of war.

With a bridgehead secured, between 18 and 21 February the lead units of IV Corps, 17th Division plus 255 Tank Brigade, were brought across the Irrawaddy. On the 21st, with rear echelons still making the crossing, the Division struck out eastwards for Meiktila.

For 5th Hikoshidan the situation from the end of the 1944 monsoon onwards became increasingly critical, with too few aircraft to cover the exceptionally large combat area. Its main priority was fixed at support for the Burma Area Army as it withdrew from Imphal to positions around Mandalay, but should the seaborne attack so feared and expected materialize operations against amphibious assaults would take precedence.

Cover for the ground forces retreat was principally the responsibility of 4th Hikodan, comprising the 50th and 8th Hikosentai (fighters and light bombers respectively). Reconnaissance patrols over the Bay of Bengal as far as Chittagong were to be maintained to give ample warning of the anticipated seaborne attack.

Demonstrating the extreme shortage of aircraft available to Japanese forces in general at this time, a proposal was put forward that 5th Hikoshidan should be withdrawn to the Philippines in its entirety to assist with the campaign to drive back MacArthur’s invasion, which had begun on 20 October. This would of course leave Burma Area Army without air cover at all and following representations to the High Command it was agreed that a skeleton force of two fighter sentai, a single light bomber sentai, and one air reconnaissance company should remain. Air strength available to the Japanese in Burma now fell well below minimum effective operational levels for the tasks at hand and comprised the following:

50th Hikosentai re-equipping with Ki-84 Frank fighters–Bangkok.

64th Hikosentai twenty Type 3 Ki-43 Oscar fighters–Central Burma.

8th Hikosentai twenty-five Ki-48 Lily light bombers–Indo China.

81st Hikosentai thirteen Type 2 & 3 Ki-46 Dinah reconnaissance aircraft—Dispersed

During the latter part of October fighter units were concentrated on the airfields around Rangoon, while 8th Hikosentai carried out a series of small-scale night raids, all that it was now capable of, across Burma and into China:

Attack by four light bombers on Myitkyina.

Three light bombers attack Chakaria and Cox’s Bazaar.

Three light bombers raid Feni & surrounding airstrips.

All of the November raids were carried out by three or four light bombers.

On 7 December, 8th Hikosentai attempted a raid on the B29 Superfortresses of 20th Bomber Command at Midonapur, near Calcutta. Blackout in the area had been discontinued, perhaps a little prematurely, even if it was close to a year since the JAAF had paid Calcutta any attention, but still the raid met with little success. Another attempt was made on 25 December but was intercepted by the fighter defence.

While 8th Hikosentai did what it could the fighters were not idle, carrying out a number of strafing raids on airfields and ground support targets. On 14 December a raid carried out by eleven Oscars of the 64th Hikosentai failed to find its target, but on their way back to base the raiders happened across a number of transport aircraft with covering fighters, claiming six transports and two Thunderbolts for the loss of two Oscars in the ensuing engagement.

As the Burma Area Army concentrated around Mandalay a decision was taken to move all railway rolling stock to the south of the city for future operations. The movement was consistently hampered by Allied aircraft bombing the Minbu bridge, and to effect the transfer the entire strength of 64th Hikosentai was sent to patrol the area of the bridge towards the end of December, as a result of which the trains were successfully moved south between the 29th and 31st of the month.

50th Hikosentai completed re-equipping during December, its final complement fourteen Ki-84 Frank fighters and four Ki-43 Oscars. The unit immediately carried out a ground support attack on an Allied mechanized column threatening to cut off the Japanese 15th Division in the Shwebo area, claiming 150 trucks destroyed, the 20 mm cannon of the Frank proving particularly effective in this role.

As the fighting along the Irrawaddy intensified the entire 50th Hikosentai and a portion of 8th Hikosentai were transferred to Indo China to counter air strikes from a US Navy carrier task force, further crippling Japanese air cover for the impending battles around Meiktila.

Despite their straitened circumstances ad hoc resistance by Japanese units continued and a deadline was growing in importance to General Slim – the six to eight weeks remaining before the onset of the monsoon. Should the weather break before the capture of Rangoon, Fourteenth Army might still be forced into a withdrawal by the weather, allowing the Japanese time to re-equip and reorganize, with all the protracted campaigning and losses in men and materiel that would entail.

The drawing up of plans for a combined air/land/sea reconquest of Burma went back almost as far as 1942, but combined operations had always been thwarted by lack of equipment, particularly amphibious craft and naval escorts. However, with the necessary resources now becoming available one such plan, code-named ‘Dracula’, had been approved by the Joint Chiefs of Staff in September 1944. With its objectives modified to the capture of Rangoon it was now proposed to put Dracula into operation combined with a landward thrust from Fourteenth Army.

By this time Akyab was fully operational as a base for transport aircraft, Nos 62, 194, 267 and 436 Squadrons RAF being based there, Nos 194 and 436 commencing operations on 20 March, and Nos 62 and 267 on 1 April. Also during the course of April, Ramree Island opened as a transport base, detachments from Nos 31, 62 and 436 Squadrons operating there from the 16th of the month. CCTF also benefited from the arrival of two additional squadrons, Nos 96 and 215 RAF.

With his manpower limited Slim organized the dash for Rangoon by advancing Fourteenth Army in two armoured columns: XXXIII Corps south-westwards along the Irrawaddy Valley and IV Corps southwards down the Mandalay–Rangoon railway. One notable date for the RAF in the advance of XXXIII Corps was 18 April when Magwe, the scene of the RAF’s greatest disaster in Burma, was retaken.

Being farther to the south and with the more direct route the main thrust for Rangoon would be that of IV Corps, and to facilitate the advance two airborne operations, ‘Gumption’ and ‘Freeborn’, were put into place. These involved the use of glider-borne engineer battalions of the US Army, forward landed to repair transport airstrips and facilitate the rapid receipt and dispersal of the supplies necessary to keep IV Corps on the move. By the middle of April materiel for Gumption – fifty-five gliders and 86,000 gallons of aviation fuel – had been stockpiled at Meiktila. Bypassing Pyinmana, forward elements of IV Corps made rapid progress to the airfield at Lewe, which was captured on 20 April and prepared by British and American engineers sufficiently for gliders from the pool at Meiktila to fly in the following day. The gliders carried with them quantities of essential equipment including bulldozers, jeeps, tractors, food and water. Skirmishing continued all day as the engineers went about their essential tasks, and on the 22nd the JAAF managed one of its fighter raids, eight Oscars strafing the gliders, five of which were destroyed. Ten minutes after the Oscars departed the first supply-dropping transports arrived overhead.

As the engineers completed their work at Lewe leading elements of 5th Indian Division pushed forward into Toungoo, capturing the town against light opposition. While 5th Division continued their advance, six of the Meiktila gliders were flown in to Tennant airfield at Toungoo, disgorging US engineers – for which the RAF had no equivalent organization – and loads similar to those at Lewe. Craters were filled, essential repairs carried out and a 6,000-foot-long airstrip made serviceable. On 24 April Tennant witnessed the landing of fifty-six heavily laden CCTF transports.

With IV Corps closing in on Rangoon and Operation Dracula scheduled to commence within a few days, on 29 April Operation Freeborn was launched. With the first storms of the monsoon beginning to blow, Freeborn entailed the airlifting of a battalion group of 9 Brigade to Pyuntaza airfield north of Pegu, itself some 40 miles north of Rangoon, to cut off any Japanese escape route eastwards from the capital. Twenty-eight transports duly ferried in infantry, ammunition, small arms, jeeps, trailers and a fully equipped mobile radio station. Immediately upon landing the troops set off for Pegu, clearing half the town of the enemy that same day, discovering as they did so some 400 British and American prisoners of war in the process of being marched by their captors from Rangoon jail, intending to take them across the Sittang River and into Siam.

The American glider-borne engineers had one more service to perform for IV Corps, flying in to Zayatkwin airfield on 8 May to prepare the airstrip there. Elsewhere, however, momentous events had taken place.

Operation Dracula, as it now stood, entailed a force of paratroops landing to neutralize seaward-facing heavy guns followed by a seaborne invasion, units of XV Corps entering the city from the Rangoon River estuary. Both operations were to be covered by extensive air support from 224 Group, with 221 Group maintaining pressure on any outlying Japanese formations. D-Day was fixed for 2 May, Air Commodore the Earl of Bandon was appointed to command the substantial tactical air operations, while Brigadier General Evans controlled the air transports. Strategic Air Force prepared the way by saturation bombing of supply dumps containing reserves sufficient for an estimated six months, these attacks including the Superfortresses of 20 Bomber Command.

Extensive photographic reconnaissance had located some 1,700 widely dispersed storage units of which approximately half were destroyed. Roads, railway yards, rolling stock, radar and gun emplacements, bridges, airfields and enemy troops all received the undivided attention of the air forces. RAF Liberators mined the river, forcing those Japanese attempting to escape to make their way either overland towards Pegu and the waiting IV Corps, or eastwards through swamps and across the Bay of Martaban.

Allied fighters and fighter bombers enjoyed something of a field day from the middle of April to early May, the rapid advance of Fourteenth Army having flushed from cover an unusual number of enemy MT units. On 19 April a Hurricane squadron attacked a heavily loaded and camouflaged convoy forty strong at a standstill just south of Pyinmana, leaving seventeen vehicles in flames and many more damaged. The same squadron located a larger column approaching the bridge over the Sittang at Mokpalin on the 30th, leaving forty-three lorries in flames. The approaches west of the Sittang Bridge in fact became a happy hunting ground for the fighters as the bridge was one of the main escape routes for the thousands of Japanese now attempting to make their way to Siam. The Mustangs of Second Air Commando Group and the Beaufighters of 224 Group made significant strikes in the area during the latter part of April.

On 1 May the initial phase of Dracula got under way when two pathfinder aircraft and thirty-eight transports of the 317th and 319th Troop Carrier Squadrons USAAF lifted off from Akyab carrying Gurkha paratroops, which they successfully dropped without opposition over their intended landing ground at Elephant Point, south of Rangoon. The following day Dakotas of Nos 194 and 267 Squadrons RAF dropped rations and ammunition at Elephant Point.

That same day, 2 May, another airborne operation took place. Wing Commander Saunders, Officer Commanding 110 Squadron RAF, took his Mosquito on a low-level reconnaissance over Rangoon. Detecting a surprising absence of Japanese he flew over Rangoon jail and saw two notices painted in large letters on the roofs of the prison blocks the first read: JAPS GONE BRITISH HERE, the second, rather more to the point, stating simply: EXTRACT DIGIT.

Landing at Mingaladon, Saunders hitch-hiked into Rangoon and released a number of prisoners of war. Then, having achieved the single-handed ‘liberation’ of Rangoon, he borrowed a native boat and rowed downriver to inform the commander of the invasion force that the Japanese had gone, which came as something of a surprise to the Army as they were convinced that the enemy had substantial forces in the city and would defend it to the death.

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The history of biological warfare

During the past century, more than 500 million people died of infectious diseases. Several tens of thousands of these deaths were due to the deliberate release of pathogens or toxins, mostly by the Japanese during their attacks on China during the Second World War. Two international treaties outlawed biological weapons in 1925 and 1972, but they have largely failed to stop countries from conducting offensive weapons research and large-scale production of biological weapons. And as our knowledge of the biology of disease-causing agents—viruses, bacteria and toxins—increases, it is legitimate to fear that modified pathogens could constitute devastating agents for biological warfare. To put these future threats into perspective, I discuss in this article the history of biological warfare and terrorism.

During the [Second World War], the Japanese army poisoned more than 1,000 water wells in Chinese villages to study cholera and typhus outbreaks

Man has used poisons for assassination purposes ever since the dawn of civilization, not only against individual enemies but also occasionally against armies ( Table 1 ). However, the foundation of microbiology by Louis Pasteur and Robert Koch offered new prospects for those interested in biological weapons because it allowed agents to be chosen and designed on a rational basis. These dangers were soon recognized, and resulted in two international declarations—in 1874 in Brussels and in 1899 in The Hague—that prohibited the use of poisoned weapons. However, although these, as well as later treaties, were all made in good faith, they contained no means of control, and so failed to prevent interested parties from developing and using biological weapons. The German army was the first to use weapons of mass destruction, both biological and chemical, during the First World War, although their attacks with biological weapons were on a rather small scale and were not particularly successful: covert operations using both anthrax and glanders ( Table 2 ) attempted to infect animals directly or to contaminate animal feed in several of their enemy countries (Wheelis, 1999). After the war, with no lasting peace established, as well as false and alarming intelligence reports, various European countries instigated their own biological warfare programmes, long before the onset of the Second World War (Geissler & Moon, 1999).

Table 1

YearEvent
1155Emperor Barbarossa poisons water wells with human bodies, Tortona, Italy
1346Mongols catapult bodies of plague victims over the city walls of Caffa, Crimean Peninsula
1495Spanish mix wine with blood of leprosy patients to sell to their French foes, Naples, Italy
1650Polish fire saliva from rabid dogs towards their enemies
1675First deal between German and French forces not to use 'poison bullets'
1763British distribute blankets from smallpox patients to native Americans
1797Napoleon floods the plains around Mantua, Italy, to enhance the spread of malaria
1863Confederates sell clothing from yellow fever and smallpox patients to Union troops, USA

It is not clear whether any of these attacks caused the spread of disease. In Caffa, the plague might have spread naturally because of the unhygienic conditions in the beleaguered city. Similarly, the smallpox epidemic among Indians could have been caused by contact with settlers. In addition, yellow fever is spread only by infected mosquitoes. During their conquest of South America, the Spanish might also have used smallpox as a weapon. Nevertheless, the unintentional spread of diseases among native Americans killed about 90% of the pre-columbian population (McNeill, 1976).

Table 2

DiseasePathogenAbused 1
Category A (major public health hazards)  
AnthraxBacillus antracis (B)First World War
  Second World War
  Soviet Union, 1979
  Japan, 1995
  USA, 2001
BotulismClostridium botulinum (T)
Haemorrhagic feverMarburg virus (V)Soviet bioweapons programme
 Ebola virus (V)
 Arenaviruses (V)
PlagueYersinia pestis (B)Fourteenth-century Europe
  Second World War
SmallpoxVariola major (V)Eighteenth-century N. America
TularemiaFrancisella tularensis (B)Second World War
Category B (public health hazards)  
BrucellosisBrucella (B)
CholeraVibrio cholerae (B)Second World War
EncephalitisAlphaviruses (V)Second World War
Food poisoningSalmonella, Shigella (B)Second World War
  USA, 1990s
GlandersBurkholderia mallei (B)First World War
  Second World War
PsittacosisChlamydia psittaci (B)
Q feverCoxiella burnetti (B)
TyphusRickettsia prowazekii (B)Second World War
Various toxic syndromesVarious bacteriaSecond World War

Category C includes emerging pathogens and pathogens that are made more pathogenic by genetic engineering, including hantavirus, Nipah virus, tick-borne encephalitis and haemorrhagic fever viruses, yellow fever virus and multidrug-resistant bacteria.

1 Does not include time and place of production, but only indicates where agents were applied and probably resulted in casualties, in war, in research or as a terror agent. B, bacterium P, parasite T, toxin V, virus.

In North America, it was not the government but a dedicated individual who initiated a bioweapons research programme. Sir Frederick Banting, the Nobel-Prize-winning discoverer of insulin, created what could be called the first private biological weapon research centre in 1940, with the help of corporate sponsors (Avery, 1999 Regis, 1999). Soon afterwards, the US government was also pressed to perform such research by their British allies who, along with the French, feared a German attack with biological weapons (Moon, 1999, Regis, 1999), even though the Nazis apparently never seriously considered using biological weapons (Geissler, 1999). However, the Japanese embarked on a largescale programme to develop biological weapons during the Second World War (Harris, 1992, 1999, 2002) and eventually used them in their conquest of China. Indeed, alarm bells should have rung as early as 1939, when the Japanese legally, and then illegally, attempted to obtain yellow fever virus from the Rockefeller Institute in New York (Harris, 2002).

The father of the Japanese biological weapons programme, the radical nationalist Shiro Ishii, thought that such weapons would constitute formidable tools to further Japan's imperialistic plans. He started his research in 1930 at the Tokyo Army Medical School and later became head of Japan's bioweapon programme during the Second World War (Harris, 1992, 1999, 2002). At its height, the programme employed more than 5,000 people, and killed as many as 600 prisoners a year in human experiments in just one of its 26 centres. The Japanese tested at least 25 different disease-causing agents on prisoners and unsuspecting civilians. During the war, the Japanese army poisoned more than 1,000 water wells in Chinese villages to study cholera and typhus outbreaks. Japanese planes dropped plague-infested fleas over Chinese cities or distributed them by means of saboteurs in rice fields and along roads. Some of the epidemics they caused persisted for years and continued to kill more than 30,000 people in 1947, long after the Japanese had surrendered (Harris, 1992, 2002). Ishii's troops also used some of their agents against the Soviet army, but it is unclear as to whether the casualties on both sides were caused by this deliberate spread of disease or by natural infections (Harris, 1999). After the war, the Soviets convicted some of the Japanese biowarfare researchers for war crimes, but the USA granted freedom to all researchers in exchange for information on their human experiments. In this way, war criminals once more became respected citizens, and some went on to found pharmaceutical companies. Ishii's successor, Masaji Kitano, even published postwar research articles on human experiments, replacing 'human' with 'monkey' when referring to the experiments in wartime China (Harris, 1992, 2002).

Although some US scientists thought the Japanese information insightful, it is now largely assumed that it was of no real help to the US biological warfare programme projects. These started in 1941 on a small scale, but increased during the war to include more than 5,000 people by 1945. The main effort focused on developing capabilities to counter a Japanese attack with biological weapons, but documents indicate that the US government also discussed the offensive use of anti-crop weapons (Bernstein, 1987). Soon after the war, the US military started open-air tests, exposing test animals, human volunteers and unsuspecting civilians to both pathogenic and non-pathogenic microbes (Cole, 1988 Regis, 1999). A release of bacteria from naval vessels off

. nobody really knows what the Russians are working on today and what happened to the weapons they produced

the coasts of Virginia and San Francisco infected many people, including about 800,000 people in the Bay area alone. Bacterial aerosols were released at more than 200 sites, including bus stations and airports. The most infamous test was the 1966 contamination of the New York metro system with Bacillus globigii— a non-infectious bacterium used to simulate the release of anthrax—to study the spread of the pathogen in a big city. But with the opposition to the Vietnam War growing and the realization that biological weapons could soon become the poor man's nuclear bomb, President Nixon decided to abandon offensive biological weapons research and signed the Biological and Toxin Weapons Convention (BTWC) in 1972, an improvement on the 1925 Geneva Protocol. Although the latter disallowed only the use of chemical or biological weapons, the BTWC also prohibits research on biological weapons. However, the BTWC does not include means for verification, and it is somewhat ironic that the US administration let the verification protocol fail in 2002, particularly in view of the Soviet bioweapons project, which not only was a clear breach of the BTWC, but also remained undetected for years.

Even though they had just signed the BTWC, the Soviet Union established Biopreparat, a gigantic biowarfare project that, at its height, employed more than 50,000 people in various research and production centres (Alibek & Handelman, 1999). The size and scope of the Soviet Union's efforts were truly staggering: they produced and stockpiled tons of anthrax bacilli and smallpox virus, some for use in intercontinental ballistic missiles, and engineered multidrug-resistant bacteria, including plague. They worked on haemorrhagic fever viruses, some of the deadliest pathogens that humankind has encountered. When virologist Nikolai Ustinov died after injecting himself with the deadly Marburg virus, his colleagues, with the mad logic and enthusiasm of bioweapon developers, re-isolated the virus from his body and found that it had mutated into a more virulent form than the one that Ustinov had used. And few took any notice, even when accidents happened. In 1971, smallpox broke out in the Kazakh city of Aralsk and killed three of the ten people that were infected. It is speculated that they were infected from a bioweapons research centre on a small island in the Aral Sea (Enserink, 2002). In the same area, on other occasions, several fishermen and a researcher died from plague and glanders, respectively (Miller et al., 2002). In 1979, the Soviet secret police orchestrated a large cover-up to explain an outbreak of anthrax in Sverdlovsk, now Ekaterinburg, Russia, with poisoned meat from anthrax-contaminated animals sold on the black market. It was eventually revealed to have been due to an accident in a bioweapons factory, where a clogged air filter was removed but not replaced between shifts ( Fig. 1 ) (Meselson et al., 1994 Alibek & Handelman, 1999).

Anthrax as a biological weapon. Light (A) and electron (B) micrographs of anthrax bacilli, reproduced from the Centers of Disease Control Public Health Image Library. The map (C) shows six villages in which animals died after anthrax spores were released from a bioweapons factory in Sverdlovsk, USSR, in 1979. Settled areas are shown in grey, roads in white, lakes in blue and the calculated contours of constant dosage of anthrax spores in black. At least 66 people died after the accident. (Reprinted with permission from Meselson et al., 1994 © (1994) American Association for the Advancement of Science.)

The most striking feature of the Soviet programme was that it remained secret for such a long time. During the Second World War, the Soviets used a simple trick to check whether US researchers were occupied with secret research: they monitored whether American physicists were publishing their results. Indeed, they were not, and the conclusion was, correctly, that the US was busy building a nuclear bomb (Rhodes, 1988, pp. 327 and 501). The same trick could have revealed the Soviet bioweapons programme much earlier ( Fig. 2 ). With the collapse of the Soviet Union, most of these programmes were halted and the research centres abandoned or converted for civilian use. Nevertheless, nobody really knows what the Russians are working on today and what happened to the weapons they produced. Western security experts now fear that some stocks of biological weapons might not have been destroyed and have instead fallen into other hands (Alibek & Handelman, 1999 Miller et al., 2002). According to US intelligence, South Africa, Israel, Iraq and several other countries have developed or still are developing biological weapons (Zilinskas, 1997 Leitenberg, 2001).

Detecting biological warfare research. A comparison of the number of publications from two Russian scientists. L. Sandakchiev (black bars) was involved, as the head of the Vector Institute for viral research, in the Soviet project to produce smallpox as an offensive biological weapon. V. Krylov (white bars) was not. Note the decrease in publications by Sandakchiev compared with those by Krylov. The data were compiled from citations from a PubMed search for the researchers on 15 August 2002.

Apart from state-sponsored biowarfare programmes, individuals and non-governmental groups have also gained access to potentially dangerous microorganisms, and some have used them (Purver, 2002). A few examples include the spread of hepatitis, parasitic infections, severe diarrhoea and gastroenteritis. The latter occurred when a religious sect tried to poison a whole community by spreading Salmonella in salad bars to interfere with a local election (Török et al., 1997 Miller et al., 2002). The sect, which ran a hospital on its grounds, obtained the bacterial strain from a commercial supplier. Similarly, a right-wing laboratory technician tried to get hold of the plague bacterium from the American Tissue Culture Collection, and was only discovered after he complained that the procedure took too long (Cole, 1996). These examples clearly indicate that organized groups or individuals with sufficient determination can obtain dangerous biological agents. All that is required is a request to 'colleagues' at scientific institutions, who share their published materials with the rest of the community (Breithaupt, 2000). The relative ease with which this can be done explains why the numerous hoaxes in the USA after the anthrax mailings had to be taken seriously, thus causing an estimated economic loss of US $100 million (Leitenberg, 2001).

These examples clearly indicate that organized groups or individuals with sufficient determination can obtain dangerous biological agents

Another religious cult, in Japan, proved both the ease and the difficulties of using biological weapons. In 1995, the Aum Shinrikyo cult used Sarin gas in the Tokyo subway, killing 12 train passengers and injuring more than 5,000 (Cole, 1996). Before these attacks, the sect had also tried, on several occasions, to distribute (non-infectious) anthrax within the city with no success. It was obviously easy for the sect members to produce the spores but much harder to disseminate them (Atlas, 2001 Leitenberg, 2001). The still unidentified culprits of the 2001 anthrax attacks in the USA were more successful, sending contaminated letters that eventually killed five people and, potentially even more seriously, caused an upsurge in demand for antibiotics, resulting in over-use and thus contributing to drug resistance (Atlas, 2001 Leitenberg, 2001 Miller et al., 2002).

One interesting aspect of biological warfare is the accusations made by the parties involved, either as excuses for their actions or to justify their political

Cuba frequently accused the USA of using biological warfare

goals. Many of these allegations, although later shown to be wrong, have been exploited either as propaganda or as a pretext for war, as recently seen in the case of Iraq. It is clearly essential to draw the line between fiction and reality, particularly if, on the basis of such evidence, politicians call for a 'pre-emptive' war or allocate billions of dollars to research projects. Examples of such incorrect allegations include a British report before the Second World War that German secret agents were experimenting with bacteria in the Paris and London subways, using harmless species to test their dissemination through the transport system (Regis, 1999 Leitenberg, 2001). Although this claim was never substantiated, it might have had a role in promoting British research on anthrax in Porton Down and on Gruinard Island. During the Korean War, the Chinese, North Koreans and Soviets accused the USA of deploying biological weapons of various kinds. This is now seen as wartime propaganda, but the secret deal between the USA and Japanese bioweapons researchers did not help to diffuse these allegations (Moon, 1992). Later, the USA accused the Vietnamese of dropping fungal toxins on the US Hmong allies in Laos. However, it was found that the yellow rain associated with the reported variety of syndromes was simply bee faeces ( Fig. 3 Seeley et al., 1985). The problem with such allegations is that they develop a life of their own, no matter how unbelievable they are. For example, the conspiracy theory that HIV is a biological weapon is still alive in some people's minds. Depending on whom one asks, KGB or CIA scientists developed HIV to damage the USA or to destabilize Cuba, respectively. Conversely, in 1997, Cuba was the first country to officially file a complaint under Article 5 of the BTWC, accusing the USA of releasing a plant pathogen (Leitenberg, 2001). Although this was never proven, the USA did indeed look into biological agents to kill Fidel Castro and Frederik Lumumba of the Democratic Republic of Congo (Miller et al., 2002).

Hmong refugees from Laos, who collaborated with the American armed forces during the Vietnam War, accused the Soviet Union of attacking them with biological or chemical weapons. However, the alleged toxin warfare agent known as yellow rain matches perfectly the yellow spots of bee faeces on leaves in the forest of the Khao Yai National Park in Thailand. (Image reprinted with permission from Seeley et al., 1985 © (1985) M. Meselson, Harvard University).

We are witnessing a renewed interest in biological warfare and terrorism owing to several factors, including the discovery that Iraq has been developing biological weapons (Zilinskas, 1997), several bestselling novels describing biological attacks, and the anthrax letters after the terrorist attacks on 11 September 2001. As history tells us, virtually no nation with the ability to develop weapons of mass destruction has abstained from doing so. And the Soviet project shows that international treaties are basically useless unless an effective verification procedure is in place. Unfortunately, the same knowledge that is needed to develop drugs and vaccines against pathogens has the potential to be abused for the development of biological weapons ( Fig. 4 Finkel, 2001). Thus, some critics have suggested that information about potentially harmful pathogens should not be made public but rather put into the hands of 'appropriate representatives' (Danchin, 2002 Wallerstein, 2002). A recent report on anti-crop agents was already self-censored before publication, and journal editors now recommend special scrutiny for sensitive papers (Mervis & Stokstad, 2002 Cozzavelli, 2003 Malakoff, 2003). Whether or not such measures are useful deterrents might be questionable, because the application of available knowledge is clearly enough to kill. An opposing view calls for the imperative publication of information about the development of biological weapons to give scientists, politicians and the interested public all the necessary information to determine a potential threat and devise countermeasures.

. virtually no nation with the ability to develop weapons of mass destruction has abstained from doing so

Intimate interactions of hosts and pathogens. (A) The face of a smallpox victim in Accra, Ghana, 1967. (Photograph from the Center of Disease Control's Public Health Image Library.) (B) A poxvirus-infected cell is shown to illustrate just one of the many intricate ways in which pathogens can interact with, abuse or mimic their hosts. The virus is shown in red, the actin skeleton of the cell in green. Emerging viruses rearrange actin into tail-like structures that push them into neighbouring cells. (Image by F. Frischknecht and M. Way, reprinted with permission from the Journal of General Virology.)

The current debate about biological weapons is certainly important in raising awareness and increasing our preparedness to counter a potential attack. It could also prevent an overreaction such as that caused in response to the anthrax letters mailed in the USA. However, contrasting the speculative nature of biological attacks with the grim reality of the millions of people who still die each year from preventable infections, we might ask ourselves just how many resources we can afford to allocate in preparation for a hypothetical human-inflicted disaster.


THE 1972 BIOLOGICAL WEAPONS CONVENTION

During the late 1960s, public and expert concerns were raised internationally regarding the indiscriminate nature of, unpredictability of, epidemiologic risks of, and lack of epidemiologic control measures for biological weapons (11, 13). In addition, more information on various nationsbiological weapons programs became evident, and it was obvious that the 1925 Geneva Protocol was ineffective in controlling the proliferation of biological weapons. In July 1969, Great Britain submitted a proposal to the UN Committee on Disarmament outlining the need to prohibit the development, production, and stockpiling of biological weapons (22). Furthermore, the proposal provided for measures for control and inspections, as well as procedures to be followed in case of violation. Shortly after submission of the British proposal, in September 1969, the Warsaw Pact nations under the lead of the Soviet Union submitted a similar proposal to the UN. However, this proposal lacked provisions for inspections. Two months later, in November 1969, the World Health Organization issued a report regarding the possible consequences of the use of biological warfare agents (Table ​ (Table3 3 ).

Table 3

Estimates of casualties produced by a hypothetical biological attack *

AgentDownwind reach (km)Number killedNumber incapacitated
Rift Valley fever140035,000
Tickborne encephalitis1950035,000
Typhus519,00085,000
Brucellosis10500125,000
Q-fever150125,000
Tularemia30,000125,000
Anthrax95,000125,000

*Release of 50 kg of agent (aerosolized) by aircraft along a 2-km line upwind of a population center of 500,000 (23).

Subsequently, the 1972 𠇌onvention on the Prohibition of the Development, Production, and Stockpiling of Bacteriological (Biological) and Toxin Weapons and on Their Destruction,” known as the BWC, was developed. This treaty prohibits the development, production, and stockpiling of pathogens or toxins in “quantities that have no justification for prophylactic, protective or other peaceful purposes” (22). Under the BWC, the development of delivery systems and the transfer of biological warfare technology or expertise to other countries are also prohibited. It further required the parties to the BWC to destroy stockpiles, delivery systems, and production equipment within 9 months of ratifying the treaty. This agreement was reached among 103 cosigning nations, and the treaty was ratified in April 1972. The BWC went into effect in March 1975 (1). Signatories that have not yet ratified the BWC are obliged to refrain from activities that would defeat the purpose of the treaty until they specifically communicate to the UN their intention not to ratify the treaty. Review conferences to the BWC were held in 1981, 1986, 1991, and 1996. Signatories to the BWC are required to submit the following information to the UN on an annual basis: facilities where biological defense research is being conducted, scientific conferences that are held at specified facilities, exchange of scientists or information, and disease outbreaks (1, 24).

However, like the 1925 Geneva Protocol, the BWC does not provide firm guidelines for inspections and control of disarmament and adherence to the protocol. In addition, there are no guidelines on enforcement and how to deal with violations. Furthermore, there are unresolved controversies about the definition of �nsive research” and the quantities of pathogens necessary for benevolent research (24, 25). Alleged violations of the BWC were to be reported to the UN Security Council, which may in turn initiate inspections of accused parties, as well as modalities of correction. The right of permanent members of the Security Council to veto proposed inspections, however, undermines this provision. More recent events in 2003 and 2004 again illustrated the complexity and the enormous difficulties the UN faces in enforcing the statutes of the BWC.

In the USA, the offensive biological weapons program was terminated by President Nixon by executive orders in 1969 and 1970 (7). The USA adopted a policy to never use biological weapons, including toxins, under any circumstances. National Security Decisions 35 and 44, issued in November 1969 (microorganisms) and February 1970 (toxins), mandated the cessation of offensive biological weapons research and production and the destruction of the biological weapons arsenal. However, research efforts continued to be allowed for the purpose of developing countermeasures, including vaccines and antisera. The entire arsenal of biological weapons was destroyed between May 1971 and February 1973 under the auspices of the US Department of Agriculture, the US Department of Health, Education, and Welfare, and the Departments of Nature Resources of Arkansas, Colorado, and Maryland. After the termination of the offensive program, USAMRIID was established to continue research for development of medical defense for the US military against a potential attack with biological weapons. The USAMRIID is an open research institution, and none of the research is classified.


What Is the Biological Warfare? Agents Use

Biological weapons include any microorganism (such as bacteria, viruses, or fungi) or toxin (poisonous compounds produced by microorganisms) found in nature that can be used to kill or injure people.

The act of bioterrorism can range from a simple hoax to the actual use of these biological weapons, also referred to as agents. A number of nations have or are seeking to acquire biological warfare agents, and there are concerns that terrorist groups or individuals may acquire the technologies and expertise to use these destructive agents. Biological agents may be used for an isolated assassination, as well as to cause incapacitation or death to thousands. If the environment is contaminated, a long-term threat to the population could be created.

  • History: The use of biological agents is not a new concept, and history is filled with examples of their use.
    • Attempts to use biological warfare agents date back to antiquity. Scythian archers infected their arrows by dipping them in decomposing bodies or in blood mixed with manure as far back as 400 BC. Persian, Greek, and Roman literature from 300 BC quotes examples of dead animals used to contaminate wells and other sources of water. In the Battle of Eurymedon in 190 BC, Hannibal won a naval victory over King Eumenes II of Pergamon by firing earthen vessels full of venomous snakes into the enemy ships.
    • During the battle of Tortona in the 12th century AD, Barbarossa used the bodies of dead and decomposing soldiers to poison wells. During the siege of Kaffa in the 14th century AD, the attacking Tatar forces hurled plague-infected corpses into the city in an attempt to cause an epidemic within enemy forces. This was repeated in 1710, when the Russians besieging Swedish forces at Reval in Estonia catapulted bodies of people who had died from plague.
    • During the French and Indian War in the 18th century AD, British forces under the direction of Sir Jeffrey Amherst gave blankets that had been used by smallpox victims to the Native Americans in a plan to spread the disease.
    • Allegations were made during the American Civil War by both sides, but especially against the Confederate Army, of the attempted use of smallpox to cause disease among enemy forces.
    • During World War I, the German Army developed anthrax, glanders, cholera, and a wheat fungus specifically for use as biological weapons. They allegedly spread plague in St. Petersburg, Russia, infected mules with glanders in Mesopotamia, and attempted to do the same with the horses of the French Cavalry.
    • The Geneva Protocol of 1925 was signed by 108 nations. This was the first multilateral agreement that extended prohibition of chemical agents to biological agents. Unfortunately, no method for verification of compliance was addressed.
    • During World War II, Japanese forces operated a secret biological warfare research facility (Unit 731) in Manchuria that carried out human experiments on prisoners. They exposed more than 3,000 victims to plague, anthrax, syphilis, and other agents in an attempt to develop and observe the disease. Some victims were executed or died from their infections. Autopsies were also performed for greater understanding of the effects on the human body.
    • In 1942, the United States formed the War Research Service. Anthrax and botulinum toxin initially were investigated for use as weapons. Sufficient quantities of botulinum toxin and anthrax were stockpiled by June 1944 to allow unlimited retaliation if the German forces first used biological agents. The British also tested anthrax bombs on Gruinard Island off the northwest coast of Scotland in 1942 and 1943 and then prepared and stockpiled anthrax-laced cattle cakes for the same reason.
    • The United States continued research on various offensive biological weapons during the 1950s and 1960s. From 1951-1954, harmless organisms were released off both coasts of the United States to demonstrate the vulnerability of American cities to biological attacks. This weakness was tested again in 1966 when a test substance was released in the New York City subway system.
    • During the Vietnam War, Viet Cong guerrillas used needle-sharp punji sticks dipped in feces to cause severe infections after an enemy soldier had been stabbed.
    • In 1979, an accidental release of anthrax from a weapons facility in Sverdlovsk, USSR, killed at least 66 people. The Russian government claimed these deaths were due to infected meat and maintained this position until 1992, when Russian President Boris Yeltsin finally admitted to the accident.

    Facts on Bioterrorism and Biowarfare Today

    • Bioterrorism and biowarfare today: A number of countries have continued offensive biological weapons research and use. Additionally, since the 1980s, terrorist organizations have become users of biological agents. Usually, these cases amount only to hoaxes. However, the following exceptions have been noted:
      • In 1985, Iraq began an offensive biological weapons program producing anthrax, botulinum toxin, and aflatoxin. During Operation Desert Storm, the coalition of allied forces faced the threat of chemical and biological agents. Following the Persian Gulf War, Iraq disclosed that it had bombs, Scud missiles, 122-mm rockets, and artillery shells armed with botulinum toxin, anthrax, and aflatoxin. They also had spray tanks fitted to aircraft that could distribute agents over a specific target.
      • In September and October of 1984, 751 people were intentionally infected with Salmonella, an agent that causes food poisoning, when followers of the Bhagwan Shree Rajneesh contaminated restaurant salad bars in Oregon.
      • In 1994, a Japanese sect of the Aum Shinrikyo cult attempted an aerosolized (sprayed into the air) release of anthrax from the tops of buildings in Tokyo.
      • In 1995, two members of a Minnesota militia group were convicted of possession of ricin, which they had produced themselves for use in retaliation against local government officials.
      • In 1996, an Ohio man attempted to obtain bubonic plague cultures through the mail.
      • In 2001, anthrax was delivered by mail to U.S. media and government offices. There were five deaths as a result.
      • In December 2002, six terrorist suspects were arrested in Manchester, England their apartment was serving as a "ricin laboratory." Among them was a 27-year-old chemist who was producing the toxin. Later, on Jan. 5, 2003, British police raided two residences around London and found traces of ricin, which led to an investigation of a possible Chechen separatist plan to attack the Russian embassy with the toxin several arrests were made.
      • On Feb. 3, 2004, three U.S. Senate office buildings were closed after the toxin ricin was found in a mailroom that serves Senate Majority Leader Bill Frist's office.

      The threat that biological agents will be used on both military forces and civilian populations is now more likely than it was at any other point in history.

      How Are Biological Agents Delivered and Detected?

      Although there are more than 1,200 biological agents that could be used to cause illness or death, relatively few possess the necessary characteristics to make them ideal candidates for biological warfare or terrorism agents. The ideal biological agents are relatively easy to acquire, process, and use. Only small amounts (on the order of pounds and often less) would be needed to kill or incapacitate hundreds of thousands of people in a metropolitan area. Biological warfare agents are easy to hide and difficult to detect or protect against. They are invisible, odorless, tasteless, and can be spread silently.

      Delivery

      Biological warfare agents can be disseminated in various ways.

      • Through the air by aerosol sprays: To be an effective biological weapon, airborne germs must be dispersed as fine particles. To be infected, a person must breathe a sufficient quantity of particles into the lungs to cause illness.
      • Used in explosives (artillery, missiles, detonated bombs): The use of an explosive device to deliver and spread biological agents is not as effective as the delivery by aerosol. This is because agents tend to be destroyed by the blast, typically leaving less than 5% of the agent capable of causing disease.
      • Put into food or water: Contamination of a city's water supplies requires an unrealistically large amount of an agent as well as introduction into the water after it passes through a regional treatment facility.
      • Absorbed through or injected into the skin: This method might be ideal for assassination, but is not likely to be used to cause mass casualties.

      Detection

      Biological agents could either be found in the environment using advanced detection devices, after specific testing or by a doctor reporting a medical diagnosis of an illness caused by an agent. Animals may also be early victims and shouldn't be overlooked.

      • Early detection of a biological agent in the environment allows for early and specific treatment and time enough to treat others who were exposed with protective medications. Currently, the U.S. Department of Defense is evaluating devices to detect clouds of biological warfare agents in the air.
      • Doctors must be able to identify early victims and recognize patterns of disease. If unusual symptoms, a large numbers of people with symptoms, dead animals, or other inconsistent medical findings are noted, a biological warfare attack should be suspected. Doctors report these patterns to public health officials.

      Protective Measures

      Protective measures can be taken against biological warfare agents. These should be started early (if enough warning is received) but definitely once it is suspected that a biological agent has been used. To read more about protective clothing, see Personal Protective Equipment.

      • Masks: Currently, available masks such as the military gas mask or high-efficiency particulate air (HEPA) filter masks used for tuberculosis exposure filter out most biological warfare particles delivered through the air. However, the face seals on ill-fitting masks often leak. For a mask to fit properly, it must be fitted to a person's face.
      • Clothing: Most biological agents in the air do not penetrate unbroken skin, and few organisms stick to skin or clothing. After an aerosol attack, the simple removal of clothing eliminates a great majority of surface contamination. Thorough showering with soap and water removes 99.99% of the few organisms that may be left on the victim's skin.
      • Medical protection: Health care professionals treating victims of biological warfare may not need special suits but should use latex gloves and take other precautions such as wearing gowns and masks with protective eye shields. Victims would be isolated in private rooms while receiving treatment. : Victims of biological warfare might be given antibiotics orally (pills) or through an IV, even before the specific agent is identified.
      • Vaccinations: Currently, protective vaccines (given as shots) are available for anthrax, Q fever, yellow fever, and smallpox. The widespread immunization of nonmilitary personnel has not been recommended by any governmental agency so far. Immune protection against ricin and staphylococcal toxins may also be possible in the near future.

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      Anthrax Exposure Symptoms, Signs, and Diagnosis

      Anthrax bacteria occur worldwide. The United States Working Group on Civilian Biodefense and the Centers for Diseases Control and Prevention (CDC) have identified anthrax as one of a few biological agents capable of causing death and disease in sufficient numbers to cripple a developed region or urban setting. The organisms known as Bacillus anthracis may ordinarily produce disease in domesticated as well as wild animals such as goats, sheep, cattle, horses, and swine. Humans become infected by contact with infected animals or contaminated animal products. Infection occurs mainly through the skin and rarely by breathing spores or swallowing them. Spores exist in the soil and become aerosolized when the microorganisms are released into the air by excavation, plowing, or other disruptive actions.

      Apart from biological warfare, anthrax in humans is rare. In the United States, only 127 cases of anthrax appeared in the early years of the 20th century and dropped to about one per year during the 1990s.

      Skin anthrax (cutaneous): Infection begins when the spores enter the skin through small cuts or abrasions. Spores then become active in the host (human or animal) and produce poisonous toxins. Swelling, bleeding, and tissue death may occur at the site of infection.

      • Most of the cases of anthrax involve the skin. After a person is exposed, the disease first appears in one to five days as a small pimple-looking sore that progresses over the next one to two days to contain fluid filled with many organisms. The sore is usually painless, and it may have swelling around it. Sometimes the swelling affects a person's entire face or limb.
      • Victims may have fever, feel tired, and have a headache. Once the sore opens, it forms a black area of tissue. The black appearance of the tissue injury gives anthrax its name from the Greek word anthrakos, meaning coal. After a period of two to three weeks, the black tissue separates, often leaving a scar. With adequate treatment, less than 1% of people infected with skin anthrax die.

      Inhalation anthrax: In inhalation anthrax, the spores are inhaled into the lungs where they become active and multiply. There they produce massive bleeding and swelling inside the chest cavity. The germs then can spread to the blood, leading to shock and blood poisoning, which may lead to death.

      • Historically known as woolsorter's disease (because it affected people who work around sheep), inhalation anthrax can appear anywhere within one to six days, or as long as 60 days after exposure. Initial symptoms are general and can include headache, tiredness, body aches, and fever. The victim may have a nonproductive cough and mild chest pain. These symptoms usually last for two to three days.
      • Some people show a short period of improvement. This is followed by the sudden onset of increased trouble breathing, shortness of breath, bluish skin color, increased chest pain, and sweating. Swelling of the chest and neck may also occur. Shock and death may follow within 24-36 hours in most people with this type of infection.
      • Anthrax is not spread from person to person. Inhalation anthrax is the most likely form of disease to follow a military or terrorist attack. Such an attack likely will involve the aerosolized delivery of anthrax spores.

      Mouth, throat, GI tract (oropharyngeal and gastrointestinal): These cases result when someone eats infected meat that has not been cooked sufficiently. After an incubation period of two to five days, victims with oropharyngeal disease develop a severe sore throat or sores in the mouth or on a tonsil. Fever and neck swelling may occur. The victim may have trouble breathing. GI anthrax begins with nonspecific symptoms of nausea, vomiting, and fever. These are followed in most victims by severe abdominal pain. The victim may also vomit blood and have diarrhea.

      Doctors will perform various tests, especially if anthrax is suspected.

      • With skin anthrax, a biopsy is taken of the sore (lesion), and lab tests are performed to look at the organism under a microscope and confirm the diagnosis of anthrax.
      • The diagnosis of inhalation anthrax is difficult to make. A chest X-ray may show certain signs in the chest cavity. A CT scan of the chest may be very helpful when there is suspected inhalational anthrax. Early in the process, when the chest X-ray is still normal, the CT scan may show pleural, pericardial, and mediastinal fluid collections, enlarged hemorrhagic mediastinal lymph nodes, and bronchial airwayedema. Cultures (growing the bacteria in a lab and then examining them under a microscope) are minimally helpful in making the diagnosis. Blood tests may also be performed.
      • GI anthrax also is difficult to diagnose because the disease is rare and symptoms are not always obvious. Diagnosis usually is confirmed only if the victim has a history of eating contaminated meat in the setting of an outbreak. Once again, cultures generally are not helpful in making the diagnosis. (brain swelling) from anthrax is difficult to distinguish from meningitis due to other causes. A spinal tap may be performed to look at the person's spinal fluid in identifying the organism.

      The most useful microbiologic test is the standard blood culture, which is almost always positive in victims with anthrax throughout their bodies. Blood cultures should show growth in six to 24 hours and if the laboratory has been alerted to the possibility of anthrax, biochemical testing should provide a preliminary diagnosis 12-24 hours later. However, if the laboratory has not been alerted to the possibility of anthrax, there is the chance that the organism may not be identified correctly.

      Rapid diagnostic tests for anthrax and its proteins include polymerase chain reaction (PCR), enzyme-linked immunosorbent assay (ELISA), and direct fluorescent antibody (DFA) testing. Currently, these tests are only available at national reference laboratories.

      Anthrax Exposure Treatment, Prevention, and Postexposure Prophylaxis

      • Inhalation anthrax: As previously stated because inhalation anthrax moves quickly throughout the body, doctors will begin antibiotic treatment right away even before a firm diagnosis is made through lab testing.
          (Cipro), doxycycline (Vibramycin), and penicillin are FDA-approved antibiotics for treatment of anthrax. Experts currently recommend ciprofloxacin or other drugs in the same class for adults who are assumed to have inhalation anthrax infection. Penicillin and doxycycline may be used once organism culture sensitivities are known.
      • Traditionally, ciprofloxacin and other antibiotics in that class are not recommended for use in children younger than 16-18 years of age because of a weak theoretical link to permanent joint disorders. Balancing these small risks against the risk of death and the possibility of infection with a resistant strain of anthrax, experts recommend that ciprofloxacin nonetheless be given to children in appropriate doses.
      • Because there is a risk the infection will recur, victims are treated with antibiotics for at least 60 days.
      • A vaccination series to protect against anthrax consists of five IM doses administered at day 0, week 4, and months 6, 12, and 18, followed by annual boosters. The CDC does not recommend vaccination for the general public, health care workers, or even people working with animals. The only groups that are recommended to receive routine vaccination are military personnel and investigators and remediation workers who are likely to enter an area with B. anthracis spores.

        Postexposure Prophylaxis

        When unvaccinated people are exposed to anthrax, it is now recommended that they receive antibiotics for 60 days and be vaccinated. The common antibiotics used for postexposure prophylaxis are ciprofloxacin and doxycycline combined. The vaccine is Anthrax Vaccine Adsorbed (AVA), and it is given as three subcutaneous doses (administered at 0, 2, and 4 weeks postexposure). These recommendations are for everyone and include pregnant women and children (although the recommendation for children will be reviewed on an event by event basis). The government has stockpiles of drugs and vaccines available and can deliver them to an affected area very quickly.

        Plague

        Plague is another infection that can strike humans and animals. It is caused by the bacteria Yersinia pestis, which has been the cause of three great human pandemics in the sixth, 14th, and 20th centuries. Throughout history, the oriental rat flea has been largely responsible for spreading bubonic plague. After the flea bites an infected animal, the organisms can multiply inside the flea. When an infected flea attempts to bite again, it vomits clotted blood and bacteria into the victim's bloodstream and passes the infection on to the next victim, whether small mammal (usually rodent) or human.

        Although the largest outbreaks of plague have been associated with the rat flea, all fleas should be considered dangerous in areas where plague may be found. The most important vector (a vector is an animal that can transmit the disease) in the United States is the most prevalent flea of rock squirrels and California ground squirrels. The black rat has been most responsible worldwide for the continuing spread of plague in urban epidemics.

        People infected with plague may suddenly develop high a fever, painful lymph nodes, and have bacteria in their blood. Some victims with the bubonic form of the disease may develop secondary pneumonic plague (a disease similar to pneumonia). Plague is contagious, and when the victim coughs, plague can spread. Pneumonic plague is the most severe form of the disease and if untreated, most people die.

        As few as one to 10 organisms are enough to infect humans or other animals including rodents. During the early phase, the germs usually spread to lymph nodes near the bite, where swelling occurs. The infection then spreads to other organs such as the spleen, liver, lungs, skin, mucous membranes, and later, the brain.

        In the United States, most victims with human plague have the bubonic form. If the organisms were used as a biological warfare agent, it most likely would be spread through the air and inhaled by victims. The result would be primary pneumonic plague (epidemic pneumonia). If fleas were used as carriers of disease, bubonic or septicemic (blood infection) plague would result.

        • Bubonic plague: Swollen lymph nodes (called buboes) develop one to eight days after exposure. Their appearance is associated with the onset of sudden fever, chills, and headache, which often are followed by nausea and vomiting several hours later. The buboes become visible within 24 hours and cause severe pain. Untreated, septicemia (blood poisoning) develops in two to six days. Up to 15% of bubonic plague victims develop secondary pneumonic plague and thus can spread illness from person to person by coughing.
        • Septicemia plague: Septicemia plague may occur with bubonic plague. The signs and symptoms of primary septicemic plague include fever, chills, nausea, vomiting, and diarrhea. Later, bleeding in the skin may develop, hands and feet may lose circulation, and tissue may die.
        • Pneumonic plague: Pneumonic plague may occur primarily from inhaling organisms in the air or from exposure to infected blood. Victims typically have a productive cough with blood-tinged sputum within 24 hours of symptom onset.

        The diagnosis of bubonic plague may be made if the victim has painful lymph glands and other common symptoms, especially if the victim has been exposed to rodents or fleas. But if the victim is not in an area where plague is present and symptoms are typical of other illnesses, the diagnosis may be difficult.

        The doctor may view under a microscope a sample of sputum from a productive cough or the fluid from a swollen lymph gland.

        Samples may grow in the laboratory and indicate plague within 48 hours and blood tests may also be performed.

        Victims of suspected plague will be isolated for the first 48 hours after treatment begins. If pneumonic plague is present, isolation may last for four more days. Since 1948, streptomycin has been the treatment of choice for plague but other antibiotics may be given.

        If treated with antibiotics, buboes typically become smaller in 10-14 days and do not require drainage. Victims are unlikely to survive primary pneumonic plague if antibiotic therapy is not begun within 18 hours of the beginning of symptoms. Without treatment, 60% of people with bubonic plague die, and 100% with pneumonic and septicemic forms die.

        Fleas always must be targeted for destruction before the rodents, because killing rodents may release into the environment massive amounts of infected fleas, which will be hungry for a blood meal and, in the absence of rodents, the fleas will seek out any warm-blooded animal, including humans and infect them. Pesticides have been successful in getting rid of rats and other animal hosts. Public education about how plague spreads is an important part of prevention.

        People who have been exposed to pneumonic plague and those who have been exposed to organisms in the air may be treated with antibiotics. Currently recommended antibiotics are streptomycin or gentamycin IM for 10 days, or until two days after the fever subsides. Alternative medications include doxycycline, ciprofloxacin, and chloramphenicol.

        Contacts with victims who have bubonic plague do not need preventive medication. But people who were in the same environment as those who are infected may need preventive antibiotics. A previously FDA-approved plague vaccine is no longer manufactured. It was useful against the bubonic form of plague but not the more serious pneumonic (lung) form of plague, which is the kind most often expected in a terrorist incident. A new vaccine effective against all varieties of plague is under development.

        Cholera

        Cholera is an acute and potentially severe gastrointestinal disease (stomach and intestines) caused by the bacteria Vibrio cholerae. This agent has been investigated in the past as a biological weapon. Cholera does not spread easily from human to human, so it appears that major drinking water supplies would have to be profusely contaminated for this agent to be effective as a biological weapon.

        Cholera normally can infect water or food that becomes contaminated by human bowel waste. The organism can survive for up to 24 hours in sewage and as long as six weeks in certain types of relatively impure water containing organic matter. It can withstand freezing for three to four days, but it is killed readily by dry heat, steam, boiling, short-term exposure to ordinary disinfectants, and chlorination of water.

        The toxin causes a person's intestines to create massive amounts of fluid that then produces thin, grayish brown diarrhea.

        Depending on how many organisms a person drinks or eats, the illness could begin within 12-72 hours. The symptoms start suddenly with intestinal cramps and painless (rice-water appearing) diarrhea. Vomiting, feeling ill, and headache often accompany the diarrhea, especially early in the illness.

        Fever is rare. If untreated, the disease generally lasts one to seven days. During the illness, the body loses great amounts of fluid, so it is important during recovery to replace fluids and balance electrolytes (such as sodium and potassium).

        Children may experience seizures and cardiovascular imbalances severe enough to cause heart problems. The rapid loss of body fluids often leads to more severe illness. If not treated, up to half of children with cholera may die.

        Although cholera can be suspected in patients with a large volume of watery diarrhea, physicians make a definitive diagnosis through stool culture on specialized culture media (thiosulfate citrate bile sucrose (TCBS) agar or taurocholate tellurite gelatin agar (TTGA). There are rapid tests that are also available for diagnosis. However, the tests lack specificity and are usually not recommended at this time.

        Fluids and electrolytes need to be replaced because the body has lost large amounts of fluids through the vomiting and diarrhea. Doctors may encourage the person to drink, but if someone continues to vomit or has frequent stools, an IV may be used to replace the fluid lost.

        Antibiotics such as tetracycline or doxycycline shorten the duration of diarrhea and reduce fluid losses. The antibiotics ciprofloxacin or erythromycin also may be used for a few days.

        There are two oral vaccines available however, the CDC does not recommend their routine use, and in fact, did not use the vaccines during the most recent severe outbreak in Haiti after the 2010 earthquake. The vaccines require two doses, and it may be weeks before the person develops immunity. The CDC does not recommend the vaccines for routine travel prophylaxis.

        Tularemia

        Tularemia is an infection that can strike humans and animals. It is caused by the bacterium Francisella tularensis. The disease causes fever, localized skin or mucous membrane ulcerations, regional swelling of lymph glands, and occasionally pneumonia.

        G.W. McCay discovered the disease in Tulare County, Calif., in 1911. The first confirmed case of human disease was reported in 1914. Edward Francis, who described transmission by deer flies via infected blood, coined the term tularemia in 1921. It has been considered an important biological warfare agent because it can infect many people if dispersed by the aerosol route.

        Rabbits and ticks most commonly spread tularemia in North America. In other areas of the world, tularemia is transmitted by water rats and other aquatic animals.

        The bacteria are usually introduced into the victim through breaks in the skin or through the mucous membranes of the eye, respiratory tract, or GI tract. Ten virulent organisms injected under the skin from a bite or 10-50 organisms breathed into the lungs can cause infection in humans. Hunters may contract this disease by trapping and skinning rabbits in some parts of the country.

        Tularemia has six major forms:

        • Ulceroglandular tularemia
        • Glandular tularemia
        • Oculoglandular tularemia
        • Pharyngeal (oropharyngeal) tularemia
        • Typhoidal tularemia
        • Pneumonic tularemia

        Victims with the most common form, ulceroglandular type, typically have a single papulo-ulcerative lesion with a central scar (often at the site of a tick bite) and associated tender regional lymphadenopathy (swollen lymph nodes). A sore up to 1 inch across may appear on the skin in a majority of people and is the most common sign of tularemia. If the bite associated with infection was from an animal carrying the disease, the sore is usually on the upper part of a person's body, such as on the arm. If the infection came from an insect bite, the sore might appear on the lower part of the body, such as on the leg.

        Enlarged lymph nodes are seen in a majority of victims and may be the initial or the only sign of infection. Although enlarged lymph nodes usually occur as single lesions, they may appear in groups. Enlarged lymph nodes may come and go and last for as long as three years. When swollen, they may be confused with buboes of bubonic plague.

        The glandular form of the disease has tender regional lymphadenopathy but no identifiable skin lesion.

        Oculoglandular tularemia presents as conjunctivitis (white of the eyes are red and inflamed), increased tearing, photophobia, and tender enlarged lymph nodes in the head and neck region. Pharyngeal tularemia presents with a sore throat, fever, and swelling in the neck.

        The most serious forms of tularemia are typhoidal and pneumonic disease. Patients with typhoidal disease can have fever, chills, anorexia, abdominal pain, diarrhea, headache, myalgias, sore throat, and cough. Patients with pneumonic tularemia have mostly pulmonary findings. Many patients with pulmonary findings have underlying typhoidal tularemia.

        Tularemia can be diagnosed by growing the bacteria in the laboratory from samples taken of blood, ulcers, sputum, and other body fluids. Serological tests (done to detect antibodies against tularemia), direct fluorescent antibody (DFA) staining of clinical specimens, and polymerase chain reaction (PCR) tests on clinical specimens are available from specialized labs.

        Victims with tularemia who do not receive appropriate antibiotics may have a prolonged illness with weakness and weight loss. Treated properly, very few people with tularemia die. If a patient has severe disease, it is recommended to give them a 14-day course of streptomycin or gentamicin. For patients with mild to moderate disease, oral ciprofloxacin or doxycycline is recommended. In children with mild to moderate disease, gentamycin is often recommended. However, despite the concerns over side effects in children, some clinicians may recommend oral treatment with ciprofloxacin or doxycycline.

        Although laboratory-related infections with this organism are common, human-to-human spread is unusual. Victims do not need to be isolated from others.

        There is no recommendation for prophylactic treatment of people going into areas where tularemia is more common. In fact, in the case of low-risk exposure, observation without antibiotics is recommended.

        There no longer exists a vaccine against tularemia. New vaccines are under development.

        Postexposure Prophylaxis

        In the event of a biological attack using Francisella tularensis, the recommendation is to treat exposed people who are not yet ill with 14 days of oral doxycycline or ciprofloxacin.

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        Brucellosis

        Brucellosis is an infection of domesticated and wild animals that can be transmitted to humans. It is caused by an organism of the genus Brucella. The organism infects mainly cattle, sheep, goats, and other similar animals, causing death of developing fetuses and genital infection. Humans, who usually are infected incidentally by contact with infected animals, may develop numerous symptoms in addition to the usual ones of fever, general illness, and muscle pain.

        The disease often becomes long-term and may return, even with appropriate treatment. The ease of transmission through the air suggests that these organisms may be useful in biological warfare.

        Each of six different strains of the bacteria infect certain animal species. Four are known to cause illness in humans. Animals may transmit organisms during a miscarriage, at the time of slaughter, and in their milk. Brucellosis is rarely, if ever, transmitted from human to human.

        Certain species can enter animal hosts through skin abrasions or cuts, the eye membranes, the respiratory tract, and the GI tract. Organisms grow rapidly and eventually go to the lymph nodes, liver, spleen, joints, kidneys, and bone marrow.

        Victims may have a fever or a long-term infection or just a local inflammation. The disease may appear suddenly or develop slowly anywhere from three days to several weeks after exposure. Symptoms include fever, sweats, fatigue, loss of appetite, and muscle or joint aches. Depression, headache, and irritability occur frequently. In addition, infection of bones, joints, or the genitourinary tract may cause pain. Cough and chest pain also may be present.

        Symptoms often last three to six months and occasionally for longer than a year. Different species of the organism can cause different symptoms from skin sores to low back pain to liver disease.

        The doctor will want to know about any exposure to animals, animal products, or environmental exposures in making the diagnosis. Those who drink unpasteurized milk are at higher risk of infection. Military troops exposed to a biological attack and who have fever are likely candidates for this illness. Environmental samples may show the presence of this organism in the attack area. Laboratory tests and cultures of blood or body fluid samples including bone marrow may be performed.

        Therapy with a single drug has resulted in a high relapse rate, so a combination of antibiotics should be prescribed. A six-week course of doxycycline along with streptomycin for the first two weeks is effective in most adults with most forms of brucellosis, but there are other alternative antibiotic options.

        Animal handlers should wear appropriate protective clothing when working with infected animals. Meat should be well cooked, and milk should be pasteurized. Laboratory workers need to take appropriate cautions in handling the organism.

        Postexposure Prophylaxis

        In the event of a biological attack, the standard gas mask should protect adequately from airborne species. No commercially available vaccine exists for humans. If the exposure is considered high risk, the CDC recommends treating with doxycycline and rifampin for three weeks.

        Q Fever

        Q fever is a disease that also affects animals and humans. It is caused by the bacteria Coxiella burnetii. A spore-like form of the organism is extremely resistant to heat, pressure, and many cleaning solutions. This allows the germs to live in the environment for long periods under harsh conditions. In contrast, the disease it causes in humans is usually not harmful, although it can be temporarily disabling. Even without treatment, most people recover.

        The organism is extremely infectious. The potential of the organism as a biological warfare agent is related directly to its ability to infect people easily. A single organism is capable of producing infection and disease in humans. Different strains have been identified worldwide.

        • Humans have been infected most commonly by contact with domestic livestock, particularly goats, cattle, and sheep. The risk of infection is increased greatly if humans are exposed while these animals are giving birth to young. Large numbers of the germs may be released into the air as an animal gives birth. Survival of the organism on surfaces, such as straw, hay, or clothing, allows for transmission to other people who are not in direct contact with infected animals.
        • People can become infected by breathing the organisms.

        Signs and Symptoms

        Humans are the only hosts that commonly develop an illness as a result of the infection. The illness may begin within 10-40 days. There is no typical pattern of symptoms, and some people show none at all. Most people appear mildly to moderately ill.

        Fever (can go up and down and last up to 13 days), chills, and headache are the most common signs and symptoms. Sweating, aches, fatigue, and loss of appetite are also common. Cough often occurs later in the illness. Chest pain occurs in a few people. Sometimes there is a rash. Other symptoms such as headache, facial pain, and hallucinations have been reported.

        Sometimes problems in the lungs are seen on chest X-rays. And some people may seem to have acute hepatitis because of their liver involvement. Others may develop a heart condition called endocarditis.

        Blood tests may help in making the diagnosis of Q fever.

        The drug of choice for treatment of Q fever is doxycycline. There are several alternative antibiotic options that may be preferred under different circumstances.

        People with chronic Q fever who develop endocarditis may die, even with appropriate treatment.

        Although an effective vaccine (Q-Vax) is licensed in Australia, all Q fever vaccines used in the United States are under study. Q fever can be prevented by immunization.

        Postexposure Prophylaxis

        In the case of bioterror attack, postexposure prophylaxis is recommended using oral doxycycline.

        Smallpox

        Variola (the virus that causes smallpox) is the most notorious of the poxviruses. Smallpox was an important cause of illness and death in the developing world until recent times. In 1980, the World Health Organization (WHO) declared that smallpox had been completely wiped out. The last case was noted in Somalia in 1977.

        Variola represents a significant threat as a biological warfare agent. Variola is highly infectious and is associated with a high death rate and secondary spread. Currently, the majority of the U.S. population has no immunity, vaccine is in short supply, and no effective treatment exists for the disease. Two WHO-approved and inspected repositories remain: One is at the Centers for Disease Control and Prevention in the United States and the other at Vector Laboratories in Russia. It is widely believed that clandestine stockpiles exist in other countries such as Iraq and North Korea.

        Variola virus is highly infectious when released into the air. It is environmentally stable and can retain its ability to infect people for long periods. Infection through contaminated objects such as clothing is infrequent. After a person is exposed to aerosolized virus, the virus multiplies in the person's respiratory tract. After a period of seven to 17 days, variola is spread through the bloodstream to lymph nodes where it continues to multiply.

        Variola then moves into smaller blood vessels near the surface of the skin where the inflammatory changes occur. The classic smallpox rash then begins. Two types of smallpox generally are recognized.

        • Variola major, the most severe form, may cause death in up to 30% of unvaccinated people who develop it (3% of people vaccinated people may also develop variola major).
        • Variola minor, a milder form of smallpox, produces death in 1% of unvaccinated people.

        The symptoms of variola major occur after a seven- to 17-day incubation period. They begin acutely with high fever, headache, chills, aches, vomiting, abdominal pain, and back pain. During the initial phase, some people develop delirium (hallucinations), and a portion of light-skinned people may develop a fleeting rash.

        After two to three days, the rash develops on the face, hands, and forearms and extends gradually to the trunk and lower part of the body. The sores progress all at once into fluid-filled sacs. The distribution of the rash is important in making the diagnosis of smallpox. A greater number of lesions will appear on the face arms and legs compared to the trunk. People with smallpox are most infectious on days three through six after the fever begins. Virus is spread to others through coughing and sneezing or by direct contact.

        With the milder form of smallpox, variola minor, the skin sores are similar but smaller and fewer in number. People are not as ill as those who have variola major.

        Most doctors have never seen a case of smallpox and may have difficulty diagnosing it. Other viral illnesses with rash, such as chickenpox or allergic contact dermatitis, can look similar. Smallpox is different from chickenpox because of the distribution of the lesions and because they are all at the same stage of development everywhere on the body. With chickenpox, sores may be forming while others are scabbing over.

        The failure to recognize mild cases of smallpox in people with partial immunity permits rapid person-to-person transmission. Exposed people may shed virus through coughing without ever showing the signs and symptoms of the disease.

        The doctor may look at scrapings of tissue under a microscope but will be unable to tell the difference between smallpox and monkeypox or cowpox. Advanced PCR techniques have been developed and may provide for more accurate diagnosis in the near future.

        People with smallpox are usually isolated from people without smallpox for 17 days. Anyone exposed to either weaponized variola or people infected with smallpox must be vaccinated immediately this may lessen or prevent the illness if done within four or five days of infection.

        Treatment of smallpox is mainly to help relieve symptoms. The antiviral agent cidofovir may be effective in treating symptoms.

        Smallpox vaccine is used to prevent people from getting smallpox. The vaccine is given as a type of shot, but a two-pronged needle is used to place the medication into the skin. This leaves a permanent scar, which many adults may still have from smallpox inoculations given to them when they were babies.

        Once the shot is given, a small fluid-filled pimple usually appears five to seven days later. A scab forms over the site during the next one to two weeks. Common side effects include low-grade fever and swollen lymph glands. People with weakened immune systems should not have the smallpox vaccination. This includes people with HIV, anyone with a history of eczema, and pregnant women.

        Postexposure Prophylaxis

        In the case of a bioterror attack, it is recommended that all people who were exposed be immunized using the vaccine as soon as possible, but at least within four days. Again, use of the vaccine is not recommended in people with skin diseases like eczema, immunocompromised individuals (like HIV), or in pregnant women.

        Monkeypox

        The monkeypox virus, which is found in Africa, is a naturally occurring relative of variola. The first case of human monkeypox was identified in 1970, but fewer than 400 cases have been diagnosed since. Some concern exists that monkeypox may be weaponized, however, human monkeypox is not as potent as smallpox. Pneumonia due to monkeypox may cause death in about half of people who develop it.

        Arboviral Encephalitides

        The arboviral encephalitides with high fatality rates include Venezuelan equine encephalitis (VEE) virus, western equine encephalitis (WEE) virus, and eastern equine encephalitis (EEE) virus. They are members of the Alphavirus genus and are regularly associated with encephalitis. These viruses were recovered from horses during the 1930s. VEE was isolated in the Guajira peninsula of Venezuela in 1930, WEE in the San Joaquin Valley of California in 1930, and EEE in Virginia and New Jersey in 1933. A more common, but milder arboviral disease, is West Nile, which is caused by a flavivirus.

        Although natural infections with these viruses occur following bites from mosquitoes, the viruses are also highly infectious when spread through the air. If intentionally released as a small particle aerosol, this virus may be expected to infect a high percentage of people exposed within a few miles.

        VEE virus has the capacity to produce epidemics. Outcomes are significantly worse for the very young and the very old. Up to 35% of people infected may die. WEE and EEE typically produce less severe and widespread disease but are associated with death rates as high as 50%-75% in those with severe illness.

        • VEE: After an incubation period of two to six days, people with VEE develop fevers, chills, headache, aches, sore throat, and sensitivity to light (eyes). They may become mildly confused, have seizures or paralysis, or go into a coma. For those who survive, their nervous system functions usually recover completely.
        • EEE: The incubation period for EEE varies from five to 15 days. Adults may have certain early symptoms up to 11 days before the onset of nervous system problems such as mild confusion, seizures, and paralysis. Signs and symptoms include fever, chills, vomiting, muscle rigidity, lethargy, slight paralysis, excess salivation, and difficulty breathing. Children frequently develop swelling on their face and near their eyes. A significant percentage of survivors of severe disease have permanent nervous system problems such as seizures and various degrees of confusion (dementia).
        • WEE: The incubation period is five to 10 days. Most people have no symptoms, or they might develop a fever. Other symptoms include nausea, vomiting, headache, a stiff neck, and drowsiness. Up to a majority of victims younger than 1 year of age have seizures. Typically, adults recover completely. Children, especially newborns, may have lasting nervous system problems.

        Laboratory tests, including nasal swab samples, may show any of the three viruses.

        No specific treatment is available. Doctors will help control symptoms. For some people, that may include medications to control fever and seizures or help breathing.

        There are no commercially available vaccines against any of the arboviral encephalitides. They are experimental and only available for researchers who work with the virus.

        Viral Hemorrhagic Fevers

        Viral hemorrhagic fevers are caused by four families of viruses.

        • Arenaviridae (Lassa, Lujo, Guanarito, Machupo, Junin, Sabia, and Chapare viruses)
        • Bunyaviridae (Rift Valley, Crimean-Congo, Hantaan)
        • Filoviridae (Marburg, Ebola)
        • Flaviviridae (Yellow, Dengue, Kyasanur Forest, Alkhurma, Omsk HFs)

        The best known of the viral hemorrhagic fevers is Ebola virus. First recognized in Zaire in 1976, the virus has been linked to at least 20 outbreaks in Africa. Earlier outbreaks in central Africa, with the Zaire species of the Ebola virus, had very high mortality rates (80%-90%). However, the most recent outbreaks with the same virus in Western Africa have had lower mortality rates (approximately 50%). The largest outbreak of Ebola virus in history began in 2014, located primarily in the Western African countries of Sierra Leone, Guinea, and Liberia. In June 2016, the WHO reported that there were 28,616 confirmed or probable cases and 11,323 deaths in those three countries, including 500 health-care workers. The World Health Organization declared Sierra Leone Ebola-free in November 2015, and in June 2016, the WHO declared Liberia and Guinea Ebola-free. However, there could me more cases identified, and there will be continued surveillance. During the outbreak, there were four cases diagnosed in the United States: One in a Liberian man who was visiting in Texas, two nurses who took care of that man, and one physician who had just returned from treating Ebola patients in Guinea.

        These viruses are each characterized by an acute generalized illness that includes feeling quite ill (flulike illness) with profound exhaustion and is sometimes associated with internal bleeding. The West African Ebola outbreak was characterized more by severe gastrointestinal illness with vomiting and large-volume diarrhea. This leads to severe volume depletion, metabolic abnormalities, and hypovolemic shock. Other symptoms include fever, body and joint pain, profound and progressive weakness, loss of appetite, sore throat, headache, and fatigue.

        Most agents are highly infectious via the aerosol route, and most are stable as respiratory aerosols. Thus, they possess characteristics that may make them attractive for use by terrorists.

        However, Ebola virus has not been demonstrated to be contagious person-to-person through an aerosol route. It is spread through direct contact with the blood or other body fluids of an infected person, including a corpse.

        The agents that produce viral hemorrhagic fever are all simple RNA viruses. They are able to survive in blood for long periods, which means they can infect people who are around animals slaughtered domestically. These viruses are linked to the rodents, bats, or insects that help to spread them, which helps in searching for a diagnosis.

        The specific viral hemorrhagic fever manifestations that develop depend on many factors such as the strength of the virus, its strain, and the route of exposure.

        The incubation period (time from exposure to onset of symptoms) ranges from two to 21 days. Although initially a classic symptom of all of the viral hemorrhagic fevers is bleeding, it actually only occurred in about 20% of Ebola patients in the most recent outbreak. Humans are not infectious until symptoms develop.

        The incubation period is the time interval from infection with the virus to onset of symptoms is two to 21 days. Humans are not infectious until they develop symptoms. The first symptoms seen are fever, muscle aches, headaches, and sore throat. Patients then go on to develop vomiting and large-volume diarrhea. This leads to severe dehydration and results in impaired kidney and liver function. Some patients develop internal and external bleeding (blood in stools and oozing from the gums).

        It is important for the doctor to know a person's travel history in making a diagnosis of viral hemorrhagic fever. These agents are linked tightly with their natural geographic area and the ecology of the species and vectors found in that specific locale. Victims often recall exposures to rodents (Arenavirus, Hantavirus), mosquitoes (Valley fever virus, yellow and dengue fever viruses), or even slaughtered horses (Rift Valley fever virus, Crimean-Congo virus).

        Laboratory tests may be helpful. Testing of whole blood or serum include antibody-capture enzyme-linked immunosorbent assay (ELISA), antigen-capture detection tests, and reverse transcriptase polymerase chain reaction (RT-PCR) assay. Testing can be conducted at the CDC in Atlanta or the U.S. Army Medical Research Institute of Infectious Disease (USAMRIID) at Fort Detrick in Frederick, Md.

        Treatment for viral hemorrhagic fevers is largely directed at easing the discomfort of the symptoms. Victims benefit from being placed in a hospital setting immediately. Air transport is not advised. Sedative and pain-relieving medications are helpful, but aspirin and similar drugs should not be given because of their tendency to make bleeding worse.

        There has been a lot of controversy surrounding the use of IV fluids for victim. At the beginning of the outbreak, the medical community was divided on the topic. However, both the CDC and WHO both recommend IV rehydration to treat patients with dehydration and bleeding problems. The improved survival in the recent outbreak was likely due to the extensive use of IV hydration. The treatment for bleeding is controversial. Generally, mild bleeding is not usually treated, but severe bleeding requires appropriate replacement therapy (blood transfusions through an IV line).

        Specific treatment with ribavirin has been used and is currently under investigation as a therapy for Lassa fever, hantavirus, Crimean-Congo, and Rift Valley fever. Treatment is most effective if begun within seven days. Ribavirin has poor activity against the filoviruses and flaviviruses.

        The only established and licensed virus-specific vaccine against any of these viruses is the yellow fever vaccine. It is mandatory for those traveling into areas of Africa and South America where the disease is commonly found. Current trials are underway for further vaccines and antibody therapies. There are ongoing trials of at least two Ebola vaccines.

        Staphylococcal Enterotoxin B

        Staphylococcal enterotoxin B (SEB) is one of the best-studied and, therefore, best-understood toxins.

        Staphylococcal enterotoxin is one of the most common causes of food poisoning. Nausea, vomiting, and diarrhea normally occur after someone eats or drinks contaminated food.

        The toxin creates different symptoms when exposure is through the air in a biological warfare situation. Only a small, inhaled dose is necessary to harm people within 24 hours of inhalation.

        After exposure, signs and symptoms begin in two to 12 hours. Mild-to-moderate exposure to SEB produces fever, chills, headache, nausea, vomiting, shortness of breath, chest pain, body aches, and a nonproductive cough. Severe exposures can lead to a toxic shock-type picture and even death. Depending on the severity of exposure, the illness may last three to 10 days.

        Diagnosis of SEB can be difficult. Laboratory tests and a chest X-ray may be performed. Nasal swabs may show the toxin for 12-24 hours after exposure.

        Doctors provide care to relieve symptoms. Close attention to oxygenation and hydration are important. People with severe SEB may need help breathing with a ventilator. Most victims are expected to do well after the initial phase, but the time to full recovery may be long.

        No approved human vaccine exists for SEB, although human trials are ongoing. Passive immunotherapy agents have demonstrated some promise when given within four hours of exposure, but such therapy is still being tested.

        Ricin

        Ricin, a plant protein toxin derived from the beans of the castor plant, is one of the most toxic and easily produced of the plant toxins. Although the lethal toxicity of ricin is about 1,000-fold less than botulinum toxin, the worldwide ready availability of castor beans and the ease with which the toxin can be produced give it significant potential as a biological weapon.

        Since ancient times, more than 750 cases of ricin intoxication have been described. Ricin may have been used in the highly published killing of Bulgarian exile Georgi Markov in London in 1978. He was attacked with a device in an umbrella that implanted a ricin-containing pellet into his thigh.

        The toxicity of ricin varies greatly with the way it is given. Ricin is extremely toxic to cells and acts by inhibiting protein synthesis. Inhalation exposure causes primarily breathing and lung problems. If eaten, ricin causes symptoms in the GI tract. If injected, the reaction takes place in that area.

        • Following inhalation exposure of ricin, toxicity is characterized by the sudden onset of nasal and throat congestion, nausea and vomiting, itching of the eyes, itching, and tightness in the chest. If exposure is significant, after 12-24 hours severe breathing problems may set in. In animal studies, death occurs 36-48 hours after severe exposure.
        • Ingestion of ricin is generally less toxic because it is not absorbed well and may degrade in the digestive tract. Out of 751 ingestions recorded, only 14 resulted in a death.
        • At low doses, injection exposures produce flulike symptoms, body aches, nausea, vomiting, and localized pain and swelling at the injection site. Severe exposure results in tissue death and GI bleeding, as well as widespread liver, spleen, and kidney problems.

        The diagnosis of ricin poisoning is made on the basis of symptoms and whether exposure was possible. In biological warfare, exposure is likely to occur by inhalation of a toxin aerosol.

        Victims may have certain signs on a chest X-ray. The diagnosis can be confirmed by lab tests on samples from a nasal swab. Ricin can be identified for up to 24 hours after exposure.

        Treatment is mainly to relieve symptoms. If exposure was by inhalation, the person may need help breathing. Those who ingested the poison may need to have their stomachs pumped (gastric lavage), or they might be given charcoal to soak up the material.

        Currently, no vaccine is available for ricin exposure. Test vaccines have proven effective in animals. Other drugs are being studied as well.

        Botulinum Toxin

        Botulinum toxins are the most deadly toxins known. Because botulinum toxin is so lethal and easy to manufacture and weaponize, it represents a credible threat as a biological warfare agent. When used in this manner, exposure is likely to occur following inhalation of aerosolized toxin or ingestion of food contaminated with the toxin or its microbial spores. Iraq admitted to active research on the offensive use of botulinum toxins and to weaponizing and deploying more than 100 munitions with botulinum toxin in 1995.

        All seven subtypes (A-G) of botulinum toxin act in similar ways. The toxin produces similar effects whether ingested, inhaled, or via a wound. The time course and severity of illness vary with route of exposure and dose received. Symptom onset is slower after inhalation exposure.

        Symptoms may occur hours to several days after exposure. Initial signs and symptoms include blurred vision, dilated pupils, difficulty swallowing, difficulty speaking, an altered voice, and muscle weakness. After 24-48 hours, muscle weakness and paralysis may cause the person to be unable to breathe. Varying degrees of muscular weakness may occur.

        Paralysis may indicate the presence of this exposure. Typical laboratory tests generally are not helpful, although special tests of nerve conduction and muscle response may be useful. Infection by inhalation can be diagnosed from nasal swabs up to 24 hours after exposure.

        The most serious complication is respiratory failure. With attention to symptoms and help breathing, sometimes with a ventilator, death occurs in fewer than 5% of cases. For confirmed exposures, an antitoxin is available from the CDC. This antitoxin has all of the disadvantages of horse serum products, including the risks for shock and serum sickness. Skin testing is performed first by injecting a small amount of the antitoxin into the skin and then monitoring the person for 20 minutes.

        The only botulinum vaccine was discontinued by the CDC in 2011.

        Mycotoxins

        The trichothecene mycotoxins are highly toxic compounds produced by certain species of fungi. Because these mycotoxins can cause massive organ damage, and because they are fairly easy to produce and can be dispersed by various methods (dusts, droplets, aerosols, smoke, rockets, artillery mines, portable sprays), mycotoxins have an excellent potential for weaponization.

        Strong evidence suggests that trichothecenes ("yellow rain") have been used as a biological warfare agent in Southwest Asia and Afghanistan. From 1974-1981, numerous attacks resulted in a minimum of 6,310 deaths in Laos, 981 deaths in Cambodia, and 3,042 deaths in Afghanistan. When taken from fungal cultures, the mycotoxins yield a yellow-brown liquid that evaporates into a yellow crystalline product (thus, the "yellow rain" appearance). These toxins require certain solutions and high heat to be completely inactivated.

        After exposure to the mycotoxins, early symptoms begin within five minutes. Full effects take 60 minutes.

        • If skin exposure occurs, the skin burns, becomes tender, swollen, and blisters. In lethal cases, large areas of skin die and slough (fall off).
        • Respiratory exposure results in nasal itching, pain, sneezing, a bloody nose, shortness of breath, wheezing, cough, and blood-tinged saliva and sputum.
        • If ingested, the person feels nausea and vomits, loses appetite, feels abdominal cramping, and has watery and/or bloody diarrhea.
        • Following entry into the eyes, pain, tearing, redness, and blurred vision occur.
        • Systemic toxicity may occur and includes weakness, exhaustion, dizziness, inability to coordinate muscles, heart problems, low or high temperature, diffuse bleeding, and low blood pressure. Death may occur within minutes to days depending on the dose and route of exposure.

        Diagnosis of an attack of trichothecene mycotoxin depends on the symptoms and identifying the toxin from biological and environmental samples. Many people with these symptoms may report being in a yellow rain or smoke attack.

        Initial laboratory tests are not always helpful. Currently, a rapid identification kit for any of the trichothecene mycotoxins does not exist. Gas-liquid chromatography has been used in the past with great success. However, chromatographic methods lack great sensitivity, and presently alternative methods of detection are under investigation.

        Treatment is mainly to help with symptoms. The immediate use of protective clothing and mask during a mycotoxin aerosol attack should prevent illness. If a soldier is unprotected during an attack, the outer clothing should be removed within four to six hours and decontaminated with 5% sodium hydroxide for six to 10 hours. The skin should be washed with copious amounts of soap and uncontaminated water. The eyes, if exposed, should be washed out with large amounts of normal saline or sterile water. U.S. military personnel can use a skin decontamination kit effectively against most chemical warfare agents, including the mycotoxins.

        No specific therapy exists for a trichothecene exposure. After appropriate skin decontamination, victims of inhalation and oral exposures may be given superactivated charcoal orally. Activated charcoal removes mycotoxins from the GI tract. Some victims may need help breathing with a ventilator. Early use of steroids increases survival time by decreasing the primary injury and shock-like state that follows significant poisoning.

        No vaccine exists for trichothecene mycotoxin exposure.

        Glanders

        Glanders is a disease mainly in horses and is caused by the bacterium Burkholderia mallei. It can be transmitted to humans and other domestic animals. However, it is only rarely seen in humans. It has been intermittently used by governments in World War I and II and by Russia in the 1980s. In humans, it causes a flu-like illness. In 2000, there was a case in a U.S. military microbiologist who recovered completely with treatment.

        Typhus

        Typhus is an acute febrile illness caused by Rickettsia typhi and Rickettsia prowazkeii. This should not be confused with typhoid fever, which is a gastrointestinal illness caused by Salmonella typhi bacteria. There are endemic and epidemic forms of the disease. The epidemic form is caused by Rickettsia prowazkeii. This is typically transmitted via lice. Rats, mice, and flying squirrels, which are asymptomatic carriers, carry the disease. The disease is spread to the human population through ticks, chiggers, fleas, and lice. There have been natural outbreaks throughout history that were usually associated with wars and famine. Poor living conditions and squalor allow spread of the disease. The typhus spread by ticks causes Rocky Mountain spotted fever. The Centers for Disease Control and Prevention (CDC) has categorized typhus as a category B biological weapons agent. While Rickettsia prowazekii is highly infectious, it cannot be passed from person to person. A number of governments have experimented with weaponizing typhus, but typhus does not appear to have ever been successfully used in a military setting.

        Anti-Crop Biological Agents

        There have been a number of agents developed during the last century to cause destruction of crops. These include wheat stem rust, rye stem rust, rice blast, cereal rust, wheat smut, and potato blight. A number of governments have experimented with using these agents, but there does not appear to have ever been a use of these agents in a military setting.


        A Brief History of Drones

        Unmanned aerial vehicles (UAVs) are aircraft with no on-board crew or passengers. They can be automated ‘drones’ or remotely piloted vehicles (RPVs). UAV’s can fly for long periods of time at a controlled level of speed and height and have a role in many aspects of aviation.

        The first pilotless vehicles were developed in Britain and the USA during the First World War . Britain’s Aerial Target, a small radio-controlled aircraft, was first tested in March 1917 while the American aerial torpedo known as the Kettering Bug first flew in October 1918. Although both showed promise in flight tests, neither were used operationally during the war.

        During the inter-war period the development and testing of unmanned aircraft continued. In 1935 the British produced a number of radio-controlled aircraft to be used as targets for training purposes. It's thought the term 'drone' started to be used at this time, inspired by the name of one of these models, the DH.82B Queen Bee. Radio-controlled drones were also manufactured in the United States and used for target practice and training.

        Reconnaissance UAVs were first deployed on a large scale in the Vietnam War. Drones also began to be used in a range of new roles, such as acting as decoys in combat, launching missiles against fixed targets and dropping leaflets for psychological operations.

        Following the Vietnam War other countries outside of Britain and the United States began to explore unmanned aerial technology. New models became more sophisticated, with improved endurance and the ability to maintain greater height. In recent years models have been developed that use technology such as solar power to tackle the problem of fuelling longer flights.

        Drones now have many functions, ranging from monitoring climate change to carrying out search operations after natural disasters, photography, filming, and delivering goods. But their most well-known and controversial use is by the military for reconnaissance, surveillance and targeted attacks. Since the 9/11 terrorist attacks, the United States in particular has significantly increased its use of drones. They are mostly used for surveillance in areas and terrains where troops are unable to safely go. But they are also used as weapons and have been credited with killing suspected militants. Their use in current conflicts and over some countries has raised questions about the ethics of this kind of weaponry, especially when it results in civilian deaths, either due to inaccurate data or because of their proximity to a ‘target’.


        An Ancient, Brutal Massacre May Be the Earliest Evidence of War

        Skulls smashed by blunt force, bodies pin-cushioned by projectile points and hapless victims—including a pregnant woman—abused with their hands bound before receiving the fatal coup de grâce.

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        This violent tableau resembles something from the darker side of modern warfare. But it instead describes the grizzly demise of a group of African hunter-gatherers some 10,000 years ago. They are the victims of the earliest scientifically dated evidence for human group conflict—a precursor to what we now know as war.

        The battered skeletons at Nataruk, west of Kenya's Lake Turkana, serve as sobering evidence that such brutal behavior occurred among nomadic peoples, long before more settled human societies arose. They also provide poignant clues that could help answer questions that have long plagued humanity: Why do we go to war, and where did our all too common practice of group violence originate?

        "The injuries suffered by the people of Nataruk—men and women, pregnant or not, young and old—shock for their mercilessness," says Marta Mirazon Lahr of the University of Cambridge, who co-authored the study published today in the journal Nature. Still, she notes, "what we see at the prehistoric site of Nataruk is no different from the fights, wars and conquests that shaped so much of our history, and indeed sadly continue to shape our lives.”

        Nataruk's prehistoric killers did not bury their victims' bodies. Instead their remains were preserved after being submerged in a now dried lagoon, near the lake shore where they lived their final, terrifying moments during the wetter period of the late Pleistocene to early Holocene.

        Researchers discovered the bones in 2012, identifying at least 27 individuals on the edge of a depression. The fossilized bodies were dated by radiocarbon dating and other techniques, as well as from samples of the shells and sediment surrounding them, to approximately 9,500 to 10,500 years ago.

        It's not clear that anyone was spared at the Nataruk massacre. Of the 27 individuals found, eight were male and eight female, with five adults of unknown gender. The site also contained the partial remains of six children. Twelve of the skeletons were in a relatively complete state, and ten of those showed very clear evidence that they had met a violent end.

        In the paper, the researchers describe “extreme blunt-force trauma to crania and cheekbones, broken hands, knees and ribs, arrow lesions to the neck, and stone projectile tips lodged in the skull and thorax of two men.” Four of them, including a late-term pregnant woman, appear to have had their hands bound. 

        This female skeleton was found reclining on her left elbow, with fractures on the knees and possibly the left foot. The position of the hands suggests her wrists may have been bound. (Marta Mirazon Lahr)

        The murderers' motives are lost in the mists of time, but there are some plausible interpretations that could challenge conventional ideas about why people go to war.  

        Warfare has often been associated with more advanced, sedentary societies that control territory and resources, farm extensively, store the foods they produce and develop social structures in which people exercise power over group actions. Conflict erupts between such groups when one wants what the other possesses.

        The bodies at Nataruk provide evidence that these conditions aren't necessary for warfare, because the hunter-gatherers of the time lived a far simpler lifestyle. Yet the killings have the hallmarks of a planned attack rather than a violent chance encounter.

        The killers carried weapons they wouldn't have used for hunting and fishing, Mirazon Lahr notes, including clubs of various sizes and a combination of close-proximity weapons like knives and distance weapons, including the arrow projectiles she calls a hallmark of inter-group conflict.

        “This suggests premeditation and planning,” Mirazon Lahr notes. Other, isolated examples of period violence have previously been found in the area, and those featured projectiles crafted of obsidian, which is rare in the area but also seen in the Nataruk wounds. This suggests that the attackers may have been from another area, and that multiple attacks were likely a feature of life at the time.

        “This implies that the resources the people of Nataruk had at the time were valuable and worth fighting for, whether it was water, dried meat or fish, gathered nuts or indeed women and children. This shows that two of the conditions associated with warfare among settled societies—control of territory and resources—were probably the same for these hunter-gatherers, and that we have underestimated their role in prehistory.”

        “This work is exciting and it suggests, at least to me, that this type behavior has deeper evolutionary roots,” says Luke Glowacki, an anthropologist with Harvard University's Department of Human Evolutionary Biology.

        We aren't the only species to engage in such behavior, he adds. Our closest relatives, chimpanzees, regularly engage in lethal attacks. “To deliberately stalk and kill members of other groups, as the chimps do, that alone is very suggestive of an evolutionary basis for warfare,” he says.

        A closeup image of the skull of a male skeleton from the Nataruk site. The skull has multiple lesions on the front and left side consistent with wounds from a blunt implement such as a club. (Marta Mirazon Lahr, enhanced by Fabio Lahr)

        But evidence to support or refute such theories has been thin on the ground. The sparse previous examples of prehistoric violence can be interpreted as individual acts of aggression, like a 430,000-year-old murder victim found in Spain last year. That makes Nataruk a valuable data point in the fossil record.

        More clues may be found among the behaviors of living peoples. Researchers can make inferences about conflict among early human hunter-gatherers by studying their closest living parallels, groups like the San of southern Africa. But such comparisons are tenuous, Glowacki notes.

        “The San are very different from our ancestors. They live in nations, they are surrounded by pastoralists and they go to markets. That limits the utility of making inferences about our own past.” Still there are other suggestions that resource competition isn't always at the root of human violence.

        “In New Guinea for example, where there are abundant resources and land, you've traditionally seen very intense warfare driven by tribal and status dynamics,” Glowacki says. “We don't have any way of knowing if that was involved at Nataruk.”

        And whatever its roots, warfare persists even in the same region of Africa: “This is still an area with a lot of intense violence in the 21st century,” Glowacki notes. “It was eye-opening from my perspective that the first really good fossil evidence for warfare among ancient hunter-gatherers comes from a place where there is still, today, this ongoing intergroup violence.”

        But, the authors point out, there is another aspect of human behavior that has also stood the test of time.

        “We should also not forget that humans, uniquely in the animal world, are also capable of extraordinary acts of altruism, compassion and caring,” Mirazon Lahr says. “Clearly both are part of our nature.”


        Quick Lime, Caltrop

        Some more unusual weapons go largely unnoticed. The caustic powder quick lime was dropped on attackers in sieges and naval battles, getting through armor and clothing to burn eyes and skin.

        The humble caltrop, a spiked metal device, was scattered on the ground to puncture enemy feet. The sharp objects were important enough that Philip the Good of Burgundy included caltrops in his niece’s dowry. 

        Unlike many medieval weapons, it is still used today, scattered across roads by drug gangs to puncture police tires.

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