How THE WEST SOLD RHODESIA TO COMMUNISM

The West has a notoriously bad habit of betraying countries which defend freedom. During President Franklin Roosevelt’s presidency, he sentenced the people of Eastern Europe to communist rule following World War II when he connived with “Uncle Joe” Stalin at the Yalta Conference. When Serbia—an ally of the United States in both World War I and World War II—sought to expel the Islamic invaders who settled in its territory of Kosovo, the United States and NATO launched a military operation to defend the Islamists from the native inhabitants of the Balkans. When Kosovo eventually seceded, the West sanctioned the secession by recognizing Kosovo as a sovereign state. If Charles Martel lived today and tried to expel the Islamic invaders from Europe, it would not be surprising if the so-called leader of the free-world—the president of the United States—held a press conference at which he announced the intention of the West to bring “war criminal” Charles Martel to justice.

They say that one should only love one’s country if one’s country is lovely. I love my country, but I fear that she has become somewhat of a whore.

The treason against freedom the West has committed is not limited to Europe, for freedom-loving African countries have been betrayed as well. When Soviet-sympathizer and terrorist Nelson Mandela desired to take South Africa away from the Afrikaners, the Western world obliged him by placing economic sanctions on South Africa in order to aid him in his ignoble goals. Instead of encouraging the South Africans to keep Mandela in the only place where he belonged—prison—the West served as an accomplice in the crime of putting Mandela in the worst place he could possibly be—in charge of South Africa.

The vilest case of treason committed by the West against freedom is arguably the case of its betrayal of Rhodesia. Rhodesia, once a colony of Great Britain, declared its independence on November 11, 1965. The British government and the United Nations declared Rhodesia’s independence to be “illegal,” because the British government desired to continue to control Rhodesia as a colony. In 1970, the United States government declared that “under no circumstances” would it recognize Rhodesia’s independence. In an article in Time entitled “Sanctions Against Rhodesia” (11/23/1966), the article states that for the first time in its history, the United Nations Security Council voted to place “mandatory economic sanctions” on a country—Rhodesia. The U.N. “declared an international embargo on 90% of Rhodesia's exports, forbade the U.N.'s 122-member nations to sell oil, arms, motor vehicles or airplanes to the rebel territory or to provide it with any form of ‘financial or other economic aid.’” God bless South Africa which announced after the U.N. placed economic sanctions against Rhodesia that “it had no intention of obeying the resolution.”

Rhodesia existed until 1980, which is the year that black Marxists seized the government and began calling the country “Zimbabwe.” The changes the Marxists implemented, however, involved more than just a change in name of the country.

According to the Central Intelligence Agency’s World Factbook, of Zimbabwe’s population of 12 million, nearly a quarter of them—24.6 percent—are infected with HIV or AIDS. The economy is in shambles: the inflation rate there is, as of August 20, 2008, at 11 million percent, the unemployment rate is approximately 80 percent, the GDP growth rate was last estimated at negative 6.1 percent, and the populace eats rodents for sustenance. In 2007, the people of Zimbabwe had the world’s shortest life expectancy—37 years for men and 34 for women. The population growth rate is currently 0.568 percent.

How great was white-controlled Rhodesia compared to black Marxist-controlled Zimbabwe? When Rhodesia existed, the country was considered the “breadbasket of Africa,” for it was an exporter of food. Until 1974 the Rhodesian economy prospered and so the country was oftentimes referred to as “the jewel of Africa.” If one does a search for “Rhodesia” on YouTube.com, one can find video footage of what Rhodesia once looked like: the cities—including the capitol city of Salisbury—appear no different than many American cities of the Midwest (excluding Detroit of course).

The telephone line system of Rhodesia was “once one of the best in Africa,” but now suffers from poor maintenance. Before the Marxist takeover of Rhodesia, the estimated population growth of the country was 4 percent, which was “perhaps the highest in the word” says Lane Flint in his book God’s Miracles Versus Marxist Terrorists. Former Prime Minister of Rhodesia Ian Smith writes in his autobiography, The Great Betrayal, that “It is difficult to find a black Zimbabwean these days who will not tell you that his standard of living has deteriorated [since the Marxists gained power].”

How was Zimbabwe able to replace prosperous Rhodesia? Mainly because the Soviet Union financed the Marxist campaign of terror and communist Chinese troops trained Zimbabwean soldiers how to wreak havoc. Flint writes:



Weapons and ammunition were hard to come by and it was apparent that the Marxist terrorists were being supplied with modern weapons from Russia to launch attacks with and fight a savage war. All the while Rhodesians were making use of the meager supply available to them and nothing could deter their determination. . . . Practically the whole world (except South Africa) [was] against them.
According to Dorothy Davies in her book Race Relations in Rhodesia: A Survey for 1972-78, the World Council of Churches granted $120,000 from the Special Fund to Combat Racism to the communist movements in Africa. To deal with political unrest, the Marxists were trained by communist North Korean military officers to suppress dissidents. While left-wing churches and leftist governments such as China, North Korea, and the Soviet Union aided the Marxist insurgency in Rhodesia, the Rhodesians received little to no help from the rest of the world.

What did the Marxists do to which the West turned a blind eye? One of the more heinous acts committed by the Marxists during their war with Rhodesia was when they used Soviet-supplied heat-seeking missiles to shoot down civilian aircraft flying from Kariba to Salisbury (now called “Harare” by the barbaric Marxists) in 1978 and 1979. The second plane crashed and everyone died instantaneously. The first plane crash-landed and some of the passengers and crew survived. Unfortunately, Smith recounts that “Before our security forces could arrive, the terrorists were on the scene and murdered everyone they could find, including women and children.”

This kind of vile activity was not an anomaly to Marxist revolution; it was central to it. One night in July of 1977, Marxist “freedom fighters” kidnapped and burned 22 people alive. There was no justification for this attack, other than that the terrorists desired to instill fear in the populace to gain power over them. When Rhodesian forces arrived, they discovered a message that had been left by the Marxists:


Zimbabwe will come through the barrel of a gun. Forward with ZANLA. Smith’s soldiers are pigs, dogs and baboons. Don’t think you are going to win this war. Forget it. On this day you are going to see how bad we are going to be!
ZANLA is the acronym for the Zimbabwe African National Liberation Army. That was the muscle behind Robert Mugabe’s Zanu-PF political party (Zimbabwe African National Union – Patriotic Front). ZANLA was based in nearby Mozambique and was largely instructed by communist Chinese troops.

Smith recollects in his autobiography:

They called themselves ‘freedom fighters.’ We referred to them as “terrorists” because they deliberately used terror to intimidate people. The record shows, without any shadow of doubt, that our terminology was correct.
Smith also notes the hypocrisy of those who criticize Rhodesia prior to the Marxist insurrection:


Terrorists destroyed [everything that was] associated with the white man. Everything associated with the white man and his civilization had to be eliminated. Many thousands of children [of all races] were thus denied the opportunity they had previously enjoyed—hardly the fault of the ‘previous white racists.’
Not only were landmines placed haphazardly throughout the country, civilian planes shot down, and people burned alive, but also “mass abductions and the indiscriminate murders of defenseless children” were common as well. Children, teenagers, and the elderly were often forced to join the ranks of the Marxist terrorists.

The “freedom” that the Marxists fought for was a perversion of the true meaning of the word. Rhodesians of all races, classes, and creeds shared the bewilderment of a daughter of an elderly woman who was “kicked, beaten, and tortured by terrorists who accused her of working against the ‘liberation forces.’” The daughter was quoted by a newspaper as asking, “Is this the freedom they are fighting for . . . the bestial and barbaric killings perpetuated in the name of freedom and justice? Heaven help us, we don’t need such freedom.”

Prime Minister Ian Smith did his very best to prevent Rhodesia from succumbing to Marxism. Smith was awarded a miniature lighthouse by the America-Rhodesia Association in New York in the late 1970’s “for so many years [of serving] as a warning beacon to the free world of the dangers of international communism.” Says Smith in his autobiography:


One must always be on guard against subversion and terrorism. Terrorists are adept at using freedom inherent in our philosophy and constitution in order to subvert freedom. Intimidation is a dreadful instrument, and it is used most expertly by those who are disciples of the philosophy of communism, or fascism, or Nazism—there is no difference between them. They are all dictatorships which believe in the “one-party state” philosophy: once power is seized, it is held forever, and anyone who dissents receives a clear message: change your mind, or else!
Smith’s dedication to opposing Marxism did not wane even in the later part of his life. In 2000, he returned to Zimbabwe from Britain, ignoring threats from leftist dictator Robert Mugabe that he would be arrested for demanding that Mugabe resign. At Harare’s international airport, Smith told reporters that “[Mugabe] must heed calls from his own people because he has destroyed this country. We cannot afford him anymore.” Mugabe’s bluff was called; Smith was not arrested.

Mugabe may not have arrested or killed Smith at the airport, but he ruined the Rhodesian economy, did away with legitimate political systems, and set loose anarchy on a once civilized society. In fact, all of the black Marxist terrorists were granted amnesty for their crimes—rapes, murders, kidnappings, arsons, and terrorism—in March of 1979 by Mugabe.

Mugabe’s regime in Zimbabwe is very similar to Soviet Russia, because a “socialist top down [governmental] structure” was established. Some of the reports that have come out of Zimbabwe are vile:


Thousands of men and women, children and elderly, were rounded up into interrogation camps where they were held for weeks. People died in these torture camps. . . . Digging graves was a daily routine for the captives. Some of the dead were loaded into trucks to be dumped in local mine shafts. At [one] police camp . . . people were held in open cages spattered with blood and human waste from previous detainees. They were exposed to the wind, rain, and sun while in adjacent interrogation cells the screams and groans of those being tortured could be heard, day and night. It was a replication of the colonial regimes, but perpetrated at a level much worse, by a black government headed by Robert Mugabe.
Hell on Earth was established in a once prosperous country, and the West is to blame, for Rhodesia was denied help in its hour of need. The West should be ashamed for all the South Africas, Rhodesias, and Serbias that it has betrayed in the past.

AN INSIGHT INTO GENERAL PETER WALLS

Extracted from SOF Magazine -a rare interview by Al J Venter with Peter Walls the Commander of the Rhodesian Army.
CLICK ON IMAGE TO ENLARGE

AMERICAN "BOUNTY" HUNTERS IN RHODESIA

An article about "Bounty Hunting" in Rhodesia towards the end of the war. Extracted from Soldier of Fortune Magazine. It appears to me that these so called Bounty Hunters were "Adventurers" with a bit of Walter Mitty in them?
CLICK ON THE IMAGES TO ENLARGEN

ANTHRAX OUTBREAK IN RHODESIA 1978-80

Anthrax Epizootic in Zimbabwe, 1978-1980: Due to Deliberate Spread?

Meryl Nass, M.D.*

Abstract
The largest recorded outbreak of anthrax in humans occurred in Zimbabwe during its civil war, in 1979 to 1980. There were a number of unusual features of the epizootic. The disease spread over time from area to area, until six of the eight provinces were affected. Yet anthrax usually appears as a point source outbreak, without significant geographic spread. Only the African-owned cattle in the Tribal Trust Lands were affected; cattle belonging to whites were uninvolved. A critical review of the scientific explanations proposed to account for these events is presented. The possibility that the epizootic could have been a biological warfare event is evaluated. Finally, suggestions are advanced for further investigations into the origin of this epizootic. [PSRQ 1992;2:198-209]


--------------------------------------------------------------------------------

The largest recorded outbreak of anthrax among humans, and possibly the largest among animals, occurred over a decade ago in Zimbabwe, formerly Rhodesia, during the time of its civil war [1]. The outbreak was reported in a series of articles by J. C. A. Davies and others in the Central African Journal of Medicine [2-8]. Little was written about it outside of Africa. Over 10,000 human cases and 182 human deaths were documented [9]. Human cases were secondary to an unprecedented outbreak in cattle [5,10].

Unusual Features of the Epizootic

There were a number of surprising aspects of this epizootic. First, the large number of cases was un usual. Ten thousand seven hundred thirty-eight human cases were documented in Zimbabwe from January 1979 through December 1980 [9]. According to Mandell's Principles and Practice of Infectious Disease, published in 1979, "about 7,000 cases are reported in the world annually" [11].The large number of human cases was particularly unusual in light of the historically low prevalence of anthrax in Zimbabwe [5]. In the 29-year period preceding the epidemic (1950-1978), the period for which records are available, a total of 334 human cases were reported in Zimbabwe. By comparison, during the same period (1950-1978) in the United States, 459 human cases were reported [12]. Clearly, anthrax was a rare disease in both countries. According to Davies, "At the beginning of what was to be a major epidemic, it is safe to say that the majority of doctors in Zimbabwe had never seen a case of anthrax" [5]. Yet during the war, anthrax became one of the country's major causes of hospital admissions.

Second, the geographic scope of this outbreak was highly unusual for anthrax. Most outbreaks are characterized by a high degree of focality [11]. Cases occur in limited areas only. Yet in Zimbabwe from 1978 to 1980, the disease spread from area to area, until six of the eight provinces were affected [13]. Anthrax needs very specialized conditions to grow in soil. Alkaline soil containing adequate nitrogen, calcium, and organic matter is required, in conjunction with extreme weather changes, such as a drought followed by heavy rains [14-19]. When these conditions are met, the organisms are thought to undergo a vegetative cycle in soil and then re sporulate. This process could generate sufficiently high soil concentrations of anthrax spores to cause disease in grazing animals, producing the occasional outbreaks separated by long disease-free intervals that have been observed. However, although this theory accounts for the periodic outbreaks exhibited by anthrax, it has yet to be proved.

Humans generally acquire the infection by handling meat or other products from infected animals. Butchering, preparing, and eating meat from an animal infected with anthrax are frequent causes of the disease in humans and accounted for many cases in Zimbabwe.

There is believed to be no significant spread from animal to animal (except through consumption of infected meat by carnivores, which are relatively resistant to infection) and no significant spread from human to human. Epizootics are generally limited both geographically and temporally [14-16]. Animal cases tend to appear in limited areas over a period of weeks to months, and the epizootic ends naturally as soil conditions change and the density of anthrax spores declines, with no spread to distant areas.

Many of the Zimbabwe cases occurred in areas where anthrax had not been recorded before. Yet in the rest of the world, epizootics generally occur in areas that are known to have produced anthrax outbreaks in the past, where there is assumed to be low-density contamination of the soil. Anthrax spores in soil may retain their virulence for decades. Epizootics do not spread beyond these areas, al though sporadic cases are seen in areas that lack a history of anthrax. The exception to this occurs when an area has become newly contaminated by animal remains or material made from tainted animal products, such as fertilizers or animal feeds made from contaminated bone meal. Such products were not generally used by rural blacks in Zimbabwe [1].

Third, if weather conditions were particularly favorable for the growth of anthrax in soils throughout much of Zimbabwe and often near its borders, then other anthrax outbreaks in adjoining countries might have been expected to occur as well. Yet none of the countries that are contiguous to Zimbabwe reported increased anthrax activity during this period [20].

Fourth, the epizootic was almost entirely confined to the Tribal Trust Lands. These were areas that had been assigned to Zimbabwe's blacks when the country was divided into distinct areas for black and white habitation by the Land Apportionment Act of 1930. Originally termed reserves, the name was changed to Tribal Trust Lands in 1969, and after 1981 they were renamed Communal Farming Areas. By the end of 1979, one-third of Tribal Trust Lands were affected with anthrax, approximately 17% of the land area of the country [10]. Davies noted that "the commercial (white-owned) farming areas appear to have been almost completely spared" [5]. Only four small outbreaks, with 11 cattle deaths, were reported in the commercial farming areas of Zimbabwe by early 1980 [10]. There are no reports of anthrax in white Zimbabweans during this period.

Fifth, the timing of the epizootic coincided with the final months of a long and particularly brutal guerrilla war. Some guerrilla activity had begun in the late 1960s, but the war did not escalate significantly until the mid 1970s. The war ended in late February 1980, when elections were held, and ZANU and ZAPU, the parties affiliated with the two guerrilla armies, won an overwhelming victory.

Human anthrax case reports by month are available for the provinces of Matabeleland, Midlands, and Mashonaland [5]. In Matabeleland and Midlands, cases peaked in November and December 1979, respectively, and decreased thereafter. In Mashonaland, there were two peaks, the first in February 1980 and a second in December 1980. After the war ended in late February 1980, only sporadic cases were seen in previously unaffected areas, and there appeared to be no further geographic spread of the epizootic. However, anthrax has remained enzootic in Zimbabwe since the war ended, a not surprising finding, given the persistence of the spores in nature.

Analyzing the Explanations

Owing to the rarity of an outbreak such as this, a number of hypotheses were put forward to account for the epizootic. These hypotheses included spread by insect vectors and contamination of new areas by infected meat that was transported long distances by the rural people. Veterinary services broke down almost completely in many communal farming areas during the war, and this lack of veterinary services was felt to contribute to the outbreak.

It was also suggested that anthrax had been more prevalent prior to the onset of the epizootic than was recorded, but, because of limited reporting from rural areas, the cases had not been documented.

Five questions that address the underlying issues in the explanations listed above have been identified. A review of the experimental and epidemiological literature on anthrax transmission was under taken to answer these questions as precisely as possible. Many questions about the natural history of anthrax still exist [21,22]. However, despite limitations in the literature, this review permits a critical evaluation of the issues involved.

QUESTION 1: What role did blowflies, horseflies, stable flies, and mosquitoes (the insects reported to be likely vectors) play in the transmission of anthrax to cattle?

Observations Opposing Vector Transmission

Sparing of Young Animals.
Several authors have noted the relative sparing of calves by anthrax [16,23]. This observation has been interpreted as supportive evidence for oral ingestion as the primary portal of entry of anthrax infection; young animals are thought to be spared by feeding primarily on their mothers' milk, thus ingesting less grass and soil.

Cutaneous Versus Systemic Disease.
The anthrax syndrome seen in cattle is almost always systemic and hyperacute, unlike the disease in horses and humans, both of which tend to develop localized areas of swelling and have a more prolonged disease course [16,24-26]. On this empirical basis alone (the absence of localized areas of swelling), most authors dispute insect vector transmission to cattle, even when they believe that it occurs in other species [26]. However, a few sources do report the existence of a cutaneous anthrax syndrome in cattle and link it to fly bites [27,28]. Still other authors report the presence of localized swelling in cattle but suggest that it is due to the systemic disease rather than local inoculation [16].

Volume of Blood Needed.
Transmission of anthrax to cattle by any species of fly would require the inoculation of organisms through the skin. How ever, in the hands of several investigators, cattle have proved notoriously difficult to infect with anthrax by parenteral injection [24]. Using intravenous, intramuscular, subcutaneous, and intradermal routes, Schlingman and colleagues gave cattle injections of up to 600 million spores but were unable to produce a fatal infection or determine an LD50 [29]. In contrast, infection by the oral route was easier to induce.

In all animal species studied, the level of terminal bacteremia of anthrax organisms ranged from about 100 million to 1 billion colony forming units/ml [30-32]. This suggests that, for a biting fly to induce anthrax infection by parenteral inoculation of blood to a cow, on the order of 1 ml of blood would need to be transferred, a herculean task for a fly. Further more, loss of large blood volumes to second hosts is unlikely in flies, since it would be unfavorable for survival.

There are two caveats to this analysis. Every study that specified the inoculum sizes employed for par enteral inoculation of anthrax used spores. Yet theoretically, insects can transmit either spores or vegetative forms of the organism. No studies exist that provide estimates or measurements of inoculum sizes needed to induce infection with the vegetative form of anthrax. Moreover, the size of the infectious dose depends on the anthrax strain employed. Yet most of the studies cited here did not identify the anthrax strain used.

Literature Review

The most complete review of more than 100 years of literature on experimental vector spread of anthrax was performed in 1971 [33]. In his summary of the data, Greenberg emphasized our lack of knowledge and concluded that the issue of vector transmission remained unresolved.

Individual Analyses by Vector

Blowflies.
The presence of hundreds of bubbles of blood resulting from insect bites, which are commonly seen on carcasses of animals that died of anthrax, has been mentioned as supporting insect vector transmission. Blowflies (Chrysomyia) are the only flies that feed on carcasses that have been suggested as anthrax vectors in Zimbabwe. Tabanids, muscids, and mosquitoes (the other suggested insect vectors in Zimbabwe's epizootic) are unable to feed on dead animals, although they may attempt to do so and acquire a small number of organisms in this fashion [34].

Because blowflies do not feed on living creatures, they cannot transmit infection to animals or humans directly via a bite. It is reported that blowflies regurgitate infectious droplets onto the leaves of trees or bushes where they perch, at a height between 1 and 3 m above ground level 135,36]. It has been further suggested that kudu develop infection after feeding on leaves contaminated with anthrax by blowflies [36,37]. With respect to cattle, however, leaves have never been implicated in anthrax out breaks.

Sen and Minett did transmit anthrax to goats through the blowfly (Calliphora erythrocephala) and the housefly (Musca domestica) [38]. Their procedure entailed bringing the flies in contact with incisions made in anthrax-infected carcasses and then transferring the flies to the cauterized skin of uninfected goats. Although it is not made explicit in the report, this transmission appears to have occurred as a result of deposition of anthrax spores present on the body parts or feces of the vectors, rather than via a bite. Twenty-four to 50 flies per goat were employed in these experiments. The authors reported that they used goats because goats are more susceptible than cattle to experimental inoculation.

Discussion of anthrax transmission to cattle by blowflies is hypothetical; no experimental evidence documents such transmission.

Stable Flies and Mosquitoes.
Sen and Minett at tempted to transmit anthrax to goats through the use of stable flies (Stomoxys calcitrans) by feeding the flies on infected goats and transferring them to the healthy skin of uninfected goats [38]. They then attempted to feed flies on incisions made in goats that died of anthrax and transferred the flies to the cauterized skin of healthy goats. Finally, they exposed the cauterized skin of healthy goats to anthrax-contaminated ny feces. In none of these experiments was anthrax transmission achieved. It was noted that application of an anthrax culture suspension to goat skin that had been cauterized or had recently received Stomoxys bites led to infection, while the same suspension applied to healthy skin caused no disease.

In 1987, Turrell and Knudson did produce anthrax by vector transmission in mice and guinea pigs [32]. Their work was initiated partly in response to the Zimbabwe epizootic to resolve whether insect vectors could account for the massive spread of disease. Mosquitoes (Aedes aegypti and Aedes taeniorhynchus) and stable flies (S calcitrans) were the vectors studied. Even under optimal conditions (feeding insects on animals immediately prior to the animals' deaths, interrupted feedings with forced transfer to a second host, shaving to remove hair from guinea pigs, and transfer of more than one infected fly to the second host), there was only occasional transmission of the disease. Twelve per cent and 17% transmission rates were reported.

Although Turrell and Knudson concluded that "various forms of evidence strongly suggest that flies play a role in the transmission of Bacillus anthracis to humans and domestic animals during an anthrax outbreak," they neglected to take into account the huge difference in susceptibility and infectious dose between mice and guinea pigs, on the one hand, and humans and cattle, on the other. Since the parenteral LD50 for mice and guinea pigs is only 5 to 50 spores [31,39], but the LD50 for cattle appears to be more than 100 million spores, the demonstration of vector transmission to mice and guinea pigs cannot be extrapolated to cattle. In fact, the opposite conclusion should be drawn: if small rodents are only occasionally infected, then cattle, with an inoculum size more than a million times greater, will rarely if ever be infected by the vectors studied.

Horseflies.
Horseflies (tabanids) are larger than the mosquitoes and stable flies studied and ingest a larger volume of blood when feeding, perhaps 100 times the volume ingested by mosquitoes and 20 times the volume of Stomoxys [40]. Yet, given the orders of magnitude involved, the likelihood of tabanid transmission of anthrax to cattle appears small.

Tabanids have been frequently reported as vectors in the transmission of tularemia. For transmission of tularemia, however, "as few as 10 to 50 organisms are sufficient to cause infection by cutaneous inoculation" [41].

QUESTION 2: Can the human consumption and trans port of infected meat be used to account for new infections in cattle?

The transport of meat can explain the occurrence of human cases in sites distant from the original outbreaks. But it does not explain cases in cattle at the secondary locations.

First, no transmission from humans to cattle by direct contact has ever been reported.

Second, since cattle are herbivorous, they would not consume meat from infected carcasses. Although infected animal bones or body parts might be discarded at the secondary sites, the areas they could contaminate would be limited, and transmission to very few animals would be expected. This is even more true if a cycle of growth in soil is needed for anthrax organisms to achieve sufficient concentrations in soil to cause disease. Most anthrax experts believe that a soil growth phase is necessary [15,16,25,42,43], though it is disputed by some and has not been proved experimentally [44,45].

Third, although the human butchering and consumption of anthrax-contaminated meat has been reported from many countries [45-51], no secondary cases in cattle have been reported as a result.

Fourth, even prior to 1978, when animals were found dead from anthrax in Zimbabwe, the meat was often consumed by the rural people [10], yet large outbreaks did not result.

QUESTION 3: Was there a precipitous increase in human and animal cases of anthrax beginning late in 1978?

Anthrax is reported to have been a rare disease in Zimbabwe in both animals and humans prior to 1978 [5-8,52]. According to Zimbabwe Veterinary Research Laboratory scientists, only about 20 cases per year in livestock had been reported annually [10].

Dr. Max Sterne, South Africa's anthrax expert and originator of the animal vaccine used worldwide, wrote that, when all animals that had died were screened for anthrax in a South African study, a fourfold rate of underreporting was found [53]. Extrapolating this figure to Zimbabwe, which may or may not be applicable, only an estimated 80 cases in livestock would have occurred annually, still a relatively small number. In Sterne's 1967 map of worldwide anthrax incidence, Zimbabwe was placed in the lowest incidence category for animal anthrax [53].

The human case numbers from the annual and monthly reports of the Zimbabwe Minister for Health from 1950 to 1985 (when publication ceased) are shown in the Table. Regular publication of yearly human anthrax cases began in 1950. The reported incidence of human cases during the period from January 1, 1979, to December 31, 1980, was more than 400 times the average incidence of the previous 29 years.

QUESTION 4: How did the cessation of veterinary services in the Tribal Trust Lands contribute to the spread of anthrax?

Routine anthrax vaccination of livestock was not practiced to a large extent in Zimbabwe before 1979, according to local veterinary experts.

Although vaccination certainly may have pre vented spread to the commercial (white-owned) farms once the outbreak was underway, if vaccination had not been practiced widely prior to the epizootic, then it cannot be credited with keeping the earlier rates so low. One must instead assume that soil contamination by anthrax was previously not widespread in Zimbabwe.

Likewise, if vaccination had not been routinely practiced on a large scale, then the breakdown in veterinary services, which accompanied the turmoil of the war, was not a factor in the early development of the anthrax outbreak, as commonly believed.

Although the well-publicized breakdown in animal dipping contributed to the increase in tick-borne diseases of livestock and was thought by many lay people in Zimbabwe to have contributed to the anthrax outbreak as well, livestock dipping by itself does not contribute to anthrax prevention. The only role that the breakdown of dipping may have played in the anthrax epizootic was in the interruption of periodic contact between villagers and veterinary workers. As a result, the reporting of anthrax cases and of unexplained animal deaths stopped. In this way there was probably interference with the usual process of identifying anthrax outbreaks, with vaccinating in response to them, and with the appropriate disposal of carcasses.

To summarize, the absence of veterinary services does not seem to account for the onset of the epidemic or its geographic spread, but, had such services functioned in the communal farming areas, there should have been fewer cases in both humans and cattle.

QUESTION 5: How can the spread to previously uninvolved areas be explained?

Stein has published perhaps the most complete epidemiological assessment of anthrax outbreaks in nature. He surveyed the entire United States for anthrax incidence and endemicity. Describing his observations of anthrax occurrences, he wrote: "In the United States anthrax occurs in epizootic form in regions in which the soil is known to be seriously infected. However, it may occur sporadically any where at any time, and thus may appear where previously not identified or where it has been quiescent for a long period" [27] (emphasis added). Whitford, who analyzed many anthrax outbreaks, made a similar observation [54]. Later, Stein examined increasing anthrax outbreaks from 1945 to 1955 throughout the United States and addressed the issue of spread to previously unaffected areas. He reported that outbreaks occurring in cattle in new areas were mainly due to infections acquired by vaccination with improperly prepared batches of vaccine. In swine, they were mostly of suspected food origin [55]. Blood, Henderson, and Radostits concur, writing that "introduction of infection into a new area is usually through contaminated animal products such as bone meal, fertilizers, hides, hair, and wool, or by contaminated concentrates or for ages" [25].

Inferred from these data is that Zimbabwe's anthrax epizootic is most consistent with the new introduction of the organism by some means into Zimbabwe.

What Do the Answers to These Five Questions Indicate?

The pattern of acquisition of anthrax in humans was consistent with its natural pattern elsewhere: secondary to contact with infected animals or animal products [5]. The only unusual epidemiological feature with respect to humans was the massive number of cases. A small number of human cases might perhaps have been secondary to spread by insect vectors [55]. (The human parenteral infectious dose is unknown, so the likelihood of vector transmission is difficult to assess.)

The disease in cattle is another story. Anthrax spread in a way that cannot be accounted for either by insect vectors or transport of infected meat. Vectors and movement of meat may have accounted for occasional, sporadic cases but would not have been expected to play a major role in the development of Zimbabwe's massive outbreak.

Lacking an identified source of anthrax contamination, the massive epizootics in previously uninvolved areas are unprecedented. Although cases elsewhere are seen in areas with no history of prior anthrax infections, these cases have consistently been only occasional and sporadic, or, when seen on a large scale, they have been traceable to a newly introduced source of infection. Weighing all available evidence, it is suggested here that a plausible explanation for the sudden peak of anthrax in the Tribal Trust Lands beginning in November, 1978, is that one or more units attached to the Rhodesian military may have air dropped anthrax spores in these territories. This action would expose cattle to the disease through ingestion or inhalation (or both) of anthrax spores. Humans would have acquired the disease from meat or meat products.

Anthrax and Biological Warfare

For the above reasons, this epidemic may not have been a natural occurrence, and might instead have been the result of deliberate spread -- employing anthrax as an agent of biological warfare. No proof exists for the deliberate use of anthrax; nor is there positive evidence of the origins of anthrax spores that may have been used or the technical means by which they may have been disseminated. The following discussion, however, attempts to put these issues into the context of what is known about anthrax and biological warfare.

Technologically, production of anthrax spores is not a difficult problem. Anthrax weapons were developed and tested by at least the Japanese, British, and United States governments during the Second World War [56-58], and it is suspected that a number of other nations have developed or acquired the technologies since [59]. The spores are stable under a wide range of conditions of temperature, pressure, and moisture. Many means exist for delivering viable anthrax spores [60,61]. Experiments on Gruinard Island (where the British tested anthrax weapons in 1942-1943) included release from exploding bombs and by airplane [62]. Either of these two methods, or other methods, could conceivably have been used in Zimbabwe. Deliberate contamination of animal feeds or fertilizers might have accomplished the same end, although these products were not widely used.

Although aerial release of anthrax spores is generally thought to result in an epidemic of inhalation anthrax in humans (which was not reported from Zimbabwe), inhalation anthrax is not necessarily what would have been seen had this method been used in Zimbabwe, for the following reasons.

Inhalation anthrax results from the intrapulmonary deposition of individual spores less than 5 microns in size. It is a rare disease, with 18 human cases reported in the United States between 1900 and 1980 [63]. This is despite the fact that some woolen mills, tanneries, and even laboratories researching anthrax have been shown to be contaminated with anthrax spores when air and surface sampling have been performed [63].

Little information is available regarding the factors that influence human susceptibility to anthrax. Besides susceptibility, the other factor that determines whether a person develops inhalation anthrax is the inoculum size to which he or she is exposed. For inhalation anthrax, this would be a function of the spore concentration, the amount of time the spores remain airborne, and spore size (larger spores are trapped before reaching the pulmonary parenchyma). Although the inhaled infectious dose for humans is unknown, studies in monkeys and estimates of spore numbers inhaled by workers in contaminated factories exist. These indicate that for 3 pound cynomolgus monkeys the LD50 is over 17,000 inhaled spores, for chimps about 40,000 spores, for rhesus monkeys about 80,000 spores, and for humans something probably greater [39,63,64].

In Zimbabwe, where "protected villages" existed in many parts of the country (which entailed the creation of new population centers by removal of blacks from their rural farms to regulated areas) and the movement of rural blacks was in some areas strictly controlled, it may have been possible to accomplish airborne spraying and yet avoid populated areas. Or, had spores been prepared as pellets or cattle cakes (as was planned by the British for a possible raid on Germany) [57], inhalation anthrax would not have occurred.

Another consideration is that, by the war's end, many of the medical facilities in the rural areas were no longer functioning. Had cases of inhalation anthrax occurred, most of the patients would probably have been unable to reach a treatment facility prior to death, which usually occurs within 24 hours of the onset of symptoms significant enough to seek medical attention.

To manufacture anthrax weapons under ideal conditions, high-containment suites are employed. However, such facilities were not available to the nations that manufactured such weapons during World War II. As pointed out, even in settings highly contaminated with anthrax spores, only rare cases of inhalation anthrax have occurred. Cutaneous anthrax was more common but could be easily treated. Therefore, use of such suites, though desirable, is not mandatory for production of anthrax weapons.

Since human anthrax vaccine has been available since the 1950s, is currently manufactured in at least three countries, and is recommended for persons with occupational exposures, procurement of the vaccine for workers who may have been engaged in researching or producing anthrax weapons should not have been difficult. Obtaining cultures of the organism is also not difficult; cultures might have been available from the American Type Culture Collection in Rockville, Maryland, or from the Centers for Disease Control [65]. Anthrax is also easily cultured from soil found in endemic areas or from some infected animal remains [19]. Methods for culturing the organism and inducing sporulation are described in the open literature.

Anthrax weapons produced by the military existed in the United States until about 1970, when President Nixon gave orders for their destruction. One cannot totally exclude the possibility that some biological munitions were transferred from the United States to other countries prior to their destruction. It is also not impossible to imagine that such weapons could have been produced by a nation that was not a complying party to the Biological Weapons Convention (which in any case only entered into force in 1975), or even by a renegade group, and could have found their way to Zimbabwe.

Political Considerations

Why would such an action be carried out? Could it possibly have benefitted the war effort? What political risks would have been faced by a possible perpetrator?

The net result of the anthrax epizootic appears to have been the impoverishment of the affected rural populations. Cattle were the major source of wealth for black farmers. Describing the effects of the out break 10 years later, Pugh and Davies paid testimony to its effects on a rural economy: "There is always hardship, but if cattle die, the family loses its source of wealth; without motive power for ploughing, crops cannot be planted, leading to no food, no money to purchase food, pay school fees, bus fares, taxes, or buy the essentials to life. The family is reduced to grinding poverty and malnutrition becomes rife" [131. Most likely, cattle would have been the objects under attack, and human cases occurred only incidentally.

One can perhaps imagine that, as the war escalated with no end in sight, and with a black population becoming ever more polarized in favor of the guerrillas, a willingness developed to use any weapon that might lead to victory. Since the many programs that had tried to stop the local populations from providing the guerrillas with support had failed [66-68], the local population itself may have come to be seen as the enemy. According to J. K. Cilliers, who published his dissertation analyzing Rhodesian counterinsurgency strategy, "by the overly aggressive use of tactics . . . Security Force actions tended rather to be aimed against the local population than in defence of them" [67].

Point 1: Food Control

The rationing and limiting of food supplies to the black population was in fact a part of the military strategy for controlling the population and restricting their support to the guerrillas. In his analysis of military strategy, Cilliers provides details of this approach:

During the final months of 1976, food control measures were instituted ... food in the Tribal Trust Lands had become less readily available to the insurgent forces owing to a general drought and the movement of locals into Protected Villages ... The intention was to further limit even these supplies by rationing the farm laborers to that which was needed . . . Farmers were to ration their laborers on a day-to-day basis with only sufficient food for a particular day. No surplus would therefore by available to feed insurgent forces, even were this demanded by force of arms. Tight food control would force insurgents to spend much time seeking sustenance, which would hasten their location and eventual elimination. A further advantage could result from hostility between the local population and insurgents as demands on limited available foodstuffs increased [67].

In late 1977, intelligence reports indicated that ZANLA (Zimbabwe African National Liberation Army) morale in the area was on the verge of collapse because of their inability to obtain either food from the local population or water from points outside Protected Villages. These had largely been destroyed by Security Forces Operations [67].

Naturally, the local population felt the effects of these policies as well as the guerrillas. "Malnutrition and disease had always been features in black rural life for numerous decades. The concentration of people (into Protected Villages) tended to exacerbate these problems" [67]. Discussing the situation in late 1978, Cilliers points out: "An increasing number of reports of malnutrition were reported by the few doctors that remained in rural areas" [67].

Point 2: Escalation of Tactics. Aerial Bombing of Zambia and Mozambique

According to Ken Flower, head of the Rhodesian Central Intelligence Organization (CIO) during the war, the guerrillas escalated a terrorism campaign beginning in June 1978 that culminated in the shooting down of a civilian Viscount airliner and massacre of many survivors in September 1978 [68]. Their actions were met by the Rhodesian government with parallel escalation: regular airborne bombing raids into Zambia and Mozambique were initiated in October 1978, attacking training camps established by the guerrillas. This was begun despite warnings from the U.S. and Britain that taking the war outside the country in a significant way could lead to a superpower conflict in southern Africa. Thousands of men, women, and children were killed in these bombing raids.

It was in November 1978, a month after initiation of the bombing raids, that the first human anthrax cases were reported following an outbreak in cattle. Thus, the epidemic did coincide with a period of escalation of tactics by the Rhodesian military.

Point 3: Chemical and Poison Weapons

Was there a parallel, well-documented use of other weapons considered abhorrent during the conflict and a willingness to overlook civilian casualties? In his memoirs, Flower admits to the deliberate distribution of poisoned clothing, which killed hundreds of black guerrillas [68]. Yet clothing can be worn by anyone. Organophosphate poisoning from tainted clothing affected civilians as well, and poisoning by this means became documented in the Zimbabwe medical literature [69,70].

Dr. Paul Epstein, an American physician practicing in Mozambique for the Ministry of Health, with support from the American Friends Service Committee in 1978, treated large numbers of Zimbabweans, who had arrived from ZANLA training camps, for a bleeding disorder. Initially a viral hemorrhagic fever was suspected. But there were many deaths despite treatment. Eventually a fat biopsy was obtained and sent for toxin analysis; this analysis revealed the presence of warfarin [71]. Thus another unconventional mode of warfare, warfarin poisoning, may have been employed by some within the Rhodesian military.

Although the use of bacteriological weapons and poisons such as organophosphates was and is prohibited by the 1925 Geneva Protocol, of which the United Kingdom is a party, the events described occurred after Rhodesia's Unilateral Declaration of Independence from the UK. Thus, whether use of such agents would have been in actual violation of the treaty is arguable. (Rhodesia was not a party to the Biological Weapons Convention, which bans the possession and use of biological weapons.) Since Rhodesia was already subject to an international embargo, which had been in force since 1965, fear of an international response to the use of chemical and biological weapons was probably not a significant deterrent.

Reporting recently in a TV documentary and magazine article on confidential interviews with former contractors for the Rhodesian military, Jeremy Brick hill, a Zimbabwe journalist and veteran of the conflict, claimed that the Rhodesian CIO and Selous Scouts (an arm of the Rhodesian military that employed blacks who successfully masqueraded as guerrillas) used anthrax, cholera, thallium-contaminated foodstuffs, and organophosphate-impregnated clothing in the later years of the war [72,73].

Conclusions

A case has been made for the possible deliberate use of anthrax as an agent of biological warfare, directed at African-owned cattle, in the final months of the Zimbabwe civil conflict.

The characteristics of Zimbabwe's anthrax epizootic are unusual. Outside Zimbabwe, outbreaks of animal anthrax have remained confined to enzootic areas or could be traced to contaminated animal products and have been generally self-limited. Zimbabwe's epizootic did not conform to this expected behavior, and the arguments put forward to explain it are unconvincing.

A military role for anthrax can be postulated, given the strategic control of food and other re sources that existed at the time. Deliberate impoverishment of rural blacks may conceivably have been a strategy as well. Desperate tactics appear to have been used by the Rhodesian military elsewhere as the war drew to a close. Finally, there have been recent reports attributed to confidential eyewitnesses that support the theory of the deliberate spread of anthrax.

Next Steps

During the past 45 years, no allegation of biological warfare has undergone careful scientific analysis and been brought to a satisfactory conclusion. There exists no generally accepted methodology to serve as a guide for the design of an investigation into the possible use of biological weapons [74-76].

A lot is known about the ecology of anthrax, and this knowledge could be employed to design studies that would help to resolve the issue of the origin of Zimbabwe's anthrax epizootic. Soil sampling could be used to detect the presence of anthrax in soils. The extent of anthrax found in communal versus commercial farming areas would be interesting. Finding high anthrax spore counts in unusual locations, such as in places that do not support its growth, would contribute to an understanding of the epizootic.

Recent developments in biotechnology can be used to resolve issues such as this. Characterization of the genetic structure of Zimbabwe anthrax strains can be used to estimate the likelihood that the strains found originated from locally occurring southern African strains, as opposed to strains that are found elsewhere or are held in laboratories.

A third approach to this question might look at the documents that are available on the military actions and strategies used during the war. For ex ample, one tactic used by the military was to assign areas of land to be "no go" or "frozen" for varying periods. This enabled certain military units to carry out special projects in the designated areas. During this time, no unassigned military units were allowed to operate within the areas and civilian access may have been restricted 167]. It would be useful to know whether land that was heavily affected by anthrax was "frozen" shortly before the first local cases of anthrax were seen.

During the time following the national elections and before transfer of power to the Mugabe government several weeks later, a large number of government records were destroyed [66]. Still, documents and sources remain. For instance, an archive of the papers retained by Ken Flower, who stayed on to work for the Mugabe government after the war, exists in Harare. Other former military and intelligence officers continue to live and work in Zimbabwe. It is now possible to design a careful and definitive investigation of this issue. The time has come for a thorough inquiry.

Acknowledgments

Thanks to Mark Wheelis, Ph.D., Ed Stanek, Ph.D., Philip S. Brachman, M.D., Morton Swartz, M.D., Howard Hu, M.D., and Jean Porwoll, M.D., for comments on earlier versions of this manuscript; to Paul Epstein, M.D., Jeremy Brickhill, Lane Foil, Ph.D., and Bruce Ivins, Ph.D., for supplying publications and supporting material; to Barbara Rosenberg, Ph.D., Arthur Serota, Esq., and Julian Perry Robinson, Ph.D., for contacts and encouragement; to Doris Alleman for untiring reference assistance; and to the many others who provided ideas, information, and inspiration, without which this analysis could not have been accomplished.

References

1. Kobuch WE, Davis J, Fleischer K, Isaacson M, Turnbull PCB. A clinical and epidemiological study of 621 patients with anthrax in western Zimbabwe. Proceedings of the international workshop on anthrax. Salisbury Medical Bulletin 1990;68(suppl):34-38.
2. Davies JCA. Transmission of anthrax. Cent Afr J Med 1980;26:47. Letter.
3. McKendrick DRA. Anthrax and its transmission to humans. Cent Afr J Med 1980;26:126-129.
4. Turner M. Anthrax in humans in Zimbabwe. Cent Afr J Med 1980;26:160-161.
5. Davies JCA. A major epidemic of anthrax in Zimbabwe, Part 1. Cent Afr J Med 1982;28:291-298.
6. Levy LM, Baker N, Meyer MP, et al. Anthrax meningitis in Zimbabwe. Cent Afr J Med 1981;27:101-104.
7. Davies JCA. A major epidemic of anthrax in Zimbabwe, Part 2. Cent Afr J Med 1983;29:8-12.
8. Davies JCA. A major epidemic of anthrax in Zimbabwe, the experience at the Beatrice Road Infectious Diseases Hospital, Harare. Cent Afr J Med 1985;31:176-180.
9. Report of the Secretary for Health. Harare, Zimbabwe: Government Printer, 1979 and 1980.
10. Lawrence JA, Foggin CM, Norval RA. The effects of war on the control of diseases of livestock in Rhodesia (Zimbabwe). Vet Rec 1980;107:82-85.
11. Poretz DM. Anthrax. In: Mandell GL, Douglas RG, Bennett JE, eds. Principles and practice of infectious diseases. 1st ed. New York: Wiley Medical, 1979,1634.
12. US Public Health Reports, reported by Whitford HW. Incidence of anthrax in the USA: 1945-1988. Proceedings of the international workshop on anthrax. Salisbury Medical Bulletin 1990;68(suppl):5-7.
13. Pugh AO, Davies JCA. Human anthrax in Zimbabwe. Proceedings of the international workshop on anthrax. Salisbury Medical Bulletin. 1990;68(suppl):32-33.
14. Van Ness G, Stein CD. Soils of the United States favorable for anthrax. J Am Vet Med Assoc January 1, 1956,7-9.
15. Van Ness GB. Ecology of anthrax. Science 1972;172:1303-1307.
16. Fox MD, Kaufman AF, Zendel SA, et al. Anthrax in Louisiana, 1971: epizootiologic study. J Am Vet Med Assoc 1973,163:446-451.
17. Kasianenko AM, Verner OM, Zaviriukha AM, Siniak KM. Mapping method in the epidemiological study of infections and infestations. II. Soil characteristics in localities permanently at risk for anthrax [in Russian]. Zhumal Mikrobiology Epidemiology Immunobiology January 1984;90-95. English abstract.
18. Kaufman AF. Observations on the occurrence of anthrax as related to soil type and rainfall. Proceedings of the international workshop on anthrax. Salisbury Medical Bulletin 1990;68(suppl):16-17.
19. Titball BW, Tumbull PC, Hutson RA. The monitoring and detection of Bacillus anthracis in the environment. J Appl Bacteriol Symp Ser 1991;70(suppl):9S-18S.
20. FAO (United Nations). Animal Health Yearbook. Kouba V, ed. Rome, Italy, 1979, 1980, 1981.
21. Nungester WJ. Problems for future study of anthrax. Federation Proceedings 1967;26:1571.
22. Smith H. Anthrax, clinical manifestations and pathogenesis: much unknown and much just forgotten. Proceedings of the international workshop on anthrax. Salisbury Medical Bulletin 1990;68(suppl):31.
23. Anthrax. In: Scanlan CM. Introduction to veterinary bacteriology. Ames: Iowa State University Press, 1988:255-257.
24. Sterne M. Anthrax. In: Dalling T, ed. International encyclopedia of veterinary medicine Edinburgh: W Green and Son, Ltd., 1966;221-230.
25. Blood DC, Henderson JA, Radostits OM. Anthrax. In: Blood DC, ed. Veterinary medicine: a textbook of the diseases of cattle, sheep, pigs, goats, and horses. Philadelphia and London: W.B. Saunders, 1979;433-436.
26. Gillespie JH, Timoney JF. The genus bacillus. In: Hagan and Bruner's infectious diseases of domestic animals. Ithaca: Cornell University Press, 1981;190-197.
27. Stein CD. Anthrax in animals and its relationship to the disease in man. Tex Rep Biol Med 1953;11:534-536.
28. Krishna Rao NS, Mohiyudeen S. Tabanus flies as transmitters of anthrax: a field experience. Indian Veterinary Journal 1958;35:348-353.
29. Schlingman AS, Devlin HB, Wright GG, et al. Immunizing activity of alum-precipitated protective antigen of Bacillus anthracis in cattle, sheep and swine. Am J Vet Res 1956;17:256-261.
30. Keppie J, Smith H, Harris-Smith PW. The chemical basis of the virulence of Bacillus anthracis. III: The role of the terminal bacteremia in death of guinea pigs from anthrax. Br J Exp Pathol 1955;136:315-322.
31. Lincoln RE, Fish DC. Anthrax toxin. In: Montie TC, Kadis S, Ajl SJ, eds. Microbial toxins. Vol. 3. New York: Academic Press, 1970;361-414.
32. Turrell MJ, Knudson GB. Mechanical transmission of Bacillus anthracis by stable flies and mosquitoes. Infect Immun 1987;155:1859-1861.
33. Greenberg B. Flies and animal disease. Vol. 2. Princeton: Princeton University Press, 1971;300-305.
34. Anthony DW. Tabanidae as disease vectors. In: Maramorosch K, ed. Biological transmission of disease agents. New York: Academic Press, 1962;93-107.
35. Braack LEO, Retief PF. Dispersal, density and habitat preference of the blow-flies Chrysomyia albiceps and Chrysomyia marginalis. Onderstepoort J Vet Res 1986;53:13-18.
36. de Vos V. The ecology of anthrax in the Kruger National Park, South Africa. Proceedings of the International Work shop on Anthrax. Salisbury Medical Bulletin 1990;68(suppl):19-23.
37. Pienaar U de V. Epidemiology of anthrax in wild animals and the control of anthrax epizootics in the Kruger National Park, South Africa. Federation Proceedings 1967;26:1496-1501.
38. Sen SK, Minett FC. Experiments on the transmission of anthrax. Indian Journal of Veterinary Science and Animal Husbandry 1944;14:149-158.
39. Lincoln RE, Walker JS, Klein F. Value of field data for extrapolation in anthrax. Federation Proceedings 1967;26:1558-1562.
40. Busvine JR. Insects and hygiene. London: Chapman and Hall, 1980.
41. Buchanan TM, Hook EW. Tularemia. In: Petersdorff RG, Adams RD, Braunwald E, Isselbacher KJ, Martin JB, Wilson JD, eds. Harrison's principles of internal medicine. New York: McGraw Hill, 1983;977-979.
42. Ferguson LC. Anthrax. In: Leman AD, ed. Diseases of swine. Ames: lowa State University Press, 1981;396-400.
43. Genus bacillus. In: Scanlan CM. Introduction to veterinary bacteriology. Ames: lowa State University Press, 1988;126-129.
44. Sterne M. Anthrax island. Nature 1982;295:362. Letter.
45. Turnbull PCB, Bell RHV, Saigawa K, et al. Anthrax in wildlife in the Luangwa Valley, Zambia, Vet Rec 1991;128:399-403.
46. Fendall NRE, Grounds JG. The incidence and epidemiology of disease in Kenya. J Trop Med Hyg 1965;68:77-83.
47. Okolo MIO. Studies on anthrax in food animals and persons occupationally exposed to the zoonoses in eastern Nigeria. International Journal of Zoology 1983;12:276-282.
48. Sirisanthana T, Navachareon N, Tharavichitkul P, et al.Outbreak of oral-oropharyngeal anthrax: an unusual manifestation of human infection with Bacillus anthracis. Am J Trop Med Hyg 1984;33:144-150.
49. Webber RH. Anthrax in Lake Rukwa Valley, Tanzania: a persistent problem. J Trop Med Hyg 1985;88:327-331.
50. Samad MA, Hoque ME. Anthrax in man and cattle in Bangladesh. J Trop Med Hyg 1986;89:43-45.
51. Doganay M. Human anthrax in Sivas, Turkey. Proceedings of the International Workshop on Anthrax. Salisbury Medical Bulletin 1990;68(suppl):13.
52. MacAdam 1. Putting anthrax into perspective. Zimbabwe Rhodesia Science News 1980;14:38-41.
53. Sterne M. Distribution and economic importance of anthrax. Federation Proceedings 1967;26:1493-1495.
54. Whitford HW. Anthrax. In: Steele JH, ed. CRC handbook in zoonoses. Boca Raton, FL: CRC Press, 1979;31-66.
55. Stein CD. Anthrax. In: Hull TG, ed. Diseases transmitted from animals to man. Springfield, IL: Charles C. Thomas, 1963;82-121.
56. Bernstein BJ. The birth of the U.S. Biological warfare program. Sci Am 1987;256:116-121.
57. Bernstein BJ. Churchill's secret biological weapons. The Bulletin of the Atomic Scientists 1987;Jan/Feb):46-50.
58. Williams P, Wallace D. Unit 731: Japan's secret biological warfare in World War II. New York: The Free Press, 1989.
59. U.S. Congress. Senate. Committee on Governmental Affairs and the Permanent Subcommittee on Investigations. Hearings on global spread of chemical and biological weapons. February 9, 10 and May 2, 17, 1989. Washington, D.C.: U.S. Government Printing Office, 1990, #24-477.
60. Hersh S. Chemical and biological warfare. New York: Bobbs Merrill, 1968;68-101.
61. Stockholm International Peace Research Institute. The problem of chemical and biological warfare. Vol. 2: CB weapons today. New York: Humanities Press, 1973;79-90.
62. Manchee RJ, Broster MG, Melling J, et al. Bacillus anthracis on Gruinard Island. Nature 1981;294:254-255.
63. Brachman PS. Inhalation anthrax. Ann NY Acad Sci 1980;353:83-93.
64. Brachman PS, Kaufman AF, Dalldorf FG. Industrial inhalation anthrax. Bacteriology Review 1966;30:646-659.
65. Nadler E, Windrem R. Deadly contagion. New Republic February 4, 1991;18-20.
66. Frederikse J. None but ourselves. Harare, Zimbabwe: Zimbabwe Publishing House, 1982.
67. Cilliers JK. Counter-insurgency in Rhodesia. London: Croom Helm, 1985.
68. Flower K. Serving secretly; Rhodesia's CIO chief on record. Alberton, South Africa: Galago, 1987.
69. Mackintosh ME, Crozier DE, Guild R, et al. A survey of the risk factors associated with organo-phosphate and carbamate pesticide poisoning. Cent Afr J Med 1978;24:41-44.
70. Laing RO. Relapse in organophosphate poisoning Cent Afr J Med 1979;25:225-226.
71. Epstein P. In southern Africa, brutality and death. Boston Globe December 26, 1987;23. Op-Ed.
72. Brickhill J. The hidden hand (videotape). London, England; Channel 4, November 14, 1991.
73. Brickhill J. Doctors of death. Horizon (Harare) March 1992;14-17.
74. Barss P. Epidemic field investigation as applied to allegations of chemical, biological or toxin warfare. Politics and Life Sciences 1992;11:5-22.
75. Nass M. Can biological, toxin, and chemical warfare be eliminated? Politics and Life Sciences 1992;11:30-32.
76. Willems JL. Difficulties in verifying the use of chemical weapons and the implications: some brief case studies. PSR Quarterly 1991;1:201-206.

©1992 Physicians for Social Responsibility

* MN, at the time of publication, was affiliated with Wing Memorial Hospital, Palmer, Massachusetts and the Department of Internal Medicine, University of Massachusetts Medical School, Worcester, MA USA.

THE LESSON OF STEVEN HATFILL

This is a well researched article which puts the Hatfill story to rest as far as his Rhodesian connections are concerned. It appears that he was afilliated to Special Brach in Rhodesia which in turn worked closely to the Selous Scouts. This story could make a good book or movie.
There are lessons to be learned here and one is the truth comes out in History.
The Lesson of Steven Hatfill

By Simon Cooper, SEED Magazine, May/June 2003

The most lethal forms of life on Earth are contained inside a small, innocuous-looking suite of laboratories at the heart of the United States Army Medical Research Institute of Infectious Diseases complex at Fort Detrick, Maryland. On September 18, 1997, microbiologist Steven Jay Hatfill walked through the gates of the facility which is known by the acronym USAMRIID, to begin work in the Virology Division.

USAMRIID grew from the ashes of an aggressive biowarfare research program run by the US until President Nixon shut it down in 1969. Afterward, the base converted to defense work. USAMRIID is home to a vast collection of nightmare pathogens and organisms—Lassa fever, monkey pox, plague, and various strains of anthrax, including the new AMES strain identified by the army in 1980. The facility is also home to the Ebola and Marburg viruses, the most feared and respected of all USAMRIID’s microscopic horrors. There are no cures and no vaccines for these viruses, whose victims bleed to death. In fact many microbiologists refuse to work with Ebola and Marburg because they are simply too dangerous. At USAMRIID, Ebola and Marburg are imprisoned in a Level Four biosafety environment, a super-secure suite of laboratories accessed through a series of airlocks, security doors, coded entry panels, and decontamination showers. In Level Four—the heart of USAMRIID—scientists wear spacesuits.

Hatfill was approved to begin work at USAMRIID after a two-year sojourn as a federally funded Fellow with the National Institutes of Child Health and Human Development (NICHD). His job was to study filoviruses, the family to which Ebola and Marburg belong. Within a month, he was authorized to access the Level Four pathogens, as well as the Level Three bugs such as anthrax and plague.

Hatfill had not been hired as an official employee of USAMRIID—which would have required a mandatory national agency security check—but as a Special Volunteer, effectively borrowed from the NICHD. His evaluation consisted of an academic review of his research, which prima facie looked both innovative and impressive. On September 2, 1997, after his resume and credentials were reviewed by the National Research Council, Hatfill received a letter from Arthur S. Levine, scientific director of the NICHD, confirming his appointment as a National Institutes of Health adjunct scientist, sponsored and paid for by USAMRIID. Now cleared to begin work at Fort Detrick, Hatfill’s resume went into an NICHD filing cabinet along with the resumes of hundreds of other scientists past and present.

It is almost certain that many of the resumes in those cabinets had been polished to present the best possible image of their owners. There’s nothing unusual about that. All resumes land on the desks of personnel departments with a bit of top-spin. But there’s a world of difference between a lick of polish and what was lurking in Hatfill’s resume.

Between 1995 and 1999, Hatfill prepared and submitted around six versions of his resume for various positions and research grants. Each resume was tailored to suit the audience it was intended for, yet together they painted a consistent portrait. Here, said the resumes, is a successful, brave, and daring man. Here is a soldier, a scientist, and a leader—an innovator with a hint of maverick, a dash of the establishment, and a splash of joie de vivre. But the resumes were not as they seemed; they were documents intended to deceive. Though they had been constructed around a skeleton of truth, they were clothed in a carefully woven concoction of lies, half-truths, and exaggerations. Hatfill’s resumes, his ticket into the NICHD and later, USAMRIID’s Level Four biocontainment labs, were misrepresentations of the man and his achievements. And yet, it appears these lies were not uncovered until Hatfill had already passed through some of America’s most sensitive and dangerous military and biological facilities.

UNITED STATES OF AMERICA
FALL 2001

The atrocity of September 11, 2001, had barely sunk into the national consciousness when another attack was unleashed. A week after more than 3,000 people died in the three plane attacks on the World Trade Center and the Pentagon, three letters were deposited into a mailbox in Trenton, New Jersey. The letters, addressed to The New York Post, NBC, and The National Enquirer all contained powdered anthrax.

On October 2, Robert Stevens, a photo editor at the Enquirer building, died of inhalation anthrax. His was to be the first of five anthrax deaths all linked to a series of letters sent in the wake of 9/11. Two more letters containing anthrax were posted on October 9, addressed to Senators Tom Daschle and Patrick Leahy.

The FBI launched a massive investigation out of its Washington, DC headquarters. One of the first tasks was to analyze the anthrax. Genetic tests revealed that all the letters contained the same AMES strain of anthrax and that at least one sample was weaponized, possibly using a process similar to one developed at Fort Detrick. On January 29, 2002, the FBI wrote to the American Society of Microbiology asking for its membership list The FBI had concluded the motivation for the anthrax attacks was criminal and not ideological. Suddenly eyes turned away from Islam terrorists abroad and toward the homefront.

According to the FBI, the perpetrator had “the technical knowledge and/or expertise to produce a highly refined and deadly product.” The attacker, the Bureau suggested, had worked at USAMRIID sometime in the past, might have worked as a CIA contractor, and could have a connection to the UN’s weapons inspectors. The attacker was probably middle-aged and might be described as stand-offish, likely preferring to “work in isolation as opposed to a group/team setting.”

In February White House spokesperson Ad Fleischer revealed that the FBI had “several suspects” before re-emphasizing: “All indications are that the source of the anthrax is domestic.”

Actually, there were some 30 individuals being scrutinized, but one name was at the top of the list, thanks to a tip about a former USAMRIID researcher. Media and Internet chatter later reported that this researcher had been heard bragging about using anthrax in the former Rhodesia.

There was no arrest, but by March, a name had been leaked. The name belonged to a man who had worked for Science Applications International Corporation (SAIC), a DC-based contractor for both the Pentagon and the CIA. Before that, he’d been a researcher at USAMR1ID.

On June 25, Hatfill signed a consent form allowing the FBI to search his apartment without a warrant. Minutes after he signed, television camera crews and reporters began to swarm into the street outside his home, which was close to the gates of Fort Detrick. Hatfill challenged an FBI agent about the remarkably rapid appearance of the press. “How the hell did they know to get here so fast?” “Sorry,” the agent told him. “Orders from above.”

On July 2, The New York Times columnist Nicholas D. Kristof named a “Mr. Z” as a “biodefense insider who intrigued investigators,” and he criticized the FBI for not pursuing “Mr. Z” more aggressively. The details of Kristof’s Mr. Z appeared to match the FBI’s profiles, as well as what was known of Hatfill.

Indeed, there were remarkable similarities between Hatfill and the suspect described in FBI profiles. Hatfill had worked at USAMRIID researching exotic pathogens; he had later worked for a company that did CIA contract work (including a study on a hypothetical anthrax mail attack); and he had trained as a UN weapons inspector.

In the weeks and months that followed, Hatfill’s life was torn apart by both the FBI and the media, yet no charges were laid. Then on August 22, live on national television, Attorney General John Ashcroft named Hatfill as a “person of interest.” The pressure on Hatfill became intense. Twice the scientist gave anguished news conferences proclaiming his innocence. Near tears at times, he addressed the television cameras stating: “I want to look my fellow Americans in the eye and declare to them, ‘I am not the anthrax killer.’ My life is being destroyed by arrogant government bureaucrats who are peddling groundless innuendo and half information.” Hatfill lashed out at Ashcroft: “In my view, he has broken the ninth commandment: thou shalt not bear false witness.”

Hatfill’s choice of commandment was interesting. Thou shalt not bear false witness. Thou shalt not lie.


FORT BRAGG, GEORGIA
JUNE 1976

Hatfill had made it. He had survived being bawled at by drill sergeants, being marched for miles and miles in full combat gear, the endless inspections, drills, and exercises. He’d been pushed out of planes, pulled up through and over every conceivable type of obstacle, man-made and natural. Finally, he’d made it to Fort Bragg, home of US Special Forces. It was the beginning of a grueling year-long training program; those who succeeded would become members of one of the world’s finest, toughest fighting units. As Hatfill passed through the gates of Fort Bragg, he must have been feeling a multitude of emotions: excitement, apprehension, pride, and maybe, a small but healthy dash of fear. He was 22 years old.

Hatfill was born in St. Louis, Missouri, on October 4, 1953, and attended Mattoon Senior High School in Illinois. He showed a flair for science, which he carried through to college, studying biology at Southwestern University in Winfield, Kansas. Partway through his degree, Hatfill halted his studies to work as a ‘health assistant’ with Methodist missionary Glenn Eschtruth at a mission Eschtruth had operated in Zaire since 1960. Through Eschtruth, Hatfill met the woman who was to become his future wife, Eschtruth’s daughter, Caroline Ruth.

After spending eight months in Zaire, Hatfill returned to Kansas and completed his degree. On June 20, 1975, at the age of 21, Hatfill enlisted in the US Army with his sights set high; he wanted to join the Special Forces. A few weeks later, Private Hatfill graduated with his BA from Southwestern, but he was already a long way from Kansas, on the road toward his Special Forces goal. Over the next year, Hatfill would complete a series of training courses that took him from Airborne school in Fort Banning,
Georgia, to West Germany and back. In the spring of 1976, Hatfill finally made it to Fort Bragg and began the Special Forces Qualification Course, a grueling five-stage selection process that takes at least a year to complete.

But on July 2, 1976, just a few weeks after starting at Fort Bragg, and just over a year after enlisting in the array, Hatfill was discharged from active duty. He spent the rest of his service period languishing, unused by the Army National Guard.

In Hatfill’s army records there is little to see; under “Medals and Citations” there is no Good Conduct Medal. There are no Special Forces tabs that he would automatically have been awarded had he completed the Special Forces course. Without completing that course he could never have “served with the US Army Special Forces” as he later would proudly claim on the resume he submitted to USAMRIID in 1997, which includes the following entry:
6/75—6/77 United States Army.
7th Special Forces Group, JFK Center for Special Warfare.

Further down the resume under the heading “Practical Experience” is the entry:
USMC [United States
Marine Corps] Officer Candidate Program... served with US Army Special Forces
after college graduation where my commanding officer was Col. Charles Beckworth (sic),
who was later to lead the abortive hostage rescue mission into Iraq (sic).

Hatfill would lie about his military experience throughout, his entire life, creating ever more elaborate accounts as time progressed. In an interview with Richard Preston, author of the internationally acclaimed The Hot Zone, Hatfill, sitting in his office at USAMRIID, claimed not only an army career spanning two decades, but also to have been a captain in the Special Forces.

Two months after his 1976 separation from Fort Bragg, Hatfill married 19-year-old Caroline Rush Eschtruth at the United Methodist Church in Pinnebog, Michigan. It was not to be a happy or a long union. In April 1977, Caroline’s father was killed at his mission during fighting between Zairian and Angolan troops. His death devastated Caroline. Hatfill too was affected deeply and in later years would often bitterly recount his father-in-law’s death.

Following his army discharge, Hatfill returned to his interest in science and, in particular, medicine. In August 1977, Hatfill gained qualification as a medical laboratory technician from the American Society of Clinical Pathology but decided he wanted to be a doctor. By this time, his marriage was under strain, and soon after, Hatfill left the United States.

HARARE, RHODESIA
EARLY MARCH 1979

The war was over—unofficially at least. After a decade and a half of fighting and the loss of more than 40,000 lives, Rhodesia’s civil war was winding down. A ceasefire had been declared. Shops and restaurants began to reopen. People scattered by the conflict picked their way home; foreigners and foreign money returned to the country, which, within a year, would be renamed Zimbabwe.

March is considered the best month in southern Africa. The rains abate and the baking heat of the African summer is still only a distant threat. Temperatures hover around a delightful 75 degrees. It is pristine weather. Weather fit for new beginnings. In March 1979, at the Godfrey Huggins School of Medicine at the University of Rhodesia, students were preparing to enroll for their first year’s study. Their first true year of peace. The university’s main hall was crowded with tables, in front of which dozens of students queued to register. As they stood in line chatting, a loud voice caught their ears, a voice that seemed to defy the hubbub of the hall, cutting through the hundreds of other voices with a forceful, unpleasant tone. Turning to see who the voice belonged to, a student in the line for the medical school saw its source was a short, stocky man with dark hair, a moustache, and dark, dark eyes; the man was corralling various groups of students, telling them where to go and what to do. His swagger and confidence struck the student. He must be a senior professor, or at least a lecturer, he thought.

‘Who’s that shouting the odds?” he asked the student next to him. “He’s an American. Don’t pay any
attention to him,” came the reply.

“Is he a professor?”



There was a snort of laughter. God no. Just some asshole who has too much to say for himself.”

Steven Hatfill would often incite this type of reaction at Godfrey Huggins, where he had enrolled a year earlier. Caroline, who had filed for divorce, remained in the US. Two months into his studies, their divorce came through, marking a year that would only get worse; Hatfill failed the first university barrier exam and was forced to repeat a year.

Many of Hatfill’s freshman class were conscripted war veterans, released early from the armed forces to start their medical training on the proviso they remained available for call-up. There were still pockets of sporadic violence in Rhodesia and, on weekends and vacations, some class members would rejoin their units and go on active duty. A few months after the start of Hatfill’s second try at first-year medical school, a small group of undergraduates were unwinding in a campus bar after a weekend call-up. The beer was cold and cheap, the company good and reassuring. Many were recounting experiences of their last missions—a kind of barroom therapy to smooth out the jitters and fatigue of a conflict that had gone on far too long. As they talked, Hatfill walked into the bar. Immediately, a few in the group grew quiet. Hatfill wandered over to the edge of the conversation. No one acknowledged his presence. Most avoided his gaze. One of the students in the bar recalls what happened next. He, like most of Hatfill’s classmates interviewed for this investigation, has asked for his name to be withheld. (Such has been the fallout of Hatfill’s “person of interest” status that former classmates have been placed under suspicion by colleagues and employers merely because they happened to go to school with him.) “We were fairly jovial, but then Steve walked into the bar. He butted in with a story of an experience he said he’d had as a pilot in Vietnam. The conversation stopped dead. A few of the guys even walked out. Everybody turned toward him. There was a real sense of animosity— some people were bristling.” “I did quick mathematics and said, ‘There’s no way, Steve. The Vietnam War ended in ‘74 and the Americans pulled out in ‘72. There’s no way you could have been there, When did you start your training—when you were 16?’” There were a couple of snickers from the group. Hatfill said nothing, turned on his heel, and left.

A classmate of Hatfill’s remembers a clever, energetic man hampered by an apparently overwhelming desire to impress at any cost. “‘That was the thing about Steve. He was an extraordinary guy and very, very bright. But he was also a real Walter Mitty kind of character, and he would tell these enormous, awful lies. He once told me his wife had died in the Congo.” “And when he told a lie like that, you were never certain if he was telling a lie to see what he could get out of it, or if he was telling a lie to see how far he could go with it, to see how gullible you were. If I ever caught him in a lie he’d just sort of wink at me and give me a nudge, as if to say ‘you caught me on that one.’”

Hatfill’s antics divided his class into two camps: those who could tolerate him and those who could not. In one incident, a few classmates were pulling late-night duty in one of Harare’s teaching hospitals. ‘We were sitting, chatting in the lounge when Hatfill walked in. Probably three quarters of the students got up and walked out,” says a classmate who was there that night. Hatfill became isolated from the rest of his year. Yet, outwardly, he seemed unaffected by his rejection. Indeed, he would go out of his way to engage, amuse, and entertain his fellow students. “He could be absolutely hilarious,” says one classmate. “I’ve seen him bring large groups of students to their knees with his antics. His speciality was to stick a small flashlight up his nose, turn off the lights in a ward, and then ‘fly’ around the ward turning the flashlight on and off to simulate an aircraft’s landing lights.”

Meanwhile, outside of medical school, Hatfill was still chasing after lost military ambitions. Sometime after arriving in Rhodesia, Hatfill turned up at the door of the Rhodesian police’s Special Branch— their equivalent of the FBI—and offered his services. At the time, the Special Branch was a part of the Selous Scouts, an elite Rhodesian Special Forces counterinsurgency unit, which spent much of its time behind enemy lines. The Scouts were an amalgam of Army Special Forces soldiers and Special Branch police officers. Intelligence was vital to Scouts operations and the mainly black officers of Special Branch undertook this function. Hatfill was 24 at the time, still an undergraduate, and struggling at medical school. He had little to offer Special Branch, other than a willingness to help. He was referred on to the medics of the Scouts and was dispatched as a volunteer junior medic to a field hospital at a base called Fort Bindura. There, he bandaged wounded guerilla fighters and acted as an assistant of sorts for the true Scouts medics. By the time 1980 arrived, the war was over, the Scouts disbanded, and Hatfill’s brief, tangential association with them ended.

Yet, in Hatfill’s mind, his Rhodesian military “service” was somewhat more grandiose. He claimed to have been a “badged” member of the Scouts and to have worked behind enemy lines. Those lies were manifested into two certificates seized by the FBI during their anthrax investigation; one purporting to show his graduation from a Scouts tracking course, the other a citation for good conduct. Both bore the forged signatures of genuine Scouts officers. A number of Hatfill’s resumes go on to claim that while in Rhodesia he served with the Rhodesian SAS. His 1997 resume elaborates, claiming he had seen “active combat experience with C Squadron Special Air Service (Rhodesia).” The regimental association of the Rhodesian SAS is adamant Hatfill never belonged to the unit. In a terse e-mail, their spokesman states, “Hatfill is not an ex-member of this unit; he was never attached to the unit in any way. If has also made claims that he was a member of an American unit giving ‘assistance’ to C Squadron. This is also untrue.”

Following the “person of interest” furor, Hatfill was accused in a number of media stories of being a protégé of Robert Symington, an anatomy professor at the University of Rhodesia’s medical school, rumoured to have been the head of an alleged secret Rhodesian biowarfare program. “Prof,” as Symington was known, was a polarizing figure on the university campus, which, despite its heritage, was solidly liberal. Silver-haired with piercing blue eyes, Symington was an unapologetic old-style Rhodesian. A student who considers himself a protégé of Symington’s recalled the following incident. “Prof had seen me talking to Steve Hatfill and invited me for a walk,” he stated. “ told me in no uncertain terms that Steve was a frigging idiot and it wasn’t going to do anyone any good, particularly me, if I became a friend of his. It seems very unlikely to me that
Steve was involved with Bob Symington—unless Bob had gone out of his way to lie to me, which wasn’t his way. He never minced words about anything.”

Symington died in 1982 while swimming in the pool at the University of Cape Town. To date, no concrete evidence has been produced proving his involvement in a Rhodesian biowarfare program. Or that a biowarfare program even existed.

UNIVERSITY OF ZIMBABWE, HARARE
NOVEMBER 11, 1983

Hatfill’s class crowded around a locked, glass-fronted wooden cabinet near the main campus halt to see the final exam results of four years of hard work. After seeing their grades, they repaired to the hall to start celebrating or commiserating. Suddenly, amid the celebrations, the sound of violent shouting and breaking glass could be heard from the hail, The students ran out to find Hatfill, his face painted with rage, fuming in front of the cabinet. Behind the shattered glass were the results indicating Hatfill’s failure. As the students looked on, a campus security guard arrived and tried to stop Hatfill from leaving the scene, but in a fit of rage, Hatfill resisted, and threw the guard into a plate glass window. The incident nearly got Hatfill arrested and thrown out of university. but he was allowed to stay on for an extra six months to re-sit his exams, and passed in 1984. By then Hatfill’s classmates had already moved on to start their careers. For many, the incident was the last they would hear of him until 2002, when, as part of the anthrax coverage, tales of his alleged African of exploits would be reported in newspaper of and television broadcasts worldwide.

QUEEN MAUD ISLAND, ANTARCTICA
DECEMBER, 1986

Hatfill stepped off the boat that had carried him south from Africa onto the desolate, frozen expanse of Antarctica. The voyage was the beginning of a phase in Hatfill’s life in which he would pursue a dream job: a position with NASA. In the autumn of 1986, Hatfill was chosen to participate in the South African National Antarctic Expedition (SANAE). and by December, was destined for a 14-month tour of duty at South Africa’s isolated base in Queen Maude Land, one of the most hostile environments on the planet. It was a perfect starting point for a would-be space scientist who, only a year earlier, had completed a 12-month internship at a small rural hospital in South Africa’s North-West Province.

In 1985, he’d registered as a medical practitioner with the South African Medical and Dental Council. His certificate to practice cited his Bachelor of Medicine qualification as M ChB (Zimbabwe) 1984. And in July 1986, Hatfill also successfully completed the process of having his medical degree recognized in the US. But mere doctoring was a million miles from Hatfill’s mind. He was headed for the stars. When the SANAE post turned up he on his resumes some ten years later, he variously records himself as the expedition’s “Research Team Leader,” “Assistant Research Team Leader,” “Science Leader and Physician,” or simply “Team Physician.” But Richard Skinner, a director of SANAE, stated Hatfill’s position had been as an “expedition doctor only.” Hatfill’s resume also claims that while at SANAE he conducted “research on pineal hypothalamic dysfunction for NASA’s Solar System Exploration Division. At the time, Mike Duke was the chief of the division, headquartered at Johnson Space Center in Houston, Texas. Duke, a geologist now retired from NASA, recounts his contact with Hatfill. “From what I remember I got a letter from him telling me about his experiences in the Antarctic. He was interested in applying his experiences in that environment to isolation in space. He then sent me a paper, which as far as I could see was part of a strategy of his for getting a job with NASA. I passed it on to the medical section people at NASA and my recollection is they didn’t do anything with it.” A year later Duke received another unsolicited paper from Hatfill. Again, Duke sent the paper along to his medical colleagues. According to Duke, “the result was that nobody paid much attention to it.”

STELLENBOSCH, SOUTH AFRICA
LATE 1988

Professor Lothar Bohm was impressed. His new student—a Dr. Steven Jay Hatfill—was proving to be quite a catch. Hatfill had thawed out from his Antarctic expedition and had completed a microbiology master’s degree at the University of Cape Town. While socializing at the UCT campus club, Hatfill met Bohm—then director of the Stellenbosch University’s radiobiology laboratory. The two discussed a second master’s this time under Bohm’s tutelage. A master’s in medical biochemistry and radiation biology would be an excellent stepping stone for Hatfill’s journey to NASA.

Bohm would later recall Hatfill as an “intellectually quick” researcher who had devised what Bohm describes as “a brilliant, brilliant concept.” Hatfill proposed that by metabolizing thalidomide with a special enzymal extract known as S-9, the drug could be used to restore leukemic cells back to normal function; it looked like a significant new treatment for leukemia. Bohm was impressed with Hatfill’s theory and requisitioned the S-9, at some expense to his laboratory.

Because of funding shortages, Hatfill’s time at Stellenbosch was not fully covered. As a result, he took a job in the university’s hematology laboratory as a clinical assistant, and this position paid his way through school.

Hatfill’s research results were impressive, Bohm says. “Because of his job, he ended up working not in my lab, but mostly in hematology He was very mature and talked with so much confidence. When he brought you data it looked right and you trusted the guy. He was very convincing and he gave these superb seminars.” Hatfill’s thesis, “Thalidomide Induction of Differentiation and Potentiation of Radiation Induced Apoptosis in Human K562 Cells,” won him his second master’s in December 1990. He immediately began a three-year hematological pathology residency at Stellenbosch and in 1992 he began to work on his PhD under the supervision of Professor Ralph Kirby at Rhodes University.

Hatfill’s resume records that in 1991, after starting his hematology residence he “established” and then “managed” or was “director” or “laboratory chief” of a “Molecular Haematology Laboratory” at the Tygerberg Hospital, which is part of the Stellenbosch medical campus. In fact, no formal molecular hematology lab was ever established at Tygerberg.

Erna Mansvelt, current director of hematology at Tygerberg. states, “Dr. Hatfill was a registrar (postgraduate student) in this department until the end of 1993. I am not aware that he had a recognized molecular laboratory in our department at that time. He did not have any official administrative duties in the department.” Interviews with numerous scientists and officials familiar with Hatfill’s work at Tygerberg confirm this statement. One such official adds, “Molecular research was performed as and when a particular individual displayed such an interest and ceased as soon as Hatfill departed in 1993. He could hardly regard himself as a director as there was nothing other than his own research project to direct. There were certainly a number of people in the academic department at the time who would have been more eligible than he for the status of ‘director,’ but such a designation simply did nor exist.”

During the same period between 1990 and 1993, Hatfill also claims to have performed “clinical rotations” at the hematology-oncology and bone marrow transplantation unit at Groote Schuur Hospital, which also acts as part of the Stellenbosch medical campus. Hospital records show that after registrar posts at Groote Schuur were advertised in October 1992, Hatfill applied for and was awarded one of them. But in January 1993, he wrote on Stellenbosch University letterhead to inform Groote Schuur that he would be unable to take up the post, citing that his research was “at a critical stage.” Subsequent checks confirm that Hatfill is not on record as being “on the staff establishment of Groote Schuur Hospital.”

Hatfill’s resume also has him working as an “Emergency Medical Officer at Conradie General Hospital, RSA.” Again, there is no record of him working there. Interviews were conducted with staff who worked there in the early 1990s. “No one remembers Hatfill,” reports an employee.

According to his resume, 1993 was an extremely busy year. In addition to completing his hematological pathology board certification, Hatfill also claims to have been chairman of a South African scientific organization, the Experimental Biology Group (EBG) and a member of the Blood Transfusion Utilization Committee at Tygerberg. Checks with current and former members of the ESG have failed to find any record of Hatfill’s chairmanship. Moreover, Tygerberg’s Blood Transfusion Committee has no records of Hatfill’s involvement. Hatfill also claims to have been a member of an AIDS advisory panel organized through the Council for Scientific Industrial Research (CSIR) on AIDS in 1994. CSIR never convened an AIDS advisory panel.

Hatfill’s penchant for the military also managed to bleed its way into the sections of his resume dealing with South Africa. Hatfill claims to have been assigned to the “2nd Medical Battalion (TA Reserve)” of the South African Defense Force during his time in South Africa. But Lieutenant Colonel Louis Kirstein, spokesperson for the South African Department for Defense states the following; ‘We have no records of a Dr. Steven Jay Hatfill on our system.”

In most of his resumes Hatfill also describes himself as a “consultant flight surgeon to 32 Squadron [changed in later resumes to 30 Squadron] Air/Sea rescue unit based at Yesterplatt (sic) Air Force Base, Cape Town.” Apart from the incorrect spelling of Ysterplaat, the main problem with this entry is that there are no such Squadrons. Ysterplaat is home to two air and sea rescue squadrons: 22 Squadron and 35 Squadron. Ysterplaat’s commanding officer Lieutenant Colonel Harry Treurnich can remember “no one of that name having served at the base.”

Hatfill attended two medical courses while in South Africa; one at the Institute of Aviation Medicine, the other at the Institute of Maritime Medicine. Both courses were only two-week certification courses, but Hatfill claims they were, respectively, eight and five weeks long, and records them under a section marked “Postgraduate Diplomas.” Neither course is considered a postgraduate qualification. While at the Maritime Institute, Hatfill claims to have gained qualification in hyperbaric medicine. Hyperbaric medicine is not part of the course he completed.

On Friday September 17, 1993, Lothar Bohm was fuming. There were major problems with Hatfill’s master’s thesis experiments. Other researchers could not reproduce the results. Also, other scientists at the laboratory were finding it impossible to extract DNA markers using a special “melting” technique Hatfill claimed to have used.

Bohm, who had coauthored a research paper with Hatfill based on the thesis work, sat down at his computer and hammered out the following e-mail to Kirby, Hatfill’s PhD supervisor and coauthor of another paper based on Hatfill’s work that had been published in the prestigious medical journal The Lancet.

Dear Ralph, 2 problems here:
We are rather disappointed if not to say PISSED OFF with so much ignorance,
carelessness and indifference. 9 months of time plus 4000 odd Rand wasted. You
are both DEEP in our memory.

A Japanese worker has
problems in reproducing the Thalidomide work on K 562. After some
correspondence relating to buffers and drug metabolism using S-9 fraction he
still cannot do it. When I discussed the problem with Steven it became clear
that he could not have done the experiment as his handling of the S-9 fraction
indicated total confusion.



Taking these observations and
the wonderful TGE melt mitochondrial DNA referred to in the Lancet paper it
also transpires that the experiment could not have been done by S. because
essential parts of the TGE machine accessories were still unopened. It goes to
show that S takes great liberties with the truth.



I think you may wish to be on
guard when you assess his PhD thesis not to risk a scandal. I can only pray
that the Japanese worker is not going to blow the whistle— but with increasing
interest in Thalidomide somebody else might. I find it utterly distasteful and
unprofessional to practice science in this way and I am reassessing my position
regarding S. and asking you again for advice.



Lothar Bohm





According to Bohm, Kirby never replied to this e-mail. Nor did Kirby reply to an e-mail from SEED about his communication from Bohm.

When a technician came to examine the TCE machine, he found the electrodes used to facilitate the DNA extraction wired the wrong way round. “The machine could never have worked,” stated a source at Stellenbosch, who witnessed the technician’s examination.

Bohm says he now regrets allowing Hatfill to do much of his research in the hematology lab where he was earning a living as a clinical assistant. “He had a job there and he wanted to work there and at he time that was fine by me. But in hindsight it would have been better to have him in [my] lab and see what he was doing. There is no doubt about it—the guy was extremely capable. But time seems to have a different meaning for him than to a normal person. He was always very fast intellectually and always racing ahead. Had he worked in my lab, the whole thing would probably have taken a different course.”

OXFORD, ENGLAND
SEPTEMBER 1994

It wasn’t quite Cape Canaveral, but Oxford in University was still a pretty big feather to have in his cap. Hatfill had left South Africa in to take up a new job as a clinical research scientist at the University’s Nuffield to Department of Pathology and Bacteriology based at the John Radcliffe Hospital. Hatfill worked in the cancer research lab.

In a resume prepared while at Oxford, Hatfill claimed that he was a “licentiate” of the “Royal College of Physicians and Surgeons, Edinburgh.” Three of his later application forms for NIH grants state Hatfill gained his MD at “Edinburgh, UK” in 1984. There is no such thing as the Royal College of Physicians and Surgeons, Edinburgh. And Hatfill does not have a UK medical degree. Scotland has three distinct medical colleges: the Royal College of Surgeons, Edinburgh, the Royal College of Physicians of Edinburgh, and the Royal College of Physicians and Surgeons of Glasgow. In the early 80’s, medical degrees from Rhodesia, like the one Hatfill was carrying, were not accepted in the UK. The University of Zimbabwe therefore made an arrangement with the Scottish colleges to let its graduates sit what was known as “The Scottish Triple,” an exam set by all three colleges. Zimbabwean graduates who passed the Triple were allowed to practice medicine in the UK.

Fiona Sinclair, membership administrator for the Royal College of Surgeons, Edinburgh, states, “A full search of our records has been conducted, both in Edinburgh and in Glasgow and there is no record of Dr. Steven Jay Hatfill having obtained any college qualification. We have no records of Dr. Hatfill at all.”

While at Oxford, Hatfill also claimed to have been elected a Fellow of the Royal Society of Medicine. Society spokesperson Rosamund Snow says that, “as far as we can tell, he has never had any association whatsoever with the society.”

In January 1995, Hatfill’s PhD was submitted for examination to Rhodes University. Bohm’s warning had, apparently gone unheard or unnoticed.

Hatfill was already applying for other jobs by the summer of 1995. He responded to an advertisement for a fellowship position placed by the NICHD in the journal Science.

The NICHD personnel charged with reviewing Hatfill’s application called Oxford University, where the NICHD say they received confirmation that Hatfill “had experience qualifying him for the position he was applying for.”

The resume accompanying Hatfill’s application claimed not only the “licentiate” Edinburgh medical qualification but, crucially, also a PhD apparently awarded by Rhodes University in 1994. Despite the fact that back in South Africa examiners were still three months from giving their decision on the PhD, Hatfill’s resume was titled “Dr. Steven Jay Hatfill M.D/Ph.D.”

Also submitted was a bundle of certificates including a PhD certificate apparently issued by Rhodes on April 16, 1994. Hatfill’s resume details the “PhD Degree in Molecular Cell Biology” but gives a contradictory date of August 1994. In fact, Hatfill’s PhD thesis was failed in November 1995. One of Hatfill’s thesis examiners—interviewed on condition of anonymity—describes his thesis as “an embarrassment to South African science,” adding, “more than once the question was asked of aspects of the thesis whether Hatfill had made a mistake, or whether he was deliberately trying to deceive?’

Hatfill also enclosed a letter of recommendation bearing the signature of his head of department at Oxford, J O’D McGee. The letter was fulsome in its praise for Hatfill. “Steven is a very valuable member of the Cancer Metastasis Laboratory” the letter reads. “He is a good molecular biologist with a good knowledge of most of the technology in this area and even more important, he can apply it to real problems.”

The letter stated McGee had gotten to know Hatfill “very well” and concludes, “As a person, he is popular, self-sufficient, and can step into any ‘crisis’ situation and deal with it effectively without demonstrating anger or any other emotion. He is also a man with a sense of driving the research team forward in a united way. I have the highest regard for Dr
Hatfill and unreservedly recommend him to you.”

When shown the letter in question, McGee stated he had no recollection of providing the reference, adding the letter was “not in the style” in which he would write a reference for a member of staff. He added he never had direct contact with Hatfill, other than one meeting where Hatfill asked him to be “a referee for him for a NASA program.”

Hatfill also submitted a letter of reference purportedly from a Tygerberg professor repeating the claim that Hatfill had established a molecular hematology laboratory there. Officials at Tygerberg dispute its authenticity.

In addition Hatfill included a certificate proving his graduation from medical school. But the certificate Hatfill present ed was issued by the “University of Rhodesia.” By the time Hatfill was recorded as graduating in 1984, Rhodesia hadn’t existed for four years. The university had changed its name to the University of Zimbabwe, and stopped issuing University of Rhodesia certificates in 1982. Those who graduated in 1983 —Hatfill’s intended year of graduation—received certificates issued by the University of Zimbabwe.

Apparently, the NICHD never picked up these discrepancies. On September 18, 1995. Hatfill was granted an Intramural Research Training Award, a fellowship that would mark the start of a four association with the US government.

SEPTEMBER 18, 1997
FORT DETRICK, MRRYLAND

The most lethal forms of life on earth are contained inside a small, innocuous-looking suite of laboratories at the heart of the United States Army Medical Research Institute of Infectious Diseases complex at Fort Detrick. Access to these Level Four labs is severely restricted. Those who are granted entry are exposed not only to the mast dangerous organisms on the planer, but also to classified information. The work USAMRIID researchers undertake could conceivably be perverted for offensive biowarfare use. The knowledge they possess is as dangerous as the pathogens they manipulate. USAMRIID should be one of the most secure locations on the face of the Earth.

After two years at NICHD, Hatfill applied to the NRC for a transfer to USAMRIID’s Level Four labs to study Ebola and Marburg viruses. His career was once again subjected to a scientific review and within a month, Hatfill was granted Level Four clearance. He was also granted clearance to access material classified as “secret.” He would spend the next two years in Level Four battling microscopic nightmares. He loved it.

In 1999, Hatfill’s research funding ended, but he traveled onward and upward to a prestigious job as a biodefense consultant with Science Applications International Corporation (SAIC), a contractor for both the Pentagon and the CIA. It was a job that gave Hatfill access to all sorts of interesting places—the FBI, CIA, and the Department of Defense.

In December 2000, after being accepted into the UNMOVIC weapons inspections training program—a process that required he submit a resume and sit for an interview—Hatfill was sent to Paris to begin basic training. While there, he boasted of his military experience to bemused fellow attendees and claimed he had access to classified documents.

In late summer 2001, Hatfill applied for a CIA contract requiring a high-level security clearance. He had to undergo a rigorous background check. When investigators questioned him about his time in Africa, the house of cards started to topple. On August 23, the secret clearance he had obtained at USAMRIID was suspended and he was removed from his full-time job at SAIC, sidelined as a “consultant.”

Still, he kept up with his UN training and in November 2001 returned to England, this time to Porton Down, home of the UK’s former chemical and biological warfare research program. By now, news of the anthrax letters was gripping the biodefensc community, Hatfill was quick to insist that Iraq was behind the attacks. What he didn’t know was that at home, the Bureau was closing in on him as a “person of interest.”

On March 4, 2002, Hatfill was fired by SAIC. On July 1, just a few days after his name was first publicized in connection with the anthrax investigation, Hatfill was hired as the associate director of Louisiana State University’s Center for Biomedical Research and Training. The money for the post, like the majority of the center’s funding, came from the federal government. On August 1, the Department of Justice sent an e-mail to the center’s director, Stephen I Gulliot, ordering him to “cease and desist” employing Hatfill. Hatfill was put on administrative leave the following day and fired from the $150,000-a-year job on September 3. Gulliot was fired a day later.

Hatfill was a month from his forty-ninth birthday when LSU fired him, and the career he’d manufactured for himself in numerous resumes was finally over. Maybe after so many years of misrepresentation, he was unable to tell what was real in his past and what had been falsified. Or maybe this was the first time his credentials were fully scrutinized.

Here is what a complete investigation uncovers: Hatfill never served with the US Special Forces, or the Rhodesian SAS. He was not a member of the Selous Scouts. The South African Department of Defense has no records of Hatfill serving in the 2nd Medical Battalion (TA Reserve) or with the Air/Sea Rescue Squadron at Ysterplaat. There is no record of Hatfill having been a casualty officer at Conradie Hospital, or working clinical rotations at Groote Schuur’s hospital. He could never have established or managed a molecular hematology laboratory at Tygerberg because there was and is no such laboratory. While in Antarctica, Hatfill was not a research team leader or even assistant research team leader. He hadn’t been commissioned to do research for NASA; he was not chairman of the Experimental Biology Group; nor was he a member of Tygerberg Blood Utilization Committee; and he couldn’t have sat on the Council for Scientific Industrial Research’s advisory panel on AIDS, because such a panel was never convened. He wasn’t a Fellow of the Royal Society of Medicine. His Edinburgh “licentiate” medical degree is nonexistent. The “University of Rhodesia” degree certificate he presented had stopped being issued two years before he graduated. His PhD is a false and there are serious questions about his previous master’s research at Stellenbosch.

Any or all of these lies and half truths should have been picked up when he was first evaluated for his job at the NICHD and then again when he applied to USAMRIID. Apparently, none of them were.

Ray Gamble is the director of the NRC awards program that vetted Hatfill for his research position at USAMRIID. The NRC is a nonprofit organization that sits between sponsors—usually federal government agencies—and researchers, Gamble admits the system is not foolproof, but says its methods are the norm in most grant review processes. Gamble explains, “We provide advice on the best quality of applicant for the awards. Our contribution is that quality review, so that the sponsors know that they are going to get the best quality people out of this process.”

But the process assumes candidates are telling the truth. “You assume that the facts stated by the applicant are in fact correct and without seeing things that seem to indicate otherwise that’s the assumption that’s made,” adds Gamble. He stresses that in addition to resumes and reviews, sealed transcripts are required to be sent directly from the applicant’s university. But he admits, “We do not individually call a thousand or so universities every time we receive an application to verify a particular document.”

It was this process that apparently failed to flag Hatfill or his falsified resumes and forged documents during the four years he spent inside the federal grants system, moving seamlessly from health to defense. At least four top officials within the federal grants system signed their names to approve grant applications on Hatfill’s behalf three times Over three consecutive years: Leonid Margolis, head of the NICHD laboratory Hatfill worked at for two years; Joshua Zimmerman, laboratory chief, NICHD; Arthur S. Levine, scientific director of the NICHD and Ruth E Mariano, the grants bid official at the NICHD. Their signatures released tens of thousands of dollars to Hatfill and allowed him access to some of the best research facilities and information in the world. Margolis and Levine also signed off on two further years of grant applications that gave Hatfill access to the USAMRIID facilities.

No one from the NIH or NICHD was prepared to be interviewed for this story. An NICHD spokesman said staff had “declined to be interviewed about Steven Hatfill’s employment at NIH.” They were, he said, “not interested in commenting about this matter.” Likewise, “Dr. Margolis does not want to be interviewed regarding Steven Hatfill.”

What about the senior officers and scientists of USAMRIID? One of the most sensitive research establishments on the planet, where Hatfill picked up “secret” level security clearance on his way to the Level Four biocontainment labs? As far as USAMRIID was concerned, the NRC had screened and passed Hatfill, and NRC says security checks are beyond their responsibility: ‘It’s a local issue,” says Gamble. “Every federal research institute has their own form of security clearance, and we can’t become involved in that because it would become too complex. It’s outside our area of responsibility.”

USAMRIID refused to respond to questions regarding Hatfill, other than to confirm his position in the Virology Division and to stress that “he did not work with anthrax” there. Hatfill also refused to comment on this investigation. But his spokesman and friend, Pat Clawson, issued a statement on his behalf:

“Dr. Steven Hatfill is not the anthrax mailer. He is a scientist and physician who has devoted his career to preserving life, not destroying it.”

The statement later continues;

“Legal considerations prevent Dr. Hatfill from responding to specific issues about his personal background and professional credentials, but the real questions the press and public should be asking are: Who perpetrated the anthrax attacks that terrorized the nation? Why is the government’s 18-month, multimillion-dollar investigation at a dead end? Why has the government conducted a public campaign to destroy the life of an innocent American patriot without having any credible evidence against him?”

In 2001, the US government spent $60 million on biodefense projects. In 2003 that figure will grow to $2 billion. Many more labs—both military and civilian—will be working with lethal pathogen, if President Bush fulfills his State of the Union promise to spend an additional $6 billion developing and stock piling biodefense vaccines.

More scientists will soon have access to anthrax, plague, monkey pox, Ebola, Marburg, and smallpox as the government’s biodefense offensive swings into action. Many of those researchers will be vetted by the same government system that vetted Hatfill.

Twice in April 2002, anthrax spores escaped from the Level Three labs of USAMRIID. USAMRIID has refused to release its report into these incidents. On February 12 this year The Los Angeles Times published a story examining USAMRIID’s safety record. The facility commander, Colonel Erik Henchal, was interviewed. He said that screening by the NRC for positions at USAMRIID was now “more stringent.” The next sentence, however, ran as follows:

But Ray Gamble, director of the council program that sponsored Hatfill, said there had been no substantive changes in how applications are reviewed. “It a scientific review that hasn’t changed in hundreds of years. It’s based on the technical proposal, the scientific merit. There are always opportunities for people to misrepresent themselves”

To date Steven Jay Hatfill remains unemployed. He now spends most of his time shut inside his girlfriend’s apartment. The frenzy of press stories about him has died. The FBI has made no public comment on the progress of the anthrax investigation in months. And no government department or agency involved in the anthrax investigation has offered any evidence of Hatfill’s guilt.