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It grows and spreads slowly in humans, too, and significant studies were only possible after it was found that armadillos are easily infected and can be used to grow large amounts of the bacteria.

I think this puts the cart before the horse: if I remember the sequence of events correctly, some armadillos were discovered to be carriers for leprosy bacteria, from which it was found that armadillos are easily infected.

To my ear, the story makes it sound more like that we went looking for an animal that was easy to infect and found the armadillo was ideal.

I did a Google search, and here is an article that seems to accord pretty much with what I remember reading before about this odd story:

Armadillo-leprosy controversy

Attachment 5

Go to armadillo-leprosy controversy home page
This material is located on Brian Martin's website on suppression of dissent

NEGLECT OF A ZOONOSIS

OVERVIEW. Discovery of leprosy in wild armadillos was one of the most bizarre and fateful coincidences in the history of medicine. For almost a century, scientists had searched vainly for an animal model in which they could grow leprosy bacilli. Storrs, a newcomer to the field, succeeded spectacularly, but unknown to anyone, hundreds of thousands of armadillos surrounding her laboratory were already infected. This came as a great cultural shock. For millennia, theologians had preached that leprosy was unique to humans, visited on them by God in punishment for sin. It was unthinkable to some that this divine scourge could afflict an animal. This second discovery by Storrs destroyed that old myth and also destroyed her program. Her finding opened up a vast natural laboratory in which the epidemiology and transmission of leprosy could be studied on an unprecedented scale. Instead of seizing this golden opportunity, USPHS embarked on a witch hunt to destroy Storrs program by accusing her of starting the zoonosis. They began a trumped-up search for leprosy in wild armadillos in 1974, but would not admit that it actually existed until 1986. They succeeded in destroying Storrs program, but in doing so destroyed the hopes of humankind for a leprosy-free world.
DISCOVERY

In December of 1972, an animal technician at Gulf South Research Institute (GSRI) reported an infected armadillo in an outdoor breeding colony to Dr. Eleanor Storrs. After a thorough examination, she concluded it had leprosy or a leprosy-like disease. This was confirmed by Lawrence L. Swan, a consulting pathologist with experience in leprosy. Dr. Chapman H. Binford also confirmed the diagnosis. Storrs was convinced the animal had acquired leprosy in the wild because it had not been inoculated with leprosy bacilli or housed near infected animals.
Her conviction was powerfully reinforced by an earlier report by Kirchheimer & Sanchez (1972). These authors had inoculated each of 16 newly captured animals at a single site on the abdomen with 1 x 10⁷ bacilli of human origin on 3 December, 1971. Four months later, a female developed two nodules teeming with acid-fast bacilli at uninoculated sites on the abdomen. Their report did not appear to make sense: the incubation period was too short and the nodules erupted far from the inoculation site. Storrs believed that the Carville animal must have been infected long before capture.
Evidence that armadillos could be infected through superficial wounds heightened her conviction. In June of 1970, she had lightly abraded the ear of an animal and topically applied a dilute suspension of M. leprae from mouse footpads. No external symptoms of leprosy developed, but in July of 1973 it was found dead (Storrs et al. 1973). On autopsy, it yielded 121 g of subcutaneous lepromas showing that armadillos could easily develop systemic infection through minor skin lacerations.
In late 1973, a second animal with nodular lesions was found in the GSRI breeding colony. Sohan Issar, GSRI pathologist, performed the autopsy. Later he was dismissed for unrelated reasons. Before leaving GSRI, he surreptitiously took slides of tissues from this animal to Carville to show to R. C. Hastings, P. W. Brand, and Kirchheimer (Issar 1976). In 1974, he took them to the annual meeting of the U. S. Leprosy Panel where he showed them to O. K. Skinsnes, Editor of International Journal of Leprosy (IJL).
Late in 1974, the GSRI group began to look for signs of infection in newly captured animals. In April of 1975, Binford was sent tissues from an armadillo which had been in captivity for only one week. He had been skeptical about the occurrence of leprosy in the wild up until then, but ten days later he telephoned to agree that the disease must have been naturally acquired and resembled human leprosy. Within a few months, GSRI had collected a sufficient number of infected animals from the wild to prove the existence of a leprosy-like disease.
Binford urged GSRI to collect as many pregnant females as possible so that future inoculations would be made on animals born in captivity. This, he believed, would minimize chances of contaminating M. leprae harvests with the then unidentified bacillus. This was a key recommendation since it ended the inoculation of wild-caught adults at GSRI.
Discovery of sylvan leprosy came at a difficult time. WHO had already announced an international program to develop a vaccine for prevention of leprosy based on armadillo-derived bacilli (Anon. 1975). Discovery of a leprosy-like disease in wild armadillos would throw their program into turmoil. Although the disease in wild armadillos looked like human leprosy, GSRI had no proof that it was human leprosy. To find out if the two diseases were identical would require lepromin testing by laboratories in Africa, South America, or Asia.
It seemed premature to announce the GSRI discovery to the scientific community without lepromin testing, but there was no alternative. GSRI could not let WHO proceed with an ambitious immunology program based on armadillo-derived bacilli without warning them of possible contamination.
A meeting of the Joint U.S.-Japan Leprosy Panels was scheduled for October of 1975. WHO representatives would attend. Therefore, Dr. Gerald P. Walsh of GSRI informed WHO delegates and others involved in the program, about the new findings. As feared, his announcement caused consternation. Charles C. Shepard, Chairman of the U.S. Leprosy Panel, formed an ad hoc committee to investigate the problem. At the meeting, R. R. Jacobson of Carville asked Walsh if inoculated armadillos had ever escaped from GSRI. A month later, Tore Godal of WHO wrote to Walsh asking the same question. These were the first indications that GSRI was going to be blamed for starting the zoonosis.
In December 1975, GSRI and Armed Forces Institute of Pathology (AFIP) published a note describing findings on seven newly captured animals with leprosy-like lesions (Walsh et al. 1975). Early publication was expedited by the editor of Journal of the Reticuloendothelial Society in a futile attempt to quell rumors about the origin of the infection. The note described a leprosy-like disease, but made no claim that the disease was human leprosy.
ACCUSATIONS

In February of 1976, Kirchheimer (1976a) published a note in LSM claiming that he had examined 138 wild armadillos without finding evidence of leprosy. On 27 February, the editor of Public Health Reports received a manuscript from Kirchheimer & Sanchez (1976a) in which they reported 141 leprosy-free animals. On 15 March, the editor of LSM received a communication from Kirchheimer (1976b) claiming 233 negative animals. In this report he also revealed that Carville staff had known since November 1973 that "an unexplained mycobacteriosis had occurred in a supposedly experimentally uninfected animal in the outdoor colony of GSRI, and that the mycobacteria were not identified." It was, of course, the animal autopsied by Issar (1976) who had shown slides from it to the Carville staff and later to the editor of IJL. Kirchheimer (1976b) concluded that
it seems evident that GSRI's claims of the existence of a mycobacteriosis and particularly leprosy in feral armadillos must be validated by unannounced trapping, handling and identification carried out only by uninvolved persons.

Shortly thereafter, Skinsnes (1976) published an editorial in IJL suggesting it was not necessary to propose escape of inoculated armadillos to account for leprosy in wild animals. He surmised that disposal of carcasses of experimental armadillos without complete incineration could spread disease if wild armadillos fed on them. He also noted that all infected animals had been found within 39 miles (52 km) of GSRI, pointing out that areas remote from the Institute had not been sampled.
Kirchheimer & Sanchez (1976b) next reported that 520 armadillos from South America had been examined without finding evidence of leprosy. Additionally, they had studied 75 animals captured by Louisiana State Wildlife and Fisheries Commission in the general neighborhood of GSRI without finding a leprosy-like disease. In March of 1978, Kirchheimer took his case against GSRI to the press. In an interview with a staff writer for the Baton Rouge Advocate (McRae 1978), he seemed to imply GSRI deliberately set diseased armadillos free to raise money to study them. The following quotation is from a feature story in the 5 March 1978 issue of the Sunday Advocate.
GSRI, which lives on research grants, offered no evidence of the source of the armadillo infection and (Kirchheimer) said further studies were needed. Dr. W. M. Meyers of the Armed Forces Institute of Pathology in Washington subsequently supported the GSRI claim, but his report was based on samples supplied to him by GSRI, and not on armadillos caught independently . . . . Last month the GSRI theory was rehashed with a new twist. A warning was issued to state residents with a fancy for armadillo meat that the animals may carry leprosy. The statement came from Dr. William Cherry, Secretary of the State Department of Health and Human Resources . . . . Cherry has asked the Legislature for $75,000 to conduct studies on the possibility of leprosy in wild armadillos. (Kirchheimer's advice: "If you catch a lepromatous armadillo and cook it, go ahead and eat it. It is no more harmful than cooking pork to get rid of trichinosis.) If a prospector were to pull gold nuggets from his pocket and tell you he had discovered gold in a mine, wouldn't you want to see the mine before you bought it?" Kirchheimer asks. "GSRI has not yet produced the gold mine," he contends.

Kirchheimer (1977, 1979) and Kirchheimer & Sanchez (1978) formalized their accusations in papers in Leprosy in India. The editor, Dharmendra (1978), endorsed their viewpoint.
VINDICATION

The first confirmations of the GSRI discovery came from two U. S. Public Health Service laboratories, Carville and Centers for Disease Control. As noted previously, Storrs' conviction that leprosy was a natural disease of armadillos was reinforced by reports that a Carville animal had developed nodules distant from inoculation sites only four months after inoculation. Next, Yoshizumi et al. (1974) reported that a Carville armadillo inoculated in the abdomen in March of 1972 had developed a walnut-sized nodule on the left thigh by mid-June. Biopsy showed it to be a leproma. It was not possible, even in armadillos, for leprosy to disseminate that rapidly (Binford 1976a, 1976b).
In late 1975 or early 1976, CDC had begun a search for naturally infected animals. According to Rees (1976), in an editorial in Leprosy Review, it was to include 600 animals. In June of 1976, CDC sent tissues from an infected armadillo to Binford and D. S. Ridley of Hospital for Tropical Diseases, London. Both confirmed that the disease was armadillo leprosy (Fox et al. 1977). The armadillo had been captured in Mississippi, 90 miles (150 km) northeast of GSRI. The authors said it confirmed observations made by GSRI. They also mentioned collaborating with Carville on examining wild armadillos for leprosy. CDC did not report another case of sylvan leprosy until October of 1978 when they found one near College Station Texas (Anon. 1978).
In October of 1977, GSRI and collaborators published three papers that should have settled the issue. They showed conclusively that (1) prevalence of leprosy in Louisiana armadillos was about 10 percent (Walsh et al. 1977), (2) the disease of wild animals was indistinguishable histologically and microbiologically from the disease produced by human bacilli (Binford et al. 1977), and (3) lepromin produced from bacilli of wild armadillos gave the same reactions as human lepromin in skin tests on patients in Venezuela, Ethiopia, Zaire, and Malaysia (Meyers et al. 1977). Scientists from Armed Forces Institute of Pathology (AFIP), National Institute for Medical Research (NIMR) of U.K., and National Institute of Dermatology (Venezuela) were co-authors of these papers. Yet, Carville rejected their findings.
Additional evidence was soon forthcoming from researchers from University of Texas who conducted an independent investigation. On 5 to 7 of April 1978, Smith et al. (1978a) collected 20 armadillos in southwest Louisiana. Two of them had leprosy. Their note to LSM was received on 1 May, 1978. Thus, it took them 26 days to confirm the GSRI findings. In the memorandum describing this work, they noted that
Rigid forensic precautions assuring continuity of animals and specimens were taken and photographically documented so that any data acquired could qualify as legally admissible evidence.

In their journal publication Smith et al. (1978b) noted that
Leprosy in wild armadillos had resulted in a heated controversy in the scientific press concerning the existence and origin of the disease: they were qualified to make an impartial study to settle the question because their group had experience with human leprosy, but had no vested interest or long term research commitment to the study of leprosy.

This group later found leprosy in wild armadillos on the Texas Gulf Coast in a belt extending from Louisiana to Mexico (Smith et al. 1983). Subsequent pathology studies gave further credence to their diagnosis of leprosy (Folse & Smith 1983).
In June of 1978, an entirely unexpected confirmation came from California (Anderson 1978). San Diego Zoo had imported two armadillos from College Station, Texas, in 1976. One of them developed symptoms of leprosy in 1978. This group had no research interests in leprosy whatsoever. Their observations resulted from routine monitoring of animal health. College Station is about 400 km from GSRI. The existence of sylvan leprosy was confirmed beyond a reasonable doubt. In early 1979, ISPHS published a fabricated map purporting to show that infected animals escaped from GSRI (Kirchheimer, 1979)
DISCUSSION

The USPHS Hospital at Carville neglected a major zoonosis hazardous to human health for 11 years despite long proximity to the largest known reservoir of leprosy bacilli in the world. The hospital was established in 1921 by annexation of the Louisiana State Home for Lepers (Gussow, 1979). Armadillos were first reported in Louisiana in 1926, and by 1943 had spread throughout the state (Talmage & Buchanan, 1954). Occurrence of leprosy in Texas animals as far south as Mexico (Smith et al., 1983) and discovery of a leprosy-like disease in Mexico (Amezcua, et al., 1984) suggest they could have brought leprosy across the border with them when they invaded South Texas in the 19th century. Serological tests show Louisiana armadillos were exposed to leprosy before 1961 (Truman et, al., 1986). Thus, Carville dozed for decades on the doorstep of a major zoonosis without realizing it.
GSRI, located only 50 air miles southwest of Carville, announced discovery of leprosy in wild armadillos (Walsh et al.,1975). Instead of taking positive action to protect the public, Carville claimed sylvan leprosy didn't exist, or if it did exist, was an artifact caused by GSRI. It took them 4 1/2 years, from January 1974 to June of 1978, before reporting an armadillo with leprosy (Kirchheimer & Sanchez, 1978). Then they did nothing about it.
The performance of CDC was only marginally better. According to Rees (1976), they began a survey of 600 armadillos in 1976. They found one leprous animal in Mississippi in 1976 (Fox et al., 1977), and another in Texas two years later (Anon. 1978). None were reported in Louisiana. Felice et al. (1977) of CDC published a paper claiming no association between armadillos and human leprosy. It was based on interviews with 19 Louisiana leprosy patients who could not recall having contacts with armadillos. C. C. Shepard and D. W. Fraser of CDC gave an interview to World Medical News (Anon. 1976) on sylvan leprosy. They stressed the possibility that the discovery might derail the WHO vaccine program, but glossed over risks to public health. Together, Carville and CDC must have examined nearly a thousand armadillos, and reported leprosy in only three.
Their performance was dismal compared to private laboratories. With no previous field experience, University of Texas confirmed leprosy in armadillos in less than a month (Smith et al., 1978a, 1978b. Workers at San Diego Zoo stumbled across it by accident during routine examination of animals imported from Texas (Anderson, 1978). Shortly after Storrs relocated to Florida, she imported 61 Louisiana armadillos. Five of them had clinically diagnosable leprosy (Storrs & Burchfield, 1984).
The leprous armadillo brought to Carville in 1978 did not spur them to action. Nothing more was heard until Job et al. (1985) reported leprosy in road kills. That Carville armadillos #16 and #34 were infected with leprosy before capture should have soon been glaringly obvious by 1972 (Burchfield, 1999). Binford 1976a, 1976b) made this crystal clear , but they did not heed him. The reluctance of Carville to accept reality has been noted by Walsh et al. (1986). Despite the powerful evident published by Binford et al. (1977) and Meyers et al. (1977), USPHS continued their onslaught on the Storrs' program. The virulence of this attack is illustrated by an interview which Kirchheimer gave to a Baton Rouge newspaper( McRae , 1978) and a forged map he published in Leprosy in India (Kirchheimer, 1979). The controversy was given world wide coverage. The downfall of Storrs' program was assured.
Good evidence now exists that armadillos transmit leprosy to humans. Eighty-nine % of native born people in United States with leprosy live or have lived in Texas and Louisiana (Mastro et al., 1992). These are the only two states where indigenous cases outnumber imported cases. The first association between armadillos and human leprosy was made by Freiberger & Fudenberg (1981) who reported on leprosy in a retired Texas rancher who had handled armadillos in his younger years. Lumpkin et al. (1983, 1984) reported six cases in Texas among people who handled armadillos regularly. West et al. (1988) reported that six people from a previously leprosy-free area of northern Louisiana had developed disease. These were isolated cases with no contacts with patients, but who lived in regions where armadillo leprosy is widespread. Holcombe (1988, 1993) reported on four people with leprosy in central Louisiana, two of whom had contacts with armadillos. Thomas et al. (1987) made a study to determine if a correlation existed between armadillo contacts and incidence of leprosy in Mexican-born residents of Los Angeles. They concluded that exposure to armadillos was an important risk factor in disease development.
Three years after Carville finally admitted sylvan leprosy existed, Job et al. (1989) published three case reports on patients who were possibly infected by bacilli from wild armadillos. The summary of their paper reads as follows:
Three case reports of patients with a single, nodular, subpolar lepromatous skin lesion, one on the left elbow, another on the posterior aspect of the left leg, and the third on the extensor ulnar aspect of the right forearm, are presented. The lesions clinically and histopathologically, resemble lepromas which develop at the site of experimental inoculation of Mycobacterium leprae in armadillos. These are sites on the body which are likely to be traumatized. With the distinct possibility of the presence of viable M. leprae in the soil of Louisiana and Texas from wild armadillos with the natural disease, it is suggested that these three patients acquired the infection from the environment and had inoculation lepromas.

It is now certain that armadillo bacilli can cause leprosy in humans. A laboratory technician at Florida Institute of Technology (FIT) accidentally jabbed her finger with a syringe containing armadillo-derived M. leprae. She developed an infection at the site of the wound. Carville confirmed the disease was leprosy.
The inoculum potential of the armadillo is enormous. Carville now reports almost a third of adult animals in Louisiana and Texas harbor leprosy bacilli (Truman et al., 1991). Severely infected animals can contain 10¹² bacilli each. Armadillos occur by the millions in these states. They are hand-captured for sport, and eaten by the indigent. Children blow in their ears to make them run faster at armadillo races. Carcasses of road kills litter the high ways. If leprosy were as infectious as tuberculosis, U.S.A. would already have a huge epidemic to contend with.
For references cited here see General references

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