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Animals and Medicine

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Jack Howard Botting

I. Treatment of Infectious Diseases

6. The Conquest of Polio and the Contribution of Animal Experiments

Note de l’auteur

An earlier version of this chapter was published as: The conquest of polio and the contribution of animal experiments. RDS News October 1991 4-5.

Texte intégral

1Any individual old enough to have even occasional recall of a childhood before World War II must be aware of the impact of antibacterial agents and vaccination on infective disease.

2With the advent of prontosil and hence the sulphonamides, followed by the antibiotics, death from common bacterial infections has become a comparative rarity. Similarly, the leg braces and iron lungs (Fig. 6.1) – a mark of the epidemics of poliomyelitis that were a regular feature of Europe and North America throughout the first half of the twentieth century – are now seen only in the countries which have not yet implemented the polio vaccination programme instituted by the WHO.

Fig. 6.1 The iron lung before vaccination, 1952? Image in the public domain.

3Those who assert that animal experiments have contributed nothing to the treatment of infectious disease claim that improvements in hygiene and sanitation are solely responsible for the lower death and morbidity from infectious disease this century.

4It is undoubtedly true that improvements in social conditions lessen the possibility of contraction of certain bacterial diseases, and that improvements in nutrition may increase resistance. It is, however, undeniable that the annual death rate from puerperal sepsis was steady at approximately 190/100,000 births from 1860 to 1938, but with the development of sulphonamides and antibiotics this had fallen to half that value within two years, and to approximately 5/100,000 by the 1960s (1).

5Similarly, the death rate from lobar pneumonia in middle-aged men averaged a steady 60/100,000 from 1910-1940, but with the application of bacterial chemotherapy had fallen to below 6 by 1970 (2).

6However, of all the contentions of the animal rights movement, its attempts to reject the contribution of animal experiments towards the reduction in death and paralysis from poliomyelitis are the most unacceptable. Thus it is claimed:

The significance of poliomyelitis had dropped as better sanitation, better housing, cleaner water and better food had been introduced in the second half of the 19th century. (3)

7This statement is quite untrue. For 4,000 years ‘infantile paralysis’ was a sporadic disease, with a very low background occurrence. A dramatic change occurred at the end of the nineteenth century, when epidemics began to occur in Scandinavia (1868-1881) and later in Vermont, USA (1894). The 1905 epidemic in Sweden (1031 cases) established the change in nature of the condition from an obscure, endemic, sporadic disease to one with a regular, almost predictable occurrence in developed countries (4) (Fig. 6.2).

8What explanation can account for this apparent paradox, that poliomyelitis only became a serious problem in those countries (e. g. in late nineteenth century Scandinavia) that boasted the highest standards of hygiene and sanitation? In fact poliomyelitis can be relatively innocuous if contracted when one is very young. Symptoms may be confined to a temperature and headache – a so-called “inapparent infection” – yet this can confer life-long immunity. It is thus obvious that infants brought up in unsanitary conditions are likely to become infected whilst very young, suffer a slight illness and become immune. As hygiene and sanitation improve children become shielded from infection during infancy, and thus may contract the condition at an age when they are particularly vulnerable to the severe, paralytic form of the disease. The infection can then easily spread among such non-immune persons and the epidemics, typical of the first half of the 20th century, will result (4).

Fig. 6.2 Comparison of infant mortality rates and the incidence of poliomyelitis.

9Animal experiments, of course, were crucial in the elucidation of the nature of poliomyelitis and inevitably in the formation of a vaccine. Although it was suspected that polio was an infectious disease, definitive proof was provided in 1908, when Landsteiner and Popper (5) managed to induce the condition in monkeys by injecting homogenates of the spinal cord of a 9-year-old boy who had died of acute polio. Since the samples of spinal cord were shown to be free of bacteria, Landsteiner and Popper surmised that poliomyelitis was caused by a virus too small to be detected by microscopic techniques at that time (in actual fact poliovirus is one of the smallest viruses). The infection was transferred from monkey to monkey and thus provided a model of the disease from which much information was gleaned.

10It is unfortunate that Landsteiner, at that time working in Vienna, was not able to continue in this field, since the enormous expense of maintaining a sufficient monkey colony to pursue this study was beyond his available funds. (Landsteiner was awarded the Nobel Prize in 1930 for his work on the classification of blood groups).

11From 1908 until the 1940s the induction of polio in monkeys was the only means of study of the disease. With this model it was established that three strains of the virus existed, that the route of infection was via the nose and mouth, and that the virus stayed and multiplied in the gut before, in more serious cases, migrating via the blood stream to the motor neurones of the spinal cord, where the destruction resulted in permanent paralysis.

12Of great significance was the observation that nasal washings from patients with a relatively trivial infection caused severe paralysis when administered to the experimental monkey, thus indicating that individuals could, in some circumstances become immune. This undoubtedly served to encourage those endeavouring to develop a vaccine.

13From an early date attempts were made to grow the virus in culture, just as bacteria were cultured in broth. Viruses of course can only replicate in cells, thus tissue culture was the only possible means of fostering the virus outside the whole animal. Progress was slow since there were few groups of workers who could afford to maintain a monkey colony. The problem was eased when, after much effort, a strain of poliovirus was transferred to the Cotton rat, and subsequently to the mouse. The maintenance of the poliovirus in mice was significant because it meant that it was now possible to use a sufficient number of animals to provide clear evidence for the existence and virulence of the poliovirus. Thus the way was paved for intensive efforts to grow the virus in culture. As animal rights literature claims:

[…] the most crucial breakthrough in preparing the vaccine came in 1949 when Enders and his colleagues showed how poliovirus could be grown in human tissue culture. (6 ),

and

animal research supporters are wrong to say that without animal experiments there would never have been a vaccine against poliomyelitis because: an early breakthrough in the development of poliomyelitis vaccine was made in 1949 with the aid of a human tissue culture. (3)

14It is certainly true that Enders and his co-workers (7) made a significant advance in showing that the poliovirus could be grown in culture and for this they were awarded the Nobel Prize in 1954. However, for animal rights groups to imply that this work was a significant departure from animal experimentation is absolutely wrong. Further it has to be said that anyone who implies as such (if they have any scientific pretensions) are either deluding themselves or deliberately attempting to mislead the general public.

15The poliovirus could not be seen, how was it therefore possible to establish that the virus was replicating in culture? Only by an animal experiment. The primary inoculum seeded by Enders was a suspension of brain tissue from a mouse that had been infected with the Lansing strain of poliovirus. (The identity of the virus was verified by the “character of the disease it produced in white mice following intracerebral injection”). Subcultures to fresh tissue were prepared at 8-20 day intervals. Replication of the virus was proven when at the end of 67 days culture the primary inoculum had been diluted by many millions. Even so, the culture fluid still: “on inoculation into mice and monkeys, produced typical paralysis.” Thus, animal experiments were crucial in these significant results. It is probably superfluous to add that the incubation fluid used by Enders et al. was “balanced salt solution (3 parts) and ox serum ultrafiltrate (1 part).”

16The ability to grow the virus in cell culture ensured the rapid development of a vaccine, and widespread vaccination was introduced in 1955 in the USA and Europe (Figs. 6.3 and 6.4).

Fig. 6.3 Deaths from poliomyelitis in the USA, 1948-1967. Data from Vital statistics of the USA; US Dept of Health, Educ. & Welfare.

Fig. 6.4 Deaths from poliomyelitis in England and Wales, 1938-1973. A. M. Ramsey and R. T. D. Emond, Infectious Diseases, London: Heinemann, 1978.

17As a result, the disease has been virtually eliminated from these areas. It has been estimated that 1.5 million cases of polio were prevented in the decade 1980-1990 due to the immunisation programme (8). Although one opponent of animal experiments claims: “Proof that the introduction of the (polio) vaccine was not the success it was made out to be comes from undeniable statistics” (3), mortality and morbidity figures do not in any way support this. Furthermore, the collective medical experience of the WHO maintains that the vaccination programme would eradicate poliomyelitis by the end of the decade (8) (Fig. 6.5).

Fig. 6.5 Polio in Latin America, confirmed cases per year, 1969-1989. Data from Medical & Health Annual, 1991, Chicago: Encycl. Britannica Inc.

Bibliographie

References

1) (1966) Disorders Which Shorten Life Report No 21. Office of Health Economics, London. https://www.ohe.org/publications/disorders-which-shorten-life

2) Anderson T (1977) The role of medicine. The Lancet i, 747.

3) Coleman V (1991) Why Animal Experiments Must Stop. London: Green Print.

4) Paul J R (1971) A History of Poliomyelitis. New Haven: Yale University Press.

5) Landsteiner K & Popper E (1908) Mikroscopische Praparate von einem menschlichen und zwei Affenruckenmarken. Wien klinWschr, 21, 1830.

6) Sharpe R (1988) The Cruel Deception: The use of Animals in Medical Research. London: Thorsons.

7) Enders J, Weller T & Robbins F (1949) Cultivation of the Lansing Strain of Poliomyelitis Virus in Cultures of Various Human Embryonic Tissues. Science, 109, 85.

8) The State of the World’s Children, UNICEF (1991), Oxford: Oxford University press. http://www.unicef.org/sowc/archive/ENGLISH/The%20State%20of%20the%20World%27s%20Children%201991.pdf

Table des illustrations

Légende Fig. 6.1 The iron lung before vaccination, 1952? Image in the public domain.
URL http://books.openedition.org/obp/docannexe/image/1977/img-1.jpg
Fichier image/jpeg, 36k
Légende Fig. 6.2 Comparison of infant mortality rates and the incidence of poliomyelitis.
URL http://books.openedition.org/obp/docannexe/image/1977/img-2.jpg
Fichier image/jpeg, 36k
Légende Fig. 6.3 Deaths from poliomyelitis in the USA, 1948-1967. Data from Vital statistics of the USA; US Dept of Health, Educ. & Welfare.
URL http://books.openedition.org/obp/docannexe/image/1977/img-3.jpg
Fichier image/jpeg, 20k
Légende Fig. 6.4 Deaths from poliomyelitis in England and Wales, 1938-1973. A. M. Ramsey and R. T. D. Emond, Infectious Diseases, London: Heinemann, 1978.
URL http://books.openedition.org/obp/docannexe/image/1977/img-4.jpg
Fichier image/jpeg, 20k
Légende Fig. 6.5 Polio in Latin America, confirmed cases per year, 1969-1989. Data from Medical & Health Annual, 1991, Chicago: Encycl. Britannica Inc.
URL http://books.openedition.org/obp/docannexe/image/1977/img-5.jpg
Fichier image/jpeg, 20k

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