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“Vertical Analysis” of
Human African
Trypanosomiasis
Guy Kegels
Studies in Health Services Organisation & Policy, 7, 1997
Studies in Health Services Organisation & Policy, 7, 1997
Series editors: W. Van Lerberghe, G. Kegels, V. De Brouwere
©ITGPress, Nationalestraat 155, B2000 Antwerp, Belgium.
E-mail : [email protected]
Author: Guy Kegels, ITM, Antwerp
Title: “Vertical analysis” of Human African Trypanosomiasis
D/1997/0450/7
ISBN 90-76070-07-5
ISSN 1370-6462
I Introduction
Sleeping sickness, as a clinical entity in humans, has been known to
Europeans for centuries. It was described in medical terms as early as 1734
by John Atkins, a surgeon of the Royal Navy, under the name 'sleeping dis-
temper'. For a long time it was thought that this disease was present only in
the African coastal areas, the only ones that were known by Europeans, and
it was regarded as something of a curiosity. Then began the penetration of
the interior, and later the colonial drive, punctuated by happenings like the
Brussels 'International Geographical Conference' in 1876, called by king
Leopold II, and in a more formally geo-political way with the Berlin Confer-
ence of 1884-1885, called by Bismarck. The African continent south of
Egypt and Sudan, and north of the Zambezi River was to be explored,
civilised, mapped, protected, occupied; the slave trade was to be suppressed
and other forms of trade were to be fostered. The European powers 'went
in'.
Quickly sleeping sickness was to be regarded as a major problem. Africa
was generally considered as an insalubrious place, but this disease was
visibly something very special. The ‘curiosity’ was taking epidemic propor-
tions and entire population groups were occasionally disappearing. In the
Senegambia, an epidemic was observed from 1876 onward, in the Upper
Volta region from 1880. A violent epidemic broke out in Nigeria in 1886,
another one around Lake Chad in the same year. In the Congo
Independent State, sleeping sickness flared up along the Congo river and
the Lualaba in the course of the 1890s, quickly followed by the more
northern territories and the Kasai region. In Angola, in 1870, sleeping
sickness broke out in the Malanje focus, east of Luanda, and again in 1895
in the plantations along the Cuanza river in the same general area. In the
French Congo the Niari region was suffering from the same problem in
1895. And so on.
But around 1900 it became a very hot issue indeed. Suddenly the
'sleepy distemper' had started to kill thousands and tens of thousands of
Studies in HSO&P, 7, 1997 1
Africans in a few years' time in the area of the Busoga District, on the
northern shores of Lake Victoria. This epidemic, the violence of which
remains to this day an enigma, was described as, and felt to be, a scourge
that was going to decimate the African populations, which for various
reasons was considered intolerable. Intervention was deemed extremely
urgent. And once interventions were selected and decided on, they were
implemented with force - of course in the context of the spirit and
prevailing values of these (early colonial) times.
How were these interventions selected? Evidently on the basis of the
understanding, at the time, of the mechanisms of transmission, propagation
and diffusion, and on the basis of what was known or thought to be known
about the 'disease entity' and its 'natural history'. In other words, on the
basis of available epidemiological and clinical understanding. Epidemiology
and clinical investigation being 'scientific' disciplines does not mean,
however, that they can be seen as entirely independent from the epoch
(and its values) in which they are practised.
The accumulation of a systematic body of observations concerning
sleeping sickness (a clinical entity not linked with the Trypanosoma parasite
before 1902) in the first decades of the 20th century is a rather epic tale. At
the origin of this huge effort must have lain an acute sense of urgency,
induced by the conjunction of a rather spectacular epidemic, (colonial)
political, economic and military considerations, and the emergence of
'tropical medicine' as a field that was establishing itself and cutting out its
rightful place in the order of things medical.
Even present day, cool headed historians investigating this period do
not escape the taste of drama and the feeling of awe inspired by what was
happening then. Witness a sentence taken from M. Lyons' book The colonial
disease: 'In the five years between the close of 1900 and the end of 1905, sleeping
sickness killed over a quarter of a million Africans in the British Protectorate of
Uganda. This tragedy sparked off one of the most dramatic chapters in the history
of medicine.' (M. Lyons, 1992) Or, to take another sample, this time by a
contemporary molecular biologist: 'Sleeping sickness was the AIDS of the turn
of the century. This disease made AIDS look like nothing. Two thirds of the
2 Studies in HSO&P, 7, 1997
people on the north shore of Lake Victoria died and no one knew what was
causing it. All the big colonial powers were there and they were worried that the
disease would disseminate to enormous numbers of people.' (J. Boothroyd,
quoted in G. Kolata, 1985).
Such was the stage at the time the Lake Victoria epidemic broke into
its full force, by 1901. A lethal disease was threatening the promises held by
Africa. This enemy had to be contained, defences had to be erected, the
knights of (Western) medical science were called in. This, I think, is the
metaphor that may allow us to make a beginning of sense of the early
history of sleeping sickness control as practised by the European colonial
powers. It has to do with political power, it has to do with economic power,
it has to do with scientific ambition and prestige, it has to do with the
drama of deadly epidemics and the basically humane willingness to do
something about it, it is at the same time very practical and eminently
romantic. But the social and political dimension should not be neglected if
one wants to understand why sleeping sickness - which had been known for
centuries - suddenly became a declared priority. Declaring an epidemic is
always somehow a political decision. An epidemic is, among other things, a
social event, not only an epidemiological one. And investigating a
threatening epidemic 'in its full force' is another kind of epidemiology than
studying the relationships between diabetes and high-density lipoproteins in
the previous generation's diet. Of course.
A second element that is needed in order to understand how sleeping
sickness control interventions were selected at the beginning of this
century, relates to the roots of epidemiological 'doctrine' in the early years
1900. We should not forget that the old dispute between 'miasmatist' and
'contagionist' theories of epidemic disease had only recently been concluded
in favour of the contagionists. The germ theory, providing an etiologic
explanation for (infectious) disease, was 'confirmed' and gained wide
acceptance from the 1860s and Pasteurian bacteriology onward. This new
and highly successful etiologic explanation, however, tended to monopolise
the attention in terms of 'causation' of disease. At the risk of caricaturing
and simplifying things out of proportion, one could say that controlling the
'disease' tended to be reduced to controlling the germ and, if that could not
Studies in HSO&P, 7, 1997 3
be envisaged, by controlling the germ-carrying host, some way or another.
This was perfectly compatible, in terms of the epidemiological doctrines of
the time, with the (implicit) assumption that epidemics are caused essentially
by germ-carriers arriving in an area where the germ was not (yet) present. In
order to avoid this, 'infected' and 'not infected' areas needed to be mapped,
and non-infected areas cordoned off. In other words, propagation of the
disease (carrying it from one geographical space to another) was the prime
concern and needed to be avoided at all cost. This could only be done, of
course, by limiting people's movements, essentially an administrative
measure - and a very difficult one to implement.
When in 1903 king Leopold II of Belgium invited the Liverpool School
of Tropical Medicine (founded in 1899) to investigate sleeping sickness in
what was then still called the 'Congo Free State', the Liverpool School sent
a team of three scientists, Cuthbert Christy, Joseph Everett Dutton and
John Lancelot Todd to the Congo. Their expedition lasted one and a half
year, at least for Todd (Christy, who joined as a volunteer, did not complete
the expedition, and Dutton died of relapsing fever in February 1905 and
was buried in Kasongo). It produced a wealth of observations, as well in the
field of scientific understanding of the disease (the scientists' prime
concern) as in terms of its 'mapping' in the Congo Free State territory.
Their advice to the colonial administration centred largely on the notion of
protecting the uninfected regions (mainly the important northern Uele region),
thus reflecting quite clearly the doctrinal bias of that time (emphasis on
containing the propagation by containing the germ-carriers). This advice
was quickly and strictly acted upon by the colonial authorities and led to a
body of control measures that pervaded almost every aspect of the native
population's social life (Lyons, 1992).
Somewhat counterbalancing the emphasis on 'germ propagation', at
least theoretically, was the then (and now) common belief that epidemics
were made possible - or were enhanced - in a situation where a set of
selected, observable, physical phenomena were produced together. This
'environmental' approach went some way in trying to understand the nature
and causation of epidemic disease, but was and is somewhat less helpful for
deciding on immediate, urgent control interventions aimed at reducing or
4 Studies in HSO&P, 7, 1997
containing the problem with quick results. It tried to identify and, if
possible, to understand the host factors in disease (resistance to infection or
vulnerability) and certain (physical) environmental factors. The importance
of these phenomena had been observed quite clearly in the European 19th
century context (the effects of crowding, poverty, climate, working
conditions, extreme nutritional status,...); however, in terms of possible
ways to change them quickly, they often were too complex to tackle
effectively and rapidly.
Applied to the West African sleeping sickness problem, it was soon
clear that occurrence of the disease is a very focal phenomenon, linked to
the environmental conditions necessary for the tsetse fly to exist and to play
a sufficiently effective role in the transmission of the disease from man to
man. Some environments (or environmental conditions) are clearly more
dangerous than others. There are basically two ways to react to this: either
change the (dangerous) environment, or separate the potential victims from
this (dangerous) environment. The first approach has been extensively
practised with the perspective of making life difficult for the tsetse flies
(bush clearing, game extermination, fly catching or poisoning), mainly in
East and South-East Africa, although it also formed one of the elements of
the French and Belgian approach in West and Central Africa. The second
one implies, if it is to be practised on a large scale, moving and resiting
human population groups or changing settlement patterns. A combination
of the two approaches was called, in the terminology of Jamot's doctrine
'agricultural prophylaxis' ('la prophylaxie agronomique'). It is not so hard to
imagine what kind of resistances are to be expected if this kind of
interventions are implemented consistently and on a large scale for
'beneficiaries' who do not really share the bio-medical paradigms on which
they are based.
Apart from the socio-political (and geopolitical) considerations, and the
prevailing epidemiological reference doctrines, a third element may be
useful in trying to understand the logic in the choice of interventions,
namely what could be called 'historically developed attitudes', themselves
largely dependent on the difference between trypanosomiases of the
savannah and those of the forest.
Studies in HSO&P, 7, 1997 5
The history of trypanosomiasis control is a complicated one. The fact
that the name of a parasite species (Trypanosoma) is used to name a variety
of distinct problems (human and animal, gambiense and rhodesiense)
certainly contributes to the confusion, especially if in the name of (African)
'trypanosomiasis' far reaching generalisations are made.
In the East and South-East Africa (savannah) fly-belts, then mainly
populated by tsetse of the morsitans variety, cattle could not survive because
of nagana - a form of animal trypanosomiasis disease - known since a long
time and by everybody to be 'caused' by tsetse flies, long before the etiologic
agent was identified as a trypanosome by Bruce in 1894-1895. Especially the
British - but before them already the Zulu - concentrated their efforts on
getting pasture land free of flies, thought to 'poison' the cattle in some
direct way. In 1890 the great rinder pest epidemic took care of both the
game and cattle animals and the flies for a while, but once it was understood
that the tsetse was only an intermediary, carrying the parasites from a
trypanotolerant game reservoir to trypano-sensitive cattle, the logic of
intervention in (animal) trypanosomiasis control was to a large extent
directed towards environmental intervention. Human trypanosomiasis in
East Africa - of the rhodesiense type - tended to be appended, as a problem,
to the animal trypanosomiases which were, historically, the first and prime
concern. The first - isolated - case of human rhodesiense sleeping sickness
was reported in 1910.
Two alternative camps developed: those who wanted to starve the
tsetse by removing their source of food (the game, which at the same time
constituted the animal reservoir of the trypanosomes) and those who
wanted to remove the tsetse without killing wild animals. For various
reasons the latter faction largely prevailed. The entomologists took a
leading role, but this does not mean that the 'British tradition' excluded all
flexibility. When and where it was judged necessary or indicated - and
notably when they were confronted with human sleeping sickness - the main
corpus of intervention or control programs was case finding and
chemotherapy.
6 Studies in HSO&P, 7, 1997
On the other hand, as John Ford puts it, 'The French and Belgians were
not impressed by the entomological argument. The great Congo epidemics still
raged. In the luxuriant West African forests, bush clearing was obviously
impossible and elimination of wild animals pointless when the reservoir of the
trypanosome was man himself. It was a problem for the doctors [...].' (Ford,
1979). These 'great Congo epidemics' were indeed far from easy to control.
Between 1920 and 1923 more than 62,000 new cases were detected in the
Kwango basin population (Belgian Congo) where average detection rates
were close to 10 %. Comparable figures were obtained in the Uele basin.
Even in 1930, the medical teams detected more than 33,000 new cases by
examining some 30 % of the population of the Belgian Congo (with the
methods available at the time). The French teams in their Central and
West African territories detected and treated hundreds of thousands of
parasite carriers in the first half of this century. This was a major and for a
long time urgent problem indeed, and obviously quite different from the
East African one, both in its nature and in its perception, and consequently
in the development of traditions to tackle it.
With the emergence of progressively more effective treatment, the
West African sleeping sickness control strategies concentrated mainly on
the notion of 'sterilising the human reservoir' while maintaining emphasis
on the containment of infected populations. Jamot's doctrine (1916) is
explicitly based on the starting point that infected people should not move;
therefore medical teams should go out and find them (and treat them where
they find them), which is the basic rationale for the mobile team (or the
'spatialist') approach as developed and operationalised by the French and
the Belgians. The prime effort is on man, through administrative and
medical measures; the environment is somewhat secondary, although not
neglected (at least in theory). Later, after the second world war, this is even
more accentuated when 'chemoprophylactic' treatment is instituted with
six-monthly pentamidine injections. The bulk of the human
trypanosomiasis control program was concentrated on the human reservoir.
In recent years a more comprehensive trend in the interpretation of the
'epidemisation' of sleeping sickness is more and more gaining attention. The
basic question always was (and still is): what is at the origin of these
Studies in HSO&P, 7, 1997 7
'epidemics'? Somewhat simplistically, one can discern two extreme
epidemiological standpoints:
(1) the 'single source' hypothesis, with an emphasis on (germ) propaga-
tion;
(2) the premise of the 'multiple dormant sources', with an emphasis on
epidemic activation by changes in the hosts' susceptibility, brought
about by changes in the social and 'ecological' environment. This is
somewhat comparable to the two-level epidemiology of (e.g.) tuber-
culosis, where infection and illness are quite distinct events for an in-
dividual, 'illness' being brought about by entirely different determi-
nants than 'infection'.
In line with the theory of propagation (the 'migratory thesis'), the first
standpoint tries to explain the onset of epidemics by identifying parasite
carriers and establishing where they came from. Its basic working question
would be: who introduced this parasite into this community? Application of
this logic ultimately leads to the notion of a single 'mother focus' of sleeping
sickness, comparable to the epidemiological understanding of other great
epidemics like influenza, plague, cholera. The focus of interest in this ap-
proach is the parasite. An example is Morris' attempt to describe 'The move-
ment of sleeping sickness across Central Africa' (Morris, 1963), by which is
meant, in fact, the movement of the parasite. Another example would be to
trace the Busoga outbreak or the spread of the Congo epidemics to move-
ments of groups of people, troops and caravan trains, during the (pre-)colo-
nial penetration. Thus the famous (or rather infamous) Busoga epidemic
has been 'traced back' by some to Stanley's rescue expedition to Emin Pasha
in 1888.
The second standpoint would state that in most cases slow circulation
of the parasite is maintained in 'endemic', 'slumbering' foci, and that from
time to time epidemic flare-ups are produced (i.e. faster circulation of the
parasite among the human population) under the influence of certain
conditions, many of which are not really known. The focus of interest in
this approach is not so much the parasite, but its interaction with the host
and the environment, in the large sense of the word. This includes not only
8 Studies in HSO&P, 7, 1997
the narrowly biological environment, but also the social, political and
economic environments, intimately linked in a dynamic equilibrium. Thus
the great epidemics which 'started' around the turn of the century would to
a large extent be ascribed to the turmoil occasioned by the colonial
conquest and occupation, producing radical changes in the human ecology.
Examples of this approach are M. Lyons' analysis of the social history of
sleeping sickness in the Belgian Congo (1992), P.G. Janssens' analysis of the
epidemisation of trypanosomiases (1992), and on a more micro-social scale
Hervouët, Meda and Laveissière's analysis of the Vavoua focus in Ivory
Coast (1991,1992). But it would be a mistake to think that this approach is
only a recent one; it was already present in the minds of control authorities,
as expressed through statements about the importance of 'improvement of the
conditions of living among the native tribes' at the Conference on Sleeping
Sickness in Entebbe, 1933 (quoted in Duke, 1936).
Then of course there are the combinations and the intermediate posi-
tions, with their greater or lesser biases, 'biomedicalising' or 'socialising'. The
(moderate) biomedical bias would lead to statements such as: 'Human
African Trypanosomiasis is in essence a biological phenomenon with, possibly or
admittedly, some serious social consequences or maybe even some social cofactors
among its determinants'. A radical social (or socio-political) bias might lead to
statements such as: 'Human African Trypanosomiasis is a social phenomenon
masquerading as a disease'. In the case of sleeping sickness the latter
statement is likely to meet with a complete mental block on the part of the
medical professions. Still, it is a useful intellectual starting point for a better
understanding of the problem. We may consider the parallelism with the
concept of famine.
Looked at from a somewhat mechanical perspective, 'famine' equals 'too
many people and too little food', or something like 'the demand for food is
far greater than its supply'. The cause may be identified as 'drought'. The so-
lution would then be to increase the supply (which is what a relief organisa-
tion would do) or, somewhat less acceptable, to reduce demand (which is
what an enemy army might do). Looked at from a socio-political
perspective, 'famine' may be said to be caused by a loss of compensatory
mechanisms to deal with food shortages (which may be induced by drought)
Studies in HSO&P, 7, 1997 9
because of disruptions of mainly social or political structures. The solution
then is somewhat less clear-cut or less easily identified. Both perspectives do
not necessarily lead to real fallacies, but the purely 'mechanical' perspective
is bound to produce solutions that may very well create new socio-political
problems which in turn may create or maintain further 'famine', as
experience has shown.
In other words, the system of logic (the perspective) that is used to
understand the problem can be expected to be a determinant of the kind of
interventions that are selected in order to solve it (together with the
formulation of their objectives), which will further have an impact on the
kind of structures that will be set up in order to implement these
interventions. What we are trying to say is that the system of logic - or the
'perspective' - is a prime determining factor; however, these systems of logic
are not always made explicit, even if they have been so at some moment in
time. What makes human trypanosomiasis such a difficult and at the same
time such an intellectually challenging and fascinating problem is precisely
the fact that different perspectives are needed in order to simply begin to
understand it. The fact that trypanosomes, tsetse flies and human beings
have to come together in order to produce the medically defined 'disease'
Human African Trypanosomiasis, thus making it one of the 'diseases caused by
protozoa' (as it still used to be called in the 17th edition of Manson's
Tropical Diseases, 1972), gives us one element of understanding: this is the
necessary condition. But it is clearly not enough; we cannot say that it is
also a sufficient condition.
This, of course, raises the question of how well we need to understand
things in general, and a problem like trypanosomiasis in particular. Again,
simplistically, we will discern two extreme positions.
The first one would state that we need to know as much as possible of
what there is to know, in order to further our knowledge about the world.
An illustrative phrase that fits in with this position would be 'to push back
the frontiers of the unknown' (a phrase that actually can be found in recent
calls for candidates for academic prizes; a certain romanticism has not yet
disappeared from the face of the academic world).
10 Studies in HSO&P, 7, 1997
The second one would state that we need to know only what is needed
in order to decide on specific action, thus reducing the notion of 'relevance'
to 'practical relevance'. Looked at from the first position, everything is
potentially relevant or 'interesting'. Looked at from the second position,
knowledge is relevant only if it gives us a sufficient basis (a sufficient
'theory') to decide on - and to implement - a course of action, or a control
strategy.
Still taking illustrations from real life, the trypanosomiasis literature and
oral tradition provides somewhat contradictory sentences like:
"The epidemiology of human African trypanosomiasis is far from
understood."
and:
"L'épidémiologie [de la trypanosomiase humaine africaine] est d'une sim-
plicité cristalline." (Lapeyssonie, 1992)
The second statement refers probably to the fact that the basically
simple Trypanosoma-Glossina life cycle provides all the elements that are
needed to justify a chosen control strategy: detection and treatment of as
many parasite carriers as possible, or eliminating as many tsetse flies as
possible, i.e. with the most effective techniques. The strategy can be made
more effective by improving the techniques, but that would not change the
stratagem in any essential way. Therefore, everything that complicates the
simple life cycle model can be judged to be 'irrelevant' or 'academic'. This
would fit in with the words of a frustrated trypanosomiasis control officer: 'I
know what to do; just give me the necessary resources to do it'. True, of course,
except for the fact that the resources are always part of the problem. But
again, both statements, although contradictory, cannot really be faulted for
obvious fallacy, at first sight, that is.
At this point, it would seem appropriate to state our position. This is, in
fact, to a large extent determined by our outlook on public health and on
the way health care (services) can be organised.
Studies in HSO&P, 7, 1997 11
It is not our position that any new element of understanding is
'relevant'. It may be 'potentially relevant', but that does not necessarily
mean that it is relevant now or that its usefulness can be foreseen. On the
other hand, it is not our position either that everything is known that needs
to be known about sleeping sickness epidemiology; our understanding of the
notion of relevance tends to place it in a somewhat wider perspective. It is
still essentially of the kind 'what is useful for decision making', but we start
from the premise that the strategic decision has not yet been made. This rests
mainly on two considerations:
- the simple (life cycle) model strategy, although it has unquestionably
accomplished an enormous breakthrough in the past, also shows
unquestionable shortcomings;
- the structural and organisational consequences of the choice of
strategy, in terms of efficiency, resource allocation and health service
organisation are very considerable, and are a determinant of relevance on
their own.
Thus the tension between '(more) complete understanding' and 'useful-
ness for decision making' results in a dynamic and changing equilibrium
that needs to be reassessed regularly, not only because of changing 'disease'
conditions, but also because the disease problem cannot be analysed
anymore outside the social and professional control systems in which it
develops and with which it interacts. For someone who needs to formulate
rational and rationally defensible action strategies, the human African
trypanosomiasis problem cannot be adequately analysed without taking into
account the environment, the population that is at risk of contracting
and/or developing the disease, the health care delivery structures, and the
interactions between them, all of which are elements of a 'system' within
reality and all of which are of practical relevance. As these dynamics
change (they always do), we may be confronted with new 'puzzles'
(inadequacies of the model used so far, or more uncertainty), but we may
also positively learn relevant things about a reality that may be or appear
more complex than we thought. The trick then appears to be to render the
increasingly complex understanding sufficiently simple to be able to act on
12 Studies in HSO&P, 7, 1997
the problem on the basis of a coherent set of practically relevant elements.
The latter could be used as a first working definition of a 'model' - in this
case a descriptive or analytic one.
Pragmatically speaking, not much is gained by a mere increase in our
awe before the wonders and complexity of the world, or by a mere increase
in our humility when faced with the insufficiencies of our understanding
however beneficial these feelings may be for the human soul. For public
health practice, better (or more profound) understanding remains relevant
only if it contributes to better decision making and implementation. 'Push-
ing back the frontiers of the unknown' therefore needs some steering, for
some frontiers are clearly more of an obstacle than others.
We hope this will clarify to some extent the structure and methodology
of the work presented here.
The first part, called Vertical Analysis, is an attempt to analyse the prob-
lem of human West-African trypanosomiasis (Trypanosoma brucei
gambiense) without prejudice, and to find out what is known (and relevant
to us) and what is not (but should, from our perspective). The second part,
the condensed summary of the Kasongo study results, will attempt to show
what we have been able to learn from this survey, and to what extent some
of the gaps in our knowledge are filled, if any. The third part will be an
attempt to draw the appropriate conclusions in terms of problem
management, from the point of view of our public health perspective and
health care organisation doctrines.
It will be clear that this may look like a somewhat presumptuous under-
taking, especially because, in fact, it intends to approach the problem of
West-African trypanosomiasis in a way that is as comprehensive as possible.
We think, however, that this 'presumptuousness' is necessary; there is a
need to establish the common ground between the epidemiological, biomedical
and health-systems-organisational disciplines, because all of them have to be
used in the interaction between communities, individuals and health care
providers. In this kind of needed exercise a synthesis needs to be made
which is possible only if a fundamentally generalist attitude is adopted and
maintained. Although we certainly cannot claim to be the only ones
Studies in HSO&P, 7, 1997 13
capable of formulating this synthesis, it is one of the specificities of our
'general public health' discipline, as we see it, to develop methods to do so
in a systematic way.
The work presented here is mainly about an application of such meth-
ods. It attempts to bring together, and to make explicit, the ways in which
decisions in health care need to be made. These ways are not restricted to
the sleeping sickness problem. They are applicable (and, in our view, should
be applied) to most if not all important health problems for which
programmes are developed. In order to be individually and socially
acceptable, the decisions must not only be based on validated knowledge
and understanding but also be subjected to an accepted set of values
expressing the ethical dimension of human health care delivery, in which
care includes - but transcends - cure.
14 Studies in HSO&P, 7, 1997
II Vertical Analysis
The vertical analysis approach
What we will call 'vertical analysis' is an intellectual exercise that
consists in the identification, description and systematic analysis of a health
problem in its various aspects, in order to make an inventory of all possible
solutions or interventions, which is expected to permit us to select, as
objectively as possible (i.e. without prejudices and without preconceived
ideas), those activities that have to be implemented with some degree of
priority in order to solve or reduce the problem.
By doing this, it is highly probable that one comes to identify areas of
uncertainty - or gaps in the knowledge that is needed for rational decision
making - which may direct our choice of research priorities.
This approach has been formulated and codified by P. Mercenier in
1972 and has been practised systematically in the Institute of Tropical
Medicine's courses in tropical medicine and the International Course for
Health Development for quite a number of years by now; one could say that
it has matured in the process. It has proven to be a useful tool, in our
experience, in order to formulate relevant questions on specific health
problems and as a 'skeleton' around which our understanding of health
problems can be 'draped', so to speak, in a comprehensive way.
Generally speaking, one could say that this approach tackles the follow-
ing questions: - is there a problem, and what is it? - where is the problem? -
what are the problem's determinants? - which elements of the problem do
we want to influence or solve? - how can we influence or solve these
elements of the problem?
In practice, the 'vertical analysis' encompasses 7 stages:
Studies in HSO&P, 7, 1997 15
1. An evaluation of the importance of the problem
2. The description of the 'system'
3. The listing of possible activities or interventions
4. The identification of the type of services necessary in order to
implement these activities
5. The identification of the type of personnel that is needed
6. The formulation of operational intervention strategies
7. The formulation of how these interventions are to be evaluated
Although unquestionably useful, this strictly systematic approach also
has its limitations, which it is appropriate to point out right from the start.
Probably the most important one is that this approach tends to force one to
isolate the health problem from its wider context. This is somehow linked
to our 'medical bias' to label a (health) problem with the name of a disease.
The latter is a nosological entity, closely linked to the medical concept of
diagnosis, a logical fiction invented by the medical profession that is
necessary, within the system of knowledge that is at the basis of modern
medicine, in order to put some order in the observed universe. It is a bio-
medical abstraction.
On the other hand, a problem, even if it is restricted to be a 'health'
problem, is a much broader and comprehensive concept than what can be
implied or covered by the name of a disease, and it is quite possible that
there exist better ways to name it or to circumscribe it than through this
rather narrow abstraction that a 'disease' is condemned to be - even if for
the moment we can do no better.
However, we think that, as long as we remain conscious of our bias, it is
possible to maintain an attitude that is as objective as possible, keeping in
mind that we are concentrating on one aspect of a much more complex
reality.
In this context, it may be of interest to note that even diagnostic
entities are not always as semantically and conceptually precise as they may
16 Studies in HSO&P, 7, 1997
give the impression to be. In fact, concerning the topic at hand, the term
Human African Trypanosomiasis, as a disease entity, is an etiologic
description, referring to a parasite-host relationship, whereas the term
sleeping sickness is a clinical description. Although the two terms are often
used interchangeably, they do not really mean the same thing. In common
parlance, an asymptomatic parasite carrier can rightly be said to be a case of
'trypanosomiasis', but it would be somewhat premature to say that he is
suffering from 'sleeping sickness' as long as he is neither 'sick' nor 'sleeping'.
Preliminary assumption
When describing the problem of Human African Trypanosomiasis
(HAT) of the gambiense variety, we will start from a basic working
hypothesis - which is basically an option we think it is necessary to take, in
order to be and remain consistent in our approach. This option is to treat the
disease as a homogeneous entity (i.e. it is considered to be one disease); it is
assumed that variations in the expression of the disease are attributable to
'epidemiological' factors related to the level of endemicity, the history and
dynamics of the endemic (in other words, observed variability can be 'explained').
In this vertical analysis we will formally take the exercise first through
steps 1, 2 and 3: the problem, the 'system' and the possible interventions.
Issues directly or indirectly related to the selection of types of services, per-
sonnel and operational interventions (steps 4, 5 and 6) will already be
touched upon in this process.
The importance of the problem
1. DEFINITION OF THE PROBLEM OF HAT
In the context of the vertical analysis approach, the 'health problem' is
neither the parasite, nor the transmission, nor the infection, but the individ-
ual and collective suffering caused by the disease, including its economic and
social cost (World Health Organization, 1964).
Studies in HSO&P, 7, 1997 17
In order to facilitate reflection, the 'overall' problem of HAT can
usefully be split in two:
- the 'actual' or 'present' problem: the suffering of symptomatic patients,
caused by their illness, and the repercussions of this on other people;
- the 'potential' health problem: the suffering that can be expected by
asymptomatic infected patients, if and when they will become symptomatic,
on the one hand, and the suffering that can be foreseen for the uninfected if
and when they become


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