Control of
Communicable Diseases in the Context of Humanitarian Aid
Dr. med. Bärbel A. Krumme
DTM&H [Liv.], M.Sc. [Heidbg.]
Missionsärztliches Institut, Würzburg
Contents
I. Introduction
III. Examples of the control of communicable diseases
a. Malaria
c. Cholera
e. Tuberculosis
27f. Measles
I. Introduction
The incidence of tuberculosis in
Europe began to decrease even before drugs were used against the disease.
We know today that this was the result of improved living conditions and
nutrition. Similarly, we observe an
increase in the incidence of TB today in regions of the world where war,
floods of refugees and poverty produce a deterioration in living standards
and people are forced into cramped living quarters. AIDS, too, is
predominantly a disease of the poor especially in countries of the
southern hemisphere. And since an HIV infection creates favourable
conditions for an opportunistic TB infection, we observe a general
increase in the incidence of TB worldwide.
The relationship between a cholera epidemic and the
context of poverty, war and other disasters is very obvious. Cholera is
transmitted via water and food that have been contaminated with
infectious faeces. Thus it is a disease caused by unhygenic living
conditions which become particularly dangerous in times of natural and
man-made disasters. Most people will remember the catastrophic cholera
outbreak in 1994, when more than one million refugees, mostly Hutus,
crossed the border into neighbouring Zaire.
Thus some knowledge of communicable diseases
especially those with epidemic potential, their mode of transmission,
their clinical picture, as well as possible control measures is
indispensable for relief workers in the field of humanitarian aid in
emergency and disaster situations. This chapter does not aim at giving a complete overview
of infectious diseases. In other words, it does not intend to replace the
many excellent books on the subject, some of which are listed and
recommended for further reading at the end of this chapter. Instead, just
a few typical infectious diseases have been selected in order to discuss
appropriate control measures by way of example. The epidemics
discussed here were experienced by the author under conditions of war and
national disaster. Hence this material is intended to serve as a starting
point, based on practical experience. It should be complemented by the
lectures and deepened by personal reading. People with medical training tend to concentrate on
the infectious agent, its virulent properties, the dosage which causes
infection, and the immune response of the subject. And these matters are
in fact essential to a correct understanding of the interreactions
between the infectious agent and the infected subject. However, these
factors cannot be isolated from the geographical and social context. In
particular, the quantity of infectious substrate causing infection in
humans and the condition and immune response of the human subject depend
to a considerable degree on the environment of the subject. Especially
the geographical and social environment in which human beings are forced
to live and move about during war and disaster situations should be given
more attention. The spread of an infectious disease within a certain
population, or within a population group, where the disease is endemic
(i.e., the number of cases remains more or less constant) or during
an epidemic (where the number of new infections increases rapidly
within a given time) is linked to factors that influence, for example,
the human-vector contact, where the disease is spread by a vector.
(Vector = an animal which transmits the infectious agent to humans.) It
is also linked to factors which influence the infection rate among
vectors, such as climate, vegetation, altitude, working and living
conditions of the human population to name but a few. Thus a better understanding of the causes of
infectious diseases and an intelligent management of public health
issues requires cooperation between the different professions and mutual
respect in order to learn from one another. The group of people for whom
this book has been written are in an excellent position to contribute to
such a dialogue. II. The effects of war on the
health of the civilian population, in particular on the spread of
contagious diseases There are 6 main scenarios associated with wars,
refugee movements and the breakdown of infrastructures: 1. Refugees in the periphery of a
neighbouring country When refugees enter the
periphery of a country, they are often confronted with poverty among the
indigenous population as it is usually an area of low income, sparcely
populated, with few natural resources and a weak infrastructure. Until
aid is given on a large scale, there is a lack of food and medical care.
If this aid is concentrated exclusively on the refugee community,
tensions are often created between the indigenous population and the
refugees because of the general poverty of the region. Before the
introduction of humanitarian aid, infectious diseases (a sudden outbreak
of cholera, followed by shigellosis and typhoid fever) have already
caused deaths in the area. This is the result of inadequate sanitation
and water, lack of hygiene, poor housing, and insufficient or unbalanced
nutrition. 2. Displaced persons in an
urban setting People who become 'displaced'
as the result of a civil war generally show a preference to flee to a
large town, where they have relatives who can take them in. During the
recent civil wars in Liberia and Sierra Leone, the international security
forces also created areas which offered more stability than the rest of
the country. This phenomenon produces overcrowding, the
infrastructure is unable to cope with the sudden influx, and food
supplies become inadequate as the surrounding countryside is not able to
keep up its production. The extended family, suddenly concentrated in the
town, is dependent on just one or a few breadwinners. Under these
conditions, infectious diseases, such as tuberculosis, are very likely
to spread. 3. The few remaining centres
become a draw-factor Areas of a country that have
suffered severe destruction during a civil war become unsafe. As people
flee from the danger, structures break down: health centres are closed
when staff no longer receive their pay or medical supplies run out. The
only centres which continue to function in such a situation are those
belonging to church and foreign organizations. Patients bear down on the
few remaining centres from far and wide. Many of them walk through the
countryside for several days. If they have a communicable disease
especially one transmitted by a droplet infection, such as measles the
outbreak of an epidemic is inevitable, especially since preventive
measures, such as immunization, have almost certainly been discontinued
for some time. The health centre has more work than it can cope with.
More patients than usually have to remain for treatment as their homes
are too far away for them to return to the centre within a few days.
Thus they have to be given accommodation. In these circumstances,
provisions of water and sanitation are generally inadequate, the
accommodation quickly becomes overcrowded, and food supplies are
insufficient. These factors, in turn, create a health threat and can lead
to the outbreak of communicable diseases. Furthermore, the reduction in
the number of health centres often means that patients seek help too
late. Some of them will die when they eventually do reach one of the
remaining health centres, and this creates even more stress for the
health workers. This scenario may also occur when humanitarian aid
organizations are forced by the local political authorities to restrict
their activities to the towns. This was the case in Ethiopia under Meguisto Haile
Miriam, whose intention was to conceal human rights violations in this
way. Some observers then blamed the relief organization, operating in one
of the Ethiopian towns, for the outbreak of cholera, and the health
workers probably were at fault for they should have foreseen that their
activities would create a draw-factor, leading to overcrowding in a town
without adequate sanitation and water.
4. Forced resettlement of
people into other parts of their country during political unrest (e.g. in former Ethiopia,
at present in Burundi) Under the pretence of providing protection for
specific population groups, people are resettled against their will.
Particular ethnic groups, thought to be directly or indirectly involved
in a conflict, are generally singled out in this way in order to prevent
them from organizing themselves. They are resettled in areas without a
functioning infrastructure, which also causes severe health hazards for
them. (e.g. the outbreak of louse-borne typhus in the
so-called regrouping camps of Burundi). In addition, they could be
exposed to diseases from which they do not have any immunity.
5. Refugee camps The general health situation
and the threat of epidemics in refugee camps depend on different factors: the available space within the
camp, the number of newcomers at a given time, the resources in the
surrounding countryside and their availability to the refugees (relations
between the refugees and the indigenous population, the official
political status of the refugees). Under the worst imaginable
circumstances, one can expect communicable diseases to occur in a
sequence: first cholera, then measles, followed by shigellosis, typhus,
and scabies; then trachoma and respiratory infections, aggravated by
malnutrition. Exposure to adverse climatic conditions, the lack of
immunity to certain diseases that are prevalent in the region, and the
absence of medical services can add to the problem. The overcrowded
living conditions also leads to the spread of tuberculosis and the
disruption of therapy gives rise to drug resistance. The vulnerability of returnees depends on
the following factors: their nutritional status, the medical care they
have received as refugees (e.g. immunization and early treatment in the
case of disease), the amount of food they are given until they are able
to grow their own crops again, and the situation with which they are
confronted on their return home. They will often discover that the
infrastructure has been weakened or even completely destroyed in their
absence. There is often a lack of water and adequate health care.
(Sanitation will be less of a problem, provided the refugees return
straight home and do not have to stay in reception centres for a long
time. The conditions in reception centres are often similar to those in
refugee camps.) Malnutrition may cause particular susceptibility to
infections. The interruption of medical supplies will be a problem,
especially in individual cases of TB. This becomes a problem for the
community when TB spreads after drug resistances developped. These scenarios must be foreseen in good time. They
can be averted by prompt and appropriate action. When an acute disaster occurs, it can best be managed
by organisations already operating in the region and familiar with the
circumstances, if they have the capacity to respond immediately. The
time it takes an international agency to negotiate an agreement with the
local goverment can often be saved by providing direct support to
partners locally. In the event of a cholera epidemic, relief workers and
their equipment from abroad will arrive too late anyway. In the autumn of 1996, when half-a-million Hutu
refugees returned home to Rwanda from Eastern Zaire within just a few
days, it was possible to prevent the outbreak of an epidemic because the
country was already receiving humanitarian aid and the relief workers
were well-organized and prepared for the return of the refugees. On the other hand, it can be an important gesture
of solidarity when a foreign agency promptly sends one or more aid
workers into a disaster area. And if the peripheral structures of the
local partner organizations are weak or even nonexistent or if their
equipment is inappropriate, such aid workers can provide significant
support. Foreigner, who are outsiders in the civil war, can also protect
the local partner from being too exposed in a politically sensitive
situation. The following qualities are essential in people who
are engaged in disaster management, especially in epidemics: they must be
well-informed about the local situation, they must have relevant
experience, they must be able to work together with others, they must be
ready to accept responsibility, they must be able to listen and adapt
quickly, and they must be politically impartial.
III. Examples of the control of communicable diseases a. Malaria Malaria is a parasitic disease caused by plasmodium
species of different types: Plasmodium falciparum causing 'malignant
malaria'; Plasmodium vivax and ovale, 'malaria tertiana'; and Plasmodium
malariae (very rare), 'malaria quartana'. It is transmitted to humans by
the bite of an infected female anopheline mosquito, that injects the
parasite with its saliva after biting through the skin and before taking
the blood meal. The parasites have different geographical preferences and
display different clinical pictures. The most common in tropical Africa
and the most dangerous disease in humans is 'malignant malaria'. It
causes many deaths if untreated. 'Malaria tertiana' shows a tendency to
relapse irregularly some time after successful treatment. 'Malignant
malaria' (P. falciparum), on the other hand, shows at most so-called
'recrudescences' after an insufficient or inappropriate regime of
treatment. During January and February 1997 a malaria epidemic
was reported from the refugee camp 'Tingi Tingi', near Lobutu, in Eastern
Zaire. Some weeks before, thousands of Rwandian refugees, who had lived
for 2 years in the camps near Goma and Bukavu, were expelled to this area
in the course of the war. Not only small children were affected by malaria, as
was usually the case in the plains around Lobutu where malaria
transmission occurs throughout the whole year. Suddenly adults, too, fell
ill with malaria, and there were also deaths reported among them. How was
it possible that the refugees reacted differently from the indigenous
population? The explanation is simple. The newcomers came from the
mountainous area around the Kivu Lake, where malaria is not generally
found. It is only sporadically seen there, due to the altitude and a
cooler climate. In contrast to the local population, the refugees
therefore lacked a protective 'semi-immunity', that only exists in people
who permanantly live in areas with continuous malaria
transmission. Semi-immunity requires constant renewal by infection.
People don't have it for life, as is the case for example with immunity
after having measles. The epidemiological expression for this type of
malaria is 'stable malaria', whereas 'unstable malaria'
occurs in areas with only seasonal malaria. The latter often has
different annual intensities of transmission or only sporadic local
epidemic outbreaks in different years. Unstable malaria affects therefore
children and adults, because the population is only able to acquire a low
level of immunity. These expressions, 'stable' and 'unstable', refer to
the degree to which the spleen is affected among different age groups
within a population. Besides this criterium, however, morbidity and
mortality rates must certainly also be considered when measuring the
severity of clinical malaria and deciding on control measures. But the expressions 'stable' and 'unstable' are
nevertheless helpful in understanding the usual connection between
mosquito density, rate of mosquitoes infected with the parasite, and the
age group in which the disease most frequently occurs and where
complications and deaths are most commonly observed. In 'holoendemic areas', a subdivision of 'stable
malaria' areas, which provide the most effective conditions for
transmission throughout the year, mostly children under the age of 5
years suffer severely from the disease. These children have an enlarged
spleen in more than 75% of the cases. In older children the disease
becomes less severe, whereas adults are often hardly aware of their
infection because of their acquired 'semi-immunity'. If such a person leaves the area where he has lived,
he loses his semi-immunity within months (to a few years). Returning
home, he might well experience severe malaria again. The same happens to
migrants and relief workers from Europe who can fall ill, no matter how
old they are, because they lack immunity. This is the phenomenon which added malaria to the
numerous other health problems of the refugee community in the
Tingi-Tingi Camp as it does in many other war zones in tropical countries
under similar conditions. After the discovery of choroquin (a medicine that is
effective against the parasite in a particular stage of its development)
and DDT (a residual insecticide), the World Health Organization made
plans to irradicate malaria completely. It was decided to organize
regular spraying campaigns of the entire walls
of houses in areas with effective transmission of malaria through
anopheline mosquitoes every 6 months. After taking a meal, mainly in the
evening and at night in (or near) human habitats, the mosquitoes tend to
rest on walls inside the house while digesting the blood. If they come
into contact with DDT, sprayed on to the walls, the mosquitoes die.
However, this project was a failure as the mosquitoes quickly developed a
resistance to DDT. Parallel to this development, the parasite also
developed a resistance to chloroquine. This created a huge health problem
in many tropical countries, where malaria was temporarily weakened, only
to return in full force a short time later. Today we would consider it a considerable success if
malaria could be just effectively controlled. Various organizations have
tried to create more effective treatment centres in the areas where the
patients live, but not surprisingly in areas of war, migration, and great
poverty, these programmes tend to fail again and again. An additional
problem is that the population density in some areas makes irrigation
schemes inevitable to increase the crops, and these schemes also create
new breeding sites for the anopheline mosquito. The mosquitoes are able to fly greater distances (e.g.
compared with tsetse flies). This explains why malaria-free areas can be
re-invaded when the conditions are opportune. The mosquito needs
stagnant water to deposit its eggs . The time for maturing into an adult
mosquito is dependent on temperature. The development of the parasite
within the infected mosquito also depends on temperature. The mosquito becomes infected when it takes a blood
meal from an infected person. When this blood, containing female and male
gametocytes, reaches the mosquitoe's gut, these parasitic stages unite
there. After going through different stages of development, the parasite
multiplies into sporozoites which invade the mosquitoes salivary glands.
The salivary fluid, containing anticoagulants, is injected into the bite
wound in order to avoid blood clotting in the mosquito's proboscis. The
sporozoites then enter the human blood stream and invade the liver cells
within 30 minutes (except in the case of malaria malariae), where they
multiply until the liver cell bursts. The parasites (called merozoites),
thus released into the circulating blood, invade the red blood cells
(erythrocytes), where they continue their asexual multiplication. When the sporozoites invade the human blood steam, the
infected person experiences an outbreak of shivering, followed by fever,
headache, backache and general malaise. In malaria tertiana, fever tends
to reappear periodically, at the beginning of the infection, on the first
day, the third day, the fifth day etc., and continues in this way if
untreated. (The name 'tertiana' describes the fever rhythm which occurs
in this type of malaria). On the other hand, the fever in malignant malaria is
usually irregular or even continuous. And while death as the result of
malaria tertiana is extremely rare, in untreated malignant malaria severe
and fatal complications quite frequently develop. In children it can
cause severe anaemia which can lead to death either in the same or in
consecutive infectious episodes. It can also cause cerebral malaria,
hypoglycaemia and acidosis. Cerebral malaria is one the most frequent
complications among adults. In addition, renal failure, liver involvement
with jaundice and lung oedema may also occur. These conditions are due to
the breakdown of microcirculation in the capillaries of the internal
organs through uninhibited parasitic multiplication and pathological
changes of red blood cells and endothelian cells (cell covering the inner
surface of blood vessels). In pregnant women semi-immunity often leads to a mild
clinical course of malaria. But anaemia often develops as well as fetal
death, miscarriage or delivery of 'small-for-date' babies (babies with a
low birth weight after a normal pregnancy period). A child can be born with malaria. On the other hand,
provided the mother is semi-imune, a baby that is fully breast-fed is
generally protected during the first months of its life through maternal
antibodies and the chemical composition of the mother's milk. (Milk does
not contain any para-amino-benzoe-acid which the parasite needs to grow.) Malaria infections may also occur in humans as the
result of blood transfusions, needle prick accidents and oculation of
infectious blood. Unfortunately the treatment of malignant malaria is
becoming increasingly difficult, as in most areas where it is common,
resistance has developed to chloroquine and other less costly
antimalarial drugs. In describing the degree of resistance we distinguish
between 3 stages: Resistance I: Malaria infection reappears
(recrudescence) after a successful response to treatment. Resistance II: The parasites are reduced but not
eliminated, thus they multiply again after treatment. Resistance III: Parasites continue to multiply as
though no treatment had been given. (They are not suppressed by the
antimalarial drug.) Resistance may also occur in the case of some of the
more expensive drugs. Although restricted at present to particular areas,
multidrug resistance is on the increase, eg. in Southeast Asia (it is
especially severe on the Cambodian-Thai border). Often a combination of
two drugs is recommended, placing an additional burden on the health
services and health budgets of poor countries. In most countries the oldest antimalarial drug,
quinine, is still used to treat complicated malaria, but it is
administered in combination with doxycyclin except for smaller children
under the age of eight. Fansidar® was given to children instead of
doxyclin in Zimbabwe. For drug-resistant areas, a chinese antimalarial drug
(artemisinin) and its derivatives (fast-acting) are recommended in
combination with mefloquine (slowly-acting), with a single oral dose on
the second day of treatment (or when the patient's condition allows.). As wide-spread prophylactic treatment would be likely
to encourage the development of drug resistance, prophylactic consumption
of artemisinin and its derivatives is prohibited on ethical grounds.
Unfortunately, however, this drug is very widely available, e.g. you can
buy it in every supermarket in Kenya. It is therefore doubtful if this
promising drug will be helpful in curing complicated malignant maleria
for very much longer. The development of resistance is especially worrying
as no malaria vaccines are yet available on the market. The more resistance there is to the drugs, the more
attention we have to give to the old simple, well-known barrier methods
which decrease malaria transmissions by reducing contact between human
beings and mosquitoes. The traditional methods include bed nets (most
effective if impregnated with pyretrum, permethrine or deltamethrine,
which must be done annually); window screening; or by wearing protective
clothing especially in the evening. Especially for small children, who
are put to bed early, mosquito nets can be very effective in reducing the
frequency of infection and thus diminishing the severity of childhood
anaemia. However the question remains: under conditions of
poverty and political unrest, where the houses are built of mud and grass
and have leaky doors and window frames, whether these measures are
really appropriate. Furthermore, other methods to fight the mosquito do
not seem to be particularly effective, especially in view of the fact
that global heating resulting in the increase of average temperatures
worldwide will favour the further spread of malaria. Methods used so
far, besides the residual spraying of the walls of houses, include the
treatment of water surfaces with little polystyrene balls to prevent the
depositing of eggs, the introduction of larvae-eating fish into infected
waters, and the sterilization of mosquito males, to mention just a few.
For the treatment schedule please consult one of the
books recommended at the end of this chapter. b. African Trypanosomiasis
(Sleeping sickness) Today, in 1997, we again hear
reports of civil unrest in northern Uganda, which could be the beginnings
of renewed civil war. The 'Lord Resistence Army', which is evidently
supported by Khartoum, is terrorizing the civil population. This population still remembers the last Ugandan civil
war only too well, where nearly the entire population from that area had
to seek refuge in neighbouring Sudan. They were only willing to return
home when the political situation had stabilized, after Museveni's coup
d'état in 1986. But in the meantime the Sudanese conflict had
deteriorated, which resulted in the enforced repatriation of the
Ugandans. During their 6 years of absence, their fields had lain fallow,
and the bush savanna had encroached and taken possession of their land.
Especially along the rivers, the dense vegetation had become an ideal
habitat for tsetse flies, and there was a growing population of them. When the UNHCR (United Nations High Commissioner for
Refugees) prepared the reception centres along the border for the
repatriation of the refugees, the lorry drivers had to close their
windows in order not to be immediately eaten up by the fies. However,
they facilitated with their lorries the wider distribution of tsetse
flies along the road parallel to the border . Without transport, the
flies are usually restricted to a small area as they cannot fly long
distances. The tsetse fly (glossina) is the vector responsible
for the transmission of the sleeping sickness, also called African
trypanosomiasis, which is caused by parasites named
trypanosomes. Three different types are known: Try
panosoma b. brucei, which only infects animals; trypanosoma b.
rhodesiense, a zoonosis with its reservoir in wild animals, which
occasionally affects humans; and Trypanosoma b. gambiense, the reservoir
being human beings and also pigs (possibly other domestic animals too).
The three different types are morphologically identical (i.e., they are
not distinguishable under the microscope). While trypanosoma rhodesiense is not well adapted to
humans, the infection follows a severe and rapid course. It quickly
involves the brain and ends fatally. On the other hand, trypanosoma
gambiense has become quite well adapted to its human host during its
evolution, and creates mild and unspecific symptoms for months and
sometimes years. But also this type will finally affect the brain and
lead to death. Because of its chronic course, it is often only in that
late stage that the disease can be diagnosed easily. For the early stage of both types of trypanosomiasis,
treatment with less severe side-effects is available (suramin and
pentamidin). But after passing into the cerebrospinal canal, the
parasites are much more difficult to eliminate. The preferred drug at
present is melarsoprol, a toxic substance causing arsenical
encephalopathy in some cases. This can result in the patients death (in
about 1-5% of cases; death is to some extent related to the physical
condition of the patient). On the other hand, without treatment in that
late stage, the patient would die anyway. Difluoromethyl ornithine (DFMO)
is used at present in treating single cases. For mass treatment the drug
is not appropriate, as it is far too expensive, more difficult to apply,
and production of the drug still falls far below the enormous demand. Therefore the solution cannot be to wait until the
final stage of the disease, responding only then with diagnosis and
treatment. One must actively search for cases in the early stages, which
not only helps the individual but also importantly reduces the
reservoir. Parallel to this activity, attempts to reduce the tsetse fly
population should also be made, e.g. by the use of fly traps. Despite the fact that a tsetse fly and
trypanosomiasis control programme was already functioning in Southern
Sudan at the time when the Ugandan refugees returned home, no exact
infection rates were known for trypanosomiasis in the indigenous
population. This was due to great differences from place to place and
even among the population of one village. The occupation of the
individual and the radius of his mobility strongly influenced the degree
of exposure and hence the risk fact or. One could only estimate an
infection rate of between 1-2%. This infection rate was also assumed to
be valid for the refugee population. Only infections with trypanosomiasis
b. gambiense with its slow development were diagnosed in that area where
the refugees had lived for the past 6 years. Thus the repatriation meant, in effect, that infected
people would be coming into an area of heavy tsetse fly infestation. One
could assume that the flies, which until then had not had much contact
with humans, could easily become infected. Even if it is true that the
rate of infection within tsetse fly populations themselves is usually
low, the great number of flies in the area would greatly facilitate the
spread of infection among the returning population in this case. Furthermore,
the entomological examination showed that the species of fly found in the
area was well able to transmit gambiense sleeping sickness to human
beings (pigs were not kept in the area and domestic animals were rare).
Uganda has had a lot of experience with sleeping
sickness in the past. Even the British colonialists ran an effective
control programme, aimed at reducing the tsetse fly populations and
detecting and treating early cases in the animal reservoirs and in
humans. In the south-east of Uganda trypanosomiasis rhodesiense had been
a common health problem in the past, then successfully controlled until,
at the end of the civil war, it reappeard in epidemic proportions. The
same was thought to happen in West Nile, North-eastern Uganda, but
exclusively with the trypanosoma gambiense infection. The Ugandian Ministry of Health, which took charge of
the situation, and its well-trained technical staff as well as the NGOs
coming from abroad were prepared to start control measures immediately.
But the doctors and nurses in the North were much more difficult to
convince, since they seldom met the disease in its late stage. (Patients
were treated separately in the Sudan, not in the normal health
institutions.) In addition, they were faced with a great number of acute
health problems which they considered much more important than the
sleeping sickness diseases such as malaria, diarrhoea, worm
infections, malnutrition, tuberculosis and many others. Also the refugees had difficulty in understanding the
neccessity for the examination procedure. In the reception camps
refugees were lined up and checked for clinical symptoms, especially for
palpable lymphnodes of the neck. Serum was
taken and a screening test the -called CATT-Test was performed on
each person, which had the disadvantage of 5 % false positive results.
Those with positive results had to be transferred to the hospital for
further examinations. Unless the parasite was found in the blood, the
diagnosis was not certain and no treatment could be started. Even with
concentration techniques (Buffycoat examination from centrifugated blood
and Lanham column provided by WHO), trypanosoma gambiense is difficult to
detect. Therefore it was recommended by WHO and the Ugandan authorities
to perform at least 7 different blood examinations on different days
before sending people home. The refugees who felt healthy often left the hospital
before this run of examinations was complete. Of course this was
understandable. They had been out of the country for many years and had
to start rebuilding their houses and cultivating their fields again. The
general population had quite different priorities from the medical
authorities and the expatriats. It became obvious that other control measures had to
be tried additionally, like vector control. Soldiers were instructed to spray passing cars at road
blocs. At first they cooperated very well, as it made their boring job
more interesting. However, after a short while, the spraying equipment
disappeared and it was obvious that it had been sold. In addition, cloth and sewing machines were bought and
women were employed to produce tsetse fly traps.
Tsetse flies are attracted by dark moving spots and
blue colours. When they approch a trap of black and blue cloth, sewn in
the form of a pyramid which is then hung from the low branch of a tree
and moves in the wind, they search for a hole in it and enter the trap.
Once in the trap, they fly towards the light in order to escape. But
their way is blocked by curtaining material at the top of the trap. When
they are exhausted, they fall into a fold of the curtaining material
under the cover of the trap and eventually they die. Impregnated with
insecticides, these traps are an effective, complementary method of
killing great numbers of vectors. In Uganda these traps were placed in the bush,
especially where people fetched water on the river bank. There the
contact between flies and humans was at its most intense. This programme, too, was not very successful at first.
The traps were stolen because the people couldnt understand the sense of
hanging such nice pieces of cloth in the bush, while some of their
children had to go naked. Looking back, we should not have been surprised
to see babies being baptized in
beautiful blue-coloured dresses, the origin of which was only too
obvious! This attitude of the people could only be
changed by posting one person next to each of the traps to guard it during
the daytime, providing him with food-for-work. (As tsetse flies only fly
during daylight, the traps could be collected in the evenings.) But the population also helped to control the
flies and the disease very effectively though unintentionally! by
clearing the bush, burning the grass and cultivating the land. Because
the area is so densely populated and because the whole population came
back within a short time, the environment that was ideal for the
multiplication of tsetse flies was quickly destroyed. The cases of sleeping sickness were registered. Cases
diagnosed in the late stage had to be treated in spite of toxic
reactions. The risk of fatal side-effects had to be accepted, and in fact
there were some deaths. However the outbreak of an epidemic was avoided.
The health problem disappeared by itself. Sadly, the story in Southern Sudan is a
different one. Here the control programme, run by Belgians, had to be
stopped because of the local political situation. Many people left the
area to seek refuge elsewhere. Their fields were left abandonned and
uncultivated . At the same time the health system broke down. Probably it
will only be possible to assess the dimensions of the problem when the
war finally comes to an end. The duration of wars in these countries is
a most significant factor, since they cause the environment for the
tsetse flies. Sleeping sickness is not the only disease that profits from
wars and unrest. But it makes the connection between disaster and disease
very clear. To see what dimensions sleeping sickness can assume
after a war of 20 years, we have only to look at Angola today.
There the disease is so wide-spread and the late stages of the disease so
common that the people don't need to be convinced that early diagnosis
and treatment would be a good thing. In spite of massive financial
support from outside the country, the capacity of the health
organizations is still inadequate. It is not even possible to provide
treatment for every person displaying symptoms. They are far removed from
the goal of actively looking for cases of the disease and slowing down
its spread. And since large areas of the country are still unsafe
in 1997, control of the disease will be very difficult to achieve in the
foreseeable future. In this setting, it is time to give less priority to
the well-being of the individual patient as painful as this decision
may be and to consider how best to use the financial resources that are
available or can be mobilized in order to stem the epidemic as a whole. c. Cholera
In 1996, when half-a-million refugees crossed the
'petite barrière', the narrow boundary between Eastern
Zaire and Rwanda, many of them were suffering from diarrhoea. Some had
typical symptoms of cholera, such as ricewater diarrhoea with great loss
of fluid and consequent dehydration (sunken eyes, decreased flexibility
of the skin, an accelerated and weak pulse, and the tendency to
collapse) as well as muscle cramps caused by electrolyte deficiencies.
These symptoms were more than sufficient reason to conduct laboratory
examinations. Twelve of these patients were found in fact to have
cholera. (This could have been merely the tip of an iceberg. Were these
cases the first of a new epidemic among the huge mass of humanity that
had passed the main road into Rwanda within just a few days?) Some of the
preconditions that had caused such an outbreak in 1994, when the same
group of people had moved in the opposite direction to Zaire, were
again present. The people were weakened by walking for so long
bare-footed. They suffered from lack of water. The possibility that the
limited water sources along the road were contaminated with cholera
couldn't be ruled out. Sanitation had been nonexistent on the Zairean
side of the border as well as on the Rwandan side. However, the disaster
which was feared did not occur. What were the circumstances that
prevented it from happening? Cholera is a disease that originated in Asia. Since
1970 there have been reports of epidemics in Africa, and since 1990
cholera is also on the increase in South America, having begun in Peru.
Cholera infection is caused by the toxin of the Gram-negative,
comma-shaped bacillus called vibrio cholera (with a number of
subtypes), which causes a secretion of Na+, Cl- and HCO3 in
the upper bowel, resulting in a massive efflux of water and preventing
reabsorption. This is the reason for the characteristic cholera diarrhoea.
The disease is transmitted from one human being to
another by the faecal-oral route. Not every one who comes into contact
with the bacteria falls ill. The quantity of bacteria transmitted, the
virulence of the bacterial subtype and the presence or absence of gastric
acid determine whether the person becomes ill. Some people become chronic
carriers of the disease. While some cases are characterized by massive
diarrhoea, causing a condition that can end in death within a few hours,
other patients only experience a mild gastro-enteritis. Therefore every
occurence of diarrhoea has to be considered as a potential symptom of
cholera during an epidemic. If a patient survives the first 24 hours, it
usually means that he has overcome the critical peak in the course of the
disease, and he then generally makes a quick recovery (usually within
another 2-3 days). Crucial intervention in the course of the disease is
the immediate replacement of the fluid (very large quantities) and
electrolytes lost, the replacement quantities strictly corresponding to
the losses. By giving the right antibiotics at once, the entire course
of the disease can usually be limited to about 2 days.
In infants, meningitis-like symptoms may occur,
sometimes accompanied by convulsions. However, these may also be due to
the mode of rehydration. Children excrete less sodium and more potassium
into the intestine than adults suffering from the disease. Therefore
oral rehydration must always be given priority even though it requires
enormous patience and oral fluids usually have to be administered
through gastric tubes. If intensive parenteral rehydration is unavoidable
because the child is also vomiting, and if under the given circumstances
different fluids are available, fluids with less sodium (such as Half
Darrow's Solution) should be administered instead of just Ringer Lactat,
which is recommended for rehydration in adults.
There is a vaccine available, which has to be injected
twice in order to give individual protection within 1-4 weeks in up to
60% of those immunized. However, it is of no use in epidemics as it does
not prevent transmission. The WHO therefore does not recommend
immunization at present. But in Sweden and Switzerland a new oral vaccine
has recently become available which may prove more effective.
Just as important as the medical treatment itself is
the mangement of the situation during or before the outbreak of
an epidemic. If the epidemic can have catastrophic results, such as is
the case with a cholera epidemic, the mangement of situation is even more
important.
In Rwanda, in the autumn of 1996, a cholera
epidemic was avoided because of preparedness and good management:
1. The humanitarian organizations were already
present, well-organized and equipped when the refugees arrived at the
border. 2. Cooperation with government officials and local
authorities was possible. 3. The communication and cooperation between
relief organizations of different types was already well-organized, and
it intensified during the following days and weeks. 4. Sufficient supply of drinking water was provided
along the road, with taps to prevent contamination. 5. In so-called 'care stations', every 5 kilometres
along the route, exhausted and sick refugees could be treated. 6. The transport of severely ill people to the nearest
possible hospital was organized. The hospitals were adequately staffed
and equipped. 7. The stream of refugees was not allowed to halt
except at night, when small grouping was permitted with limited numbers
of people along the roadside. Forcing the majority of the refugees to
continue walking, which some observers simplistically considered cruel
or likened to a kind of punishment, was the only way to achieve a rapid
and safe repatriation. If this mass of humanity had come to a halt during
the first few days, this would certainly have resulted in a chaotic
situation and increased the risk of an epidemic outbreak of cholera. (It
became possible within a few days to provide lorries for a more human and
even more effective rapid repatriation). 8. The most vulnerable groups were identified as such
beforehand e.g. unaccompanied children, the elderly, and disabled
people and organizations were appointed to take care of them. 9. Food was provided exclusively in the form of dry
rations, protein biscuits providing all the nutritional requirements of
the human organism. They were only distributed in the evening in order to
avoid large, uncontrolled gatherings of people. Inevitably the people
would have come together in this way if other types of food had been
distributed, which needed cooking or diluting and couldn't be consumed
while moving. 10. Finally, there were special cholera units placed
near hospitals, which were prepared and equipped to take care of small
numbers of patients (10 to 15) in the early stage of a possible epidemic.
This was merely a preventive measure, and fortunately it was never
required.
There are different views on how to set up a cholera
unit. In his thesis, Ure (1988) gives an example of how such a situation
in Somalia was effectively managed some years ago. His account provides
very useful guidelines for similar situations.
For someone who might at some future date be
confronted with an outbreak of cholera which he/she has to help manage,
it is a most useful exercise to reflect on the special conditions within
a given geographical and social environment where you have worked before.
You should consider ways of setting up and mangaging a cholera unit under
pressure of time and consequently, if possible, with resources that are
already available locally.
Against this background, the following questions
should be answered:
Cholera is often considered to be merely a medical problem, but the epidemic is of general concern and in no way can it be managed by the physician-in-charge alone. The above list of questions that have to be answered and decisions made has little in common with the curriculum that doctors follow in medical schools! It should be obvious that other professionals can also be involved people who are used to clear thinking and decision-making, those with management skills and authority within the community.
Returning to our starting-point: it must be stressed that the conditions in which a cholera epidemic is likely to occur should, at best, be foreseen and eliminated before the actual epidemic breaks out. Worldwide there is still a lot to do in this respect.
In Freetown, Sierra Leone, a three-storeyed children's hospital, situated close to the habour and ironically planned as a referral centre for cases of cholera, had all its toilets blocked or destroyed when it was visited in 1996. This is a disasterous situation, and it is sad that potential donor organizations know of such a situation and hesitate or find no way to intervene.
Of course intervention in such a situation earns much less public acclaim and fewer public donations than the management of a cholera epidemic, once it has started! This is the situation and the frustration which a relief worker might be faced with, once he has understood the whole context of cholera.
d. Meningococcal Meningitis Meningitis is an inflamatory infection of the
meninges, causing symptoms of fever, headache, nausea, vomiting and
neck-stiffness. In infants (under the age of 2 years) the neck-stiffness
can be less pronounced or even missing. But the fontanell is seen to be
bulging in the fully-developed disease. Symptoms like drowsiness,
confusion and even convulsions may occur.
Different sorts of infectious agents can cause these
symptoms. The most frequent in southern countries where living
conditions are poor are probably:
1.
2. viral meningitis or viral meningo-encephalitis (mostly diagnosed after excluding the others)
3. bacterial meningitis :
Besides clinical symptoms, microscopic examination of the CSF (cerebral spinal fluid) is important for the diagnosis. The CSF in viral meningitis and in cerebral malaria is mostly clear (like water), even if the microscopic cell count is increased. In bacterial meningitis, the CSF is cloudy (except in TB-meningitis!). (Malaria can be diagnosed in a thick film of peripheral blood, for differentiation of bacterial meningitis, special staining methods are available.)
4. cerebral toxic reaction: neonatal tetanus (after delivery in unhygienic conditions,
3-10 days after delivery when the cord care is inapproprate; when the mother is not immunized)
In 1981, at the end of the dry season in the region known as West Nile, in Northern Uganda, a sudden outbreak of purulent meningitis occurred in children and young adults. This region belongs to the south-eastern extension of the so-called 'Meningitis belt of Africa'. Therefore it was immediately suspected that these meningitis cases were the beginning of an epidemic.
The microscopic examination of the CSF-sediment (staining with Methylene blue and Gram Staining) in the only functioning hospital of the district showed diplococcae which were "Gram negative". Together with the clinical signs, the time of onset (during the dry season) and the geographical characteristics, the diagnosis was quite certain. Other diagnostic procedures, that may usually help to provide 100% confirmation of the diagnosis in individual cases, were not available.
A spread of disease among patients and the relatives taking care of them had to be avoided. In addition, waiting for the patients to be brought to hospital would have involved carrying patients very long distances, delaying treatment (with the risk of more deaths and cerebral complications) and also risking new infections among contacts on the way.
Meningococcae are transmitted by droplet infections. They may be present in the pharyngonasal cavity without producing symptoms. But from there they can also invade the blood stream and infect the membranes of the brain and the spinal cord. The incubation period (the time between infection and the appearance of symptoms) usually lasts between 1 day to 1 week. Two types of meningococcae are usually responsible for epidemic outbreaks : Type A and C. Vaccines are normally available from centres in capital cities.
But in 1981 Uganda was involved in a civil war. Radio communication was not as wide-spread then as it is nowadays in southern countries, even in war zones. Consequently action had to be taken which did not include vaccination.
At first those villages and compounds were registered, where meningitis cases had occurred. On a detailed map of the area the center of the epidemic could be identified. Then a small team of hospital personnel went there and met with the local authorities (chief, clergy, headmaster).
The team succeeded in informing and persuading the authorities that control measures had to be taken by the community. These included the closing of schools and the temporary prohibition of markets and other public assemblies in the affected region. General information was distributed to facilitate the early diagnosis of new cases within the community. The school and church compound were turned into a centre for the diagnosis and treatment of meningitis patients. Shortly after this meeting, two medical staff (a doctor and a nurse) were moved to the church compound where they were helped by the teachers of the neighbouring school. Within a short time, such a great number of patients were brought to them that a microscopic CSF-excamination of all suspected cases was impossible. Instead all patients with clinical signs of the disease received a lumbar puncture.
If the spinal fluid was clear (like water), the patient was transported to the hospital, but if it was cloudy the patient was admitted to the emergency ward set up in the church and given intravenous antibiotic treatment (penicillin) immediately. (Of all the patients diagnosed in this way (about 400), only one diagnosis was false-negative for meningitis. And this false diagnosis was corrected the next day, when the lumbar puncture was repeated.)
The second dose of antibiotic treatment was then administered at the same time as the other patients received their treatment, 6-hourly (at 6 a.m., at 12 noon, at 6 p.m. and at midnight) for 5 days. In the case of vomiting, infusions were applied, the bottles being hung from wires stretched down both aisles of the church. A small truck brought a tank of clean drinking water every day for the patients and the relatives taking care of them. Each patient was permitted only one relative to stay. These people and the other direct contacts were given prophylactic antibiotic treatment daily.
Provided the patient's condition had improved and he returned to full conciousness, intravenous treatment was discontinued after 5 days and substituted with orally administered Choramphenicol (for children a pleasant tasting syrup is available). At this point the patient was moved to the neighbouring school for another 5 days.
Parallel to these activities, the local authorities also organized an active search for further cases, visiting every family in the community.
It may be assumed that this swift and well-organized response to the occurence of meningitis cases during a relatively early stage of the epidemic significantly limited the spread of the disease, saved the lives of many patients, and prevented complications with only a few exceptions. The number of cases decreased after just two weeks, and with the beginning of the rainy season, the epidemic ended within 3-4 weeks, and there were no further cases.
(Unfortunately the meningitis epidemic was immediately followed by an outbreak of typhoid fever, which typically develops during the rains.)
In this particular case of an epidemic of meningococcal meningitis in Uganda, fortunately (petechial) bleedings in the skin and mucous membranes did not occur. These are due to capillary damage and caused by toxins occasionally elaborated by the micro-organism (Waterhouse-Friderichsen Syndrom, sometimes associated with shock especially in small children and babies).
The preferred therapy in disaster areas nowadays is Chloramphenicol (in oil-suspension) administered intramuscularly. It can be given once every 24-48 hours during large outbreaks and is very cost-effective.
Sometimes resistence develops, as with Penicillin. Ampicillin, given 3-4 times daily, and Cephalosporines are also effective but much more expensive.
The incidence of 20 meningococcal meningitis cases per week in a population of 100,000 is considered an epidemic. They occur mainly in the Sahel Zone, in northern India, Nepal and the slum areas of South American megatowns. The frequency of epidemic outbreaks in one specific area influences the average age of those afflicted in the area (the shorter the intervals between the epidemics, the younger the patients).
e. Tuberculosis
The civil war in Liberia caused large numbers of the rural population to seek refuge in the two major towns, Monrovia and Buchanan. Many of them were taken in by relatives. Others took shelter in public buildings that were still under construction. But when the fighting spread to Monrovia itself in April and May 1996 and the urban population and their homes were attacked, whole districts of the town became uninhabitable. Living space became even more cramped.
Not surprisingly under these conditions, tuberculosis spread rapidly. The tuberculosis control programme that had been operating in Liberia before the war had collapsed with the outbreak of hostilities. Thus on a field trip to the war-torn region in the summer of 1996, an important question to be assessed was whether, despite the civil war, it would be reasonable to start a new tuberculosis control programme in Monrovia and/or Buchanan. In both cases the answer was yes.
The following preconditions must be fulfilled before a tuberculosis programme can be started:
Tuberculosis is caused by tubercular bacteria, which are mostly conveyed through droplet infection, by coughing, from one infected person to another (and occasionally through fresh milk from infected cattle). The infection usually disappears by itself. Only in a small percentage of cases, it causes a local infectious inflamatory reaction of the lymph nodes (primary complex), which again mostly passes unnoticed. The early haematogenic scattering can lead to miliary tuberculosis and tuberculous meningitis, mostly in children.
The tubercular bacteria remain infectious in the lymph nodes but are encapsulated in granulomatous tissue. When the organism has been weakened as the result of other diseases (e.g., measles, HIV infection, diabetes mellitus), drugs (e.g., cortisone) or malnourishment, such sources of infection can be reactivated. (The disease develops in 15% of infected persons.) Thus the tubercular bacteria reach the lungs but also other organs, such as the kidneys; the spine, the meninges etc. via the blood circulation and can cause an organic tuberculosis there. In the lungs it is often the apex that is infected. If the infectious reaction spreads into the branches of the bronchial tree and the infamed tissue dissolves in the course of the infection, bacteria can be emitted from the body through the bronchial tubes, and other people in the vicinity of the diseased person can be infected. This is termed open tuberculosis.
Control programmes in countries where the disease is widespread aim at the fastest possible diagnosis and effective treatment of patients with open tuberculosis. However, such a programme involves considerable responsibility. When the therapy is disrupted as is often the case in war zones the TB germ develops resistances to the available medicines and poses a greater threat to human society worldwide.
There are many ways of preventing the disruption of therapy. Since tuberculosis is also a disease of the poor, it is not suficient to hand out medicines; feeding must also be monitored. Little work programmes to accompany the therapy, or rewards for fulfilling part of the regime sometimes provide motivation. The importance of the therapy can be emphasized by signing a contract with the patient in the presence of an official witness before the regime starts.
It is a matter of controversy, whether patients should pay money for being treated. One often places more value on the things one has to pay for. But when patients find it difficult to pay fees, they may tend to delay appointments or discontinue the therapy altogether.
The patients often include teachers. Such people are often well-suited for training as assistant health workers (during the time that they are released from teaching). They can then spread information about tuberculosis control. TB sufferers in many countries are discriminated against; knowledge combats such discrimination. Education programmes can result in a rapid increase in the number of patients requesting diagnosis and treatment, thus increasing the effectiveness of the control programme.
The programme in Liberia fulfilled all the criteria, listed above. Nevertheless the work in Monrovia was disrupted after just a short while. It had been guaranteed exclusively by foreign workers, and these had to leave the country on account of the security situation. Before departing, they tried to ensure a continuation of the medical treatment during the first 2 months the intensive phase of treatment. Happily, the programme in Buchanan, on the other hand, continues uninterrupted.
The example of Monrovia, however, shows how careful one must be when starting a tuberculosis control programme, especially under the unpredictable conditions of war.
A note on immunization and tuberculin tests:
The BCG immunization with weakened bacteria from a species of cattle, intradermally injected, does not prevent infection or the later reactivation of the bacteria. However, it does prevent the haematogenic development of miliary tuberculosis and tuberculous meningitis. Especially in developing countries, it should be given to all children as early as possible.
Immunized children living with an infectious person in the same household should be given 3 months' chemoprophylaxis, while non-immunized children should be given a course of 6 months. (Children with a failure to thrive, which cannot explained by another reason and successfully treated, should be considered as TB and treated with a combination of three different drugs.)
The tuberculin test, which consists of a special tuberculosis protein or a refined protein derivative, is injected intradermally. When positive, it causes a hypersensitive reaction in the form of a small area of hardened skin. This indicates that an infection has occurred (acute, symptomatic or asymptomatic), or that the subject has been immunized. However, when the immune system is defective particularly in advanced HIV infection and severe malnutrition the test is mostly negative, even when the subject is infected with tubercular bacteria.
f. Measles
The Luwero Triangle, about 70 km northwest of Kampala, was one of the most dangerous places to live in 1984, during the civil war. Nevertheless a great number of the civil population had no alternative but to stay and try to survive, sometimes hiding in the bush, sometimes cultivating land as far as possible away from the roads in order to avoid being harrassed by the soldiers.
To re-open a hospital in the middle of the Luwero Triangle in such a situation and after it had not operated for years was a risky enterprise. It was evident that people would come from all directions to the only place where they could expect to find medical care. Thus contagious diseases could easily spread in a population that had already suffered so much, were not immunized, and whose nutritional status was worse than simply insufficient. Some of them lived in camps, especially the descendants of Rwandan refugees from the south of Uganda, after losing their cattle.
The medical team from abroad was well aware of the potential risks of their work. They immediately started immunization of children in the hospital, especially against measles. Every child that was brought for medical treatment, no matter what the complaint, was vaccinated against measles before the specific case was even examined.
In addition, the team organized mobile health services in order to make their services more readily available to the people in need, especially those living in camps.
But despite all these measures, the hospital still became a draw-factor for the sick. Instead of the maximum 120 in-patients, the number of admissions to the hospital more than doubled in a short time. In addition, many more were seen daily in the out-patients' department.
In spite of the immediate vaccination and the careful handling of the measles vaccine (which is extremely sensitive to gradual changes of temperature and short interruptions of the cold chain), an epidemic of measles occured.
Why?
Looking back, one can ask if every one of the new patients was really vaccinated immediately after admission, or if perhaps a few of them escaped immediate vaccination when they came in the middle of other emergencies or late in the evening. The number of trained medical staff was of course limited, and obviously they could not be everywhere they were needed at the same time.
But these considerations alone cannot explain the dimensions of the measles epidemic that blew up.
It became a horror scenario for about 6 weeks and a very traumatic experience for all involved. 10 % of the children admitted to the hospital with measles died. On one single day, at the peak of the epidemic, which no one from the medical team will probably ever forget, ten children died mostly after the onset of the disease, with severe laryngitis, creating a terrible sense of helplessness and even a feeling of responsibility and guilt.
'Measles is an acute, highly contagious viral disease which is a scourge of children in all the developing countries'. It is transmitted from person to person by droplet infection and usually starts with symptoms easily confused with a severe common cold: soryza, pyrexia, conjunctivitis, coughing and loss of appetite, and these symptoms are often accompanied by dehydration as the result of diarrhoea and vomiting.
On dark skin the common skin rash is more difficult to recognize before it causes desquamation at a late stage. But little white-grey spots with a reddish base, called 'Koplik dots', appearing on the inside of the cheeks, make a firm diagnosis possible at an early stage. Common symptoms during a severe attack are also sores in the mouth (which can prevent breast-fed children from sucking), laryngitis, bronchopneumonia, extensive weight loss and bleeding of the nose and gums. Sometimes convulsions may occur during bouts of high fever and also the brain can be affected in small children. The most striking problem is that the children become very prone to bacterial infections, such as pneumonia, otitis media and tuberculosis. They often continue to lose weight after the acute measle infection and show signs of marasme or kwashiorkor, accompanied by iron and vitamin A deficiency.
As in most virus infections, only symptomatic treatment is available once the infection is acquired. Much emphasis has to be given to immediate rehydration and prophylactic treatment of the mouth (with gentian violet) as well as supplementary vitamin A (to avoid eye complications). Therapeutic feeding with a lot of patience is the most crucial response, as these children have no appetite at all. One person is required just to instruct the mothers and to insist on continuing breast-feeding right from the beginning, combining this with food supplementation as well as constant feeding of small amounts of an appropriate solid food mixture (in increasing concentration) to the weaned and older children as soon as the vomiting has stopped.
Secondary infections require early diagnosis and antibiotic treatment. If tuberculosis is suspected in these severely malnourished children after the acute measles infection, one should not wait for a positive tuberculine reaction (skin reaction after inocculation of toxines, produced by tuberculous bacilli or its purified protein derivatives). These children too often lack the capacity to give an appropriate skin immune reaction. A positive test is only possible later when the childs condition has improved.
Immediate active immunization (with the measles vaccine, an attenuated living virus vaccine) usually prohibits the infection of contacts.
The most probable reason why immunization was not effective in many children during the measles epidemic of war-torn Uganda in 1984 was their poor nutritional status at the time when they were exposed to the infection. This probably resulted in a very severe immune suppression, with little or no antibody production against the attenuated virus in the vaccine within the incubation period. Thus passive immunization (serum already containing antibodies of a person that had gone through the infection) would have been the only effective protection at that time. Unfortunately in the given situation it was not available.
The highest percentage of infections in Uganda happened to occur among children of the Rwandan refugee community. As they were mainly restricted to camps, their cattle taken by the Ugandan soldiers, the Rwandans were the most vulnerable group in the Luwero Triangle and further south of it at that time. But even this identification and the special emphasis put on their care from the side of the medical professionals didnt have the expected effect. Their political marginalization, which was the root cause of their vulnerability, couldn't be changed. It is therefore not surprising that they helped Museveni to take over the country in the hope of improving their own situation in this way, with the ultimate goal of returning to their own country, Rwanda, as soon as possible.
After the war the immunization programme was successfully intensified in Uganda (by the Ugandan Ministry of Health, supported by UNICEF) . Today measles occurs extremely rarely in that country, and mortality as the result of measles no longer plays a role in the health statistics of Uganda.
IV. Other diseases, possibly occuring in disaster situations, their mode of infection, treatment and control:
|
DISEASE |
MODE OF INFECTION |
TREATMENT |
CONTROL |
|
Scabies |
skin to skin contact (mites) |
repeated treatment of the patient and the contacts |
adequate water supply |
|
Respiratory infections |
droplet (viral, bacterial) |
virus: symptomatic bacterial: antibiotic |
ventilation, avoid overcrowding |
|
Whooping cough
|
droplet |
antibiotic |
routine immunization |
|
Worms e.g. ascaris, hookworms |
faecal-oral (eggs) faecal-skin (larvae) |
antihelmintica (worm medicines) |
lavatories personal hygiene shoes |
|
Trachoma |
eye-hand-hand-eye |
antibiotic ointment |
water supply personal hygiene |
|
Hepatitis A |
food contamination (virus) |
symptomatic |
water supply food preparation (immunization) |
|
Hepatitis B/ HIV infection |
sexual intercourse blood, needle sharing, mother-to-child |
symptomatic |
behaviour change STD-Control, Transfusion care, (immunization) |
|
Syphilis |
as above |
penicillin |
as above |
|
Gonorrhea |
sexual intercourse mother-to-child (ophthalmia neonat.) |
antibiotic treatment (antibiotic eye ointment) |
STD-Control, routine silver nitrate, prophylaxis |
|
Typhoid Fever |
faecal-oral (or by food contaminated e.g. by flies, contaminated water salmonella)
|
antibiotic |
lavatories, personal hygiene, treatment of food, safe water |
|
DISEASE |
MODE OF INFECTION |
TREATMENT |
CONTROL |
|
Amoebic Dysentery |
faecal-oral (contamination of food with amoebic cysts) |
amoebicides |
as above |
|
Bacillar Dysentery |
smear infection, contaminated food, faecal-oral |
rehydration, selective chemo-therapy |
as above |
|
Dengue Fever |
mosquitoes (viruses) |
symptomatic |
vector control |
|
Lassa Fever |
mammals (mice), viruses |
antiviral |
source control (mammals) |
|
Tetanus |
contaminated soil - skin wounds |
symptomatic Tetanushyperim-mun-globulin, antibiotics |
routine immunization |
|
Relapsing Fever |
lice or ticks (borrelliosis) |
Doxytetracycline Tetracycline |
clothing lice: delousing, insecticides |
|
Epidemic Typhus |
louse-borne (rickettsia) |
Doxytetracycline |
as above |
|
Endemic Typhus |
flea-borne |
Doxytetracycline |
as above |
Further Reading
Publications in German
|
1997: |
Kraus, H., et al., Zoonosen, Von Tier zu Mensch übertragbare Infektionskrankheiten. Deutscher Ärzte Verlag, Köln. |
|
1996: |
Knoblauch, Jürgen (Hrsg.), Tropen- und Reisemedizin. Gustav Fischer Verlag, Jena/Stuttgart/Ulm/Lübeck. |
|
1996: |
Metzger, C.E. und Ries, Renate, 'Verkannt und heimtückisch': Die ungebrochene Macht der Seuchen. Birkhauser Verlag, Basel/Boston/Berlin. |
|
1990: |
Warrell, D.A. (Hrsg.), [Übers. Kleinheinz, Andreas), Infektionskrankheiten. Edition Medizin, Weinheim. |
|
1981: |
Stürchler, Dieter, Epidemiegebiete tropischer Infektionskrankheiten: Karte und Texte für die Praxis. Verlag Hans Huber, Bern/Stuttgart/Wien. |
Publications in English
|
1997: |
Bell, Dion R., Lecture Notes on Tropical Medicine. Blackwell Scientific Publications, Oxford. |
|
1996: |
, Tuberculosis Guide for Low Income Countries. International Union Against Tuberculosis and Lung Disease, Paris. [See address list, below.] |
|
1995: |
Krawinkel, M., and Renz-Polster, H., Medical Practice in Developing Countries. Jungjohannverlagsgesellschaft, Lübeck/Ulm. |
|
1993: |
, The Control of Schistosomiasis, WHO Technical Report Series 830, Geneva. |
|
1993: |
Desenclos, J.C. (ed.), Clinical Guidelines: Diagnostic and Clinical Manual. Medicins Sans Frontières, Paris. |
|
1991: |
Hendrickse, R.G., Barr, D.G.D., Matthews, T.S., Paediatrics in the Tropics. Blackwell Scientific Publications, London. |
|
1990: |
Cook, G. C., Parasitic Disease in Clinical Practice. The Bloomsbury Series in Clinical Science. Springer Verlag. |
|
1990: |
Mandell/Douglas/Bennet, Principles and Practice of Infectious Diseases. Churchill Livingson, New York/Edinburgh/London/Melbourne. |
|
1988: |
Werner, David, Where There Is No Doctor. A village health care handbook. MacMillan Tropical Community Health Manuals [T.A.L.C.] |
|
1987: |
Jong, E.C., The Travel and Tropical Medicine Manual. W.B. Saunders Co., Philadelphia, London, Toronto. |
|
1987: |
Manson-Bahr, P.E.C. and Bell, D.R., Manson's Tropical Diseases. Baillière Tindall, London. |
|
1987: |
Ross, P.W. and Peutherer, Clinical Microbiology. Churchill Livingstone, New York/Edinburgh/London/Melbourne. |
|
1987: |
Sandler, R.H. and Jones, T.C., Medical Care of Refugees. Oxford University Press. |
|
1987: |
Schull, C.R., Common Medical Problems in the Tropics. MacMillan [T.A.L.C.]. |
|
1987: |
, Epidemiology and Control of African Trypanosomiasis. WHO, Geneva |
|
1986: |
Sandford-Smith, J., Eye Diseases in Hot Climates. Wright, Bristol. |
|
1986: |
Jelliffe, D.B. (ed.), Child Health in the Tropics. English Language Book Society, Edward Arnold, London. |
|
1985: |
Morley, David, Paediatric Priorities in the Developing World, English Language Book Society/Butterworths [supplied by T.A.L.C., see address list, below] |
|
1983: |
Brown, H.W., Franklin A.N., Basic Clinical Parasitology. Prentice Hall International, INC, Englewood Cliffs. |
Addresses
|
International Union Against Tuberculosis and Lung Disease |
68 Boulevard Saint Michel 75006 Paris France |
|
Medical Mission Institute Cooperation in Need and Disaster |
Salvatorstrasse 22 97074 Würzburg Germany |
|
T.A.L.C. (Teaching-aids at Low Cost) |
P.O. Box 49 St. Albans Herts AL1 5TX United Kingdom |
|
World Health Organization |
20 Avenue Appia CH-1211 Geneva 27 Switzerland |
Arbeitsgruppe: Zusammenarbeit in Not und Katastrophen Missionsärztliches Institut, Salvatorstraße 22, D-97074 Würzburg Germany
The author can be contacted by E-mail: miss040@rzhub.uni-wuerzburg.de
© 1997 Bδrbel Krumme